"and feeder minnows are susceptible to developing thiamine deficiency. This is often a problem observed in captivity when keeping garter and ribbon snakes that are fed a goldfish-exclusive diet, as these fish contain thiaminase, an enzyme that breaks down thiamine. Thiamine deficiency has been identified as the cause of a paralytic disease affecting wild birds in the Baltic Sea area dating back to 1982. In this condition, there is difficulty in keeping the wings folded along the side of the body when resting, loss of the ability to fly and voice, with eventual paralysis of the wings and legs and"
"Thiamine responsive megaloblastic anemia syndrome Thiamine responsive megaloblastic anemia syndrome (also known as Rogers Syndrome) is a very rare genetic disorder affecting a thiamine transporter, which is characterized by megaloblastic anemia, diabetes mellitus and hearing loss. The condition is treated with high doses of thiamine (vitamin B1). In most cases (80-99%), people with this condition experience poor appetite (anorexia), diarrhea, headache, and lethargy. Thiamine responsive megaloblastic anemia syndrome is associated with progressive sensorineural hearing loss. Additional manifestations include optic atrophy, short stature, enlarged liver, and an enlarged spleen. Some cases may affect the heart, leading to abnormal heart rhythms. Treatment"
"teeth grinding, trismus, salivation, drooling, convulsions, nystagmus, clonic convulsions, and recumbency. Early administration of thiamine may be curative, but if the lesion is more advanced, then surviving animals may remain partially blind and mentally dull. Polioencephalomalacia Polioencephalomalacia (PEM), also referred to as cerebrocortical necrosis (CCN), is a neurological disease seen in ruminants that is caused by disrupted thiamine production in the body. Thiamine is a key chemical in glucose metabolism that, when definicient, is most threatening to neurological activity. Cattles, sheep, goat, and other ruminants that are diagnosed with PEM or pre-PEM suffer opishotonus, cortical blindness, disoriented movement, and eventually"
"That is, patients could be led to believe certain things had happened which actually had not, but so could people without alcoholic Korsakoff syndrome. Conditions resulting in thiamine deficiency and its effects include chronic alcoholism and severe malnutrition. Alcoholism may co-occur with poor nutrition, which in addition to inflammation of the stomach lining, causes thiamine deficiency. Other causes include dietary deficiencies, prolonged vomiting, eating disorders, and the effects of chemotherapy. It can also occur in pregnant women who have a form of extreme morning sickness known as hyperemesis gravidarum. Mercury poisoning can also lead to Korsakoff's syndrome. Though it does"
"ganglia disease which is treated with pharmacological doses of thiamine and biotin, another B vitamin. Other disorders in which a putative role for thiamine has been implicated include subacute necrotising encephalomyelopathy, opsoclonic cerebellopathy (a paraneoplastic syndrome), and Nigerian seasonal ataxia. In addition, several inherited disorders of ThDP-dependent enzymes have been reported, which may respond to thiamine treatment. Thiamine in the human body has a half-life of 18 days and is quickly exhausted, particularly when metabolic demands exceed intake. A derivative of thiamine, thiamine pyrophosphate (TPP), is a cofactor involved in the citric acid cycle, as well as connecting the breakdown"
"intake. Clinical signs of B deficiency include mental changes such as apathy, decrease in short-term memory, confusion, and irritability. Moderate deficiency in thiamine may reduce growth in young populations, in increase chronic illness in both young and middle-aged adults. In addition, moderate deficiency of thiamine may increase rates of depression, dementia, falls, and fractures in old age. The lingering symptoms of neuropathy associated with cerebral beriberi are known as Korsakoff's syndrome, or the chronic phase of Wernicke-Korsakoff's. Wernicke encephalopathy is a neurological disorder resulting from a deficiency in thiamine, sharing the same predominant features of cerebral beriberi, as characterized by"
"intake has been interrupted by trauma or surgery. This can occur after childbirth. A severe mental disorder was described by Wernicke and Korsakoff. Its most striking feature is loss of memory, which can be permanent. The cause is vitamin B (thiamine) deficiency, usually found in severe alcoholics. It can also result from pernicious vomiting of pregnancy (hyperemesis gravidarum). Over 125 cases have been reported in the world literature and, although thiamine treatment has been available since 1936, these cases still occur in countries with advanced medical services, due to rehydration without vitamin supplements. A few patients have developed symptoms after"
"NYX (nyctalopin). CSNB-2 involves mutations of CACNA1F, a voltage-gated calcium channel that, when mutated, does not conduct ions. Nystagmus that occurs later in childhood or in adulthood is called acquired nystagmus. The cause is often unknown, or idiopathic, and thus referred to idiopathic nystagmus. Other common causes include diseases and disorders of the central nervous system, metabolic disorders and alcohol and drug toxicity. In the elderly, stroke is the most common cause. Some of the diseases that present nystagmus as a pathological sign or symptom are as follows: Sources of toxicity that could lead to nystagmus: Risk factors for thiamine"
"Polioencephalomalacia Polioencephalomalacia (PEM), also referred to as cerebrocortical necrosis (CCN), is a neurological disease seen in ruminants that is caused by disrupted thiamine production in the body. Thiamine is a key chemical in glucose metabolism that, when definicient, is most threatening to neurological activity. Cattles, sheep, goat, and other ruminants that are diagnosed with PEM or pre-PEM suffer opishotonus, cortical blindness, disoriented movement, and eventually fatality, if left untreated. Current data shows that the onset of PEM can range from birth to late adulthood. Thiamine availability is controlled by the direct dietary consumption of thiamine. Thiamine availability is also regulated"
"1 (HT-1) in combination with dietary restriction of tyrosine and phenylalanine. Liver transplant is indicated for patients with tyrosinemia type I who do not respond to nitisinone, as well as those with acute liver failure and hepatomas. Tyrosinemia Tyrosinemia or tyrosinaemia is an error of metabolism, usually inborn, in which the body cannot effectively break down the amino acid tyrosine. Symptoms include liver and kidney disturbances and intellectual disability. Untreated, tyrosinemia can be fatal. Most inborn forms of tyrosinemia produce hypertyrosinemia (high levels of tyrosine). All tyrosinemias result from dysfunction of various genes in the phenylalanine and tyrosine catabolic pathway,"
"use of monoamine oxidase inhibitors (MAOIs) and foods high in tyramine are ingested, a hypertensive crisis can result, as tyramine also can displace stored monoamines, such as dopamine, norepinephrine, and epinephrine, from pre-synaptic vesicles. The first signs of this were discovered by a British pharmacist who noticed his wife, who at the time was on MAOI medication, had severe headaches when eating cheese. For this reason, the crisis is still called the ""cheese effect"" or ""cheese crisis"", though other foods can cause the same problem. Most processed cheeses do not contain enough tyramine to cause hypertensive effects, although some aged"
"liver cancer. Heart failure, growth impairment, diabetes and osteoporosis are life-threatening contributors brought upon by TM. The main cardiac abnormalities seen to have resulted from thalassemia and iron overload include left ventricular systolic and diastolic dysfunction, pulmonary hypertension, valveulopathies, arrhythmias, and pericarditis. Increased gastrointestinal iron absorption is seen in all grades of beta thalassemia and increased red blood cell destruction by the spleen due to ineffective erythropoiesis further releases additional iron into the bloodstream. Two major groups of mutations can be distinguished: Beta thalassemia is a hereditary disease affecting hemoglobin. As with about half of all hereditary diseases, an inherited"
"by the use of alcohol, there have been several cases where it has developed from other instances of thiamine deficiency resulting from gross malnutrition due to conditions such as; stomach cancer, anorexia nervosa, and gastrectomy. Several cases have been documented where Wernicke–Korsakoff syndrome has been seen on a large scale. In 1947, 52 cases of WKS were documented in a prisoner of war hospital in Singapore where the prisoners' diets included less than 1 mg of thiamine per day. Such cases provide an opportunity to gain an understanding of what effects this syndrome has on cognition. In this particular case,"
"cycle and the pentose phosphate shunt. Thiamine is first metabolised to its more active form, thiamine diphosphate (TDP), before it is used. The body only has 2–3 weeks of thiamine reserves, which are readily exhausted without intake, or if depletion occurs rapidly, such as in chronic inflammatory states or in diabetes. Thiamine is involved in: The primary neurological-related injury caused by thiamine deficiency in WE is three-fold: oxidative damage, mitochondrial injury leading to apoptosis, and directly stimulating a pro-apoptotic pathway. Thiamine deficiency affects both neurons and astrocytes, glial cells of the brain. Thiamine deficiency alters the glutamate uptake of astrocytes,"
"12.5% or more. Mortality caused by Wernicke's disease reaches 17% of diseases, which means 3.4/1000 or about 25 million contemporaries. The number of people with Wernicke's disease may be even higher, considering that early stages may have dysfunctions prior to the production of observable lesions at necropsy. In addition, uncounted numbers of people can experience fetal damage and subsequent diseases. Genetic diseases of thiamine transport are rare but serious. Thiamine responsive megaloblastic anemia (TRMA) with diabetes mellitus and sensorineural deafness is an autosomal recessive disorder caused by mutations in the gene SLC19A2, a high affinity thiamine transporter. TRMA patients do"
"weakness, muscle cramps, abnormal heart rhythms, increased irritability of the nervous system with tremors, paresthesias, palpitations, low potassium levels in the blood, hypoparathyroidism which might result in low calcium levels in the blood, chondrocalcinosis, spasticity and tetany, migraines, epileptic seizures, basal ganglia calcifications and in extreme and prolonged cases coma, intellectual disability or death. Magnesium plays an important role in carbohydrate metabolism and its deficiency may worsen insulin resistance, a condition that often precedes diabetes, or may be a consequence of insulin resistance. People being treated on an intensive care unit who have a low magnesium level may have a"
"that causes uremic breath to smell fishy). Trimethylamine is oxidized in the liver to trimethylamine ""N""-oxide (TMAO), which causes atherosclerosis in animal models. Patients in the top quartile of TMAO had a 2.5-fold increase in the 3-year risk of stroke, death, or myocardial infarction. A key issue is that vegans who consumed -carnitine did not produce TMAO because they did not have the intestinal bacteria that produce TMA from carnitine. Chemotherapy and radiation treatment adverse effects such as fatigue, mood and sleep disturbances, are common in cancer patients. A deficiency in carnitine may also occur, some studies were done on"
"Vascular dementia is often considered the second-most common form of dementia and is the reduction of blood flow to parts of the brain most often caused by many very small strokes that have an accumulative effect on cognitive abilities including memory. Korsakoff's is caused by a severe thiamine (vitamin B) deficiency due to chronic alcoholism or malnourishment. Thiamine is necessary for the body to process carbohydrates. This thiamine dificiency can lead to symptoms such as: confusion, loss of balance, drowsiness, and some specific problems with vision. When the deficiency is considered severe, the memory loss may be accompanied by agitation"
"Leigh syndrome Leigh syndrome (also called Leigh disease and subacute necrotizing encephalomyelopathy) is an under-recognized inherited neurometabolic disorder that affects the central nervous system. It is named after Denis Archibald Leigh, a British neuropsychiatrist who first described the condition in 1951. Normal levels of thiamine, thiamine monophosphate, and thiamine diphosphate are commonly found but there is a reduced or absent level of thiamine triphosphate. This is thought to be caused by a blockage in the enzyme thiamine-diphosphate kinase, and therefore treatment in some patients would be to take thiamine triphosphate daily. The symptoms of Leigh syndrome are classically described as"
"consists of high doses of oral thiamine. Treatment can delay the onset of diabetes mellitus, and reverses anemia. If treatment is initiated early, thiamine may be prevented. The condition is inherited in an autosomal recessive fashion, and is caused by a mutation in the SLC19A2 gene. The condition was first described in 1969 by Rogers. Thiamine responsive megaloblastic anemia syndrome Thiamine responsive megaloblastic anemia syndrome (also known as Rogers Syndrome) is a very rare genetic disorder affecting a thiamine transporter, which is characterized by megaloblastic anemia, diabetes mellitus and hearing loss. The condition is treated with high doses of thiamine"
"and/or digestive disorders during their lifetime (called ""determinate"" chronic Chagas disease). In 10% of individuals, the disease progresses directly from the acute form to a symptomatic clinical form of chronic Chagas disease. The symptomatic (determinate) chronic stage affects the nervous system, digestive system and heart. About two-thirds of people with chronic symptoms have cardiac damage, including dilated cardiomyopathy, which causes heart rhythm abnormalities and may result in sudden death. About one-third of patients go on to develop digestive system damage, resulting in dilation of the digestive tract (megacolon and megaesophagus), accompanied by severe weight loss. Swallowing difficulties (secondary achalasia) may"
"growth, muscle cramps, and skeletal deformities. Many South Africans also have a Thiamine (Vitamin B1) deficiency. A serious deficiency in this vital nutrient can cause beriberi, which has the immediate symptom of severe lethargy. If left untreated, Beriberi can cause inflammation of the nervous system and even heart failure. Heart failure associated with beriberi is especially prominent in Johannesburg, the capital of South Africa. Another disease common to South Africa is pellagra. Dr. D Blumhson, a physician, notes a high rate of pellagra among the patients of a hospital in Soweto, South Africa. Pellagra seems to be especially common in"
"life-threatening disease associated with early mortality and significant morbidity. LAL Deficiency is a chronic disease in which genetic mutations result in decreased activity of the LAL enzyme; this leads to marked accumulation of lipids in vital organs, blood vessels, and other tissues, resulting in progressive and multi-systemic organ damage including fibrosis, cirrhosis, liver failure, accelerated atherosclerosis, cardiovascular disease, and other devastating consequences. LAL Deficiency affects patients of all ages with sudden and unpredictable clinical complications manifesting from infancy through adulthood. The disease can be diagnosed with a simple blood test. Kanuma was granted orphan designation by the U.S. Food and"
"Tyrosinemia Tyrosinemia or tyrosinaemia is an error of metabolism, usually inborn, in which the body cannot effectively break down the amino acid tyrosine. Symptoms include liver and kidney disturbances and intellectual disability. Untreated, tyrosinemia can be fatal. Most inborn forms of tyrosinemia produce hypertyrosinemia (high levels of tyrosine). All tyrosinemias result from dysfunction of various genes in the phenylalanine and tyrosine catabolic pathway, and are inherited in an autosomal-recessive pattern. Type I tyrosinemia results from a mutation in the ""FAH"" gene, which encodes the enzyme fumarylacetoacetase. As a result of ""FAH"" deficiency, the substrate fumarylacetoacetate can accumulate in proximal renal"
"is a high-affinity transporter specific to the intake of thiamine. Thiamine transport is not inhibited by other organic cations nor affected by sodium ion concentration; it is stimulated by a proton gradient directed outward, with an optimal pH between 8.0 and 8.5. TC1 is transported to the cell membrane by intracellular vesicles via microtubules. Mutations in the ""SLC19A2"" gene can cause thiamine-responsive megaloblastic anemia syndrome (TRMA), which is an autosomal recessive disease characterized by megaloblastic anemia, diabetes mellitus, and sensorineural deafness. Onset is typically between infancy and adolescence, but all of the cardinal findings are often not present initially. The"
"may also be used. The vitamin thiamine is recommended. Mortality without treatment is between 15% and 40%. Currently death occurs in about 1% to 4% of cases. About half of people with alcoholism will develop withdrawal symptoms upon reducing their use. Of these, three to five percent develop DTs or have seizures. The name delirium tremens was first used in 1813; however, the symptoms were well described since the 1700s. The word ""delirium"" is Latin for ""going off the furrow,"" a plowing metaphor. It is also called shaking frenzy and Saunders-Sutton syndrome. Nicknames include the shakes, barrel-fever, blue horrors, bottleache,"
"Hypervalinemia Hypervalinemia, also called valinemia or valine transaminase deficiency, is a rare autosomal recessive metabolic disorder in which urinary and serum levels of the branched-chain amino acid valine are elevated, without related elevation of the branched-chain amino acids leucine and isoleucine. It is caused by a deficiency of the enzyme valine transaminase. Presenting in infancy, symptoms include lack of appetite, vomiting, dehydration, hypotonia and failure to thrive. Hypervalinemia is inherited in an autosomal recessive manner. This means the defective gene responsible for the disorder is located on an autosome, and two copies of the defective gene (one inherited from each"
"is a set of symptoms caused by thiamine deficiency. Hypoesthesia Hypoesthesia (also spelled as hypesthesia) is a common side effect of various medical conditions which manifests as a reduced sense of touch or sensation, or a partial loss of sensitivity to sensory stimuli. In everyday speech this is generally referred to as numbness. Hypoesthesia primarily results from damage to nerves, and from blockages in blood vessels, resulting in ischemic damage to tissues supplied by the blocked blood vessels. This damage is detectable through the use of various imaging studies. Damage in this way is caused by a variety of different"
"the effects of thiamine deficiency that would result from ingesting the leaves raw. In the explorers' journals they noted many symptoms of thiamine deficiency, so it is thought that they did not soak the nardoo long enough. Eventually thiamine deficiency could have led to their demise. It is noteworthy to mention that there are several other hypotheses regarding what may have killed Burke and Wills and it is widely disagreed upon by historians and scientists alike. Thiaminase Thiaminase () is an enzyme that metabolizes or breaks down thiamine into two molecular parts. The old name was ""aneurinase"". There are two"
"to death, yet this is very rarely seen. Thyrotoxic myopathy Thyrotoxic myopathy (TM) is a neuromuscular disorder that develops due to the overproduction of the thyroid hormone thyroxine. Also known as hyperthyroid myopathy, TM is one of many myopathies that lead to muscle weakness and muscle tissue breakdown. Evidence indicates the onset may be caused by hyperthyroidism. There are two known causes of hyperthyroidism that lead to development thyrotoxic myopathy including a multinodular goiter and Graves' disease. Physical symptoms of TM may include muscle weakness, the breakdown of muscle tissue, fatigue, and heat intolerance. Physical acts such as lifting objects"
"respiratory distress syndrome, acute kidney failure, encephalitis, gastrointestinal bleeding, hepatitis, meningitis, myocarditis, pancreatitis, pneumonia, septic shock, sub-acute thyroiditis, and multi-organ dysfunctions. Harmful symptoms involving multiple organ failure and neurological impairment are difficult to treat, and can be lifelong debilitation or directly fatal. The central nervous system is often affected and result in various complications including cerebellitis, cranial nerve palsies, meningoencephalitis, plexopathy, transverse myelitis, neuroleptic malignant syndrome, and Guillan-Barré syndrome. Death rates due to complications can be up to 14% in brain infections, and 24% with multiple organ failure. It is the major cause of acute encephalitis syndrome in India, where"
"personality disorder (BPD), Neurological disorders such as attention-deficit hyperactivity disorder (ADHD), Parkinson's disease as well as chronic pain, neuralgia or neuropathic pain, and fibromyalgia, headache, or migraine, smoking cessation, tourette syndrome, trichotillomania, irritable bowel syndrome (IBS), interstitial cystitis (IC), nocturnal enuresis (NE), narcolepsy, insomnia, pathological crying and/or laughing, chronic hiccups, ciguatera poisoning, and as an adjunct in schizophrenia. For many years the TCAs were the first choice for pharmacological treatment of clinical depression. Although they are still considered to be highly effective, they have been increasingly replaced by antidepressants with an improved safety and side effect profile, such as the"
"Grass tetany Grass tetany or hypomagnesemic tetany, also known as grass staggers and winter tetany, is a metabolic disease involving magnesium deficiency, which can occur in such ruminant livestock as beef cattle, dairy cattle and sheep, usually after grazing on pastures of rapidly growing grass, especially in early spring. Progressive symptoms may include grazing away from the herd, irritability, muscle twitching, staring, incoordination, staggering, collapse, thrashing, head thrown back, and coma, followed by death. However, clinical signs are not always evident before the animal is found dead. The condition results from hypomagnesemia (low magnesium concentration in blood) which may reflect"