Cheap kamagra supplier reviews

Dear Reader, Thank you for following the Me&MyDoctor blog cheap kamagra supplier reviews. I'm writing to let you know we are moving the public health stories authored by Texas physicians, residents, and medical students, and patients to the Texas Medical Association's social media channels. Be sure to follow us cheap kamagra supplier reviews on all our social media accounts (Facebook, Twitter, Instagram) as well as Texas Medicine Today to access these stories and more. We look forward to seeing you there.Best, Olivia Suarez Me&My Doctor EditorSravya Reddy, MDPediatric Resident at The University of Texas at Austin Dell Medical SchoolMember, Texas Medical AssociationHow does the erectile dysfunction treatment kamagra factor into potentially abusive situations?.

To stop the spread of erectile dysfunction treatment, we have isolated ourselves into small family units to avoid catching and transmitting the kamagra. While saving so many from succumbing to a severe illness, socially isolating has unfortunately posed its cheap kamagra supplier reviews own problems. Among those is the increased threat of harm from intimate partner violence, which includes physical violence, sexual violence, stalking, or psychological harm by a current or former partner or spouse. Potential child abuse is an increased threat as well.

The impact of this kamagra happened cheap kamagra supplier reviews so rapidly that society did not have time to think about all the consequences of social isolation before implementing it. Now those consequences are becoming clear.Social isolation due to the kamagra is forcing victims to stay home indefinitely with their abusers. Children and adolescents also have been forced to stay at home since many school districts have made education virtual to keep everyone safe from the kamagra. Caregivers are also home because they are working cheap kamagra supplier reviews remotely or because they are unemployed.

With the increase in the number of erectile dysfunction treatment cases, financial strain due to the economic downturn, and concerns of contracting the kamagra and potentially spreading it to family members, these are highly stressful times. Stress leads to an increase in the rate of intimate partner violence. Even those who suffer from it can begin to become abusive to other household members, thus amplifying the abuse in the household cheap kamagra supplier reviews. Some abuse may go unrecognized by the victims themselves.

For example, one important and cheap kamagra supplier reviews less well-known type of abuse is coercive control. It’s the type of abuse that doesn’t leave a physical mark, but it’s emotional, verbal, and controlling. Victims often know that something is wrong – but can’t quite identify what it is. Coercive control can still lead to violent physical abuse, and murder cheap kamagra supplier reviews.

The way in which people report abuse has also been altered by the kamagra.People lacking usual in-person contacts (with teachers, co-workers, or doctors) and the fact that some types of coercive abuse are less recognized lead to fewer people reporting that type of abuse. Child abuse often is discovered during pediatricians’ well-child visits, but the kamagra has limited those visits. Many teachers, who might also notice signs of abuse, also cheap kamagra supplier reviews are not able to see their students on a daily basis. Some abuse victims visit emergency departments (EDs) in normal times, but ED visits are also down due to erectile dysfunction treatment.Local police in China report that intimate partner violence has tripled in the Hubei province.

The United Nations reports it also increased 30% in France as of March 2020 and increased 25% in Argentina. In the cheap kamagra supplier reviews U.S. The conversation about increased intimate partner violence during these times has just now started, and we are beginning to gather data. Preliminary analysis shows police reports of intimate partner violence have increased by 18% to 27% across several U.S.

Cities. Individuals affected by addiction have additional stressors and cannot meet with support groups. Children and adolescents who might otherwise use school as a form of escape from addicted caregivers are no longer able to do so. Financial distress can also play a factor.

According to research, the rate of violence among couples with more financial struggles is nearly three and a half times higher than couples with fewer financial concerns.Abuse also can come from siblings. Any child or adolescent with preexisting behavioral issues is more likely to act out due to seclusion, decreased physical activity, or fewer positive distractions. This could increase risk for others in the household, especially in foster home situations. These other residents might be subject to increased sexual and physical abuse with fewer easy ways to report it.

What can we do about this while abiding by the rules of the kamagra?. How can physicians help?. Patients who are victims of intimate partner violence are encouraged to reach out to their doctor. A doctor visit may be either in person or virtual due to the safety precautions many doctors’ offices are enforcing due to erectile dysfunction treatment.

During telehealth visits, physicians should always ask standard questions to screen for potential abuse. They can offer information to all patients, regardless of whether they suspect abuse.People could receive more support if we were to expand access to virtual addiction counseling, increase abuse counseling, and launch more campaigns against intimate partner violence. The best solution might involve a multidisciplinary team, including psychiatrists, social workers, child abuse teams and Child Protective Services, and local school boards. Physicians can help in other ways, too.

Doctors can focus on assessing mental health during well-child and acute clinic visits and telehealth visits. A temporary screening tool for behavioral health during the kamagra might be beneficial. Governments could consider allocating resources to telepsychiatry. Many paths can be taken to reduce the burden of mental health issues, and this is an ongoing discussion.

How should physicians approach patients who have or may have experienced intimate partner violence?. Victims of domestic assault can always turn to their physician for guidance on next steps. In response, doctors can:Learn about local resources and have those resources available to your patients;Review safety practices, such as deleting internet browsing history or text messages. Saving abuse hotline information under other listings, such as a grocery store or pharmacy listing.

And creating a new, confidential email account for receiving information about resources or communicating with physicians.If the patient discloses abuse, the clinician and patient can establish signals to identify the presence of an abusive partner during telemedicine appointments.To my fellow physicians, I suggest recognizing and talking about the issue with families.Medical professionals take certain steps if they suspect their patient’s injuries are a result of family violence, or if the patient discloses family violence. Physicians will likely screen a patient, document their conversation with the patient, and offer support and inform the patient of the health risks of staying in an abusive environment, such as severe injuries or even death. A doctor’s priority is his or her patient’s safety, regardless of why the victim might feel forced to remain in an abusive environment. While physicians only report child and elderly abuse, they should encourage any abused patient to report her or his own case, while also understanding the complexity of the issue.

Under no circumstance should any form of abuse be tolerated or suffered. Any intimate partner violence should be avoided, and reported if possible and safe. My hope is that with more awareness of this rising public health concern, potential victims can better deal with the threat of abuse during this stressful kamagra – and hopefully avoid it..

What is kamagra pills

Biogen, placing a major bet what is kamagra pills on a once-failed treatment, is paying $1.53 billion for the commercial rights to a Sage Therapeutics’ oral depression drug that disappointed in its last major he has a good point clinical trial.Under the agreement, announced Friday, Biogen will give Sage $875 million in cash and buy $650 million worth of its stock at a 40% premium. In exchange, Biogen is entitled to 50% of the U.S. Profits from zuranolone, a depression drug that could win approval in 2022 if what is kamagra pills proven safe and effective, and an earlier-stage treatment for movement disorders. Unlock this article by subscribing to STAT+ and enjoy your first 30 days free!. GET STARTED Log In what is kamagra pills | Learn More What is it?.

STAT+ is STAT's premium subscription service for in-depth biotech, pharma, policy, and life science coverage and analysis. Our award-winning team covers news on Wall Street, policy developments in Washington, early science breakthroughs and clinical trial results, and health care disruption what is kamagra pills in Silicon Valley and beyond. What's included?. Daily reporting and analysis The most comprehensive industry coverage from a powerhouse team of reporters Subscriber-only newsletters Daily newsletters to brief you on the most important industry news of the day STAT+ Conversations Weekly opportunities to engage with our reporters and leading industry experts in live video conversations Exclusive industry events Premium access to subscriber-only networking events around the country The best reporters in the industry The most trusted and well-connected newsroom in the health care industry what is kamagra pills And much more Exclusive interviews with industry leaders, profiles, and premium tools, like our CRISPR Trackr.My painful excursion into the world of dueling s started on a Tuesday afternoon with a scratchy throat and a mild-yet-annoying cough. I chalked it up to fall in Kentucky, where sunny afternoons in the mid 70s can be followed by freezing temperatures at night.

I’m no stranger to what is kamagra pills respiratory s, having lived for years with the triple threat of allergies, asthma, and low immunity.On Wednesday morning, I was having coughing fits that made me dizzy. I went to see my doctor, who assured me that I almost certainly didn’t have erectile dysfunction treatment, even though our county had been considered a “red” one for more than a month and the case count was climbing.I was a bit suspicious of my doctor’s reassurance because I had learned that morning of a student who had tested positive for erectile dysfunction treatment the week before in the high school where I am a Spanish and social studies teacher.advertisement As a precaution, I was tested for strep, influenza, and erectile dysfunction treatment. I was shocked when the nurse let me know that I had tested positive for the flu, and I left with a prescription for Tamiflu and instructions to stay home for a week. On Thursday, I was tired and achy — both mild what is kamagra pills flu-like symptoms — but was able to complete all my work virtually. Aside from the occasional coughing fit, one of which brought me to my knees, I believed I just had the flu.advertisement The next day I got a call that I had also tested positive for erectile dysfunction treatment.

I should have expected that news, what is kamagra pills because the night before I had lit a pumpkin-scented candle but didn’t realize until later that I hadn’t smelled its fragrance.I was extremely scared. But I was also angry. I was angry at my school for not following state recommendations to keep students home and use remote learning, at my doctor for downplaying the increasing threat of the kamagra, at my family members and friends who brushed off what is kamagra pills my concerns, and even angry at myself for creating a false sense of security that using an N95 mask, an air purifier, and a plexiglass shield in my classroom would keep me safe.I was angry, and still am, that the response to a worldwide kamagra has become so deeply politicized in the U.S. And that even though I took every precaution, it still wasn’t enough. I began taking nebulizer treatments four times a day to keep my lungs clear and began taking zinc and vitamin what is kamagra pills D.

Over the weekend, it was difficult to know which symptoms were due to erectile dysfunction treatment and which ones were due to the flu. The coughing began to slowly improve, and I had a temperature above 99.9° only once, though I experienced extreme fatigue, chills, aches, a severe headache, and diarrhea.By Monday, the coughing had stopped and my what is kamagra pills fever was down, but I felt even worse than before. I believe that was the point where I was over the flu and erectile dysfunction treatment was taking over. I slept so much that my sister dropped in on my Alexa because I didn’t answer calls or texts for hours at a time. I didn’t leave my bedroom except to use the bathroom and drank room-temperature orange Gatorade Zero that my mom had bought in what is kamagra pills bulk and I kept next to my bed.

Trips beyond the bathroom were carefully planned for efficiency as they required all of my strength and a nap immediately after.I watched TV, but found I couldn’t focus or would fall asleep. After trying to watch the first episode of Lovecraft Country four times, I resorted to browsing TikTok or what is kamagra pills re-watching The Office as I couldn’t keep up with the simplest plot. I had several rounds of severe abdominal pain and experienced a completely new sensation. Small tingles that would randomly move throughout my lower and upper abdomen.Over the next few days, I constantly checked my oxygen saturation, knowing that if it dropped below 93% I would need to what is kamagra pills go to the hospital. From a starting point of 98%, the pulse oximeter readings crept down to 93% on Wednesday, at which point I was having mild shortness of breath and chest pain when I took a full breath.

That said, I was what is kamagra pills feeling a little better. My doctor ordered a chest X-ray, which I got at a hospital a three-minute drive from where I live. It was normal what is kamagra pills. I started to take oral steroids, which helped immensely.It wasn’t until Friday — a full week after I first learned that I had erectile dysfunction treatment plus the flu — that I made the move from my bed to the couch. It felt like a momentous occasion.During that week, I had lost 12 pounds.

After a few bites of food, I what is kamagra pills would feel nauseous and completely full, and there were days when I ate nothing even though my family and friends delivered food to my porch. It took me two full days to eat one donut, taking just one or two bites at a time.During the time when I felt the worst, anxiety compounded my physical symptoms. I wondered every time I fell asleep if I would wake up wheezing or unable to what is kamagra pills breathe. I am incredibly grateful that my respiratory symptoms were mild and that I was able to get through it without hospitalization.The day I was diagnosed with erectile dysfunction treatment, the news was full of the record-breaking number of cases. More than 85,000 that what is kamagra pills day.

Now, the record is nearly 140,000, and increasing by the day.I still don’t know for sure how or when or where I contracted erectile dysfunction treatment or the flu, though I suspect it was at school. I haven’t been in a grocery store or eaten in a restaurant since March what is kamagra pills because of my low immunity and asthma. My only close contacts have been my mother and my sister, both of whom tested negative for erectile dysfunction treatment and have had no symptoms. I always wear a mask and use an N95 respirator at school.The simple fact is that we still have a lot to learn about this airborne what is kamagra pills kamagra. How it is transmitted, how it is best treated, what its long-term effects are, and more.Now that I’m on the other side, I’m feeling better physically and am far less anxious.

I take no pride in knowing that I’m special. It’s rare to be diagnosed with both erectile dysfunction treatment what is kamagra pills and the flu, especially when taking significant precautions for erectile dysfunction treatment and receiving a flu shot. While I am teaching virtually for the rest of the semester and still am following public health guidance, I have a sense of relief — for now. I can’t wait to be back in the physical classroom with my students, and I am hoping that any immunity will last long enough until I can get vaccinated.No one knows how long immunity to erectile dysfunction treatment lasts, whether it is 90 days what is kamagra pills or a year or longer, and I am still worried about potential long-term effects. The fatigue and digestive issues lasted long after quarantine, and I have experienced worrisome chest pain.

To me, the bottom line from my experience is that all of us must be serious about protecting the people around us who need and deserve extra precautions, since protective measures are no guarantee (as I learned the hard way), especially in the face of what looks to be a serious spike in what is kamagra pills erectile dysfunction treatment this winter.Lauren Hines teaches Spanish and social studies in Kentucky.With more than 250,000 Americans killed by erectile dysfunction treatment, it’s time to think about reimagining Black Friday.Police officers in Philadelphia gave the Friday after Thanksgiving its dark name in 1966 as zealous shoppers mobbed streets and sidewalks. But it quickly came to mean a day when business owners could expect their accounts to be in the black, as opposed to in the red.If Black Friday celebrates American consumers spending in order to live well, we could also adopt it as a day to consider what it means to die well. As the ancient Greek philosopher Epicurus ostensibly put it, “The art of living well and the art of dying well are what is kamagra pills one.”advertisement As a physician, I’ve met countless patients who were ill-prepared for death. The “trajectories of decline” described by geriatrician Joann Lynn make it easy not to prepare. Some people live for what is kamagra pills years with chronic illnesses but feel no need to ponder their mortality.

Hospital tune-ups enable them to live seemingly forever. Others enjoy relative health until being caught off guard by a deadly illness. Still others live good long what is kamagra pills lives only to succumb to dementia, which robs them of their ability to plan.We are habituated to living with hope for intervention or cure. To accept the impossibility of treatment is to admit defeat, which most people are loathe to do.advertisement How and where we die underscores how unprepared we are. Most Americans have never had end-of-life conversations or what is kamagra pills formalized their wishes for medical treatments at the end of life.

Despite existing in some form since the 1970s, only 37% of Americans report having formalized their wishes through an advance directive. What’s more, most Americans say they want to die what is kamagra pills at home, yet roughly 60 percent die in hospitals, nursing homes, and hospices. There’s no question that institutional care can be a lifesaver for families not equipped to care for their loved ones at home.If we are to realize the ideal of death at home surrounded by family, we’ve got work to do. Making a home death possible requires difficult decisions — in what is kamagra pills end-of-life conversations with family members and health care professionals — about which treatments and hospitalizations to forgo, whether homes can accommodate hospital beds, and who will do the hard work of caring for the dying.That’s where taking a new approach to Black Friday comes in. On that day, families could pivot from giving thanks to giving thought to ending well.

A simple prompt for starting end-of-life conversations what is kamagra pills might be, “Mom, Dad, if you become so sick that you can’t speak for yourself, who would you want to make medical decisions on your behalf?. € And the natural follow-up would be, “Help me know how to advocate for you. Let’s talk about the benefits and burdens of particular medical interventions.” Conversation can then move to broader community-based issues such as funeral, burial, and religious or existential concerns.It’s not the easiest conversation to have, but the payoff can be worth the effort. And since Black Friday comes every year, it’s a discussion that can build on itself over time.A reimagined Black Friday could help Americans formalize their wishes for what is kamagra pills care at the end of life. Advance care planning documents allow people to identify health care proxies to make medical decisions if they lose decision-making capacity.

Living wills specify an individual’s what is kamagra pills choice to have — or not have — cardiac resuscitation, mechanical ventilation, and other invasive procedures.To be fair, there are good reasons why some people don’t want to prepare for death. Many of my patients fear that talk of death might “jinx” them. Some are reluctant to put their wishes in writing because they what is kamagra pills worry that doctors will give up on them. Others are concerned they’ll change their minds down the road but be too sick to say so. These concerns are real, but the potential exists for much greater harm by ignoring finitude entirely.Reflecting on death has the potential what is kamagra pills to bring into relief that which matters most, and it can empower us to change how we live for the better.

Ask anyone who is fully engaged in the process of dying. When our days are numbered, we value our relationships what is kamagra pills differently. We spend our time and money differently. We ponder life’s mysteries.In ordinary times, we fool ourselves into thinking that the preparation for death can wait. But these what is kamagra pills are not ordinary times.

When I was caring for hospitalized erectile dysfunction treatment patients this past Spring in New York City, they were frequently astonished that they had become so sick. They had not understood, as did Epicurus, that the art of dying is wrapped up in the art of what is kamagra pills living. But the kamagra has taught us that sickness and death do not happen only to other people. All of us must live with a view to our finitude.This Black what is kamagra pills Friday, after the feasting has subsided and before the shopping begins, take a few minutes to talk with those you love about how to die well. Be frank about end-of-life wishes.

Complete and sign documents.At the same time, it also makes sense to talk what is kamagra pills about living. If Epicurus is right, to die well one must live well. And attending to what it means to live well — in light of the precarity of life — can make what is kamagra pills all the difference.L.S. Dugdale is a physician and ethicist at Columbia University, director of the Columbia Center for Clinical Medical Ethics, and author of “The Lost Art of Dying. Reviving Forgotten Wisdom” (HarperOne, 2020)..

Biogen, placing a major bet on a once-failed treatment, is paying $1.53 billion for the commercial rights to a Sage Therapeutics’ oral depression drug that disappointed in its last major clinical trial.Under the agreement, announced Friday, Biogen will give Sage $875 cheap kamagra supplier reviews million in cash and buy $650 million worth of its stock at a 40% premium. In exchange, Biogen is entitled to 50% of the U.S. Profits from zuranolone, a depression drug that could win approval in 2022 if proven safe and effective, and an earlier-stage treatment cheap kamagra supplier reviews for movement disorders. Unlock this article by subscribing to STAT+ and enjoy your first 30 days free!.

GET STARTED cheap kamagra supplier reviews Log In | Learn More What is it?. STAT+ is STAT's premium subscription service for in-depth biotech, pharma, policy, and life science coverage and analysis. Our award-winning team covers news on Wall Street, policy cheap kamagra supplier reviews developments in Washington, early science breakthroughs and clinical trial results, and health care disruption in Silicon Valley and beyond. What's included?.

Daily reporting and analysis The most comprehensive industry coverage from a powerhouse team of reporters Subscriber-only newsletters Daily newsletters to brief you on the most important industry news of the day STAT+ Conversations Weekly opportunities to engage with our reporters and leading industry experts in live video conversations Exclusive industry events Premium access to subscriber-only networking events around the country The best reporters in the industry The most trusted and well-connected newsroom in the health care industry And much more Exclusive interviews with industry cheap kamagra supplier reviews leaders, profiles, and premium tools, like our CRISPR Trackr.My painful excursion into the world of dueling s started on a Tuesday afternoon with a scratchy throat and a mild-yet-annoying cough. I chalked it up to fall in Kentucky, where sunny afternoons in the mid 70s can be followed by freezing temperatures at night. I’m no stranger to respiratory s, having lived for years with the triple threat of allergies, asthma, and low immunity.On cheap kamagra supplier reviews Wednesday morning, I was having coughing fits that made me dizzy. I went to see my doctor, who assured me that I almost certainly didn’t have erectile dysfunction treatment, even though our county had been considered a “red” one for more than a month and the case count was climbing.I was a bit suspicious of my doctor’s reassurance because I had learned that morning of a student who had tested positive for erectile dysfunction treatment the week before in the high school where I am a Spanish and social studies teacher.advertisement As a precaution, I was tested for strep, influenza, and erectile dysfunction treatment.

I was shocked when the nurse let me know that I had tested positive for the flu, and I left with a prescription for Tamiflu and instructions to stay home for a week. On Thursday, I was cheap kamagra supplier reviews tired and achy — both mild flu-like symptoms — but was able to complete all my work virtually. Aside from the occasional coughing fit, one of which brought me to my knees, I believed I just had the flu.advertisement The next day I got a call that I had also tested positive for erectile dysfunction treatment. I should have expected that news, because the night before I had lit a pumpkin-scented candle but didn’t realize until later that I hadn’t smelled its fragrance.I was extremely scared cheap kamagra supplier reviews.

But I was also angry. I was angry at my school for not following state recommendations to keep students home and use remote learning, at my doctor for downplaying the increasing threat of the kamagra, at my family members and friends who brushed off my concerns, and even angry at myself for creating a false sense of security cheap kamagra supplier reviews that using an N95 mask, an air purifier, and a plexiglass shield in my classroom would keep me safe.I was angry, and still am, that the response to a worldwide kamagra has become so deeply politicized in the U.S. And that even though I took every precaution, it still wasn’t enough. I began taking nebulizer treatments four times a day to keep cheap kamagra supplier reviews my lungs clear and began taking zinc and vitamin D.

Over the weekend, it was difficult to know which symptoms were due to erectile dysfunction treatment and which ones were due to the flu. The coughing began to slowly improve, and I had a temperature above 99.9° only once, though I experienced extreme fatigue, chills, aches, a severe headache, and diarrhea.By Monday, the coughing had stopped and my fever cheap kamagra supplier reviews was down, but I felt even worse than before. I believe that was the point where I was over the flu and erectile dysfunction treatment was taking over. I slept so much that my sister dropped in on my Alexa because I didn’t answer calls or texts for hours at a time.

I didn’t leave my bedroom except to use the bathroom and drank room-temperature cheap kamagra supplier reviews orange Gatorade Zero that my mom had bought in bulk and I kept next to my bed. Trips beyond the bathroom were carefully planned for efficiency as they required all of my strength and a nap immediately after.I watched TV, but found I couldn’t focus or would fall asleep. After trying to watch the first episode of Lovecraft Country four times, I resorted to browsing TikTok or re-watching The Office as I couldn’t keep up with the cheap kamagra supplier reviews simplest plot. I had several rounds of severe abdominal pain and experienced a completely new sensation.

Small tingles that would randomly move throughout my lower and upper cheap kamagra supplier reviews abdomen.Over the next few days, I constantly checked my oxygen saturation, knowing that if it dropped below 93% I would need to go to the hospital. From a starting point of 98%, the pulse oximeter readings crept down to 93% on Wednesday, at which point I was having mild shortness of breath and chest pain when I took a full breath. That said, I was feeling a cheap kamagra supplier reviews little better. My doctor ordered a chest X-ray, which I got at a hospital a three-minute drive from where I live.

It was cheap kamagra supplier reviews normal. I started to take oral steroids, which helped immensely.It wasn’t until Friday — a full week after I first learned that I had erectile dysfunction treatment plus the flu — that I made the move from my bed to the couch. It felt like a momentous occasion.During that week, I had lost 12 pounds. After a few bites of food, I would feel nauseous and completely full, and there were days when I ate nothing even though my cheap kamagra supplier reviews family and friends delivered food to my porch.

It took me two full days to eat one donut, taking just one or two bites at a time.During the time when I felt the worst, anxiety compounded my physical symptoms. I wondered every time I fell asleep if I would wake up cheap kamagra supplier reviews wheezing or unable to breathe. I am incredibly grateful that my respiratory symptoms were mild and that I was able to get through it without hospitalization.The day I was diagnosed with erectile dysfunction treatment, the news was full of the record-breaking number of cases. More than 85,000 cheap kamagra supplier reviews that day.

Now, the record is nearly 140,000, and increasing by the day.I still don’t know for sure how or when or where I contracted erectile dysfunction treatment or the flu, though I suspect it was at school. I haven’t been cheap kamagra supplier reviews in a grocery store or eaten in a restaurant since March because of my low immunity and asthma. My only close contacts have been my mother and my sister, both of whom tested negative for erectile dysfunction treatment and have had no symptoms. I always wear a mask and use an N95 respirator cheap kamagra supplier reviews at school.The simple fact is that we still have a lot to learn about this airborne kamagra.

How it is transmitted, how it is best treated, what its long-term effects are, and more.Now that I’m on the other side, I’m feeling better physically and am far less anxious. I take no pride in knowing that I’m special. It’s rare to be diagnosed with both erectile dysfunction treatment and cheap kamagra supplier reviews the flu, especially when taking significant precautions for erectile dysfunction treatment and receiving a flu shot. While I am teaching virtually for the rest of the semester and still am following public health guidance, I have a sense of relief — for now.

I can’t wait to be back in the physical classroom with my students, and I am hoping that any immunity will last long cheap kamagra supplier reviews enough until I can get vaccinated.No one knows how long immunity to erectile dysfunction treatment lasts, whether it is 90 days or a year or longer, and I am still worried about potential long-term effects. The fatigue and digestive issues lasted long after quarantine, and I have experienced worrisome chest pain. To me, the bottom line from my experience is that all of us must be serious about protecting the people around us who need and deserve extra precautions, since protective measures are no guarantee cheap kamagra supplier reviews (as I learned the hard way), especially in the face of what looks to be a serious spike in erectile dysfunction treatment this winter.Lauren Hines teaches Spanish and social studies in Kentucky.With more than 250,000 Americans killed by erectile dysfunction treatment, it’s time to think about reimagining Black Friday.Police officers in Philadelphia gave the Friday after Thanksgiving its dark name in 1966 as zealous shoppers mobbed streets and sidewalks. But it quickly came to mean a day when business owners could expect their accounts to be in the black, as opposed to in the red.If Black Friday celebrates American consumers spending in order to live well, we could also adopt it as a day to consider what it means to die well.

As the ancient Greek philosopher cheap kamagra supplier reviews Epicurus ostensibly put it, “The art of living well and the art of dying well are one.”advertisement As a physician, I’ve met countless patients who were ill-prepared for death. The “trajectories of decline” described by geriatrician Joann Lynn make it easy not to prepare. Some people live for cheap kamagra supplier reviews years with chronic illnesses but feel no need to ponder their mortality. Hospital tune-ups enable them to live seemingly forever.

Others enjoy relative health until being caught off guard by a deadly illness. Still others live good long lives only to succumb to dementia, which robs them of their ability to plan.We are habituated to living with hope for intervention cheap kamagra supplier reviews or cure. To accept the impossibility of treatment is to admit defeat, which most people are loathe to do.advertisement How and where we die underscores how unprepared we are. Most Americans cheap kamagra supplier reviews have never had end-of-life conversations or formalized their wishes for medical treatments at the end of life.

Despite existing in some form since the 1970s, only 37% of Americans report having formalized their wishes through an advance directive. What’s more, most Americans say they cheap kamagra supplier reviews want to die at home, yet roughly 60 percent die in hospitals, nursing homes, and hospices. There’s no question that institutional care can be a lifesaver for families not equipped to care for their loved ones at home.If we are to realize the ideal of death at home surrounded by family, we’ve got work to do. Making a home death possible requires difficult decisions — in end-of-life conversations with family members and health care professionals — about which treatments and hospitalizations to forgo, whether homes can accommodate hospital beds, and who will do the hard work of caring for the dying.That’s where taking a new approach to cheap kamagra supplier reviews Black Friday comes in.

On that day, families could pivot from giving thanks to giving thought to ending well. A simple prompt for starting end-of-life conversations might be, “Mom, Dad, if you cheap kamagra supplier reviews become so sick that you can’t speak for yourself, who would you want to make medical decisions on your behalf?. € And the natural follow-up would be, “Help me know how to advocate for you. Let’s talk about the benefits and burdens of particular medical interventions.” Conversation can then move to broader community-based issues such as funeral, burial, and religious or existential concerns.It’s not the easiest conversation to have, but the payoff can be worth the effort.

And since Black Friday comes every year, it’s a discussion that can build on cheap kamagra supplier reviews itself over time.A reimagined Black Friday could help Americans formalize their wishes for care at the end of life. Advance care planning documents allow people to identify health care proxies to make medical decisions if they lose decision-making capacity. Living wills specify an individual’s cheap kamagra supplier reviews choice to have — or not have — cardiac resuscitation, mechanical ventilation, and other invasive procedures.To be fair, there are good reasons why some people don’t want to prepare for death. Many of my patients fear that talk of death might “jinx” them.

Some are reluctant to put their wishes in writing because cheap kamagra supplier reviews they worry that doctors will give up on them. Others are concerned they’ll change their minds down the road but be too sick to say so. These concerns are real, but the potential exists for much greater harm by ignoring finitude entirely.Reflecting on death has the potential to bring into relief that which matters most, and it cheap kamagra supplier reviews can empower us to change how we live for the better. Ask anyone who is fully engaged in the process of dying.

When our days are numbered, we value our relationships cheap kamagra supplier reviews differently. We spend our time and money differently. We ponder life’s mysteries.In ordinary times, we fool ourselves into thinking that the preparation for death can wait. But these cheap kamagra supplier reviews are not ordinary times.

When I was caring for hospitalized erectile dysfunction treatment patients this past Spring in New York City, they were frequently astonished that they had become so sick. They had not understood, as did Epicurus, that the art of dying is wrapped up in the art of cheap kamagra supplier reviews living. But the kamagra has taught us that sickness and death do not happen only to other people. All of us must live with a view to our finitude.This Black Friday, after the feasting has subsided and before the shopping begins, take a few minutes to talk with those you cheap kamagra supplier reviews love about how to die well.

Be frank about end-of-life wishes. Complete and sign documents.At the same time, it also makes sense cheap kamagra supplier reviews to talk about living. If Epicurus is right, to die well one must live well. And attending to what it means to live well — in light of the precarity of life — can make all the difference.L.S.

Dugdale is a physician and ethicist at Columbia University, director of the Columbia Center for Clinical Medical Ethics, and author of “The Lost Art of Dying. Reviving Forgotten Wisdom” (HarperOne, 2020)..

Where can I keep Kamagra?

Keep out of reach of children. Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F). Throw away any unused medicine after the expiration date.

Kamagra oral jelly melbourne

3 February 2022 Members are invited to go to this site submit questions around erectile dysfunction treatment and Haemostasis to our Congress panel in advance Congress goers, this is your chance to take part in the discussion - what did kamagra oral jelly melbourne we learn about erectile dysfunction treatment and haemostasis throughout the kamagra?. Delegates are asked to submit questions kamagra oral jelly melbourne to Congress@ibms.org. Then, join Professor Gary Moore, Director of Clinical Diagnostic Research, Technoclone, Dr Steve Kitchen, Clinical Scientist, The Royal Hallamshire Hospital and Dr Annette Bowyer, Clinical Scientist, The Royal Hallamshire Hospital at 11am on Wednesday 16 March 2022 for the ‘Q&A.

What we learnt from kamagra oral jelly melbourne erectile dysfunction treatment’. Changes in knowledge of the haemostatic system after the kamagra How the kamagra interferes with haemostasis What did we learn from the kamagra and its effects.2 February 2022 In February's statement, David Wells talks about how the IBMS is working to broaden awareness of the value our members bring to society As the professional body for biomedical science, the IBMS has a responsibility that stretches beyond supporting the practice and careers of our members. We must also make sure that the government and public understand the value of what our members bring to society.Throughout the kamagra, key decision makers did not appear to understand the value or complexities of having an accredited workforce in a diagnostics laboratory – or how our profession ensures safety, quality, well-being and peace of mind for patients across kamagra oral jelly melbourne the UK.

However, after continually informing the press and public, we began to make headway and started meeting with policy makers.With the increased visibility that the IBMS helped to foster, things are looking better, backed up with a wave of funding. More people understand the value of what we do and how we do it but a big part of our next strategy kamagra oral jelly melbourne is rightly focussed on taking further action to broaden this awareness.In order to change the way government and key decision makers think and respond to our role in society, it is essential that we start to build a body of peer reviewed evidence. This is why the IBMS is looking to offer funding for academic research that focuses on the value of having an accredited workforce in the biomedical science professions.

Many other areas of the healthcare services are supported by such studies and we want to make sure that our profession is better represented in this regard.The IBMS is also in the process kamagra oral jelly melbourne of employing a Policy Lead. This means that we will have a dedicated expert whose sole responsibility will be to build stronger bridges and increase reach with the government and the relevant healthcare, academic and industrial leaders – constantly making sure that our profession’s concerns, information and advice are reaching the right people in the right ways.The inroads made over the last couple of years by Past-President Allan Wilson and others on our Council and Specialist Panels were hard won and we have learnt from this that the IBMS needs to establish the evidence and capability to put us on the front foot with politicians, government and policy officials going forward.While there are challenges ahead, rest assured that the IBMS is busy establishing and building upon our new strengths for the future benefit and support of our members, the profession and patient care..

3 February 2022 Members are invited to submit questions around erectile dysfunction treatment and Haemostasis to our Congress cheap kamagra supplier reviews panel in advance Congress goers, this is your chance to take part in the discussion - what did we learn about erectile dysfunction treatment and haemostasis throughout the kamagra?. Delegates are asked to cheap kamagra supplier reviews submit questions to Congress@ibms.org. Then, join Professor Gary Moore, Director of Clinical Diagnostic Research, Technoclone, Dr Steve Kitchen, Clinical Scientist, The Royal Hallamshire Hospital and Dr Annette Bowyer, Clinical Scientist, The Royal Hallamshire Hospital at 11am on Wednesday 16 March 2022 for the ‘Q&A. What we cheap kamagra supplier reviews learnt from erectile dysfunction treatment’.

Changes in knowledge of the haemostatic system after the kamagra How the kamagra interferes with haemostasis What did we learn from the kamagra and its effects.2 February 2022 In February's statement, David Wells talks about how the IBMS is working to broaden awareness of the value our members bring to society As the professional body for biomedical science, the IBMS has a responsibility that stretches beyond supporting the practice and careers of our members. We must also make sure that the government and public understand the value of what our members bring to society.Throughout the kamagra, key decision makers did not appear to understand the value or complexities of having an accredited workforce in a diagnostics laboratory – or how our profession ensures safety, cheap kamagra supplier reviews quality, well-being and peace of mind for patients across the UK. However, after continually informing the press and public, we began to make headway and started meeting with policy makers.With the increased visibility that the IBMS helped to foster, things are looking better, backed up with a wave of funding. More people understand the value of what we do and how we do it but a big part of our next strategy is rightly focussed on taking further action to broaden this awareness.In order to change the way government and key decision makers think and respond to our role in society, it is essential that we cheap kamagra supplier reviews start to build a body of peer reviewed evidence.

This is why the IBMS is looking to offer funding for academic research that focuses on the value of having an accredited workforce in the biomedical science professions. Many other areas of the healthcare services are supported by such cheap kamagra supplier reviews studies and we want to make sure that our profession is better represented in this regard.The IBMS is also in the process of employing a Policy Lead. This means that we will have a dedicated expert whose sole responsibility will be to build stronger bridges and increase reach with the government and the relevant healthcare, academic and industrial leaders – constantly making sure that our profession’s concerns, information and advice are reaching the right people in the right ways.The inroads made over the last couple of years by Past-President Allan Wilson and others on our Council and Specialist Panels were hard won and we have learnt from this that the IBMS needs to establish the evidence and capability to put us on the front foot with politicians, government and policy officials going forward.While there are challenges ahead, rest assured that the IBMS is busy establishing and building upon our new strengths for the future benefit and support of our members, the profession and patient care..

Kamagra ingredients

How to cite this kamagra ingredients kamagra oral jelly wholesalers article:Singh OP. The National Commission for Allied and Healthcare Professions Act, 2020 and its implication for mental health. Indian J Psychiatry 2021;63:119-20The National Commission for Allied and Healthcare Professions Act, 2020 has been notified on March 28, 2021, kamagra ingredients by the Gazette of India published by the Ministry of Law and Justice.

This bill aims to “provide for regulation and maintenance of standards of education and services by allied and healthcare professionals, assessment of institutions, maintenance of a Central Register and State Register and creation of a system to improve access, research and development and adoption of latest scientific advancement and for matters connected therewith or incidental thereto.”[1]This act has created a category of Health Care Professionals which is defined as. €œhealthcare professional” includes a scientist, therapist, or other professional who studies, advises, researches, supervises or provides preventive, curative, rehabilitative, therapeutic or promotional health services and who has obtained any qualification of degree under this Act, the duration of which shall not be <3600 h spread over a period of 3 years to 6 years divided into specific semesters.[1]According to the act, “Allied health professional” includes an associate, technician, or technologist who is trained to perform any technical and practical task to support diagnosis and treatment of illness, disease, injury or impairment, and to support implementation of any healthcare treatment and referral plan recommended by a medical, nursing, or any other healthcare professional, and who has obtained any qualification of diploma or degree under this Act, the duration of which shall not be less than 2000 h spread over a period of 2 years to 4 years divided into specific semesters.”[1]It is noticeable that while the term “Health Care Professionals” does not include doctors who are registered under National Medical Council, Mental Health Care Act (MHCA), 2017 includes psychiatrists under the ambit of Mental Health Care Professionals.[2] This discrepancy needs to be corrected - psychiasts, being another group of medical specialists, should be kept out of the broad umbrella of “Mental Healthcare Professionals.”The category of Behavioural Health Sciences Professional has been included and defined as “a person who undertakes scientific study of the emotions, behaviours and biology relating to a person's mental well-being, their kamagra ingredients ability to function in everyday life and their concept of self. €œBehavioural health” is the preferred term to “mental health” and includes professionals such as counselors, analysts, psychologists, educators and support workers, who provide counseling, therapy, and mediation services to individuals, families, groups, and communities in response to social and personal difficulties.”[1]This is a welcome step to the extent that it creates a diverse category of trained workforce in the field of Mental Health (Behavioural Health Science Professionals) and tries to regulate their training although it mainly aims to promote mental wellbeing.

However there is a kamagra ingredients huge lacuna in the term of “Mental Illness” as defined by MHCA, 2017. Only severe disorders are included as per definition and there is no clarity regarding inclusion of other psychiatric disorders, namely “common mental disorders” such as anxiety and depression. This leaves a strong possibility of concept of “psychiatric illnesses” being limited to only “severe psychiatric disorders” (major psychoses) thus perpetuating the kamagra ingredients stigma and alienation associated with psychiatric patients for centuries.

Psychiatrists being restricted to treating severe mental disorders as per MHCA, 2017, there is a strong possibility that the care of common mental disorders may gradually pass on under the care of “behavioural health professionals” as per the new act!. There is need to look into this kamagra ingredients aspect by the leadership in psychiatry, both organizational and academic psychiatry, and reduce the contradictions between the MHCA, 2017 and this nascent act. All disorders classified in ICD 10 and DSM 5 should be classified as “Psychiatric Disorders” or “Mental Illness.” This will not only help in fighting the stigma associated with psychiatric illnesses but also promote the integration of psychiatry with other specialties.

References kamagra ingredients 1.The National Commission for Allied and Healthcare Professions Act, 2021. The Gazette of India. Published by kamagra ingredients Ministry of Law and Justice.

28 March, 2021. 2.The Mental Healthcare Act, 2017 kamagra ingredients. The Gazette of India.

Published by Ministry of Law and kamagra ingredients Justice. April 7, 2017. Correspondence Address:Om Prakash SinghAA 304, Ashabari Apartments, kamagra ingredients O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support.

None, Conflict of Interest. NoneDOI. 10.4103/indianjpsychiatry.indianjpsychiatry_268_21Abstract Thiamine is essential for the activity of kamagra ingredients several enzymes associated with energy metabolism in humans.

Chronic alcohol use is associated with deficiency of thiamine along with other vitamins through several mechanisms. Several neuropsychiatric syndromes have been associated with thiamine deficiency in the context of alcohol use kamagra ingredients disorder including Wernicke–Korsakoff syndrome, alcoholic cerebellar syndrome, alcoholic peripheral neuropathy, and possibly, Marchiafava–Bignami syndrome. High-dose thiamine replacement is suggested for these neuropsychiatric syndromes.Keywords.

Alcohol use disorder, alcoholic cerebellar kamagra ingredients syndrome, alcoholic peripheral neuropathy, Marchiafava–Bignami syndrome, thiamine, Wernicke–Korsakoff syndromeHow to cite this article:Praharaj SK, Munoli RN, Shenoy S, Udupa ST, Thomas LS. High-dose thiamine strategy in Wernicke–Korsakoff syndrome and related thiamine deficiency conditions associated with alcohol use disorder. Indian J Psychiatry 2021;63:121-6How to cite this kamagra ingredients URL:Praharaj SK, Munoli RN, Shenoy S, Udupa ST, Thomas LS.

High-dose thiamine strategy in Wernicke–Korsakoff syndrome and related thiamine deficiency conditions associated with alcohol use disorder. Indian J Psychiatry [serial kamagra ingredients online] 2021 [cited 2021 Jun 11];63:121-6. Available from.

Https://www.indianjpsychiatry.org/text.asp?. 2021/63/2/121/313716 Introduction Thiamine is a water-soluble vitamin (B1) that plays a key role in the activity of several enzymes associated with energy metabolism. Thiamine pyrophosphate (or diphosphate) is the active form that acts as a cofactor for enzymes.

The daily dietary requirement of thiamine in adults is 1–2 mg and is dependent on carbohydrate intake.[1],[2] The requirement increases if basal metabolic rate is higher, for example, during alcohol withdrawal state. Dietary sources include pork (being the major source), meat, legume, vegetables, and enriched foods. The body can store between 30 and 50 mg of thiamine and is likely to get depleted within 4–6 weeks if the diet is deficient.[2] In those with alcohol-related liver damage, the ability to store thiamine is gradually reduced.[1],[2]Lower thiamine levels are found in 30%–80% of chronic alcohol users.[3] Thiamine deficiency occurs due to poor intake of vitamin-rich foods, impaired intestinal absorption, decreased storage capacity of liver, damage to the renal epithelial cells due to alcohol, leading to increased loss from the kidneys, and excessive loss associated with medical conditions.[2],[3] Furthermore, alcohol decreases the absorption of colonic bacterial thiamine, reduces the enzymatic activity of thiamine pyrophosphokinase, and thereby, reducing the amount of available thiamine pyrophosphate.[4] Since facilitated diffusion of thiamine into cells is dependent on a concentration gradient, reduced thiamine pyrophosphokinase activity further reduces thiamine uptake into cells.[4] Impaired utilization of thiamine is seen in certain conditions (e.g., hypomagnesemia) which are common in alcohol use disorder.[2],[3],[4] This narrative review discusses the neuropsychiatric syndromes associated with thiamine deficiency in the context of alcohol use disorder, and the treatment regimens advocated for these conditions.

A PubMed search supplemented with manual search was used to identify neuropsychiatric syndromes related to thiamine deficiency in alcohol use disorder patients. Neuropsychiatric Syndromes Associated With Thiamine Deficiency Wernicke–Korsakoff syndromeWernicke encephalopathy is associated with chronic alcohol use, and if not identified and treated early, could lead to permanent brain damage characterized by an amnestic syndrome known as Korsakoff syndrome. Inappropriate treatment of Wernicke encephalopathy with lower doses of thiamine can lead to high mortality rates (~20%) and Korsakoff syndrome in ~ 80% of patients (ranges from 56% to 84%).[5],[6] The classic triad of Wernicke includes oculomotor abnormalities, cerebellar dysfunction, and confusion.

Wernicke lesions are found in 12.5% of brain samples of patients with alcohol dependence.[7] However, only 20%–30% of them had a clinical diagnosis of Wernicke encephalopathy antemortem. It has been found that many patients develop Wernicke–Korsakoff syndrome (WKS) following repeated subclinical episodes of thiamine deficiency.[7] In an autopsy report of 97 chronic alcohol users, only16% had all the three “classical signs,” 29% had two signs, 37% presented with one sign, and 19% had none.[8] Mental status changes are the most prevalent sign (seen in 82% of the cases), followed by eye signs (in 29%) and ataxia (23%).[8] WKS should be suspected in persons with a history of alcohol use and presenting with signs of ophthalmoplegia, ataxia, acute confusion, memory disturbance, unexplained hypotension, hypothermia, coma, or unconsciousness.[9] Operational criteria for the diagnosis of Wernicke encephalopathy have been proposed by Caine et al.[10] that requires two out of four features, i.e., (a) dietary deficiency (signs such as cheilitis, glossitis, and bleeding gums), (b) oculomotor abnormalities (nystagmus, opthalmoplegia, and diplopia), (c) cerebellar dysfunction (gait ataxia, nystagmus), and (d) either altered mental state (confusion) or mild memory impairment.As it is very difficult to clinically distinguish Wernicke encephalopathy from other associated conditions such as delirium tremens, hepatic encephalopathy, or head injury, it is prudent to have a lower threshold to diagnose this if any of the clinical signs is seen. Magnetic resonance imaging (MRI) brain scan during Wernicke encephalopathy shows mammillary body atrophy and enlarged third ventricle, lesions in the medial portions of thalami and mid brain and can be used to aid diagnosis.[11],[12] However, most clinical situations warrant treatment without waiting for neuroimaging report.

The treatment suggestions in the guidelines vary widely. Furthermore, hardly any evidence-based recommendations exist on a more general use of thiamine as a preventative intervention in individuals with alcohol use disorder.[13] There are very few studies that have evaluated the dose and duration of thiamine for WKS, but higher doses may result in a greater response.[6],[14] With thiamine administration rapid improvement is seen in eye movement abnormalities (improve within days or weeks) and ataxia (may take months to recover), but the effects on memory, in particular, are unclear.[4],[14] Severe memory impairment is the core feature of Korsakoff syndrome. Initial stages of the disease can present with confabulation, executive dysfunction, flattened affect, apathy, and poor insight.[15] Both the episodic and semantic memory are affected, whereas, procedural memory remains intact.[15]Thomson et al.[6] suggested the following should be treated with thiamine as they are at high risk for developing WKS.

(1) all patients with any evidence of chronic alcohol misuse and any of the following. Acute confusion, decreased conscious level, ataxia, ophthalmoplegia, memory disturbance, and hypothermia with hypotension. (2) patients with delirium tremens may often also have Wernicke encephalopathy, therefore, all of these patients should be presumed to have Wernicke encephalopathy and treated, preferably as inpatients.

And (3) all hypoglycemic patients (who are treated with intravenous glucose) with evidence of chronic alcohol ingestion must be given intravenous thiamine immediately because of the risk of acutely precipitating Wernicke encephalopathy.Alcoholic cerebellar syndromeChronic alcohol use is associated with the degeneration of anterior superior vermis, leading to a clinical syndrome characterized by the subacute or chronic onset of gait ataxia and incoordination in legs, with relative sparing of upper limbs, speech, and oculomotor movements.[16] In severe cases, truncal ataxia, mild dysarthria, and incoordination of the upper limb is also found along with gait ataxia. Thiamine deficiency is considered to be the etiological factor,[17],[18] although direct toxic effects of alcohol may also contribute to this syndrome. One-third of patients with chronic use of alcohol have evidence of alcoholic cerebellar degeneration.

However, population-based studies estimate prevalence to be 14.6%.[19] The effect of alcohol on the cerebellum is graded with the most severe deficits occurring in alcohol users with the longest duration and highest severity of use. The diagnosis of cerebellar degeneration is largely clinical. MRI can be used to evaluate for vermian atrophy but is unnecessary.[20] Anterior portions of vermis are affected early, with involvement of posterior vermis and adjacent lateral hemispheres occurring late in the course could be used to differentiate alcoholic cerebellar degeneration from other conditions that cause more diffuse involvement.[21] The severity of cerebellar syndrome is more in the presence of WKS, thus could be related to thiamine deficiency.[22],[23] Therefore, this has been considered as a cerebellar presentation of WKS and should be treated in a similar way.[16] There are anecdotal evidence to suggest improvement in cerebellar syndrome with high-dose thiamine.[24]Alcoholic peripheral neuropathyPeripheral neuropathy is common in alcohol use disorder and is seen in 44% of the users.[25] It has been associated predominantly with thiamine deficiency.

However, deficiency of other B vitamins (pyridoxine and cobalamin) and direct toxic effect of alcohol is also implicated.[26] Clinically, onset of symptoms is gradual with the involvement of both sensory and motor fibers and occasionally autonomic fibers. Neuropathy can affect both small and large peripheral nerve fibers, leading to different clinical manifestations. Thiamine deficiency-related neuropathy affects larger fiber types, which results in motor deficits and sensory ataxia.

On examination, large fiber involvement is manifested by distal limb muscle weakness and loss of proprioception and vibratory sensation. Together, these can contribute to the gait unsteadiness seen in chronic alcohol users by creating a superimposed steppage gait and reduced proprioceptive input back to the movement control loops in the central nervous system. The most common presentations include painful sensations in both lower limbs, sometimes with burning sensation or numbness, which are early symptoms.

Typically, there is a loss of vibration sensation in distal lower limbs. Later symptoms include loss of proprioception, gait disturbance, and loss of reflexes. Most advanced findings include weakness and muscle atrophy.[20] Progression is very gradual over months and involvement of upper limbs may occur late in the course.

Diagnosis begins with laboratory evaluation to exclude other causes of distal, sensorimotor neuropathy including hemoglobin A1c, liver function tests, and complete blood count to evaluate for red blood cell macrocytosis. Cerebrospinal fluid studies may show increased protein levels but should otherwise be normal in cases of alcohol neuropathy and are not recommended in routine evaluation. Electromyography and nerve conduction studies can be used to distinguish whether the neuropathy is axonal or demyelinating and whether it is motor, sensory, or mixed type.

Alcoholic neuropathy shows reduced distal, sensory amplitudes, and to a lesser extent, reduced motor amplitudes on nerve conduction studies.[20] Abstinence and vitamin supplementation including thiamine are the treatments advocated for this condition.[25] In mild-to-moderate cases, near-complete improvement can be achieved.[20] Randomized controlled trials have showed a significant improvement in alcoholic polyneuropathy with thiamine treatment.[27],[28]Marchiafava–Bignami syndromeThis is a rare but fatal condition seen in chronic alcohol users that is characterized by progressive demyelination and necrosis of the corpus callosum. The association of this syndrome with thiamine deficiency is not very clear, and direct toxic effects of alcohol are also suggested.[29] The clinical syndrome is variable and presentation can be acute, subacute, or chronic. In acute forms, it is predominantly characterized by the altered mental state such as delirium, stupor, or coma.[30] Other clinical features in neuroimaging confirmed Marchiafava–Bignami syndrome (MBS) cases include impaired gait, dysarthria, mutism, signs of split-brain syndrome, pyramidal tract signs, primitive reflexes, rigidity, incontinence, gaze palsy, diplopia, and sensory symptoms.[30] Neuropsychiatric manifestations are common and include psychotic symptoms, depression, apathy, aggressive behavior, and sometimes dementia.[29] MRI scan shows lesions of the corpus callosum, particularly splenium.

Treatment for this condition is mostly supportive and use of nutritional supplements and steroids. However, there are several reports of improvement of this syndrome with thiamine at variable doses including reports of beneficial effects with high-dose strategy.[29],[30],[31] Early initiation of thiamine, preferably within 2 weeks of the onset of symptoms is associated with a better outcome. Therefore, high-dose thiamine should be administered to all suspected cases of MBS.

Laboratory Diagnosis of Thiamine Deficiency Estimation of thiamine and thiamine pyrophosphate levels may confirm the diagnosis of deficiency. Levels of thiamine in the blood are not reliable indicators of thiamine status. Low erythrocyte transketolase activity is also helpful.[32],[33] Transketolase concentrations of <120 nmol/L have also been used to indicate deficiency, while concentrations of 120–150 nmol/L suggest marginal thiamine status.[1] However, these tests are not routinely performed as it is time consuming, expensive, and may not be readily available.[34] The ETKA assay is a functional test rather than a direct measurement of thiamin status and therefore may be influenced by factors other than thiamine deficiency such as diabetes mellitus and polyneuritis.[1] Hence, treatment should be initiated in the absence of laboratory confirmation of thiamine deficiency.

Furthermore, treatment should not be delayed if tests are ordered, but the results are awaited. Electroencephalographic abnormalities in thiamine deficiency states range from diffuse mild-to-moderate slow waves and are not a good diagnostic option, as the prevalence of abnormalities among patients is inconsistent.[35]Surrogate markers, which reflect chronic alcohol use and nutritional deficiency other than thiamine, may be helpful in identifying at-risk patients. This includes gamma glutamate transferase, aspartate aminotransferase.

Alanine transaminase ratio >2:1, and increased mean corpuscular volume.[36] They are useful when a reliable history of alcohol use is not readily available, specifically in emergency departments when treatment needs to be started immediately to avoid long-term consequences. Thiamine Replacement Therapy Oral versus parenteral thiamineIntestinal absorption of thiamine depends on active transport through thiamine transporter 1 and 2, which follow saturation kinetics.[1] Therefore, the rate and amount of absorption of thiamine in healthy individuals is limited. In healthy volunteers, a 10 mg dose results in maximal absorption of thiamine, and any doses higher than this do not increase thiamine levels.

Therefore, the maximum amount of thiamine absorbed from 10 mg or higher dose is between 4.3 and 5.6 mg.[37] However, it has been suggested that, although thiamine transport occurs through the energy-requiring, sodium-dependent active process at physiologic concentrations, at higher supraphysiologic concentrations thiamine uptake is mostly a passive process.[38] Smithline et al. Have demonstrated that it is possible to achieve higher serum thiamine levels with oral doses up to 1500 mg.[39]In chronic alcohol users, intestinal absorption is impaired. Hence, absorption rates are expected to be much lower.

It is approximately 30% of that seen in healthy individuals, i.e., 1.5 mg of thiamine is absorbed from 10 mg oral thiamine.[3] In those consuming alcohol and have poor nutrition, not more than 0.8 mg of thiamine is absorbed.[2],[3],[6] The daily thiamine requirement is 1–1.6 mg/day, which may be more in alcohol-dependent patients at risk for Wernicke encephalopathy.[1] It is highly likely that oral supplementation with thiamine will be inadequate in alcohol-dependent individuals who continue to drink. Therefore, parenteral thiamine is preferred for supplementation in deficiency states associated with chronic alcohol use. Therapy involving parenteral thiamine is considered safe except for occasional circumstances of allergic reactions involving pruritus and local irritation.There is a small, but definite risk of anaphylaxis with parenteral thiamine, specifically with intravenous administration (1/250,000 intravenous injections).[40] Diluting thiamine in 50–100 mg normal saline for infusion may reduce the risk.

However, parenteral thiamine should always be administered under observation with the necessary facilities for resuscitation.A further important issue involves the timing of administration of thiamine relative to the course of alcohol abuse or dependence. Administration of thiamine treatment to patients experiencing alcohol withdrawal may also be influenced by other factors such as magnesium depletion, N-methyl-D-aspartate (NMDA) receptor upregulation, or liver impairment, all of which may alter thiamine metabolism and utilization.[6],[14]Thiamine or other preparations (e.g., benfotiamine)The thiamine transporters limit the rate of absorption of orally administered thiamine. Allithiamines (e.g., benfotiamine) are the lipid-soluble thiamine derivatives that are absorbed better, result in higher thiamine levels, and are retained longer in the body.[41] The thiamine levels with orally administered benfotiamine are much higher than oral thiamine and almost equals to intravenous thiamine given at the same dosage.[42]Benfotiamine has other beneficial effects including inhibition of production of advanced glycation end products, thus protecting against diabetic vascular complications.[41] It also modulates nuclear transcription factor κB (NK-κB), vascular endothelial growth factor receptor 2, glycogen synthase kinase 3 β, etc., that play a role in cell repair and survival.[41] Benfotiamine has been found to be effective for the treatment of alcoholic peripheral neuropathy.[27]Dosing of thiamineAs the prevalence of thiamine deficiency is very common in chronic alcohol users, the requirement of thiamine increases in active drinkers and it is difficult to rapidly determine thiamine levels using laboratory tests, it is prudent that all patients irrespective of nutritional status should be administered parenteral thiamine.

The dose should be 100 mg thiamine daily for 3–5 days during inpatient treatment. Commonly, multivitamin injections are added to intravenous infusions. Patients at risk for thiamine deficiency should receive 250 mg of thiamine daily intramuscularly for 3–5 days, followed by oral thiamine 100 mg daily.[6]Thiamine plasma levels reduce to 20% of peak value after approximately 2 h of parenteral administration, thus reducing the effective “window period” for passive diffusion to the central nervous system.[6] Therefore, in thiamine deficient individuals with features of Wernicke encephalopathy should receive thiamine thrice daily.High-dose parenteral thiamine administered thrice daily has been advocated in patients at risk for Wernicke encephalopathy.[43] The Royal College of Physicians guideline recommends that patients with suspected Wernicke encephalopathy should receive 500 mg thiamine diluted in 50–100 ml of normal saline infusion over 30 min three times daily for 2–3 days and sometimes for longer periods.[13] If there are persistent symptoms such as confusion, cerebellar symptoms, or memory impairment, this regimen can be continued until the symptoms improve.

If symptoms improve, oral thiamine 100 mg thrice daily can be continued for prolonged periods.[6],[40] A similar treatment regimen is advocated for alcoholic cerebellar degeneration as well. Doses more than 500 mg intramuscular or intravenous three times a day for 3–5 days, followed by 250 mg once daily for a further 3–5 days is also recommended by some guidelines (e.g., British Association for Psychopharmacology).[44]Other effects of thiamineThere are some data to suggest that thiamine deficiency can modulate alcohol consumption and may result in pathological drinking. Benfotiamine 600 mg/day as compared to placebo for 6 months was well tolerated and found to decrease psychiatric distress in males and reduce alcohol consumption in females with severe alcohol dependence.[45],[46] Other Factors During Thiamine Therapy Correction of hypomagnesemiaMagnesium is a cofactor for many thiamine-dependent enzymes in carbohydrate metabolism.

Patients may fail to respond to thiamine supplementation in the presence of hypomagnesemia.[47] Magnesium deficiency is common in chronic alcohol users and is seen in 30% of individuals.[48],[49] It can occur because of increased renal excretion of magnesium, poor intake, decreased absorption because of Vitamin D deficiency, the formation of undissociated magnesium soaps with free fatty acids.[48],[49]The usual adult dose is 35–50 mmol of magnesium sulfate added to 1 L isotonic (saline) given over 12–24 h.[6] The dose has to be titrated against plasma magnesium levels. It is recommended to reduce the dose in renal failure. Contraindications include patients with documented hypersensitivity and those with heart block, Addison's disease, myocardial damage, severe hepatitis, or hypophosphatemia.

Do not administer intravenous magnesium unless hypomagnesemia is confirmed.[6]Other B-complex vitaminsMost patients with deficiency of thiamine will also have reduced levels of other B vitamins including niacin, pyridoxine, and cobalamin that require replenishment. For patients admitted to the intensive care unit with symptoms that may mimic or mask Wernicke encephalopathy, based on the published literature, routine supplementation during the 1st day of admission includes 200–500 mg intravenous thiamine every 8 h, 64 mg/kg magnesium sulfate (≈4–5 g for most adult patients), and 400–1000 μg intravenous folate.[50] If alcoholic ketoacidosis is suspected, dextrose-containing fluids are recommended over normal saline.[50] Precautions to be Taken When Administering Parenteral Thiamine It is recommended to monitor for anaphylaxis and has appropriate facilities for resuscitation and for treating anaphylaxis readily available including adrenaline and corticosteroids. Anaphylaxis has been reported at the rate of approximately 4/1 million pairs of ampoules of Pabrinex (a pair of high potency vitamins available in the UK containing 500 mg of thiamine (1:250,000 I/V administrations).[40] Intramuscular thiamine is reported to have a lower incidence of anaphylactic reactions than intravenous administration.[40] The reaction has been attributed to nonspecific histamine release.[51] Administer intravenous thiamine slowly, preferably by slow infusion in 100 ml normal saline over 15–30 min.

Conclusions Risk factors for thiamine deficiency should be assessed in chronic alcohol users. A high index of suspicion and a lower threshold to diagnose thiamine deficiency states including Wernicke encephalopathy is needed. Several other presentations such as cerebellar syndrome, MBS, polyneuropathy, and delirium tremens could be related to thiamine deficiency and should be treated with protocols similar to Wernicke encephalopathy.

High-dose thiamine is recommended for the treatment of suspected Wernicke encephalopathy and related conditions [Figure 1]. However, evidence in terms of randomized controlled trials is lacking, and the recommendations are based on small studies and anecdotal reports. Nevertheless, as all these conditions respond to thiamine supplementation, it is possible that these have overlapping pathophysiology and are better considered as Wernicke encephalopathy spectrum disorders.Figure 1.

Thiamine recommendations for patients with alcohol use disorder. AHistory of alcohol use, but no clinical features of WE. BNo clinical features of WE, but with risk factors such as complicated withdrawal (delirium, seizures).

CClinical features of WE (ataxia, opthalmoplegia, global confusion)Click here to viewFinancial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Frank LL. Thiamin in clinical practice.

JPEN J Parenter Enteral Nutr 2015;39:503-20. 2.Thomson AD, Marshall EJ. The natural history and pathophysiology of Wernicke's Encephalopathy and Korsakoff's Psychosis.

Alcohol Alcohol 2006;41:151-8. 3.Thomson AD, Guerrini I, Marshall EJ. Wernicke's encephalopathy.

Role of thiamine. Pract Gastroenterol 2009;33:21-30. 4.Isenberg-Grzeda E, Kutner HE, Nicolson SE.

Wernicke-Korsakoff-syndrome. Under-recognized and under-treated. Psychosomatics 2012;53:507-16.

5.Wood B, Currie J, Breen K. Wernicke's encephalopathy in a metropolitan hospital. A prospective study of incidence, characteristics and outcome.

Med J Aust 1986;144:12-6. 6.Thomson AD, Cook CC, Touquet R, Henry JA, Royal College of Physicians, London. The Royal College of Physicians report on alcohol.

Guidelines for managing Wernicke's encephalopathy in the accident and Emergency Department. Alcohol Alcohol 2002;37:513-21. 7.Harper C.

Thiamine (vitamin B1) deficiency and associated brain damage is still common throughout the world and prevention is simple and safe!. Eur J Neurol 2006;13:1078-82. 8.Harper CG, Giles M, Finlay-Jones R.

Clinical signs in the Wernicke-Korsakoff complex. A retrospective analysis of 131 cases diagnosed at necropsy. J Neurol Neurosurg Psychiatry 1986;49:341-5.

9.Cook CC. Prevention and treatment of Wernicke-Korsakoff syndrome. Alcohol Alcohol 2000;35:19-20.

10.Caine D, Halliday GM, Kril JJ, Harper CG. Operational criteria for the classification kamagra online purchase of chronic alcoholics. Identification of Wernicke's encephalopathy.

J Neurol Neurosurg Psychiatry 1997;62:51-60. 11.Sullivan EV, Pfefferbaum A. Neuroimaging of the Wernicke-Korsakoff syndrome.

Alcohol Alcohol 2009;44:155-65. 12.Jung YC, Chanraud S, Sullivan EV. Neuroimaging of Wernicke's encephalopathy and Korsakoff's syndrome.

Neuropsychol Rev 2012;22:170-80. 13.Pruckner N, Baumgartner J, Hinterbuchinger B, Glahn A, Vyssoki S, Vyssoki B. Thiamine substitution in alcohol use disorder.

A narrative review of medical guidelines. Eur Addict Res 2019;25:103-10. 14.Day E, Bentham PW, Callaghan R, Kuruvilla T, George S.

Thiamine for prevention and treatment of Wernicke-Korsakoff Syndrome in people who abuse alcohol. Cochrane Database Syst Rev 2013;7:CD004033. Doi.

10.1002/14651858.CD004033.pub3. 15.Arts NJ, Walvoort SJ, Kessels RP. Korsakoff's syndrome.

A critical review. Neuropsychiatr Dis Treat 2017;13:2875-90. 16.Laureno R.

Nutritional cerebellar degeneration, with comments on its relationship to Wernicke disease and alcoholism. Handb Clin Neurol 2012;103:175-87. 17.Maschke M, Weber J, Bonnet U, Dimitrova A, Bohrenkämper J, Sturm S, et al.

Vermal atrophy of alcoholics correlate with serum thiamine levels but not with dentate iron concentrations as estimated by MRI. J Neurol 2005;252:704-11. 18.Mulholland PJ, Self RL, Stepanyan TD, Little HJ, Littleton JM, Prendergast MA.

Thiamine deficiency in the pathogenesis of chronic ethanol-associated cerebellar damage in vitro. Neuroscience 2005;135:1129-39. 19.Del Brutto OH, Mera RM, Sullivan LJ, Zambrano M, King NR.

Population-based study of alcoholic cerebellar degeneration. The Atahualpa Project. J Neurol Sci 2016;367:356-60.

20.Hammoud N, Jimenez-Shahed J. Chronic neurologic effects of alcohol. Clin Liver Dis 2019;23:141-55.

21.Lee JH, Heo SH, Chang DI. Early-stage alcoholic cerebellar degeneration. Diagnostic imaging clues.

J Korean Med Sci 2015;30:1539. 22.Phillips SC, Harper CG, Kril JJ. The contribution of Wernicke's encephalopathy to alcohol-related cerebellar damage.

Drug Alcohol Rev 1990;9:53-60. 23.Baker KG, Harding AJ, Halliday GM, Kril JJ, Harper CG. Neuronal loss in functional zones of the cerebellum of chronic alcoholics with and without Wernicke's encephalopathy.

Neuroscience 1999;91:429-38. 24.Graham JR, Woodhouse D, Read FH. Massive thiamine dosage in an alcoholic with cerebellar cortical degeneration.

Lancet 1971;2:107. 25.Julian T, Glascow N, Syeed R, Zis P. Alcohol-related peripheral neuropathy.

A systematic review and meta-analysis. J Neurol 2018;22:1-3. 26.Chopra K, Tiwari V.

Alcoholic neuropathy. Possible mechanisms and future treatment possibilities. Br J Clin Pharmacol 2012;73:348-62.

27.Woelk H, Lehrl S, Bitsch R, Köpcke W. Benfotiamine in treatment of alcoholic polyneuropathy. An 8-week randomized controlled study (BAP I Study).

Alcohol Alcohol 1998;33:631-8. 28.Peters TJ, Kotowicz J, Nyka W, Kozubski W, Kuznetsov V, Vanderbist F, et al. Treatment of alcoholic polyneuropathy with vitamin B complex.

A randomised controlled trial. Alcohol Alcohol 2006;41:636-42. 29.Fernandes LM, Bezerra FR, Monteiro MC, Silva ML, de Oliveira FR, Lima RR, et al.

Thiamine deficiency, oxidative metabolic pathways and ethanol-induced neurotoxicity. How poor nutrition contributes to the alcoholic syndrome, as Marchiafava-Bignami disease. Eur J Clin Nutr 2017;71:580-6.

30.Hillbom M, Saloheimo P, Fujioka S, Wszolek ZK, Juvela S, Leone MA. Diagnosis and management of Marchiafava-Bignami disease. A review of CT/MRI confirmed cases.

J Neurol Neurosurg Psychiatry 2014;85:168-73. 31.Nemlekar SS, Mehta RY, Dave KR, Shah ND. Marchiafava.

Bignami disease treated with parenteral thiamine. Indian J Psychol Med 2016;38:147-9. [Full text] 32.Brin M.

Erythrocyte transketolase in early thiamine deficiency. Ann N Y Acad Sci 1962;98:528-41. 33.Dreyfus PM.

Clinical application of blood transketolase determinations. N Engl J Med 1962;267:596-8. 34.Edwards KA, Tu-Maung N, Cheng K, Wang B, Baeumner AJ, Kraft CE.

Thiamine assays – Advances, challenges, and caveats. ChemistryOpen 2017;6:178-91. 35.Chandrakumar A, Bhardwaj A, 't Jong GW.

Review of thiamine deficiency disorders. Wernicke encephalopathy and Korsakoff psychosis. J Basic Clin Physiol Pharmacol 2018;30:153-62.

36.Torruellas C, French SW, Medici V. Diagnosis of alcoholic liver disease. World J Gastroenterol 2014;20:11684-99.

37.Thomson AD, Leevy CM. Observations on the mechanism of thiamine hydrochloride absorption in man. Clin Sci 1972;43:153-63.

38.Hoyumpa AM Jr., Strickland R, Sheehan JJ, Yarborough G, Nichols S. Dual system of intestinal thiamine transport in humans. J Lab Clin Med 1982;99:701-8.

39.Smithline HA, Donnino M, Greenblatt DJ. Pharmacokinetics of high-dose oral thiamine hydrochloride in healthy subjects. BMC Clin Pharmacol 2012;12:4.

40.Latt N, Dore G. Thiamine in the treatment of Wernicke encephalopathy in patients with alcohol use disorders. Intern Med J 2014;44:911-5.

41.Raj V, Ojha S, Howarth FC, Belur PD, Subramanya SB. Therapeutic potential of benfotiamine and its molecular targets. Eur Rev Med Pharmacol Sci 2018;22:3261-73.

42.Xie F, Cheng Z, Li S, Liu X, Guo X, Yu P, et al. Pharmacokinetic study of benfotiamine and the bioavailability assessment compared to thiamine hydrochloride. J Clin Pharmacol 2014;54:688-95.

43.Cook CC, Hallwood PM, Thomson AD. B Vitamin deficiency and neuropsychiatric syndromes in alcohol misuse. Alcohol Alcohol 1998;33:317-36.

44.Lingford-Hughes AR, Welch S, Peters L, Nutt DJ, British Association for Psychopharmacology, Expert Reviewers Group. BAP updated guidelines. Evidence-based guidelines for the pharmacological management of substance abuse, harmful use, addiction and comorbidity.

Recommendations from BAP. J Psychopharmacol 2012;26:899-952. 45.Manzardo AM, He J, Poje A, Penick EC, Campbell J, Butler MG.

Double-blind, randomized placebo-controlled clinical trial of benfotiamine for severe alcohol dependence. Drug Alcohol Depend 2013;133:562-70. 46.Manzardo AM, Pendleton T, Poje A, Penick EC, Butler MG.

Change in psychiatric symptomatology after benfotiamine treatment in males is related to lifetime alcoholism severity. Drug Alcohol Depend 2015;152:257-63. 47.Dingwall KM, Delima JF, Gent D, Batey RG.

Hypomagnesaemia and its potential impact on thiamine utilisation in patients with alcohol misuse at the Alice Springs Hospital. Drug Alcohol Rev 2015;34:323-8. 48.Flink EB.

Magnesium deficiency in alcoholism. Alcohol Clin Exp Res 1986;10:590-4. 49.Grochowski C, Blicharska E, Baj J, Mierzwińska A, Brzozowska K, Forma A, et al.

Serum iron, magnesium, copper, and manganese levels in alcoholism. A systematic review. Molecules 2019;24:E1361.

50.Flannery AH, Adkins DA, Cook AM. Unpeeling the evidence for the banana bag. Evidence-based recommendations for the management of alcohol-associated vitamin and electrolyte deficiencies in the ICU.

Crit Care Med 2016;44:1545-52. 51.Lagunoff D, Martin TW, Read G. Agents that release histamine from mast cells.

Annu Rev Pharmacol Toxicol 1983;23:331-51. Correspondence Address:Samir Kumar PraharajDepartment of Psychiatry, Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal, Karnataka IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_440_20 Figures [Figure 1].

How to cheap kamagra supplier reviews cite this kamagra online purchase article:Singh OP. The National Commission for Allied and Healthcare Professions Act, 2020 and its implication for mental health. Indian J Psychiatry 2021;63:119-20The National Commission for Allied and Healthcare Professions Act, 2020 has been notified on March 28, 2021, by the Gazette of India published by the Ministry of Law and Justice cheap kamagra supplier reviews.

This bill aims to “provide for regulation and maintenance of standards of education and services by allied and healthcare professionals, assessment of institutions, maintenance of a Central Register and State Register and creation of a system to improve access, research and development and adoption of latest scientific advancement and for matters connected therewith or incidental thereto.”[1]This act has created a category of Health Care Professionals which is defined as. €œhealthcare professional” includes a scientist, therapist, or other professional who studies, advises, researches, supervises or provides preventive, curative, rehabilitative, therapeutic or promotional health services and who has obtained any qualification of degree under this Act, the duration of which shall not be <3600 h spread over a period of 3 years to 6 years divided into specific semesters.[1]According to the act, “Allied health professional” includes an associate, technician, or technologist who is trained to perform any technical and practical task to support diagnosis and treatment of illness, disease, injury or impairment, and to support implementation of any healthcare treatment and referral plan recommended by a medical, nursing, or any other healthcare professional, and who has obtained any qualification of diploma or degree under this Act, the duration of which shall not be less than 2000 h spread over a period of 2 years to 4 years divided into specific semesters.”[1]It is noticeable that while the term “Health Care Professionals” does not include doctors who are registered under National Medical Council, Mental Health Care Act (MHCA), 2017 includes psychiatrists under the ambit of Mental Health Care Professionals.[2] This discrepancy needs to be corrected - psychiasts, being another group of medical specialists, should be kept out of the broad umbrella of “Mental cheap kamagra supplier reviews Healthcare Professionals.”The category of Behavioural Health Sciences Professional has been included and defined as “a person who undertakes scientific study of the emotions, behaviours and biology relating to a person's mental well-being, their ability to function in everyday life and their concept of self. €œBehavioural health” is the preferred term to “mental health” and includes professionals such as counselors, analysts, psychologists, educators and support workers, who provide counseling, therapy, and mediation services to individuals, families, groups, and communities in response to social and personal difficulties.”[1]This is a welcome step to the extent that it creates a diverse category of trained workforce in the field of Mental Health (Behavioural Health Science Professionals) and tries to regulate their training although it mainly aims to promote mental wellbeing.

However there is a huge lacuna in the term of “Mental Illness” as defined cheap kamagra supplier reviews by MHCA, 2017. Only severe disorders are included as per definition and there is no clarity regarding inclusion of other psychiatric disorders, namely “common mental disorders” such as anxiety and depression. This leaves a strong possibility of concept of “psychiatric illnesses” being limited to only cheap kamagra supplier reviews “severe psychiatric disorders” (major psychoses) thus perpetuating the stigma and alienation associated with psychiatric patients for centuries.

Psychiatrists being restricted to treating severe mental disorders as per MHCA, 2017, there is a strong possibility that the care of common mental disorders may gradually pass on under the care of “behavioural health professionals” as per the new act!. There is need to look into this aspect by cheap kamagra supplier reviews the leadership in psychiatry, both organizational and academic psychiatry, and reduce the contradictions between the MHCA, 2017 and this nascent act. All disorders classified in ICD 10 and DSM 5 should be classified as “Psychiatric Disorders” or “Mental Illness.” This will not only help in fighting the stigma associated with psychiatric illnesses but also promote the integration of psychiatry with other specialties.

References 1.The National Commission for Allied cheap kamagra supplier reviews and Healthcare Professions Act, 2021. The Gazette of India. Published by Ministry of Law and Justice cheap kamagra supplier reviews.

28 March, 2021. 2.The Mental Healthcare Act, 2017 cheap kamagra supplier reviews. The Gazette of India.

Published by cheap kamagra supplier reviews Ministry of Law and Justice. April 7, 2017. Correspondence Address:Om Prakash SinghAA 304, Ashabari Apartments, O/31, cheap kamagra supplier reviews Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support.

None, Conflict of Interest. NoneDOI. 10.4103/indianjpsychiatry.indianjpsychiatry_268_21Abstract Thiamine is essential for cheap kamagra supplier reviews the activity of several enzymes associated with energy metabolism in humans.

Chronic alcohol use is associated with deficiency of thiamine along with other vitamins through several mechanisms. Several neuropsychiatric cheap kamagra supplier reviews syndromes have been associated with thiamine deficiency in the context of alcohol use disorder including Wernicke–Korsakoff syndrome, alcoholic cerebellar syndrome, alcoholic peripheral neuropathy, and possibly, Marchiafava–Bignami syndrome. High-dose thiamine replacement is suggested for these neuropsychiatric syndromes.Keywords.

Alcohol use disorder, alcoholic cheap kamagra supplier reviews cerebellar syndrome, alcoholic peripheral neuropathy, Marchiafava–Bignami syndrome, thiamine, Wernicke–Korsakoff syndromeHow to cite this article:Praharaj SK, Munoli RN, Shenoy S, Udupa ST, Thomas LS. High-dose thiamine strategy in Wernicke–Korsakoff syndrome and related thiamine deficiency conditions associated with alcohol use disorder. Indian J Psychiatry 2021;63:121-6How to cite this URL:Praharaj SK, Munoli RN, Shenoy S, Udupa ST, Thomas LS cheap kamagra supplier reviews.

High-dose thiamine strategy in Wernicke–Korsakoff syndrome and related thiamine deficiency conditions associated with alcohol use disorder. Indian J Psychiatry [serial online] 2021 [cited 2021 cheap kamagra supplier reviews Jun 11];63:121-6. Available from.

Https://www.indianjpsychiatry.org/text.asp?. 2021/63/2/121/313716 Introduction Thiamine is a water-soluble vitamin (B1) that plays a key role in the activity of several enzymes associated with energy metabolism. Thiamine pyrophosphate (or diphosphate) is the active form that acts as a cofactor for enzymes.

The daily dietary requirement of thiamine in adults is 1–2 mg and is dependent on carbohydrate intake.[1],[2] The requirement increases if basal metabolic rate is higher, for example, during alcohol withdrawal state. Dietary sources include pork (being the major source), meat, legume, vegetables, and enriched foods. The body can store between 30 and 50 mg of thiamine and is likely to get depleted within 4–6 weeks if the diet is deficient.[2] In those with alcohol-related liver damage, the ability to store thiamine is gradually reduced.[1],[2]Lower thiamine levels are found in 30%–80% of chronic alcohol users.[3] Thiamine deficiency occurs due to poor intake of vitamin-rich foods, impaired intestinal absorption, decreased storage capacity of liver, damage to the renal epithelial cells due to alcohol, leading to increased loss from the kidneys, and excessive loss associated with medical conditions.[2],[3] Furthermore, alcohol decreases the absorption of colonic bacterial thiamine, reduces the enzymatic activity of thiamine pyrophosphokinase, and thereby, reducing the amount of available thiamine pyrophosphate.[4] Since facilitated diffusion of thiamine into cells is dependent on a concentration gradient, reduced thiamine pyrophosphokinase activity further reduces thiamine uptake into cells.[4] Impaired utilization of thiamine is seen in certain conditions (e.g., hypomagnesemia) which are common in alcohol use disorder.[2],[3],[4] This narrative review discusses the neuropsychiatric syndromes associated with thiamine deficiency in the context of alcohol use disorder, and the treatment regimens advocated for these conditions.

A PubMed search supplemented with manual search was used to identify neuropsychiatric syndromes related to thiamine deficiency in alcohol use disorder patients. Neuropsychiatric Syndromes Associated With Thiamine Deficiency Wernicke–Korsakoff syndromeWernicke encephalopathy is associated with chronic alcohol use, and if not identified and treated early, could lead to permanent brain damage characterized by an amnestic syndrome known as Korsakoff syndrome. Inappropriate treatment of Wernicke encephalopathy with lower doses of thiamine can lead to high mortality rates (~20%) and Korsakoff syndrome in ~ 80% of patients (ranges from 56% to 84%).[5],[6] The classic triad of Wernicke includes oculomotor abnormalities, cerebellar dysfunction, and confusion.

Wernicke lesions are found in 12.5% of brain samples of patients with alcohol dependence.[7] However, only 20%–30% of them had a clinical diagnosis of Wernicke encephalopathy antemortem. It has been found that many patients develop Wernicke–Korsakoff syndrome (WKS) following repeated subclinical episodes of thiamine deficiency.[7] In an autopsy report of 97 chronic alcohol users, only16% had all the three “classical signs,” 29% had two signs, 37% presented with one sign, and 19% had none.[8] Mental status changes are the most prevalent sign (seen in 82% of the cases), followed by eye signs (in 29%) and ataxia (23%).[8] WKS should be suspected in persons with a history of alcohol use and presenting with signs of ophthalmoplegia, ataxia, acute confusion, memory disturbance, unexplained hypotension, hypothermia, coma, or unconsciousness.[9] Operational criteria for the diagnosis of Wernicke encephalopathy have been proposed by Caine et al.[10] that requires two out of four features, i.e., (a) dietary deficiency (signs such as cheilitis, glossitis, and bleeding gums), (b) oculomotor abnormalities (nystagmus, opthalmoplegia, and diplopia), (c) cerebellar dysfunction (gait ataxia, nystagmus), and (d) either altered mental state (confusion) or mild memory impairment.As it is very difficult to clinically distinguish Wernicke encephalopathy from other associated conditions such as delirium tremens, hepatic encephalopathy, or head injury, it is prudent to have a lower threshold to diagnose this if any of the clinical signs is seen. Magnetic resonance imaging (MRI) brain scan during Wernicke encephalopathy shows mammillary body atrophy and enlarged third ventricle, lesions in the medial portions of thalami and mid brain and can be used to aid diagnosis.[11],[12] However, most clinical situations warrant treatment without waiting for neuroimaging report.

The treatment suggestions in the guidelines vary widely. Furthermore, hardly any evidence-based recommendations exist on a more general use of thiamine as a preventative intervention in individuals with alcohol use disorder.[13] There are very few studies that have evaluated the dose and duration of thiamine for WKS, but higher doses may result in a greater response.[6],[14] With thiamine administration rapid improvement is seen in eye movement abnormalities (improve within days or weeks) and ataxia (may take months to recover), but the effects on memory, in particular, are unclear.[4],[14] Severe memory impairment is the core feature of Korsakoff syndrome. Initial stages of the disease can present with confabulation, executive dysfunction, flattened affect, apathy, and poor insight.[15] Both the episodic and semantic memory are affected, whereas, procedural memory remains intact.[15]Thomson et al.[6] suggested the following should be treated with thiamine as they are at high risk for developing WKS.

(1) all patients with any evidence of chronic alcohol misuse and any of the following. Acute confusion, decreased conscious level, ataxia, ophthalmoplegia, memory disturbance, and hypothermia with hypotension. (2) patients with delirium tremens may often also have Wernicke encephalopathy, therefore, all of these patients should be presumed to have Wernicke encephalopathy and treated, preferably as inpatients.

And (3) all hypoglycemic patients (who are treated with intravenous glucose) with evidence of chronic alcohol ingestion must be given intravenous thiamine immediately because of the risk of acutely precipitating Wernicke encephalopathy.Alcoholic cerebellar syndromeChronic alcohol use is associated with the degeneration of anterior superior vermis, leading to a clinical syndrome characterized by the subacute or chronic onset of gait ataxia and incoordination in legs, with relative sparing of upper limbs, speech, and oculomotor movements.[16] In severe cases, truncal ataxia, mild dysarthria, and incoordination of the upper limb is also found along with gait ataxia. Thiamine deficiency is considered to be the etiological factor,[17],[18] although direct toxic effects of alcohol may also contribute to this syndrome. One-third of patients with chronic use of alcohol have evidence of alcoholic cerebellar degeneration.

However, population-based studies estimate prevalence to be 14.6%.[19] The effect of alcohol on the cerebellum is graded with the most severe deficits occurring in alcohol users with the longest duration and highest severity of use. The diagnosis of cerebellar degeneration is largely clinical. MRI can be used to evaluate for vermian atrophy but is unnecessary.[20] Anterior portions of vermis are affected early, with involvement of posterior vermis and adjacent lateral hemispheres occurring late in the course could be used to differentiate alcoholic cerebellar degeneration from other conditions that cause more diffuse involvement.[21] The severity of cerebellar syndrome is more in the presence of WKS, thus could be related to thiamine deficiency.[22],[23] Therefore, this has been considered as a cerebellar presentation of WKS and should be treated in a similar way.[16] There are anecdotal evidence to suggest improvement in cerebellar syndrome with high-dose thiamine.[24]Alcoholic peripheral neuropathyPeripheral neuropathy is common in alcohol use disorder and is seen in 44% of the users.[25] It has been associated predominantly with thiamine deficiency.

However, deficiency of other B vitamins (pyridoxine and cobalamin) and direct toxic effect of alcohol is also implicated.[26] Clinically, onset of symptoms is gradual with the involvement of both sensory and motor fibers and occasionally autonomic fibers. Neuropathy can affect both small and large peripheral nerve fibers, leading to different clinical manifestations. Thiamine deficiency-related neuropathy affects larger fiber types, which results in motor deficits and sensory ataxia.

On examination, large fiber involvement is manifested by distal limb muscle weakness and loss of proprioception and vibratory sensation. Together, these can contribute to the gait unsteadiness seen in chronic alcohol users by creating a superimposed steppage gait and reduced proprioceptive input back to the movement control loops in the central nervous system. The most common presentations include painful sensations in both lower limbs, sometimes with burning sensation or numbness, which are early symptoms.

Typically, there is a loss of vibration sensation in distal lower limbs. Later symptoms include loss of proprioception, gait disturbance, and loss of reflexes. Most advanced findings include weakness and muscle atrophy.[20] Progression is very gradual over months and involvement of upper limbs may occur late in the course.

Diagnosis begins with laboratory evaluation to exclude other causes of distal, sensorimotor neuropathy including hemoglobin A1c, liver function tests, and complete blood count to evaluate for red blood cell macrocytosis. Cerebrospinal fluid studies may show increased protein levels but should otherwise be normal in cases of alcohol neuropathy and are not recommended in routine evaluation. Electromyography and nerve conduction studies can be used to distinguish whether the neuropathy is axonal or demyelinating and whether it is motor, sensory, or mixed type.

Alcoholic neuropathy shows reduced distal, sensory amplitudes, and to a lesser extent, reduced motor amplitudes on nerve conduction studies.[20] Abstinence and vitamin supplementation including thiamine are the treatments advocated for this condition.[25] In mild-to-moderate cases, near-complete improvement can be achieved.[20] Randomized controlled trials have showed a significant improvement in alcoholic polyneuropathy with thiamine treatment.[27],[28]Marchiafava–Bignami syndromeThis is a rare but fatal condition seen in chronic alcohol users that is characterized by progressive demyelination and necrosis of the corpus callosum. The association of this syndrome with thiamine deficiency is not very clear, and direct toxic effects of alcohol are also suggested.[29] The clinical syndrome is variable and presentation can be acute, subacute, or chronic. In acute forms, it is predominantly characterized by the altered mental state such as delirium, stupor, or coma.[30] Other clinical features in neuroimaging confirmed Marchiafava–Bignami syndrome (MBS) cases include impaired gait, dysarthria, mutism, signs of split-brain syndrome, pyramidal tract signs, primitive reflexes, rigidity, incontinence, gaze palsy, diplopia, and sensory symptoms.[30] Neuropsychiatric manifestations are common and include psychotic symptoms, depression, apathy, aggressive behavior, and sometimes dementia.[29] MRI scan shows lesions of the corpus callosum, particularly splenium.

Treatment for this condition is mostly supportive and use of nutritional supplements and steroids. However, there are several reports of improvement of this syndrome with thiamine at variable doses including reports of beneficial effects with high-dose strategy.[29],[30],[31] Early initiation of thiamine, preferably within 2 weeks of the onset of symptoms is associated with a better outcome. Therefore, high-dose thiamine should be administered to all suspected cases of MBS.

Laboratory Diagnosis of Thiamine Deficiency Estimation of thiamine and thiamine pyrophosphate levels may confirm the diagnosis of deficiency. Levels of thiamine in the blood are not reliable indicators of thiamine status. Low erythrocyte transketolase activity is also helpful.[32],[33] Transketolase concentrations of <120 nmol/L have also been used to indicate deficiency, while concentrations of 120–150 nmol/L suggest marginal thiamine status.[1] However, these tests are not routinely performed as it is time consuming, expensive, and may not be readily available.[34] The ETKA assay is a functional test rather than a direct measurement of thiamin status and therefore may be influenced by factors other than thiamine deficiency such as diabetes mellitus and polyneuritis.[1] Hence, treatment should be initiated in the absence of laboratory confirmation of thiamine deficiency.

Furthermore, treatment should not be delayed if tests are ordered, but the results are awaited. Electroencephalographic abnormalities in thiamine deficiency states range from diffuse mild-to-moderate slow waves and are not a good diagnostic option, as the prevalence of abnormalities among patients is inconsistent.[35]Surrogate markers, which reflect chronic alcohol use and nutritional deficiency other than thiamine, may be helpful in identifying at-risk patients. This includes gamma glutamate transferase, aspartate aminotransferase.

Alanine transaminase ratio >2:1, and increased mean corpuscular volume.[36] They are useful when a reliable history of alcohol use is not readily available, specifically in emergency departments when treatment needs to be started immediately to avoid long-term consequences. Thiamine Replacement Therapy Oral versus parenteral thiamineIntestinal absorption of thiamine depends on active transport through thiamine transporter 1 and 2, which follow saturation kinetics.[1] Therefore, the rate and amount of absorption of thiamine in healthy individuals is limited. In healthy volunteers, a 10 mg dose results in maximal absorption of thiamine, and any doses higher than this do not increase thiamine levels.

Therefore, the maximum amount of thiamine absorbed from 10 mg or higher dose is between 4.3 and 5.6 mg.[37] However, it has been suggested that, although thiamine transport occurs through the energy-requiring, sodium-dependent active process at physiologic concentrations, at higher supraphysiologic concentrations thiamine uptake is mostly a passive process.[38] Smithline et al. Have demonstrated that it is possible to achieve higher serum thiamine levels with oral doses up to 1500 mg.[39]In chronic alcohol users, intestinal absorption is impaired. Hence, absorption rates are expected to be much lower.

It is approximately 30% of that seen in healthy individuals, i.e., 1.5 mg of thiamine is absorbed from 10 mg oral thiamine.[3] In those consuming alcohol and have poor nutrition, not more than 0.8 mg of thiamine is absorbed.[2],[3],[6] The daily thiamine requirement is 1–1.6 mg/day, which may be more in alcohol-dependent patients at risk for Wernicke encephalopathy.[1] It is highly likely that oral supplementation with thiamine will be inadequate in alcohol-dependent individuals who continue to drink. Therefore, parenteral thiamine is preferred for supplementation in deficiency states associated with chronic alcohol use. Therapy involving parenteral thiamine is considered safe except for occasional circumstances of allergic reactions involving pruritus and local irritation.There is a small, but definite risk of anaphylaxis with parenteral thiamine, specifically with intravenous administration (1/250,000 intravenous injections).[40] Diluting thiamine in 50–100 mg normal saline for infusion may reduce the risk.

However, parenteral thiamine should always be administered under observation with the necessary facilities for resuscitation.A further important issue involves the timing of administration of thiamine relative to the course of alcohol abuse or dependence. Administration of thiamine treatment to patients experiencing alcohol withdrawal may also be influenced by other factors such as magnesium depletion, N-methyl-D-aspartate (NMDA) receptor upregulation, or liver impairment, all of which may alter thiamine metabolism and utilization.[6],[14]Thiamine or other preparations (e.g., benfotiamine)The thiamine transporters limit the rate of absorption of orally administered thiamine. Allithiamines (e.g., benfotiamine) are the lipid-soluble thiamine derivatives that are absorbed better, result in higher thiamine levels, and are retained longer in the body.[41] The thiamine levels with orally administered benfotiamine are much higher than oral thiamine and almost equals to intravenous thiamine given at the same dosage.[42]Benfotiamine has other beneficial effects including inhibition of production of advanced glycation end products, thus protecting against diabetic vascular complications.[41] It also modulates nuclear transcription factor κB (NK-κB), vascular endothelial growth factor receptor 2, glycogen synthase kinase 3 β, etc., that play a role in cell repair and survival.[41] Benfotiamine has been found to be effective for the treatment of alcoholic peripheral neuropathy.[27]Dosing of thiamineAs the prevalence of thiamine deficiency is very common in chronic alcohol users, the requirement of thiamine increases in active drinkers and it is difficult to rapidly determine thiamine levels using laboratory tests, it is prudent that all patients irrespective of nutritional status should be administered parenteral thiamine.

The dose should be 100 mg thiamine daily for 3–5 days during inpatient treatment. Commonly, multivitamin injections are added to intravenous infusions. Patients at risk for thiamine deficiency should receive 250 mg of thiamine daily intramuscularly for 3–5 days, followed by oral thiamine 100 mg daily.[6]Thiamine plasma levels reduce to 20% of peak value after approximately 2 h of parenteral administration, thus reducing the effective “window period” for passive diffusion to the central nervous system.[6] Therefore, in thiamine deficient individuals with features of Wernicke encephalopathy should receive thiamine thrice daily.High-dose parenteral thiamine administered thrice daily has been advocated in patients at risk for Wernicke encephalopathy.[43] The Royal College of Physicians guideline recommends that patients with suspected Wernicke encephalopathy should receive 500 mg thiamine diluted in 50–100 ml of normal saline infusion over 30 min three times daily for 2–3 days and sometimes for longer periods.[13] If there are persistent symptoms such as confusion, cerebellar symptoms, or memory impairment, this regimen can be continued until the symptoms improve.

If symptoms improve, oral thiamine 100 mg thrice daily can be continued for prolonged periods.[6],[40] A similar treatment regimen is advocated for alcoholic cerebellar degeneration as well. Doses more than 500 mg intramuscular or intravenous three times a day for 3–5 days, followed by 250 mg once daily for a further 3–5 days is also recommended by some guidelines (e.g., British Association for Psychopharmacology).[44]Other effects of thiamineThere are some data to suggest that thiamine deficiency can modulate alcohol consumption and may result in pathological drinking. Benfotiamine 600 mg/day as compared to placebo for 6 months was well tolerated and found to decrease psychiatric distress in males and reduce alcohol consumption in females with severe alcohol dependence.[45],[46] Other Factors During Thiamine Therapy Correction of hypomagnesemiaMagnesium is a cofactor for many thiamine-dependent enzymes in carbohydrate metabolism.

Patients may fail to respond to thiamine supplementation in the presence of hypomagnesemia.[47] Magnesium deficiency is common in chronic alcohol users and is seen in 30% of individuals.[48],[49] It can occur because of increased renal excretion of magnesium, poor intake, decreased absorption because of Vitamin D deficiency, the formation of undissociated magnesium soaps with free fatty acids.[48],[49]The usual adult dose is 35–50 mmol of magnesium sulfate added to 1 L isotonic (saline) given over 12–24 h.[6] The dose has to be titrated against plasma magnesium levels. It is recommended to reduce the dose in renal failure. Contraindications include patients with documented hypersensitivity and those with heart block, Addison's disease, myocardial damage, severe hepatitis, or hypophosphatemia.

Do not administer intravenous magnesium unless hypomagnesemia is confirmed.[6]Other B-complex vitaminsMost patients with deficiency of thiamine will also have reduced levels of other B vitamins including niacin, pyridoxine, and cobalamin that require replenishment. For patients admitted to the intensive care unit with symptoms that may mimic or mask Wernicke encephalopathy, based on the published literature, routine supplementation during the 1st day of admission includes 200–500 mg intravenous thiamine every 8 h, 64 mg/kg magnesium sulfate (≈4–5 g for most adult patients), and 400–1000 μg intravenous folate.[50] If alcoholic ketoacidosis is suspected, dextrose-containing fluids are recommended over normal saline.[50] Precautions to be Taken When Administering Parenteral Thiamine It is recommended to monitor for anaphylaxis and has appropriate facilities for resuscitation and for treating anaphylaxis readily available including adrenaline and corticosteroids. Anaphylaxis has been reported at the rate of approximately 4/1 million pairs of ampoules of Pabrinex (a pair of high potency vitamins available in the UK containing 500 mg of thiamine (1:250,000 I/V administrations).[40] Intramuscular thiamine is reported to have a lower incidence of anaphylactic reactions than intravenous administration.[40] The reaction has been attributed to nonspecific histamine release.[51] Administer intravenous thiamine slowly, preferably by slow infusion in 100 ml normal saline over 15–30 min.

Conclusions Risk factors for thiamine deficiency should be assessed in chronic alcohol users. A high index of suspicion and a lower threshold to diagnose thiamine deficiency states including Wernicke encephalopathy is needed. Several other presentations such as cerebellar syndrome, MBS, polyneuropathy, and delirium tremens could be related to thiamine deficiency and should be treated with protocols similar to Wernicke encephalopathy.

High-dose thiamine is recommended for the treatment of suspected Wernicke encephalopathy and related conditions [Figure 1]. However, evidence in terms of randomized controlled trials is lacking, and the recommendations are based on small studies and anecdotal reports. Nevertheless, as all these conditions respond to thiamine supplementation, it is possible that these have overlapping pathophysiology and are better considered as Wernicke encephalopathy spectrum disorders.Figure 1.

Thiamine recommendations for patients with alcohol use disorder. AHistory of alcohol use, but no clinical features of WE. BNo clinical features of WE, but with risk factors such as complicated withdrawal (delirium, seizures).

CClinical features of WE (ataxia, opthalmoplegia, global confusion)Click here to viewFinancial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Frank LL. Thiamin in clinical practice.

JPEN J Parenter Enteral Nutr 2015;39:503-20. 2.Thomson AD, Marshall EJ. The natural history and pathophysiology of Wernicke's Encephalopathy and Korsakoff's Psychosis.

Alcohol Alcohol 2006;41:151-8. 3.Thomson AD, Guerrini I, Marshall EJ. Wernicke's encephalopathy.

Role of thiamine. Pract Gastroenterol 2009;33:21-30. 4.Isenberg-Grzeda E, Kutner HE, Nicolson SE.

Wernicke-Korsakoff-syndrome. Under-recognized and under-treated. Psychosomatics 2012;53:507-16.

5.Wood B, Currie J, Breen K. Wernicke's encephalopathy in a metropolitan hospital. A prospective study of incidence, characteristics and outcome.

Med J Aust 1986;144:12-6. 6.Thomson AD, Cook CC, Touquet R, Henry JA, Royal College of Physicians, London. The Royal College of Physicians report on alcohol.

Guidelines for managing Wernicke's encephalopathy in the accident and Emergency Department. Alcohol Alcohol 2002;37:513-21. 7.Harper C.

Thiamine (vitamin B1) deficiency and associated brain damage is still common throughout the world and prevention is simple and safe!. Eur J Neurol 2006;13:1078-82. 8.Harper CG, Giles M, Finlay-Jones R.

Clinical signs in the Wernicke-Korsakoff complex. A retrospective analysis of 131 cases diagnosed at necropsy. J Neurol Neurosurg Psychiatry 1986;49:341-5.

9.Cook CC. Prevention and treatment of Wernicke-Korsakoff syndrome. Alcohol Alcohol 2000;35:19-20.

10.Caine D, Halliday GM, Kril JJ, Harper CG. Operational criteria for the classification of chronic alcoholics. Identification of Wernicke's encephalopathy.

J Neurol Neurosurg Psychiatry 1997;62:51-60. 11.Sullivan EV, Pfefferbaum A. Neuroimaging of the Wernicke-Korsakoff syndrome.

Alcohol Alcohol 2009;44:155-65. 12.Jung YC, Chanraud S, Sullivan EV. Neuroimaging of Wernicke's encephalopathy and Korsakoff's syndrome.

Neuropsychol Rev 2012;22:170-80. 13.Pruckner N, Baumgartner J, Hinterbuchinger B, Glahn A, Vyssoki S, Vyssoki B. Thiamine substitution in alcohol use disorder.

A narrative review of medical guidelines. Eur Addict Res 2019;25:103-10. 14.Day E, Bentham PW, Callaghan R, Kuruvilla T, George S.

Thiamine for prevention and treatment of Wernicke-Korsakoff Syndrome in people who abuse alcohol. Cochrane Database Syst Rev 2013;7:CD004033. Doi.

10.1002/14651858.CD004033.pub3. 15.Arts NJ, Walvoort SJ, Kessels RP. Korsakoff's syndrome.

A critical review. Neuropsychiatr Dis Treat 2017;13:2875-90. 16.Laureno R.

Nutritional cerebellar degeneration, with comments on its relationship to Wernicke disease and alcoholism. Handb Clin Neurol 2012;103:175-87. 17.Maschke M, Weber J, Bonnet U, Dimitrova A, Bohrenkämper J, Sturm S, et al.

Vermal atrophy of alcoholics correlate with serum thiamine levels but not with dentate iron concentrations as estimated by MRI. J Neurol 2005;252:704-11. 18.Mulholland PJ, Self RL, Stepanyan TD, Little HJ, Littleton JM, Prendergast MA.

Thiamine deficiency in the pathogenesis of chronic ethanol-associated cerebellar damage in vitro. Neuroscience 2005;135:1129-39. 19.Del Brutto OH, Mera RM, Sullivan LJ, Zambrano M, King NR.

Population-based study of alcoholic cerebellar degeneration. The Atahualpa Project. J Neurol Sci 2016;367:356-60.

20.Hammoud N, Jimenez-Shahed J. Chronic neurologic effects of alcohol. Clin Liver Dis 2019;23:141-55.

21.Lee JH, Heo SH, Chang DI. Early-stage alcoholic cerebellar degeneration. Diagnostic imaging clues.

J Korean Med Sci 2015;30:1539. 22.Phillips SC, Harper CG, Kril JJ. The contribution of Wernicke's encephalopathy to alcohol-related cerebellar damage.

Drug Alcohol Rev 1990;9:53-60. 23.Baker KG, Harding AJ, Halliday GM, Kril JJ, Harper CG. Neuronal loss in functional zones of the cerebellum of chronic alcoholics with and without Wernicke's encephalopathy.

Neuroscience 1999;91:429-38. 24.Graham JR, Woodhouse D, Read FH. Massive thiamine dosage in an alcoholic with cerebellar cortical degeneration.

Lancet 1971;2:107. 25.Julian T, Glascow N, Syeed R, Zis P. Alcohol-related peripheral neuropathy.

A systematic review and meta-analysis. J Neurol 2018;22:1-3. 26.Chopra K, Tiwari V.

Alcoholic neuropathy. Possible mechanisms and future treatment possibilities. Br J Clin Pharmacol 2012;73:348-62.

27.Woelk H, Lehrl S, Bitsch R, Köpcke W. Benfotiamine in treatment of alcoholic polyneuropathy. An 8-week randomized controlled study (BAP I Study).

Alcohol Alcohol 1998;33:631-8. 28.Peters TJ, Kotowicz J, Nyka W, Kozubski W, Kuznetsov V, Vanderbist F, et al. Treatment of alcoholic polyneuropathy with vitamin B complex.

A randomised controlled trial. Alcohol Alcohol 2006;41:636-42. 29.Fernandes LM, Bezerra FR, Monteiro MC, Silva ML, de Oliveira FR, Lima RR, et al.

Thiamine deficiency, oxidative metabolic pathways and ethanol-induced neurotoxicity. How poor nutrition contributes to the alcoholic syndrome, as Marchiafava-Bignami disease. Eur J Clin Nutr 2017;71:580-6.

30.Hillbom M, Saloheimo P, Fujioka S, Wszolek ZK, Juvela S, Leone MA. Diagnosis and management of Marchiafava-Bignami disease. A review of CT/MRI confirmed cases.

J Neurol Neurosurg Psychiatry 2014;85:168-73. 31.Nemlekar SS, Mehta RY, Dave KR, Shah ND. Marchiafava.

Bignami disease treated with parenteral thiamine. Indian J Psychol Med 2016;38:147-9. [Full text] 32.Brin M.

Erythrocyte transketolase in early thiamine deficiency. Ann N Y Acad Sci 1962;98:528-41. 33.Dreyfus PM.

Clinical application of blood transketolase determinations. N Engl J Med 1962;267:596-8. 34.Edwards KA, Tu-Maung N, Cheng K, Wang B, Baeumner AJ, Kraft CE.

Thiamine assays – Advances, challenges, and caveats. ChemistryOpen 2017;6:178-91. 35.Chandrakumar A, Bhardwaj A, 't Jong GW.

Review of thiamine deficiency disorders. Wernicke encephalopathy and Korsakoff psychosis. J Basic Clin Physiol Pharmacol 2018;30:153-62.

36.Torruellas C, French SW, Medici V. Diagnosis of alcoholic liver disease. World J Gastroenterol 2014;20:11684-99.

37.Thomson AD, Leevy CM. Observations on the mechanism of thiamine hydrochloride absorption in man. Clin Sci 1972;43:153-63.

38.Hoyumpa AM Jr., Strickland R, Sheehan JJ, Yarborough G, Nichols S. Dual system of intestinal thiamine transport in humans. J Lab Clin Med 1982;99:701-8.

39.Smithline HA, Donnino M, Greenblatt DJ. Pharmacokinetics of high-dose oral thiamine hydrochloride in healthy subjects. BMC Clin Pharmacol 2012;12:4.

40.Latt N, Dore G. Thiamine in the treatment of Wernicke encephalopathy in patients with alcohol use disorders. Intern Med J 2014;44:911-5.

41.Raj V, Ojha S, Howarth FC, Belur PD, Subramanya SB. Therapeutic potential of benfotiamine and its molecular targets. Eur Rev Med Pharmacol Sci 2018;22:3261-73.

42.Xie F, Cheng Z, Li S, Liu X, Guo X, Yu P, et al. Pharmacokinetic study of benfotiamine and the bioavailability assessment compared to thiamine hydrochloride. J Clin Pharmacol 2014;54:688-95.

43.Cook CC, Hallwood PM, Thomson AD. B Vitamin deficiency and neuropsychiatric syndromes in alcohol misuse. Alcohol Alcohol 1998;33:317-36.

44.Lingford-Hughes AR, Welch S, Peters L, Nutt DJ, British Association for Psychopharmacology, Expert Reviewers Group. BAP updated guidelines. Evidence-based guidelines for the pharmacological management of substance abuse, harmful use, addiction and comorbidity.

Recommendations from BAP. J Psychopharmacol 2012;26:899-952. 45.Manzardo AM, He J, Poje A, Penick EC, Campbell J, Butler MG.

Double-blind, randomized placebo-controlled clinical trial of benfotiamine for severe alcohol dependence. Drug Alcohol Depend 2013;133:562-70. 46.Manzardo AM, Pendleton T, Poje A, Penick EC, Butler MG.

Change in psychiatric symptomatology after benfotiamine treatment in males is related to lifetime alcoholism severity. Drug Alcohol Depend 2015;152:257-63. 47.Dingwall KM, Delima JF, Gent D, Batey RG.

Hypomagnesaemia and its potential impact on thiamine utilisation in patients with alcohol misuse at the Alice Springs Hospital. Drug Alcohol Rev 2015;34:323-8. 48.Flink EB.

Magnesium deficiency in alcoholism. Alcohol Clin Exp Res 1986;10:590-4. 49.Grochowski C, Blicharska E, Baj J, Mierzwińska A, Brzozowska K, Forma A, et al.

Serum iron, magnesium, copper, and manganese levels in alcoholism. A systematic review. Molecules 2019;24:E1361.

50.Flannery AH, Adkins DA, Cook AM. Unpeeling the evidence for the banana bag. Evidence-based recommendations for the management of alcohol-associated vitamin and electrolyte deficiencies in the ICU.

Crit Care Med 2016;44:1545-52. 51.Lagunoff D, Martin TW, Read G. Agents that release histamine from mast cells.

Annu Rev Pharmacol Toxicol 1983;23:331-51. Correspondence Address:Samir Kumar PraharajDepartment of Psychiatry, Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal, Karnataka IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_440_20 Figures [Figure 1].