Thiamine Deficiency
Pyrithiamine
Transketolase
Wernicke Encephalopathy
Beriberi
Korsakoff Syndrome
Thiamine Pyrophosphate
Thiamine Monophosphate
Alcohol Amnestic Disorder
Diencephalon
Ketoglutarate Dehydrogenase Complex
Laos
Thiamin Pyrophosphokinase
Antimetabolites
Amnesia
Clinical Enzyme Tests
Polyneuropathies
Thiamine deficiency is prevalent in a selected group of urban Indonesian elderly people. (1/195)
This cross-sectional study involved 204 elderly individuals (93 males and 111 females). Subjects were randomly recruited using a list on which all 60-75 y-old-people living in seven sub-villages in Jakarta were included. The usual food intake was estimated using semiquantitative food frequency questionnaires. Hemoglobin, plasma retinol, vitamin B-12, red blood cell folate and the percentage stimulation of erythrocyte transketolase (ETK), as an indicator of thiamine status, were analyzed. Median energy intake was below the assessed requirement. More than 75% of the subjects had iron and thiamine intakes of approximately 2/3 of the recommended daily intake, and 20.2% of the study population had folate intake of approximately 2/3 of the recommended daily intake. Intakes of vitamins A and B-12 were adequate. Biochemical assessments demonstrated that 36.6% of the subjects had low thiamine levels (ETK stimulation > 25%). The elderly men tended to have lower thiamine levels than the elderly women. The overall prevalence of anemia was 28.9%, and the elderly women were affected more than the elderly men. Low biochemical status of vitamins A, B-12 and RBC folate was found in 5.4%, 8.8 % and 2.9% of the subjects, respectively. Dietary intakes of thiamine and folate were associated with ETK stimulation and plasma vitamin B-12 concentration (r = 0.176, P = 0.012 and r = 0.77, P = 0.001), respectively. Results of this study suggest that anemia, thiamine and possibly vitamin B-12 deficiency are prevalent in the elderly living in Indonesia. Clearly, micronutrient supplementation may be beneficial for the Indonesian elderly population living in underprivileged areas. (+info)Biochemical evidence of thiamin deficiency in young Ghanian children. (2/195)
Detailed biochemical studies for nutritional status were carried out on 146 Ghanaian children ages 6 months to 6 years over a 2-year period. Study children comprised three main groups: severe protein-calorie malnutrition; mild to moderate protein-calorie malnutrition and apparently healthy children. Erythrocyte transketolase activity and the percentage of erythrocyte transketolase pyrophosphate effect were also determined. In the first year of the study elevated percentage of transketolase pyrophosphate effect indicative of thiamin deficiency was found in all three of the above-mentioned groups, with the most widespread deficiency in the normal groups. In year 2, repeat studies of the severely malnourished group after 2 weeks of nutritional therapy with the administration of vitamin capsules, which included thiamin, resulted in the normalization of transketolase pyrophosphate effect. Apoenzyme activity was comparable in all groups studied. There were no obvious clinical signs of thiamin deficiency, although sensory testing was not performed. A relatively large number of children with high percentage of transketolase pyrosphosphate effect also had serum folic acid deficiency. This evidence of widespread biochemical thiamin deficiency is indicative of an at-risk population among young children for clinical thiamin deficiency. Further studies are needed to identify whether the problem is inadequate thiamin intake, destruction of thiamin by thiaminases or food preparation methods, or malabsorption of thiamin. (+info)Thiamin and pyridoxine requirements during intravenous hyperalimentation. (3/195)
Studies were undertaken to determine rational dosages of vitamin B1 and B6 during long-term intravenous hyperalimentation, using more sensitive techniques than formerly used to evaluate B1 and B6 status. A standard vitamin combination, type A, (usually commercially available products) has been used up to now because of convenience, disregarding the effects of long-term administration. This combination lacks biotin, folic acid, and vitamin E and contains from 10 to 100 times the dietary allowances of such vitamins as B1, B2, B6, B12, and C. In response to the possibility of vitamin overdose, two new vitamin combinations, type B (from commercial products) and type C (a convenient and easily administered combination produced at the hospital) were developed in order to provide the normal dietary allowances and at the same time eliminate any harmful side-effects. From the results obtained, 5 mg/day for thiamin HCl and 3 mg/day for pyridoxine HCl in type B and type C were found to be a sufficient and safe level as opposed to 55 mg/day for thiamin HCl and 102 mg/day for pyridoxine HCl in type A. (+info)Is thiamine deficiency in elderly people related to age or co-morbidity? (4/195)
OBJECTIVES: to compare erythrocyte thiamine pyrophosphate concentrations in elderly people with those in healthy younger people; to determine if any differences can be attributed to age or to co-morbidities. DESIGN: cross-sectional and 3-year longitudinal surveys. SETTING: primary care. PATIENTS: 100 volunteer blood donors and 222 elderly people from a general practice register. MEASUREMENTS: thiamine pyrophosphate concentrations using high performance liquid chromatography; physical examination, medical and medication history; grip strength, body mass index and plasma albumin. RESULTS: the mean [95% confidence interval (CI)] thiamine pyrophosphate concentration was 152 nmol/l (147-158) in the elderly group and 224 (213-235) nmol/l in the younger group (P < 0.001). Ninety-six (43.4%) of the elderly subjects had thiamine pyrophosphate concentrations below the fifth percentile of the younger subjects (140 nmol/l). Over 3 years thiamine pyrophosphate concentrations fell in the elderly cohort by 20% (95% CI: 14.5-24.5%; P < 0.01). Thiamine pyrophosphate concentrations in 39 healthy older people were no different from those in elderly people with co-morbidity but were significantly lower than those in the younger people. Elderly people with absent vibration sense in their feet had a lower thiamine pyrophosphate concentration than the rest of the group [129 (117-142)nmol/l compared with 156 (150-162)nmol/l; P < 0.01)]. Thiamine pyrophosphate concentrations were not related to prevalent diseases, common medications, body mass index, grip strength or plasma albumin. CONCLUSION: lower thiamine pyrophosphate concentrations in elderly people appear to be related more to age itself than to co-existent illnesses. (+info)Glucose uptake in the brainstem of thiamine-deficient rats. (5/195)
Acute dietary deficiency of thiamine was produced in immature female rats. Uptake of glucose by brainstem nuclei was determined by autoradiographic examination of tissue concentrations of 14-C-3-O-methyl-d-glucose following a test dose, and compared with levels in normal and isocaloric control animals. The experiment showed that glucose uptake was depressed in the lesions of thiamine deficiency as compared with the controls, that the depression occurred with the occurrence of morphologic evidence of tissue edema, and that the depression was temporally independent of the breakdown of the blood-brain barrier to protein which is found in the late, necrotic lesions. (+info)Metabolic changes in rats during developing thiamin deficiency. (6/195)
Determinations of rectal temperature, blood glucose, plasma free fatty acids, liver acetyl-CoA and carcass fat of thiamin-deficient rats indicated that during the ensuing anorexia they metabolized their fat reserves more rapidly than did pair-fed normal controls. Their lower metabolic rate indicates that the reserves mobilized are utilized inefficiently. (+info)Postgastrectomy polyneuropathy with thiamine deficiency. (7/195)
OBJECTIVE: Polyneuropathy has been reported after gastrectomy performed to treat various lesions. Although thiamine deficiency is a possible cause of this neuropathy, the pathogenesis still remains to be clarified. Seventeen patients with peripheral neuropathy with thiamine deficiency after gastrectomy are described. METHODS: Seventeen patients with polyneuropathy after gastrectomy accompanied by thiamine deficiency were selected. Patients were restricted to those with total or subtotal gastric resection to treat ulcer or neoplasm. Patients who had undergone operations to treat morbid obesity were excluded. RESULTS: Intervals between the operation and onset of neuropathy varied from 2 months to 39 years. Most patients did not seem malnourished. Serum concentrations of B vitamins other than thiamine were nearly normal. Symmetric motor-sensory polyneuropathy, predominantly involving the lower limbs, had progressed over intervals varying from 3 days to 8 years. Relative degrees of motor and sensory impairment also varied extensively. Some cases that progressed rapidly mimicked Guillain-Barre syndrome. Electrophysiological and pathological findings were those of axonal neuropathy. Substantial functional recovery from polyneuropathy was seen in most patients by 3 to 6 months after initiating thiamine supplementation. Motor recovery was better than sensory recovery. CONCLUSIONS: Various symptoms were seen in patients with postgastrectomy neuropathy. Thiamine deficiency should be considered in the differential diagnosis of motor-sensory polyneuropathy after gastrectomy. (+info)Thiamine deficiency in patients with B-chronic lymphocytic leukaemia: a pilot study. (8/195)
Malignancy associated primary thiamine deficiency has been documented in several experimental tumours, sporadic clinical case reports, and in a number of patients with fast growing haematological malignancies. Thiamine status was assessed prospectively in 14 untreated B-chronic lymphocytic leukaemia (CLL) patients, and in 14 age matched control patients with non-malignant disease. Patients with any known cause of absolute, relative, or functional thiamine deficiency were excluded. High (>15%) thiamine pyrophosphate effect (TPPE), indicating thiamine deficiency, was found in five out of 14 CLL patients (35.7%) and in none of the controls (p=0.057). Mean (SD) TPPE in the thiamine deficient patients group was 21.6 (3.4)%. In all the patients, thiamine deficiency was subclinical. No correlates for the thiamine deficiency have been found save for an increment of more than 20% in the total leucocyte count over the preceding three months, which was found in all five thiamine deficient patients compared with only one of the nine non-thiamine deficient CLL patients. Thus, CLL patients may be prone to develop primary thiamine deficiency possibly promoted by the increased leucocytes span, which may increase thiamine consumption. Since even subclinical thiamine deficiency may be detrimental to the patient's clinical course, and in view of the theoretical danger of thiamine promoted tumour cell proliferation, further large scale studies are warranted to confirm this observation, and to elucidate the issue of thiamine supplementation to CLL patients. (+info)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.
Pyrithiamine is not typically considered a medical term, but it is a chemical compound that has been used in scientific research. It's an antivitamin, specifically an analog of thiamine (vitamin B1), which means it can interfere with the metabolism of thiamine in the body.
Here's a more specific definition from a biochemical perspective:
Pyrithiamine is a synthetic organic compound with the formula C6H7N2O2S. It is an analog of thiamine, where the aminomethyl group of thiamine is replaced by a pyridine ring. This structural modification makes pyrithiamine unable to act as a vitamin, but it can still interact with the enzymes and transport proteins involved in thiamine metabolism. As a result, pyrithiamine has been used as a tool to study thiamine deficiency and its effects on various organisms, including mammals.
Please note that pyrithiamine is not a term commonly used in clinical medicine or patient care. If you have any concerns about vitamins, nutrition, or health-related topics, it's best to consult a healthcare professional for accurate information and advice tailored to your specific situation.
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.
Wernicke Encephalopathy is a neuropsychiatric disorder that is caused by a deficiency of thiamine (vitamin B1). It is characterized by a classic triad of symptoms: confusion, oculomotor dysfunction (such as nystagmus and ophthalmoplegia), and gait ataxia. Other symptoms can include memory loss, apathy, and hypothermia.
Wernicke Encephalopathy is most commonly seen in alcoholics due to poor nutrition, but it can also occur in people with conditions that cause malabsorption or increased thiamine requirements, such as AIDS, cancer, and chronic diarrhea. Immediate treatment with thiamine replacement therapy is necessary to prevent progression of the disease and potential permanent neurological damage. If left untreated, Wernicke Encephalopathy can lead to Korsakoff's syndrome, a chronic memory disorder.
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.
Korsakoff syndrome is a neuropsychiatric disorder typically caused by alcohol abuse, specifically thiamine (vitamin B1) deficiency in the brain. It's often associated with Wernicke encephalopathy, and the two together are referred to as Wernicke-Korsakoff syndrome.
The main features of Korsakoff syndrome include severe memory impairment, particularly anterograde amnesia (inability to form new memories), confabulation (making up stories due to gaps in memory), and a lack of insight into their condition. Other cognitive functions like intelligence and perception are usually preserved.
The syndrome is believed to result from damage to the mammillary bodies and other structures in the diencephalon, particularly the thalamus. Treatment involves abstinence from alcohol, thiamine replacement, and a balanced diet. The prognosis varies but often includes some degree of permanent memory impairment.
Thiamine pyrophosphate (TPP) is the active form of thiamine (vitamin B1) that plays a crucial role as a cofactor in various enzymatic reactions, particularly in carbohydrate metabolism. TPP is essential for the functioning of three key enzymes: pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and transketolase. These enzymes are involved in critical processes such as the conversion of pyruvate to acetyl-CoA, the oxidative decarboxylation of alpha-ketoglutarate in the Krebs cycle, and the pentose phosphate pathway, which is important for generating reducing equivalents (NADPH) and ribose sugars for nucleotide synthesis. A deficiency in thiamine or TPP can lead to severe neurological disorders, including beriberi and Wernicke-Korsakoff syndrome, which are often observed in alcoholics due to poor nutrition and impaired thiamine absorption.
Oxythiamine is not a medication or a condition, but rather a chemical compound. It is an oxidized form of thiamine (vitamin B1), which means it has been changed by the addition of oxygen molecules. Oxythiamine is used in research to study the effects of thiamine deficiency and to investigate the role of thiamine in various biological processes. It is not used as a medication in humans or animals.
Amprolium is an antiprotozoal medication used primarily in veterinary medicine to prevent and treat coccidiosis, which is a parasitic infection caused by protozoa of the Eimeria species. It works as a competitive inhibitor of thiamine (vitamin B1) absorption in the coccidian parasites, leading to their eventual death. Amprolium is available in various formulations, including powders, pellets, and solutions, for use in animals such as chickens, turkeys, and calves. It is not typically used in human medicine.
Thiamine monophosphate (TMP) is a biochemical compound that is a derivative of thiamine (vitamin B1). It is a cofactor for several enzymes involved in key metabolic processes, particularly in the conversion of carbohydrates into energy. TMP plays an essential role in the metabolism of carbohydrates, amino acids, and neurotransmitters.
Thiamine monophosphate is formed when thiamine undergoes phosphorylation by the enzyme thiamine pyrophosphokinase. This reaction adds a phosphate group to the thiamine molecule, resulting in the formation of TMP. Thiamine monophosphate can then be further phosphorylated to form thiamine triphosphate (TTP) or dephosphorylated back to thiamine.
Deficiency in thiamine and its derivatives, including TMP, can lead to several medical conditions, such as beriberi, Wernicke-Korsakoff syndrome, and other neurological disorders. These conditions are often associated with impaired energy metabolism, nerve damage, and cognitive decline. Proper intake of thiamine through diet or supplementation is crucial for maintaining normal physiological functions and preventing these health issues.
Alcohol Amnestic Disorder is not listed as a separate disorder in the current edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), which is used by mental health professionals to diagnose mental conditions. However, it was previously included in earlier editions as a subtype of Amnestic Disorder due to the effects of substance use or exposure to toxins.
Alcohol Amnestic Disorder is characterized by significant memory impairment that is directly caused by alcohol consumption. This disorder can result in anterograde amnesia, which is the inability to form new memories after drinking, and/or retrograde amnesia, which involves forgetting previously learned information or personal experiences.
The diagnosis of Alcohol Amnestic Disorder typically requires a comprehensive medical and neuropsychological evaluation to determine the extent and nature of memory impairment, as well as to rule out other potential causes for cognitive decline. Treatment usually involves a combination of abstinence from alcohol, pharmacotherapy, and psychosocial interventions to address substance use disorder and any co-occurring mental health conditions.
The diencephalon is a term used in anatomy to refer to the part of the brain that lies between the cerebrum and the midbrain. It includes several important structures, such as the thalamus, hypothalamus, epithalamus, and subthalamus.
The thalamus is a major relay station for sensory information, receiving input from all senses except smell and sending it to the appropriate areas of the cerebral cortex. The hypothalamus plays a crucial role in regulating various bodily functions, including hunger, thirst, body temperature, and sleep-wake cycles. It also produces hormones that regulate mood, growth, and development.
The epithalamus contains the pineal gland, which produces melatonin, a hormone that helps regulate sleep-wake cycles. The subthalamus is involved in motor control and coordination.
Overall, the diencephalon plays a critical role in integrating sensory information, regulating autonomic functions, and modulating behavior and emotion.
The Ketoglutarate Dehydrogenase Complex (KGDC or α-KGDH) is a multi-enzyme complex that plays a crucial role in the Krebs cycle, also known as the citric acid cycle. It is located within the mitochondrial matrix of eukaryotic cells and functions to catalyze the oxidative decarboxylation of α-ketoglutarate into succinyl-CoA, thereby connecting the Krebs cycle to the electron transport chain for energy production.
The KGDC is composed of three distinct enzymes:
1. α-Ketoglutarate dehydrogenase (E1): This enzyme catalyzes the decarboxylation and oxidation of α-ketoglutarate to form a thioester intermediate with lipoamide, which is bound to the E2 component.
2. Dihydrolipoyl succinyltransferase (E2): This enzyme facilitates the transfer of the acetyl group from the lipoamide cofactor to CoA, forming succinyl-CoA and regenerating oxidized lipoamide.
3. Dihydrolipoyl dehydrogenase (E3): The final enzyme in the complex catalyzes the reoxidation of reduced lipoamide back to its disulfide form, using FAD as a cofactor and transferring electrons to NAD+, forming NADH.
The KGDC is subject to regulation by several mechanisms, including phosphorylation-dephosphorylation reactions that can inhibit or activate the complex, respectively. Dysfunction of this enzyme complex has been implicated in various diseases, such as neurodegenerative disorders and cancer.
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!
Thiamin pyrophosphokinase (TPK) is an enzyme that plays a crucial role in the metabolism of thiamin, also known as vitamin B1. Thiamin is essential for the body's energy production and nerve function. TPK catalyzes the conversion of thiamin into its active form, thiamin pyrophosphate (TPP), by adding two phosphate groups to thiamin. This reaction is the rate-limiting step in the synthesis of TPP, which serves as a cofactor for several enzymes involved in carbohydrate metabolism, particularly in the process of decarboxylation of alpha-keto acids.
TPK exists in two isoforms: cytoplasmic and mitochondrial. The cytoplasmic form (cTPK) is primarily responsible for maintaining intracellular TPP levels, while the mitochondrial form (mTPK) helps regulate TPP concentrations within the mitochondria. Proper functioning of TPK is vital for overall cellular health and energy production, as well as for preventing neurological disorders associated with thiamin deficiency, such as beriberi and Wernicke-Korsakoff syndrome.
Antimetabolites are a class of drugs that interfere with the normal metabolic processes of cells, particularly those involved in DNA replication and cell division. They are commonly used as chemotherapeutic agents to treat various types of cancer because many cancer cells divide more rapidly than normal cells. Antimetabolites work by mimicking natural substances needed for cell growth and division, such as nucleotides or amino acids, and getting incorporated into the growing cells' DNA or protein structures, which ultimately leads to the termination of cell division and death of the cancer cells. Examples of antimetabolites include methotrexate, 5-fluorouracil, and capecitabine.
Amnesia is a condition characterized by memory loss, which can be temporary or permanent. It may result from brain damage or disease, and it can affect various aspects of memory, such as the ability to recall past events (retrograde amnesia), the ability to form new memories (anterograde amnesia), or both. Amnesia can also affect a person's sense of identity and their ability to learn new skills.
There are several types of amnesia, including:
1. Anterograde amnesia: This type of amnesia affects the ability to form new memories after an injury or trauma. People with anterograde amnesia may have difficulty learning new information and remembering recent events.
2. Retrograde amnesia: Retrograde amnesia affects the ability to recall memories that were formed before an injury or trauma. People with retrograde amnesia may have trouble remembering events, people, or facts from their past.
3. Transient global amnesia: This is a temporary form of amnesia that usually lasts for less than 24 hours. It is often caused by a lack of blood flow to the brain, and it can be triggered by emotional stress, physical exertion, or other factors.
4. Korsakoff's syndrome: This is a type of amnesia that is caused by alcohol abuse and malnutrition. It is characterized by severe memory loss, confusion, and disorientation.
5. Dissociative amnesia: This type of amnesia is caused by psychological factors, such as trauma or stress. People with dissociative amnesia may have trouble remembering important personal information or events that are emotionally charged.
The treatment for amnesia depends on the underlying cause. In some cases, memory may improve over time, while in other cases, it may be permanent. Treatment may involve medication, therapy, or rehabilitation to help people with amnesia cope with their memory loss and develop new skills to compensate for their memory impairments.
Clinical enzyme tests are laboratory tests that measure the amount or activity of certain enzymes in biological samples, such as blood or bodily fluids. These tests are used to help diagnose and monitor various medical conditions, including organ damage, infection, inflammation, and genetic disorders.
Enzymes are proteins that catalyze chemical reactions in the body. Some enzymes are found primarily within specific organs or tissues, so elevated levels of these enzymes in the blood can indicate damage to those organs or tissues. For example, high levels of creatine kinase (CK) may suggest muscle damage, while increased levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) can indicate liver damage.
There are several types of clinical enzyme tests, including:
1. Serum enzyme tests: These measure the level of enzymes in the blood serum, which is the liquid portion of the blood after clotting. Examples include CK, AST, ALT, alkaline phosphatase (ALP), and lactate dehydrogenase (LDH).
2. Urine enzyme tests: These measure the level of enzymes in the urine. An example is N-acetyl-β-D-glucosaminidase (NAG), which can indicate kidney damage.
3. Enzyme immunoassays (EIAs): These use antibodies to detect and quantify specific enzymes or proteins in a sample. They are often used for the diagnosis of infectious diseases, such as HIV or hepatitis.
4. Genetic enzyme tests: These can identify genetic mutations that cause deficiencies in specific enzymes, leading to inherited metabolic disorders like phenylketonuria (PKU) or Gaucher's disease.
It is important to note that the interpretation of clinical enzyme test results should be done by a healthcare professional, taking into account the patient's medical history, symptoms, and other diagnostic tests.
Polyneuropathy is a medical condition that refers to the damage or dysfunction of peripheral nerves (nerves outside the brain and spinal cord) in multiple areas of the body. These nerves are responsible for transmitting sensory, motor, and autonomic signals between the central nervous system and the rest of the body.
In polyneuropathies, this communication is disrupted, leading to various symptoms depending on the type and extent of nerve damage. Commonly reported symptoms include:
1. Numbness or tingling in the hands and feet
2. Muscle weakness and cramps
3. Loss of reflexes
4. Burning or stabbing pain
5. Balance and coordination issues
6. Increased sensitivity to touch
7. Autonomic dysfunction, such as bowel, bladder, or digestive problems, and changes in blood pressure
Polyneuropathies can be caused by various factors, including diabetes, alcohol abuse, nutritional deficiencies, autoimmune disorders, infections, toxins, inherited genetic conditions, or idiopathic (unknown) causes. The treatment for polyneuropathy depends on the underlying cause and may involve managing underlying medical conditions, physical therapy, pain management, and lifestyle modifications.
Thiamine deficiency
Heterocyclic amine
Wernicke encephalopathy
Thiamine
Anaphe venata
Oxidative decarboxylation
Causes of seizures
Feeder fish
Wernicke-Korsakoff syndrome
Ōoku: The Inner Chambers
Russell Morse Wilder
Ophthalmoparesis
M74 syndrome
The great imitator
Dementia
Postpartum psychosis
Ataxia
Sensory ataxia
Thiaminase
Toxic and nutritional optic neuropathy
Long-term effects of alcohol
Thiamine responsive megaloblastic anemia syndrome
Malnutrition in South Africa
Alcohol-related brain damage
Sulbutiamine
Carl Wernicke
Abducens nerve
Cat food
Francisco Xavier de Mendonça Furtado
Furosemide
Thiamine deficiency - Wikipedia
Beriberi (Thiamine Deficiency): Practice Essentials, Pathophysiology, Etiology
Vitamin B1 (Thiamine) Deficiency - StatPearls - NCBI Bookshelf
Beriberi (Thiamine Deficiency) Treatment & Management: Approach Considerations, Activity
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Thiamine deficiency in Cambodian infants with and without beriberi. - Texas A&M University (TAMU) Scholar
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Levels of thiamine6
- Thiamine deficiency is a medical condition of low levels of thiamine (Vitamin B1). (wikipedia.org)
- Diagnosis is based on symptoms, low levels of thiamine in the urine, high blood lactate, and improvement with thiamine supplementation. (wikipedia.org)
- Recently there have been a few recalls that have occurred as a result of pet foods not reaching the required levels of thiamine. (nutritionrvn.com)
- Thiamine is recommended for people with low levels of thiamine, including those with thiamine deficiency syndromes and pregnant women. (webmd.com)
- The Procter & Gamble Co. is recalling some lots of its Iams canned cat food because they may have insufficient levels of thiamine -- the vitamin B1. (aol.com)
- Low levels of thiamine reflect malabsorption states, poor nutritional status, or inadequate oral intake, while high levels suggest excessive intake or absorption issues. (medscape.com)
Lead to thiamine deficiency3
- It plays a key role in several important health functions, and not getting enough of it can lead to thiamine deficiency. (feelgoodpal.com)
- Not getting enough thiamine can lead to thiamine deficiency, which can happen in as little as 3 weeks and affect your heart, nervous, and immune systems. (feelgoodpal.com)
- Chronic alcohol use can lead to thiamine deficiency, which sometimes causes brain damage and memory loss. (webmd.com)
Beriberi12
- Thiamine deficiency, or beriberi, refers to a lack of thiamine pyrophosphate, the biologically active form of the vitamin known as thiamine (also spelled thiamin), or vitamin B-1 (see the image below). (medscape.com)
- With other causes of beriberi, once the primary problem has been addressed, an appropriate diet providing more-than-adequate thiamine levels should be adopted by the patient. (medscape.com)
- Thiamine deficiency can affect the cardiovascular, nervous, and immune systems, as commonly seen in wet beriberi, dry beriberi, or Wernicke-Korsakoff syndrome. (nih.gov)
- The deficiency of this vitamin in women can cause infantile beriberi, which this article will not specifically address. (nih.gov)
- Support for cardiac function is necessary in cases of wet beriberi, because lack of cardiac support leads to low-output cardiac failure when the thiamine deficiency is corrected. (medscape.com)
- Thiamin deficiency (causing beriberi) is most common among people subsisting on white rice or highly refined carbohydrates in countries with high rates of food insecurity and among people with alcohol use disorder. (msdmanuals.com)
- Dry beriberi refers to peripheral neurologic deficits due to thiamin deficiency. (msdmanuals.com)
- This deficiency is known as beriberi if it's severe and chronic. (feelgoodpal.com)
- Among the most well-known side effects of prolonged, severe thiamine deficiency (beriberi) is nerve damage, also known as neuropathy. (feelgoodpal.com)
- The reason Japanese developed Beriberi is because while polishing and processing rice, they were essentially removing most of its Vitamin B content and hence making the people thiamine deficient. (ithrivein.com)
- Thiamine deficiency in Cambodian infants with and without beriberi. (tamu.edu)
- STUDY DESIGN: In a case-control study, thiamine diphosphate (TDP) blood concentrations were measured in 27 infants diagnosed with beriberi at a rural clinic, as well as their mothers and healthy Cambodian and American controls. (tamu.edu)
Riboflavin2
- Overview of Vitamins Vitamins may be Fat soluble (vitamins A, D, E, and K) Water soluble (B vitamins and vitamin C) The B vitamins include biotin, folate, niacin, pantothenic acid, riboflavin (B2), thiamin (B1). (msdmanuals.com)
- Thiamine and Riboflavin [i] play a major role in regenerating your gut microbiota. (ipsnews.net)
Folate3
- Less well established but plausible signs and symptoms include improvements in energy or neurological health on a low-carbohydrate diet, low levels of neurotransmitters, and apparent deficiencies of folate and vitamin K that do not respond well to dietary or supplemental corrections. (ithrivein.com)
- Your cat's nutritional needs (2006) National Research Council states 'Human patients with CKD apparently are especially prone to pyridoxine and folate deficiency (Gilmour et al, 1993). (felinecrf.org)
- A chronic dietary deficiency of either folate or vitamin B12 causes macrocytic anemia, although strict dietary deficiencies are rare. (cdc.gov)
Pyrophosphate6
- Thiamine pyrophosphate acts as a coenzyme in carbohydrate metabolism through the decarboxylation of alpha ketoacids. (medscape.com)
- It functions as a catalyst in the generation of energy through decarboxylation of branched-chain amino acids and alpha-ketoacids and acts as a coenzyme for transketolase reactions in the form of thiamine pyrophosphate. (nih.gov)
- Thiamine pyrophosphate, the biologically active form of thiamine, acts as a coenzyme in carbohydrate metabolism through the decarboxylation of alpha ketoacids. (duckdvm.com)
- Thiamine pyrophosphokinase (TPK) produces thiamine pyrophosphate, a cofactor for a number of enzymes, including pyruvate dehydrogenase and 2-ketoglutarate dehydrogenase. (ox.ac.uk)
- Furthermore, we have established the assays for TPK enzyme activity measurement and thiamine pyrophosphate quantification in frozen muscle and blood. (ox.ac.uk)
- A stimulation of over 20%-25% during a red blood cell transketolase measurement using thiamine pyrophosphate (TTP) indicates deficiency. (medscape.com)
Lack of thiamine1
- While some products have been recalled over concerns of a lack of thiamine, is this something we need to be concerned abut when selecting a pet food? (nutritionrvn.com)
Amount of thiamine3
- Alcoholics may have thiamine deficiency because of: Inadequate nutritional intake: Alcoholics tend to intake less than the recommended amount of thiamine. (wikipedia.org)
- Some researchers suggest that the excess biotin given along with thiamine as treatment for the disorder may increase the amount of thiamine transporter that is produced, partially compensating for the impaired efficiency of the abnormal protein. (medlineplus.gov)
- In meat, liver has the highest amount of thiamine. (webmd.com)
Deficient in thiamine4
- How can a diet be deficient in thiamine? (nutritionrvn.com)
- Being deficient in thiamine (vitamin B1) can cause subtle and often overlooked symptoms. (feelgoodpal.com)
- For instance, one study found that rats ate significantly less food after receiving a diet deficient in thiamine for 16 days. (feelgoodpal.com)
- Being deficient in thiamine can show up as fatigue (tiredness), which may come on quickly or over time, depending on the severity of the deficiency. (feelgoodpal.com)
Risk for thiamine deficiency1
- Special populations of individuals also at risk for thiamine deficiency include pregnant women, those requiring parental feeding, individuals who have undergone bariatric surgery, those with overall poor nutritional status, and patients on chronic diuretic therapy as it increases urinary losses. (nih.gov)
Causes of thiamine deficiency3
- Include education regarding Korsakoff syndrome (which arises from thiamine deficiency) for patients being treated for alcohol dependency, one of the causes of thiamine deficiency. (medscape.com)
- This activity reviews the causes of thiamine deficiency, the associated pathophysiology, and typical patient presentation and highlights the role of the interprofessional team in its management. (nih.gov)
- Outline the causes of thiamine deficiency. (nih.gov)
Patients with thiamine deficiency2
- Follow-up care until delivery of current pregnancy, intensive care for advanced cardiomyopathy, definitive care for hyperthyroidism, or further workup of intestinal derangement may be warranted in patients with thiamine deficiency. (medscape.com)
- We describe two hematological pediatric patients with thiamine deficiency and hemodynamic instability who improved following thiamine supplements. (thieme-connect.de)
Supplementation7
- Treatment is by thiamine supplementation, either by mouth or by injection. (wikipedia.org)
- Wernicke's encephalopathy is the most frequently encountered manifestation of thiamine deficiency in Western society, though it may also occur in patients with impaired nutrition from other causes, such as gastrointestinal disease, those with HIV/AIDS, and with the injudicious administration of parenteral glucose or hyperalimentation without adequate B-vitamin supplementation. (wikipedia.org)
- The most common route to fixing thiamine deficiency is supplementation, which are typically taken orally. (ithrivein.com)
- We recommend that children with hematological malignancies admitted to a pediatric intensive care unit with low blood pressure and lactic acidosis should be considered for thiamine-level screening and receive supplementation accordingly. (thieme-connect.de)
- 9 Manzanares W, Hardy G. Thiamine supplementation in the critically ill. (thieme-connect.de)
- Early thiamine supplementation prevented encephalopathic episodes and improved developmental progression of Patient 1, emphasizing the importance of early diagnosis and treatment of TPK deficiency. (ox.ac.uk)
- We present evidence suggesting that thiamine supplementation may rescue TPK enzyme activity. (ox.ac.uk)
Enough thiamine4
- Thiamine deficiency occurs when ducks aren't getting enough thiamine (vitamin B1) in their diet. (duckdvm.com)
- Ensure ducks are getting enough thiamine in their diet. (duckdvm.com)
- Not having enough thiamine in the body means it cannot produce as much energy as fuel. (feelgoodpal.com)
- If a patient is unable to eat a regular diet to begin with, can only hold down liquids due to being nauseas, and has continued vomiting, gagging and/or sinus drainage, the body can simply be unable to absorb enough thiamine. (medmal1.com)
Pyridoxine2
- A modified rotarod technique is used to determine if dietary deficiencies in pyridoxine (65236) or thiamine (59438), bilateral adrenalectomy or cortisol (50237) treatment and pretreatment with microsomal enzyme inducers (DDT (50293) or phenobarbital (57307)) would modify the course of onset and recovery from functional acrylamide neuropathy in rats. (cdc.gov)
- Neither pyridoxine nor thiamine deficiency nor daily injections of cortisol is found to have any measurable effect on the cumulative dose of acrylamide required to produce functional impairment. (cdc.gov)
Severe10
- The level of activity and the presence of a high energy consumption state (eg, hyperthyroidism, pregnancy, lactation, severe disease) increase the daily requirements of thiamine. (medscape.com)
- Very severe thiamine deficiency may cause seizures, paralysis, and death. (ithrivein.com)
- Tragically, severe thiamin deficiency is underdiagnosed in emergency medicine and often diagnosed at autopsy. (ithrivein.com)
- Poor glucose tolerance may occur in less severe thiamin deficits. (ithrivein.com)
- In severe cases, thiamine may be given intravenously. (ithrivein.com)
- A severe thiamine deficiency can result in potentially serious complications involving the nervous system, brain, muscles, heart, and gastrointestinal system. (medmal1.com)
- Acute decompensation in thiamine-deficient patients may manifest as neurologic or cardiovascular changes, with severe lactic acidosis as the presenting symptom. (thieme-connect.de)
- 1 Svahn J, Schiaffino MC, Caruso U, Calvillo M, Minniti G, Dufour C. Severe lactic acidosis due to thiamine deficiency in a patient with B-cell leukemia/lymphoma on total parenteral nutrition during high-dose methotrexate therapy. (thieme-connect.de)
- Xerophthalmia is particularly common among children who have a severe deficiency of calories and protein, which includes inadequate intake of vitamin A . Foamy deposits (Bitot spots) may appear in the whites of the eyes. (merckmanuals.com)
- A stimulation exceeding 20%-25% after the addition of TTP indicates severe thiamine deficiency (an activity coefficient of 1.25). (medscape.com)
Disorders7
- Following these reports SCF established surveillance of micro-nutrient deficiency disorders. (ennonline.net)
- The New York Academy of Sciences: "National control and prevention programs for thiamine deficiency disorders. (webmd.com)
- Introduction Diagnosis of infantile thiamine deficiency disorders (TDD) is challenging due to the non-specific, highly variable clinical presentation, often leading to misdiagnosis. (bmj.com)
- Our primary objective is to develop a case definition for thiamine responsive disorders (TRD) to determine among hospitalised infants and young children, which clinical features and risk factors identify those who respond positively to thiamine administration. (bmj.com)
- Some 740 million people - both children and adults - in 130 countries are affected by iodine deficiency disorders , still the greatest single cause of preventable brain damage to the fetus, infant and young child. (who.int)
- Disorders that impair the intestine's absorption of fats can reduce the absorption of the fat-soluble vitamin A and increase the risk of vitamin A deficiency. (merckmanuals.com)
- Subtly reduced cognitive function resulting from early vitamin B12 deficiency is sometimes the only symptom of these intestinal disorders. (cdc.gov)
Inadequate2
- Worldwide, thiamine deficiency is primarily due to inadequate dietary intake, specifically in diets comprised mainly of polished rice and grains. (nih.gov)
- Inadequate thiamine stores may disrupt how well this process works, making you feel full even when you may not be. (feelgoodpal.com)
Vitamins10
- Thiamine is a type of vitamin B. Several different substances belong to the group of vitamins known as the B vitamins. (patient.info)
- Thiamine, also known as vitamin B1, is one of the eight essential B vitamins. (feelgoodpal.com)
- Like the other B vitamins, thiamine is water-soluble. (feelgoodpal.com)
- As its name suggests, the condition may improve if the vitamins biotin and thiamine are given as treatment. (medlineplus.gov)
- Thiamine , which is also called thiamin or vitamin B1, is one of the vitamins that are found in many vitamin B complex products. (webmd.com)
- Like other B vitamins, thiamine helps the body break down food and turn it into energy. (webmd.com)
- Legumes are a rich source of thiamine and other B vitamins. (webmd.com)
- Vitamin B1, or thiamine, is one of the most relevant vitamins in obtaining energy for the nervous system. (mdpi.com)
- Deficiencies of these vitamins may exacerbate anemia and increase erythropoietin resistance. (felinecrf.org)
- This condition is a medical emergency and should be treated in a hospital with injectable Thiamin along with other oral vitamins. (health-disease.org)
Vitamin deficiencies2
- Vitamin deficiencies in acutely intoxicated patients in the ED. The American Journal of Emergency Medicine. (wikem.org)
- it often occurs with other B vitamin deficiencies. (msdmanuals.com)
Signs and symptoms6
- This article examines the functions of thiamine, the signs and symptoms of deficiency, and how to ensure you're getting enough of this essential nutrient in your diet. (feelgoodpal.com)
- Signs and symptoms of thiamine deficiency can be easy to overlook, as they can be nonspecific and vague, sometimes mimicking symptoms of other conditions. (feelgoodpal.com)
- Despite that, and despite numerous signs and symptoms of a thiamine deficiency, every doctor in this case ultimately admitted that they never did anything to rule out or treat a thiamine deficiency as the potential cause. (medmal1.com)
- The signs and symptoms of a thiamine deficiency include an unsteady gate, vision problems (notably nystagmus which is involuntary eye movement), hearing problems, swelling, tingling, or a numbness sensation in the hands and feet, and fatigue. (medmal1.com)
- however, since its known to occur following gastric bypass surgery, any combination of the signs and symptoms on a patient that recently had this surgery should immediately place a thiamine deficiency not only on a doctor's differential diagnosis list, but immediately at the top to be ruled out or treated. (medmal1.com)
- The signs and symptoms of biotin-thiamine-responsive basal ganglia disease usually begin between the ages of 3 and 10, but the disorder can appear at any age. (medlineplus.gov)
Cases of thiamine2
- In suspected cases of thiamine deficiency, prompt administration of parenteral thiamine is indicated. (medscape.com)
- No cases of thiamine toxicity have been reported from the use of thiamine at the dosages indicated, even in patients in critical condition. (medscape.com)
Intake6
- When thiamine stores are depleted (which takes about 4 weeks after stopping intake), symptoms start to appear. (nih.gov)
- Furthermore, they increased appetite and returned to usual food intake once thiamine was added to their diet. (feelgoodpal.com)
- These antithiamine compounds can result in thiamine deficiency in a person with limited thiamine intake. (medicalalgorithms.com)
- In industrial countries where fortification is widespread, fortified foods provide about 50% of the total thiamine intake. (webmd.com)
- Worldwide, poor oral intake is the most cause of thiamine deficiency , whereas alcoholism or chronic illnesses (eg, cancer) are more common in Western nations. (medscape.com)
- The State recognizes that food fortification is vital where there is a demonstrated need to increase the intake of an essential nutrient by one or more population groups, as manifested in dietary, biochemical or clinical evidences of deficiency. (who.int)
Role of thiamine3
- The role of thiamine and effects of deficiency in dogs and cats. (nutritionrvn.com)
- This symptom makes sense, given the role of thiamine in converting food into energy. (feelgoodpal.com)
- The Role of Thiamine Deficiency in Alcoholic Brain Disease. (webmd.com)
Malnutrition3
- See 21 Hidden Clues to Diagnosing Nutritional Deficiencies , a Critical Images slideshow, to help identify clues to conditions associated with malnutrition. (medscape.com)
- She is the co-author of the book "Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition" and the author of over 200 articles on various topics, from women's health and hormones, medication reactions, to mitochondrial function and dysfunction. (betterhealthguy.com)
- To that end, thiamine deficiencies are caused by malnutrition where the body isn't absorbing enough vitamin B-1. (medmal1.com)
Absorption of thiamine2
- Might toxic mold exposure interfere with the absorption of thiamine? (betterhealthguy.com)
- Feeding food that is rich in thiaminase activity such as some raw fish blocks the absorption of thiamine in the diet, which is why an all-raw fish diet in cats can be a cause of thiamine deficiency. (nutritionrvn.com)
Neurological disorder caused2
- Expanding the clinical and molecular spectrum of thiamine pyrophosphokinase deficiency: a treatable neurological disorder caused by TPK1 mutations. (ox.ac.uk)
- BACKGROUND: Wernicke encephalopathy (WE) is a devastating acute or subacute neurological disorder caused by thiamine deficiency. (bvsalud.org)
Form of thiamine1
- What form of thiamine is most health-supporting? (betterhealthguy.com)
Biologically active form1
- Whole blood is the preferred specimen (as opposed to plasma or serum), as 90% of vitamin B1 in whole blood is thiamine diphosphate (the biologically active form) and 80% of thiamine in whole blood is found in red blood cells. (medscape.com)
Phosphorylation of thiamine2
- Ethanol per se inhibits thiamine transport in the gastrointestinal system and blocks phosphorylation of thiamine to its cofactor form (ThDP). (wikipedia.org)
- The small intestine is where phosphorylation of thiamine takes place. (medscape.com)
Diphosphate1
- Clinical follow-up with measurement of thiamine diphosphate activity may be warranted if relapse or noncompliance is suspected. (medscape.com)
Parenteral thiamine1
- If Wernicke's encephalopathy is suspected, immediately interrupt arsenic trioxide and initiate parenteral thiamine. (nih.gov)
Encephalopathy7
- Symptoms may occur concurrently with those of Wernicke's encephalopathy, a primarily neurological thiamine deficiency-related condition. (wikipedia.org)
- In this case, a 39 year old woman suffered from a thiamine deficiency following bariatric surgery which led to Wernicke's encephalopathy (a permanent brain injury). (medmal1.com)
- Everyone in this case agreed, even the Defendant physicians did in their depositions, that the earlier a thiamine deficiency/Wernicke's encephalopathy is diagnosed and treated, the better chance there is of reversing its effects. (medmal1.com)
- 4 Isenberg-Grzeda E, Alici Y, Hatzoglou V, Nelson C, Breitbart W. Nonalcoholic thiamine-related encephalopathy (Wernicke-Korsakoff syndrome) among inpatients with cancer: a series of 18 cases. (thieme-connect.de)
- Thiamine deficiency secondary to anorexia nervosa: an uncommon cause of peripheral neuropathy and Wernicke encephalopathy in adolescence. (thieme-connect.de)
- Episodic encephalopathy type thiamine metabolism dysfunction (OMIM 614458) due to TPK1 mutations is a recently described rare disorder. (ox.ac.uk)
- Its deficiency leads to mitochondrial dysfunction, lactate and pyruvate accumulation, and consequently to focal thalamic degeneration, manifested as Wernicke's encephalopathy or Wernicke-Korsakoff syndrome. (bvsalud.org)
Little thiamine2
- Because there is very little thiamine (vitamin B-1) stored in the body, thiamine depletion can occur quickly, within 14 days. (medmal1.com)
- Since very little thiamine is actually stored in the body (approximately 25-30 mg), depletion can take place in 14 days to one month. (medscape.com)
Irritability1
- Babies with thiamine deficiency frequently express increased irritability as a symptom. (feelgoodpal.com)
Pathophysiology1
- Describe the pathophysiology of thiamine deficiency. (nih.gov)
Lactic Acidosis2
- Shah, S & Wald, E 2015, ' Type B lactic acidosis secondary to thiamine deficiency in a child with malignancy ', Pediatrics , vol. 135, no. 1, pp. e221-e224. (northwestern.edu)
- Thiamine is an essential component of cellular metabolism and its deficiency results in potentially life-threatening events and profound lactic acidosis through anaerobic metabolism. (thieme-connect.de)
Chronic1
- Impaired thiamine utilization: Magnesium, which is required for the binding of thiamine to thiamine-using enzymes within the cell, is also deficient due to chronic alcohol consumption. (wikipedia.org)
Lactate2
- After administration of intravenous thiamine, his lactate level rapidly normalized and remained stable. (northwestern.edu)
- specifically, lower thiamine levels were related to higher lactate levels. (thieme-connect.de)
Neurologic1
- Hematologic signs, however, are not always present in vitamin B12 deficiency and hematologic signs and neurologic abnormalities can be inversely correlated (Baik, et al. (cdc.gov)
Glucose4
- Does thiamine play a role in glucose regulation? (betterhealthguy.com)
- Because thiamine is an important cofactor for pyruvate dehydrogenase, he was unable to use glucose through aerobic metabolism pathways. (northwestern.edu)
- Thiamin is involved in carbohydrate, fat, amino acid, glucose, and alcohol metabolism and is particularly important in the function of central and peripheral nerve cells and the myocardium. (msdmanuals.com)
- In addition, it participates in the cellular respiration and oxidation of fatty acids: in malnourished people, high doses of glucose result in acute thiamine deficiency. (bvsalud.org)
Bariatric surgery1
- Vitamin D deficiency is very common after bariatric surgery, and something you have to monitor on a regular basis. (medscape.com)
Thiaminase4
- Thiaminase is also deactivated through heat and cooking, so a commercial product that is fish flavoured or contains fish is unlikely to cause a deficiency. (nutritionrvn.com)
- This can occur due to a lack of adaquate amounts of vitamin B1 in the diet or from being fed foods that contain thiaminase, which decreases the absorption of vitamin B1 (thiamine). (duckdvm.com)
- OBJECTIVES: To test the hypothesis that heavy metal toxicity and consumption of thiaminase-containing foods predispose to symptomatic thiamine deficiency. (tamu.edu)
- Neither heavy metal toxicity nor consumption of thiaminase-containing foods account for thiamine deficiency in this region. (tamu.edu)
Enzymes2
- Additionally, certain food products such as tea, coffee, raw fish, and shellfish contain thiaminases - enzymes that destroy thiamine. (nih.gov)
- A number of chemicals or enzymes may destroy or degrade thiamine (vitamin B1). (medicalalgorithms.com)
Alcohol3
- Decreased uptake of thiamine from the GI tract: Active transport of thiamine into enterocytes is disturbed during acute alcohol exposure. (wikipedia.org)
- Depending on the cause of the vitamin deficiency, a referral to an alcohol dependency clinic may be needed. (medscape.com)
- Specific items like fast food, sugar, tea, coffee, alcohol make the body Thiamine-depleted due to absorption by the gut. (ithrivein.com)
Acute1
- Acute thiamine deficiency and refeeding syndrome: Similar findings but different pathogenesis. (thieme-connect.de)
Syndrome2
- In fact, neuropathy from thiamine deficiency was among the first deficiency syndrome identified in humans. (feelgoodpal.com)
- 1. AIDS: Acquired immune deficiency syndrome Acquired immunodeficiency syndrome 2. (cdc.gov)
Nervous5
- Thiamine, also known as Vitamin B1 is an essential nutrient that plays a vital role in the body's metabolism and function of the Central Nervous System (CNS). (ithrivein.com)
- Biotin-thiamine-responsive basal ganglia disease is a disorder that affects the nervous system, including a group of structures in the brain called the basal ganglia, which help control movement. (medlineplus.gov)
- Thiamine, also known as vitamin B1, is obtained from the diet and is necessary for proper functioning of the nervous system. (medlineplus.gov)
- Thiamine, or vitamin B1, is involved in a number of functions in the body, including nervous system (axonal conduction) and muscular functioning (electrolyte flow in these cells), carbohydrate metabolism, enzymatic processes, and production of hydrochloric acid needed for digestion. (medscape.com)
- Untreated deficiencies will lead to megaloblastic anemia and vitamin B12 deficiency results in irreversible central nervous system degeneration. (cdc.gov)
Liver2
- Liver thiamine stores are reduced due to hepatic steatosis or fibrosis. (wikipedia.org)
- Vitamin A deficiency can result from a diet low in vitamin A or an absorption or liver disorder. (merckmanuals.com)
Nutritional Deficiencies2
- and known current and past nutritional deficiencies. (cdc.gov)
- Nutritional deficiencies. (healthwise.net)
Pyruvate1
- Mutations in E3 cause additional deficiencies of pyruvate and alpha-ketoglutarate dehydrogenases. (medscape.com)
Water-soluble vitamin1
- Thiamine is a water-soluble vitamin that is absorbed in the jejunum by 2 processes. (medscape.com)
Intravenous1
- Children will be treated with intravenous or intramuscular thiamine (100 mg daily for a minimum of 3 days) alongside other interventions deemed appropriate. (bmj.com)
Metabolism1
- Thiamine plays a special role in the body as a coenzyme necessary for the metabolism of carbohydrates, fats and proteins. (bvsalud.org)
Cardiac failure1
- High-output cardiac failure should prompt investigation of thiamine deficiency as a cause. (medscape.com)
Occurs2
- First, we need to look at how thiamine deficiency occurs and where fish fits into this picture. (nutritionrvn.com)
- For example, vitamin A deficiency occurs in southern and eastern Asia, where regular rice, which contains no vitamin A , is the main food. (merckmanuals.com)
Dysfunction1
- Mutations in the SLC19A3 gene likely result in a protein with impaired ability to transport thiamine into cells, resulting in decreased absorption of the vitamin and leading to neurological dysfunction. (medlineplus.gov)
Abnormalities1
- The relationship between these specific brain abnormalities and the abnormal thiamine transporter is unknown. (medlineplus.gov)
Among infants1
- CONCLUSIONS: Thiamine deficiency is endemic among infants and nursing mothers in rural southeastern Cambodia and is often clinically inapparent. (tamu.edu)
Deficits1
- If left untreated, even though some symptoms may improve over time once treatment is started, memory impairment and cognitive deficits are typically permanent (i.e. high doses of thiamine can improve muscle coordination and confusion, but rarely improves memory loss). (medmal1.com)
Metabolic2
- Thiamin is essential to the metabolic utilisation of carbohydrates. (ennonline.net)
- In cats small bowel disease inhibits cobalamin uptake, and cobalamin deficiency can result in metabolic acidosis. (vin.com)
Loss of appet2
- Experiencing an atypical loss of appetite can be one of the earliest symptoms of thiamine deficiency. (feelgoodpal.com)
- Early signs of thiamine deficiency can include loss of appetite, drooling, vomiting and weight loss. (aol.com)