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» Home » CAD » Endocrinology » Metabolic Disorders » Beriberi (Thiamine Deficiency)
Background
Many years ago, vitamin B1 thiamine was the first vitamin to be discovered. Through the decarboxylation of alpha-ketoacids and long-chain amino acid residues, it serves as a catalyst for the production of energy. ThPP (Thiamine pyrophosphate), which it takes the form of, also serves as a coenzyme for transketolase processes.
Additionally, thiamine participates in maintaining the medullary sheath as well as an undetermined involvement in the transmission of nerve signals. Despite the fact that milled paddy and cereals only contain trace levels of thiamine due to the removal of thiamine during processing, thiamine is present in nuts, pork, meat, whole grains, legumes, and cattle.
Additionally, several foods include thiaminases, which are enzymes that degrade thiamine, including coffee, tea, shellfish, and uncooked fish. Dry beriberi, wet beriberi, and WKS (Wernicke-Korsakoff condition) are all common manifestations of thiamine deficit, which can also have an impact on the immune, neurological, and cardiovascular systems.
It is most frequently reported in areas where finished grains and processed cereals are the main sources of diet, as well as in those who suffer from severe alcohol dependence. In contrast to wet beriberi, which manifests as high-output cardiac failure, dry beriberi first appears as symmetric peripheral neuropathy. CNS abnormalities such as impaired mental state, aberrant ocular development, and gait problems might appear in WKS patients.
Epidemiology
Thiamine insufficiency is mostly brought on by insufficient food intake worldwide, particularly in diets high in refined wheat and refined rice. It typically manifests in individuals who are chronically ill or drinking in Western nations.
Special categories of people are also at risk for thiamine deficiency, including pregnant women, those who need parental care, those who have had gastric bypass, those with generally low nutrition, and inpatients’ continuous diuretic medication since it increases urine losses.
This page will not directly cover juvenile beriberi, which can result from this vitamin deficit in women.
Anatomy
Pathophysiology
Symptoms begin to emerge after thiamine levels become exhausted, which takes place approximately four weeks after use has stopped. The CNS is affected when there is dry beriberi. Usually, poor ingestion is the cause of this illness. Reflexes are among the neurological symptoms, as are symmetrical sensory and motor impairments in the extremity.
Myelin loss occurs without any immediate inflammation. Wernicke encephalopathy is a different type of dry beriberi. This disorder manifests in clearly defined steps beginning with vomiting and nausea and then moving on to fever, horizontal nystagmus, progressively worsening mental disability, ataxia, and ocular palsy leading directly to the Korsakoff syndrome.
Only patients who have not had the Korsakoff syndrome can improve. Less than half of patients significantly improve after therapy. When the cardiac system is affected, wet beriberi is evident. Fluid retention and edema result from the heart’s dysfunction.
Injury from overuse is the main cause of cardiac dysfunction. Without medication, wet beriberi is a life-threatening emergency that can cause death within weeks. Thiamine can aid with recovery gradually, although the majority of patients need intensive care unit (ICU)-style supportive care.
Etiology
Thiamine deficiency may be linked to:
A poor diet
Inadequate absorption
Greater loss
Increased use of thiamine
Medications that may cause thiamine insufficiency
Genetics
Prognostic Factors
Thiamine insufficiency is easily curable, and most indications and symptoms of the deficit completely disappear with thiamine supplementation. Therefore, the prognosis for individuals with the condition is often positive. After starting medication, wet beriberi-related heart dysfunction should start to improve within 24hrs.
The symptoms of dry beriberi may become better or go away. Unfortunately, the patient may only somewhat improve after early treatment if the deficiency has developed into Korsakoff disease, as well as the remaining signs may be permanent.
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
5-30 mg intramuscularly thrice daily if critical
Later, continue 5-30 mg thrice daily for a month
Duration depends on ongoing symptoms
10-25 mg intramuscularly or intravenously each day or 10-50 mg per dose orally each day for a minimum of 2 weeks
Later, 5-10 mg/day orally for a month
Duration of treatment depends on symptoms
Future Trends
References
https://www.ncbi.nlm.nih.gov/books/NBK537204/
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» Home » CAD » Endocrinology » Metabolic Disorders » Beriberi (Thiamine Deficiency)
Many years ago, vitamin B1 thiamine was the first vitamin to be discovered. Through the decarboxylation of alpha-ketoacids and long-chain amino acid residues, it serves as a catalyst for the production of energy. ThPP (Thiamine pyrophosphate), which it takes the form of, also serves as a coenzyme for transketolase processes.
Additionally, thiamine participates in maintaining the medullary sheath as well as an undetermined involvement in the transmission of nerve signals. Despite the fact that milled paddy and cereals only contain trace levels of thiamine due to the removal of thiamine during processing, thiamine is present in nuts, pork, meat, whole grains, legumes, and cattle.
Additionally, several foods include thiaminases, which are enzymes that degrade thiamine, including coffee, tea, shellfish, and uncooked fish. Dry beriberi, wet beriberi, and WKS (Wernicke-Korsakoff condition) are all common manifestations of thiamine deficit, which can also have an impact on the immune, neurological, and cardiovascular systems.
It is most frequently reported in areas where finished grains and processed cereals are the main sources of diet, as well as in those who suffer from severe alcohol dependence. In contrast to wet beriberi, which manifests as high-output cardiac failure, dry beriberi first appears as symmetric peripheral neuropathy. CNS abnormalities such as impaired mental state, aberrant ocular development, and gait problems might appear in WKS patients.
Thiamine insufficiency is mostly brought on by insufficient food intake worldwide, particularly in diets high in refined wheat and refined rice. It typically manifests in individuals who are chronically ill or drinking in Western nations.
Special categories of people are also at risk for thiamine deficiency, including pregnant women, those who need parental care, those who have had gastric bypass, those with generally low nutrition, and inpatients’ continuous diuretic medication since it increases urine losses.
This page will not directly cover juvenile beriberi, which can result from this vitamin deficit in women.
Symptoms begin to emerge after thiamine levels become exhausted, which takes place approximately four weeks after use has stopped. The CNS is affected when there is dry beriberi. Usually, poor ingestion is the cause of this illness. Reflexes are among the neurological symptoms, as are symmetrical sensory and motor impairments in the extremity.
Myelin loss occurs without any immediate inflammation. Wernicke encephalopathy is a different type of dry beriberi. This disorder manifests in clearly defined steps beginning with vomiting and nausea and then moving on to fever, horizontal nystagmus, progressively worsening mental disability, ataxia, and ocular palsy leading directly to the Korsakoff syndrome.
Only patients who have not had the Korsakoff syndrome can improve. Less than half of patients significantly improve after therapy. When the cardiac system is affected, wet beriberi is evident. Fluid retention and edema result from the heart’s dysfunction.
Injury from overuse is the main cause of cardiac dysfunction. Without medication, wet beriberi is a life-threatening emergency that can cause death within weeks. Thiamine can aid with recovery gradually, although the majority of patients need intensive care unit (ICU)-style supportive care.
Thiamine deficiency may be linked to:
A poor diet
Inadequate absorption
Greater loss
Increased use of thiamine
Medications that may cause thiamine insufficiency
Thiamine insufficiency is easily curable, and most indications and symptoms of the deficit completely disappear with thiamine supplementation. Therefore, the prognosis for individuals with the condition is often positive. After starting medication, wet beriberi-related heart dysfunction should start to improve within 24hrs.
The symptoms of dry beriberi may become better or go away. Unfortunately, the patient may only somewhat improve after early treatment if the deficiency has developed into Korsakoff disease, as well as the remaining signs may be permanent.
5-30 mg intramuscularly thrice daily if critical
Later, continue 5-30 mg thrice daily for a month
Duration depends on ongoing symptoms
10-25 mg intramuscularly or intravenously each day or 10-50 mg per dose orally each day for a minimum of 2 weeks
Later, 5-10 mg/day orally for a month
Duration of treatment depends on symptoms
https://www.ncbi.nlm.nih.gov/books/NBK537204/
Many years ago, vitamin B1 thiamine was the first vitamin to be discovered. Through the decarboxylation of alpha-ketoacids and long-chain amino acid residues, it serves as a catalyst for the production of energy. ThPP (Thiamine pyrophosphate), which it takes the form of, also serves as a coenzyme for transketolase processes.
Additionally, thiamine participates in maintaining the medullary sheath as well as an undetermined involvement in the transmission of nerve signals. Despite the fact that milled paddy and cereals only contain trace levels of thiamine due to the removal of thiamine during processing, thiamine is present in nuts, pork, meat, whole grains, legumes, and cattle.
Additionally, several foods include thiaminases, which are enzymes that degrade thiamine, including coffee, tea, shellfish, and uncooked fish. Dry beriberi, wet beriberi, and WKS (Wernicke-Korsakoff condition) are all common manifestations of thiamine deficit, which can also have an impact on the immune, neurological, and cardiovascular systems.
It is most frequently reported in areas where finished grains and processed cereals are the main sources of diet, as well as in those who suffer from severe alcohol dependence. In contrast to wet beriberi, which manifests as high-output cardiac failure, dry beriberi first appears as symmetric peripheral neuropathy. CNS abnormalities such as impaired mental state, aberrant ocular development, and gait problems might appear in WKS patients.
Thiamine insufficiency is mostly brought on by insufficient food intake worldwide, particularly in diets high in refined wheat and refined rice. It typically manifests in individuals who are chronically ill or drinking in Western nations.
Special categories of people are also at risk for thiamine deficiency, including pregnant women, those who need parental care, those who have had gastric bypass, those with generally low nutrition, and inpatients’ continuous diuretic medication since it increases urine losses.
This page will not directly cover juvenile beriberi, which can result from this vitamin deficit in women.
Symptoms begin to emerge after thiamine levels become exhausted, which takes place approximately four weeks after use has stopped. The CNS is affected when there is dry beriberi. Usually, poor ingestion is the cause of this illness. Reflexes are among the neurological symptoms, as are symmetrical sensory and motor impairments in the extremity.
Myelin loss occurs without any immediate inflammation. Wernicke encephalopathy is a different type of dry beriberi. This disorder manifests in clearly defined steps beginning with vomiting and nausea and then moving on to fever, horizontal nystagmus, progressively worsening mental disability, ataxia, and ocular palsy leading directly to the Korsakoff syndrome.
Only patients who have not had the Korsakoff syndrome can improve. Less than half of patients significantly improve after therapy. When the cardiac system is affected, wet beriberi is evident. Fluid retention and edema result from the heart’s dysfunction.
Injury from overuse is the main cause of cardiac dysfunction. Without medication, wet beriberi is a life-threatening emergency that can cause death within weeks. Thiamine can aid with recovery gradually, although the majority of patients need intensive care unit (ICU)-style supportive care.
Thiamine deficiency may be linked to:
A poor diet
Inadequate absorption
Greater loss
Increased use of thiamine
Medications that may cause thiamine insufficiency
Thiamine insufficiency is easily curable, and most indications and symptoms of the deficit completely disappear with thiamine supplementation. Therefore, the prognosis for individuals with the condition is often positive. After starting medication, wet beriberi-related heart dysfunction should start to improve within 24hrs.
The symptoms of dry beriberi may become better or go away. Unfortunately, the patient may only somewhat improve after early treatment if the deficiency has developed into Korsakoff disease, as well as the remaining signs may be permanent.
https://www.ncbi.nlm.nih.gov/books/NBK537204/
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