Cases reported "Thiamine Deficiency"

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1/29. Lactic acidosis caused by thiamine deficiency in a pregnant alcoholic patient.

    BACKGROUND: Metabolic acidosis from accumulation of lactic acid is a relatively common condition, whereas its causation by thiamine deficiency is not. methods: We studied a pregnant alcoholic patient who presented with hyperemesis and a high anion gap acidosis. RESULTS: Lactic acidosis and thiamine deficiency were confirmed. The patient's symptoms and acidosis resolved with thiamine administration. CONCLUSIONS: Lactic acidosis caused by thiamine deficiency must be suspected when pregnant patients at risk for thiamine deficiency present with a high anion gap acidosis. A large dose of thiamine must be administered immediately.
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2/29. A common cause of altered mental status occurring at an uncommon age.

    Wernicke's encephalopathy is a neurologic disorder due to a nutritional deficiency of thiamine, characterized by ocular palsies, ataxia, and altered mental activity. While Wernicke's encephalopathy is commonly attributed to alcoholism in the adult population, it has been described in children receiving prolonged parenteral nutrition and those with malignancies and AIDS. The disease, however, is rarely diagnosed in the pediatric population during life. We report a case of Wernicke's encephalopathy in a child with prolonged starvation and aim to improve awareness of a potentially fatal but treatable disease.
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3/29. 'Iatrogenic' Wernicke's encephalopathy in japan.

    'Iatrogenic' Wernicke's encephalopathy has appeared to occur more frequently in japan, probably induced by the change of our Japanese national health insurance policy in 1992. We report 4 nonalcoholic patients with such Wernicke's encephalopathy, which occurred during the early postoperative oral food intake period following intravenous nutrition without vitamin supplements. We analyzed the medical records of 4 patients, 3 men and 1 woman, aged between 55 and 71 years, who were admitted to our hospital between 1992 and 1995. Three patients underwent gastrointestinal surgery and 1 suffered chronic pyothorax. We diagnosed our patients as having Wernicke's encephalopathy based on typical neurological abnormalities, in addition to typical cranial magnetic resonance image findings, low serum vitamin B(1) levels, or both. Although all of the patients were treated with vitamin B(1) and showed some improvement, 1 patient developed korsakoff syndrome, 2 made incomplete neurological recovery, and 1 died. We speculated that the body vitamin B(1) stores had been decreasing in our patients who did not receive any vitamin supplements during intravenous hyperalimentation or hydration. Subsequent administration of high calorie and high carbohydrate oral diets increased the demand for vitamin B(1), further depleting the vitamin stores, thereby causing 'iatrogenic' Wernicke's encephalopathy. The change of our national health insurance policy in 1992 discouraged the routine administration of vitamins, probably causing Wernicke's encephalopathy in our patients.
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4/29. chorea induced by thiamine deficiency in hemodialysis patients.

    thiamine deficiency is mainly encountered in alcoholics or food faddists, but it may complicate chronic dialysis because of low intake and accelerated loss of thiamine in dialysis patients. We report here 2 hemodialysis (HD) patients who developed chorea induced by thiamine deficiency. We propose that thiamine deficiency, with a consequent dysfunction of the basal ganglia, may induce chorea in HD patients.
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5/29. Wernicke's encephalopathy in a non-alcoholic man: case report and brief review.

    Wernicke's encephalopathy, a serious neurological disorder caused by thiamine deficiency, is most commonly found in chronic alcoholics. We present a typical case of Wernicke's encephalopathy in a non-alcoholic man. Our patient presented with altered mental status, slurred speech, fever, vomiting and headache of one-week duration. An infectious etiology of the symptoms was ruled out by spinal fluid cultures. The patient improved dramatically within 24 hours of administration of thiamine.
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6/29. Wernicke-korsakoff syndrome following small bowel obstruction.

    We report a case of a 64-year-old lady who developed clinical features of Wernicke-korsakoff syndrome following a laparotomy for small bowel obstruction. Following the operation she developed paralytic ileus and required total parenteral nutrition for one month. A suspected history of average 40 units of weekly alcohol consumption prior to the operation could not be confirmed and the patient did not show any sign of alcohol dependence. Within a few months of treatment with a daily oral dose of thiamine 200 mgs supplemented by multivitamins the patient showed subjective evidence of improvement in confusion, confabulation, and anterograde amnesia, although objective tests showed residual deficits in many areas of cognitive functioning, including immediate and delayed recall of verbal and non-verbal materials, planning and switching of attention.
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ranking = 0.027248544779038
keywords = alcohol
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7/29. wernicke encephalopathy: unusual findings in nonalcoholic patients.

    We report the unique findings on magnetic resonance imaging (MRI) in two cases of diet-related wernicke encephalopathy (WE). There was no relation to alcohol in either case. The first patient presented with seizures and showed changes of WE on diffusion-weighted MRI with involvement of the motor strip. The second case illustrates extensive changes in the thalamus caused by WE, resulting in obstructive hydrocephalus requiring shunting.
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8/29. Fatal metabolic acidosis caused by thiamine deficiency.

    Acute thiamine deficiency, an uncommon cause of hemodynamic instability in Western countries, may be manifested by acute heart failure and neurological deficits. Severe metabolic acidosis is one of its least recognized features. We present a report of foreign workers who complained of weakness and lower limb edema and were found to have acute thiamine deficiency. One died of refractory metabolic acidosis and shock, and the diagnosis was reached post mortem. thiamine deficiency should be considered in every case of severe lactic acidosis without an obvious cause, especially in high-risk populations (malnourished, alcoholics, Far-East workers, etc). Whenever it is suspected, empiric treatment with thiamine should be initiated immediately. physicians who care for populations at risk should be familiar with the clinical spectrum of nutritional deficits, and monitor the nutritional habits of these patients carefully. The treatment is inexpensive and devoid of adverse effects. Moreover, delaying thiamine administration in patients with deficiency may cause severe life-threatening metabolic acidosis and affect recovery. The prophylactic use of thiamine in a high-risk population, even before blood levels are received, may be cost effective.
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9/29. Occidental beriberi and sudden death.

    beriberi, thiamine deficiency, is classified as "dry" (neurologic) or "wet" (cardiovascular) and may be mixed. Deficiency of this vitamin may be nutritional or secondary to alcohol intoxication. In Western societies (occidental beriberi), the disorder is more commonly observed in long-term alcohol abusers. However, it may go undiagnosed because it is relatively uncommon. In some cases (acute cardiovascular beriberi), early treatment with parenteral vitamin B1 is required to prevent the development of low-output state and sudden death. We report a case of occidental beriberi with fatal outcome despite therapy.
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10/29. thiamine deficiency in hematologic malignant tumors.

    The case is reported of a patient with acute myeloid leukemia with severe right-sided congestive heart failure that responded to treatment with thiamine. leukocytes cells contain relatively high concentrations of thiamine-dependent enzymes compared with erythrocytes. Because no other cause could be found, it was postulated that consumption of thiamine by blast cells was responsible for the deficiency. After studying this patient, the thiamine pyrophosphate (TPP) effect was measured in five other consecutive patients with fast-growing hematologic malignant tumors. In two patients, the TPP effect was elevated slightly, but another patient had a definite thiamine deficiency with severe cardiac failure. It is suggested that the clinician be alert for this underdiagnosed potentially fatal but easily treatable deficiency in nonalcoholic patients with fast-growing hematologic cancers.
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