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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats were maintained on a thiamine-deficient diet to deplete skeletal muscle of thiamine pyrophosphate, and thus decrease the oxidative metabolism of pyruvate. The blood lactate concentration was significantly elevated in thiamine-deficient (TD) animals when compared with pair-fed (TP) controls. Analysis of diaphragm strips from these animals revealed that tissue lactate and pyruvate concentrations were not affected by any of the treatments employed. The rate of lactate efflux from TD tissues was, however, twice that from TP and 4.5 times that from weight-control (WC) tissues. The H+ efflux rate was also much greater in the TD muscle preparation than either of the control groups. Following 3 min of stimulation (150-Hz, 200-ms pulse train every 0.5 s), the degree of fatigue of tissues from each of these three treatment groups was not different. The observation in this study that glycolysis becomes the predominant metabolic pathway in thiamine deficiency without increasing the intracellular level of products, indicates that this treatment also has other effects which increase the effective lactate permeability of the fibre membranes.
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PMID:Lactate and pyruvate production in isolated thiamine-deficient rat diaphragm strips. 672 53

High cardiac output failure/state (HCOF) is regular feature of some illnesses e.g. thiamine deficiency, hyperthyroidism, severe anemia, Paget's disease or arteriovenous fistulae. HCOF in multiple myeloma is reported quite rarely. 31-year-old man was admitted because of fatigue, dyspnea and subfebrilities. Heart rate was 116/min, sinus rythm blood pressure 110/60 mmHg. Chest film showed cardiomegaly with sings of interstitial pulmonary edema, echocardiography mild dilatation of the left ventricle with hyperkinetic wall motion and small pericardial effusion. Hemoglobin was 104 g/l, leukocyte count 13.5 x 10(9)/l with 30% of plasmatic cells. Serum protein electrophoresis demonstrated a monoclonal gammapathy, X ray studies of the skelet multiple osteolytic lesions. Diagnosis of plasmocytic leukemia-form of multiple myeloma was established and chemotherapy (vincristine + adriamycine + dexamethason) was started. Patient cardiac status deteriorated. Cardiac catheterisation demonstrated mean righ atrial pressure of 25 mmHg, mean pulmonary artery pressure of 28 mmHg and pulmonary artery wedge pressure of 24 mmHg. Co was 20.0 l/min (C.I. 11.5 l/min/m2). In continuing of chemotherapy and symptomatic therapy for heart failure patients status gradually improved and complete remission of the myeloma and normalisation of cardiac parameters was achieved. Heart failure in multiple myeloma patients has been attributed to amyloidosis of myocardium, hyperviscosity syndrome, co-existing CAD or anthracycline toxicity. HCOF should be considered in patients with clinical evidence of heart failure and normal left ventricular function.
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PMID:[Hypercirculatory heart failure in a patient with plasmacytic leukemia]. 855 97

The most common symptoms of chronic beriberi due to thiamine deficiency include dyspnoea, fatigue, leg oedema, lower extremity weakness and numbness. When collapsed peripheral circulation, metabolic acidosis, or shock are present, the disease has advanced from chronic beriberi to pernicious or fulminating beriberi heart failure (Shoshin beriberi). We report two patients with fulminating beriberi; both of whom had been incarcerated at a detention centre for 5 months before hospitalization. A prolonged monotonous diet, low in thiamine, was a major risk factor in both patients. Thiamine deficiency should be considered for any patient with symptoms and signs compatible with beriberi.
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PMID:Cardiac beriberi among illegal mainland Chinese immigrants. 1127 46

Wernicke's Encephalopathy is an acute neuro-psychiatric condition caused by an insufficient supply of thiamine (Vitamin B1) to the brain. If undiagnosed or inadequately treated, it is likely to proceed to Korsakoff's Syndrome. Wernicke's Encephalopathy can result from dietary deficiency alone and this form is usually successfully treated, with little chance of Korsakoff's Syndrome supervening. On the other hand, thiamine deficiency associated with alcohol misuse/dependence may require up to 1 gram of thiamine IV in the first 24 hours to be treated successfully. The reasons for this difference in treatment will be discussed. Thiamine diphosphate acts as a co-factor for a number of thiamine-dependent enzymes. Thiamine deficiency leads to a reduction in the activity of these enzymes, and this leads to alterations in mitochondrial activity, impairment of oxidative metabolism, decreased energy status and eventually selective neuronal death. The damage caused by the combination of thiamine deficiency and alcohol metabolism probably interferes with adequate thiamine transport at a number of sites in the body, including the blood-brain barrier, as well as causing damage to the apoenzymes which then require higher concentrations of thiamine to work normally. The accumulated damage is likely to render the use of oral thiamine therapeutically inadequate since the body is unable to produce high enough concentrations of thiamine in the blood to traverse the blood-brain barrier. Some individuals are probably genetically predisposed to develop Wernicke's. Long before individuals with alcohol misuse or dependence develop Wernicke's Encephalopathy the neurons and other cells of the body are functioning sub-optimally because of the inadequate supply of thiamine and the neurotoxic effect of alcohol. This relative deficiency initiates a series of pathological changes which accumulate and further interfere with the supply of thiamine and its utilisation at a time when the requirements are increased. The best treatment for Korsakoff's Syndrome is timely recognition of Wernicke's Encephalopathy and appropriate intervention and prevention.
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PMID:The evolution and treatment of Korsakoff's syndrome: out of sight, out of mind? 2256 70

Spinocerebellar ataxia type 2 is a genetic disorder characterised by the degeneration of the cerebellum, its connections and degeneration in brainstem areas. Some observations indicate that high doses of thiamine may lead to the partial regression of the symptoms. One patient was under rehabilitative treatment from June 2011 to July 2012. We assessed the level of fatigue using the Fatigue Severity Scale. We performed the Scale for Assessment and Rating of Ataxia and Robertson Profile for Dysarthria (Italian version). Thiamine and thiamine pyrophosphate levels in the blood were within the healthy reference range. We started a parenteral therapy with 100 mg intramuscular every 7 days. The therapy led to a partial regression of fatigue within a few days. After about 3 months, a discreet improvement of motor symptoms especially in speech was observed. The symptoms could derive from a focal thiamine deficiency that could determine a selective neuronal loss.
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PMID:Thiamine and spinocerebellar ataxia type 2. 2331 45

Living with fibromyalgia means living with chronic pain, fatigue, sleep disorders and other associated key symptoms. To date, pharmacotherapy generally produces modest benefits. Some observations indicate that the large majority of symptoms of fibromyalgia could be the clinical manifestation of a mild thiamine deficiency due to a dysfunction of the active transport of thiamine from the blood to the mitochondria or to enzymatic abnormalities. Between June and July 2011, we recruited three female patients affected by fibromyalgia. We proceeded with the study of the patients' history, a physical examination, an evaluation of chronic widespread pain using the Visual Numeric Scale and an evaluation of the fatigue using the Fatigue Severity Scale were also performed. The levels of thiamine and thiamine pyrophosphate in the blood were determined. After the therapy with high doses of thiamine, in the patients, there was an appreciable improvement of the symptoms.
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PMID:High-dose thiamine improves the symptoms of fibromyalgia. 2369 41

The majority of the patients with multiple sclerosis (MS) experience fatigue. Some observations indicate that fatigue and related manifestations concomitant with MS could be associated with an intracellular mild thiamine deficiency. We recruited 15 patients with MS who also experience fatigue and assessed the severity of the fatigue using the Fatigue Severity Scale. Although blood thiamine and thiamine pyrophosphate levels were within normal limit in all the patients, high-dose thiamine therapy administered orally or parenterally led to an appreciable improvement of the fatigue. The absence of apparent decrease in blood thiamine despite the presence of symptoms referable to a mild thiamine deficiency suggests that these patients may have a dysfunction of the mechanisms of intracellular transport or structural enzymatic abnormalities. The administration of large quantities of thiamine was effective in reversing the fatigue in MS, suggesting that the abnormalities in thiamine-dependent processes could be overcome by diffusion-mediated transport at supranormal thiamine concentrations.
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PMID:High dose thiamine improves fatigue in multiple sclerosis. 2386 Dec 80

A 43-year-old man was admitted with end-stage renal disease caused by IgA nephropathy, and was treated with maintenance peritoneal dialysis. The patient developed general fatigue and appetite loss, and his symptoms were gradually aggravated by depression. After approximately 2 months on dialysis, the patient presented with altered consciousness and ophthalmoplegia. Wernicke's encephalopathy was diagnosed based on the presence of classic symptoms and the findings on magnetic resonance imaging. Thiamine replacement therapy was immediately initiated. The patient recovered from most of his neurological symptoms; however, the sequela of Korsakoff syndrome remained. A marginal thiamine deficiency in combination with predisposing factors must be considered when treating dialysis patients.
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PMID:Wernicke's encephalopathy that developed during the introduction period of peritoneal dialysis. 2404 19

The food habit is involved in the onset and development of lifestyle-related diseases. In this review I would like to describe a historical case of vitamin B1 deficiency, as well as our case study of fatty acid metabolism abnormality due to carnitine deficiency. In history, the army and navy personnel in Japan at the end of the 19th century received food rations based on a high-carbohydrate diet including white rice, resulting in the onset of beriberi. An epidemiological study by Kenkan Takaki revealed the relationship between the onset of beriberi and rice intake. Then, Takaki was successful in preventing the onset of beriberi by changing the diet. However, the primary cause had yet to be elucidated. Finally, Christian Eijkman established an animal model of beriberi (chickens) showing peripheral neuropathy, and he identified the existence of an anti-beriberi substance, vitamin B1. This is an example of the successful control of a disease by integrating the results of epidemiological and experimental studies. In our study using a murine model of fatty acid metabolism abnormality caused by carnitine deficiency, cardiac abnormality and fatty liver developed depending on the amount of dietary fat. In addition, the mice showed disturbance of orexin neuron activity related to the sleep-arousal system, which is involved in fatigue symptoms under fasting condition, one of the states showing enhanced fatty acid metabolism. These findings suggest that fatty acid toxicity is enhanced when the mice are more dependent on fatty acid metabolism. Almost simultaneously, a human epidemiological study showed that narcolepsy, which is caused by orexin system abnormality, is associated with the polymorphism of the gene coding for carnitine palmitoyltransferase 1B, which is involved in carnitine metabolism. To understand the pathological mechanism of fatty acid toxicity, not only an experimental approach using animal models, but also an epidemiological approach is necessary. The results will be applied to preventing and treating lifestyle-related diseases associated with fatty acid metabolism abnormality.
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PMID:[Experimental Approach to Analysis of the Relationship between Food Environments and Lifestyle-Related Diseases, Including Cardiac Hypertrophy, Fatty Liver, and Fatigue Symptoms]. 2599 41