Beriberi
Thiamine Deficiency
Transketolase
Cardiomyopathy, Alcoholic
Fursultiamin
Shoshin beriberi with vasospastic angina pectoris possible mechanism of mid-ventricular obstruction: possible mechanism of mid-ventricular obstruction. (1/26)
A 73-year-old heavy drinker was admitted to hospital in a state of shock. He had been suffering from frequent angina at rest, causing him to drink more heavily in an effort to overcome his anginal chest pain. He had been drinking hard each day and had not eaten for 4 weeks. His hemodynamic state on admission showed high-output heart failure. Echocardiography revealed hyperkinesis of the left ventricle and mid-ventricular obstruction with peak intraventricular gradients of 30 mmHg. Although no improvement was seen despite administering the maximal dose in catecholamine therapy, his condition improved rapidly after vitamin B(1) was administered. Cardiac catheterization revealed mid-ventricular obstruction with an apical aneurysm. Coronary artery spasm was induced by injecting acetylcholine in the distal site of the left anterior descending artery, which perfused the area of the apical aneurysm. In the present case, both left ventricular hyperkinesis caused by shoshin beriberi and apical myocardial infarction caused by frequent coronary spasms produced mid-ventricular obstruction with an apical aneurysm. (+info)Outbreak of beriberi among illegal mainland Chinese immigrants at a detention center in Taiwan. (2/26)
OBJECTIVE: The authors describe an outbreak of beriberi in a detention center in Taiwan and examine risk factors for illness. METHODS: A survey was conducted among a sample of 176 randomly selected detainees. A menu-assisted dietary recall method was used to obtain diet information from nine hospitalized detainees. A probable case patient was defined as an individual who had at least two of the following characteristics: leg edema, weakness of the extremities, poor appetite, and dyspnea. Possible case patients were those who had only one of these characteristics. RESULTS: Of the 176 survey respondents, 19% were classified as probable case patients and 40% as possible case patients. The mortality rate based on probable cases was 1.1%. Body Mass Index (BMI) was negatively associated with illness (p < 0.0001), and length of stay in the detention center was independently positively associated with illness (p < 0.05). The average intake of dietary thiamine among the nine hospitalized case patients who completed three-day dietary recall surveys was 0.49 +/- 0.1 mg/day. After thiamine administration, all symptoms and signs of beriberi resolved. CONCLUSION: This outbreak is a reminder of the importance of ensuring adequate diets for poor, institutionalized, or refugee populations who are unable to supplement their diets. (+info)Gene-environment interactions in wet beriberi: effects of thiamine depletion in CD36-defect rats. (3/26)
Selective vulnerability to thiamine deficiency is known to occur between individuals and within different tissues. However, no comprehensive explanation for this has been found, and there are no reports that reproduce the cardiovascular manifestations of human wet beriberi in animals. We hypothesized that the distinction of substrate reliance, namely, the primary dependency on glucose as substrate, could be an underlying factor in the selective vulnerability of thiamine deficiency. In the setting of impaired fatty acid entry, which occurs in CD36-defect rats, substrate reliance shifts from fatty acid to glucose, which would be expected to lead to a susceptibility to thiamine deficiency. Genomic DNA was analyzed for CD36 defects in three cognate strains of rats [spontaneously hypertensive rats (SHR)/NCrj, SHR/Izm, and Wistar-Kyoto (WKY)/NCrj], which identified the presence of a CD36 defect in SHR/NCrj rats but not in SHR/Izm and WKY/NCrj rats. Treatment with 2 wk of thiamine-depleted chow on 4-wk-old rats of each of these strains resulted in increased body and lung weight in the SHR/NCrj rats but not in the SHR/Izm and WKY/NCrj rats. The increased lung weight in the SHR/NCrj rats was accompanied with histological changes of congestive vasculopathy, which were not observed in either the SHR/Izm or the WKY/NCrj rats. Thiamine-deficient 12-wk-old SHR/NCrj rats demonstrated increased body weight (305.6 +/- 6.2 g in thiamine-deficient rats vs. 280.8 +/- 9.1 g in control; P < 0.0001), lactic acidemia (pH, 7.322 +/- 0.026 in thiamine-deficient rats vs. 7.443 +/- 0.016 in control; P < 0.0001; lactate, 2.42 +/- 0.28 mM in thiamine-deficient rats vs. 1.20 +/- 0.11 mM in control; P < 0.0001) and reduced systemic vascular resistance (4.61 +/- 0.42 x 104 dyn.s.cm-5 in thiamine-deficient rats vs. 6.55 +/- 1.36 x 104 dyn.s.cm-5 in control; P < 0.0001) with high cardiac output (186.0 +/- 24.7 ml in thiamine-deficient rats vs. 135.4 +/- 27.2 ml in control; P < 0.0019). In conclusion, SHR/NCrj rats harboring a genetic defect of long-chain fatty acid uptake present the relevant clinical cardiovascular signs of human wet beriberi, strongly indicating a close gene-environment interaction in wet beriberi. (+info)Cardiovascular complications of parenteral nutrition. (4/26)
During a 3 year period, 1987-1989, we encountered three major complications associated with parenteral nutrition leading to congestive cardiac failure--acute beriberi, right atrial and superior vena caval thrombosis, and fungal endocarditis. Unrecognized, these are invariably fatal. Persistent vomiting from intestinal obstruction led to the development of thiamine deficiency in the patient with beriberi. Recurrent catheter tip sepsis probably accounted for thrombosis and endocarditis in the second and third cases, respectively. These conditions are preventable with careful attention to nutritional replenishment and aseptic technique. In patients with catheter-related sepsis early, repeated blood culture is of diagnostic value. Patients with Staphylococcus aureus catheter-associated bacteraemia require at least 4 weeks of appropriate antibiotic therapy. Recurrent sepsis, especially when associated with pulmonary embolic phenomena, is an indication for echocardiography. (+info)ST-segment elevation of electrocardiogram in a patient with Shoshin beriberi. (5/26)
We report a case of a 58-year-old man with Shoshin beriberi who demonstrated ST-segment elevation and myocardial damage without coronary artery stenosis. The patient subsequently recovered with thiamine treatment. We conclude that it is important to consider Shoshin beriberi as part of the differential diagnosis in patients with shock and ST-segment elevation. (+info)Histopathological changes of biopsied myocardium in Shoshin beriberi. (6/26)
Cardiovascular beriberi is caused by thiamine deficiency and usually arises for one of two reasons: alcoholism or diet. Shoshin beriberi is a fulminant form of cardiac beriberi. We investigated the histopathological features of biopsied myocardial tissue samples from two patients with Shoshin beriberi (one patient with nonalcoholic beriberi and another patient with alcoholic beriberi). Interstitial fibrosis and a variation in size of the myocardial fibers were the main findings in the sample from these patients after thiamine treatment. These findings are persistent histopathological features in the myocardium of patients with Shoshin beriberi after thiamine treatment. (+info)Lactate in a laubenpieper. (7/26)
Acid-base disorders seldom kill; however, the mechanisms and associated complications certainly do. We recently encountered a patient with a mysterious lactic acidosis. The patient proved to be a most capable teacher of important lessons. (+info)Thiamin deficiency and uncomplicated falciparum malaria in Laos. (8/26)
OBJECTIVE: Thiamin deficiency complicates severe Plasmodium falciparum malaria in Thailand and may contribute to acidosis. We therefore estimated the frequency of biochemical thiamin deficiency in patients presenting with uncomplicated falciparum malaria in southern Laos. METHODS: Red cell transketolase activation coefficients (alpha) were measured in 310 patients presenting with uncomplicated falciparum malaria and 42 days after starting treatment. RESULTS: Twelve per cent of patients had biochemical evidence of severe deficiency (alpha values >1.31) at presentation, declining to 3% 42 days later. CONCLUSION: Thiamin deficiency was common in Lao patients admitted with uncomplicated P. falciparum infection and was reduced following treatment of malaria and multivitamin supplementation. The role of this preventable and treatable disorder in malaria and other acute infections, and the incidence of beriberi in rural Laos, needs further investigation. (+info)Beriberi is a medical condition caused by a deficiency in thiamine (vitamin B1). This deficiency can lead to various symptoms, including peripheral neuropathy, muscle wasting, and heart failure. There are two main types of beriberi: wet beriberi, which affects the cardiovascular system, and dry beriberi, which primarily affects the nervous system.
Wet beriberi can cause symptoms such as shortness of breath, rapid heart rate, and fluid accumulation in the legs and lungs. Dry beriberi, on the other hand, is characterized by symptoms such as numbness, tingling, and weakness in the hands and feet, muscle wasting, and difficulty walking.
Beriberi can be prevented through a balanced diet that includes adequate amounts of thiamine-rich foods, such as whole grains, legumes, pork, beef, and fortified cereals. Treatment for beriberi typically involves administering thiamine supplements to restore normal levels of the vitamin in the body. In severe cases, hospitalization may be necessary to provide supportive care and monitor the patient's condition.
Thiamine deficiency, also known as beriberi, is a condition that results from inadequate intake or impaired absorption of thiamine (vitamin B1), which is essential for energy metabolism and nerve function. This deficiency can lead to various symptoms such as peripheral neuropathy, muscle weakness, heart failure, and in severe cases, Wernicke-Korsakoff syndrome, a neurological disorder associated with alcoholism. Thiamine deficiency is commonly found in populations with poor nutrition, alcohol dependence, and gastrointestinal disorders affecting nutrient absorption.
Thiamine, also known as vitamin B1, is a water-soluble vitamin that plays a crucial role in certain metabolic reactions, particularly in the conversion of carbohydrates into energy in the body. It is essential for the proper functioning of the heart, nerves, and digestive system. Thiamine acts as a cofactor for enzymes involved in the synthesis of neurotransmitters and the metabolism of carbohydrates, lipids, and proteins. Deficiency in thiamine can lead to serious health complications, such as beriberi (a disease characterized by peripheral neuropathy, muscle wasting, and heart failure) and Wernicke-Korsakoff syndrome (a neurological disorder often seen in alcoholics due to chronic thiamine deficiency). Thiamine is found in various foods, including whole grains, legumes, pork, beef, and fortified foods.
Transketolase is an enzyme found in most organisms, from bacteria to humans. It plays a crucial role in the pentose phosphate pathway (PPP), which is a metabolic pathway that runs alongside glycolysis in the cell cytoplasm. The PPP provides an alternative way of generating energy and also serves to provide building blocks for new cellular components, particularly nucleotides.
Transketolase functions by catalyzing the transfer of a two-carbon ketol group from a ketose (a sugar containing a ketone functional group) to an aldose (a sugar containing an aldehyde functional group). This reaction forms a new ketose and an aldose, effectively converting three-carbon sugars into five-carbon sugars, or vice versa.
In humans, transketolase is essential for the production of NADPH, an important reducing agent in the cell, and for the synthesis of certain amino acids and nucleotides. Deficiencies in this enzyme can lead to metabolic disorders such as pentosuria.
Alcoholic cardiomyopathy is a type of cardiomyopathy (a disease of the heart muscle) that is caused by excessive alcohol consumption. The condition is characterized by the progressive weakening and enlargement of the heart muscle, which can lead to heart failure. Over time, alcoholic cardiomyopathy can cause the heart to become weakened and unable to pump blood efficiently throughout the body. This can result in symptoms such as shortness of breath, fatigue, irregular heartbeat, and fluid retention.
The exact mechanism by which alcohol causes cardiomyopathy is not fully understood, but it is thought to involve a combination of factors, including direct toxic effects of alcohol on the heart muscle, nutritional deficiencies, and genetic predisposition. Treatment for alcoholic cardiomyopathy typically involves lifestyle changes such as abstaining from alcohol, as well as medications to manage symptoms and improve heart function. In severe cases, hospitalization or surgery may be necessary.
I'm sorry for any confusion, but "Fursultiamin" is not a recognized term in medicine or pharmacology. It seems there might be a spelling mistake or a misunderstanding of the name. If you meant "Fursultiamine," it is a medication that contains a combination of thiamine (vitamin B1) and furmaric acid. It is used to treat alcoholism and symptoms related to vitamin B1 deficiency, such as beriberi or Wernicke-Korsakoff syndrome. However, I must emphasize that the use of any medication should be under the guidance and supervision of a healthcare professional.
I'm sorry for any confusion, but "Laos" is not a medical term. It is the name of a country, the Lao People's Democratic Republic, located in Southeast Asia. If you have any questions about medical terms or health-related topics, I'd be happy to try and help answer them!