Cases reported "Thiamine Deficiency"

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1/35. Metabolic acidosis and thiamine deficiency.

    We describe a 19-year-old patient who was receiving home parenteral nutrition in whom lactic acidosis developed. A review of her home parenteral nutrition formula revealed the absence of multivitamins, most significantly thiamine. After thiamine administration, the acidosis resolved, and the patient experienced pronounced clinical improvement. Clinicians must be aware that thiamine is essential for normal glucose metabolism and that thiamine deficiency can lead to lactic acidosis. thiamine deficiency should be included in the differential diagnosis of lactic acidosis. The recent shortage of intravenous multivitamin preparations has led to documented cases of lactic acidosis as a result of thiamine deficiency, and a previous shortage led to several deaths due to lactic acidosis as a consequence of thiamine deficiency. All patients receiving parenteral nutrition must also receive adequate vitamin supplementation.
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2/35. 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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3/35. '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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4/35. Efficacy of hemodiafiltration in a child with severe lactic acidosis due to thiamine deficiency.

    We report the case of a child in whom severe lactic acidosis (LA) and hyperammonemia developed after twenty days of total parenteral nutrition (TPN) for diffuse esophageal damage due to caustic ingestion. The revision of TPN preparation revealed that thiamine was never included and the hypothesis of thiamine deficiency was later confirmed measuring the serum thiamine level. Because severe metabolic acidosis the dialytic treatment with hemodiafiltration (HDF) and bicarbonate infusion were performed: the patient very quickly recovered with dramatic reestablishment of the acid-basic balance. Thiamine administration restored lactate metabolism. We emphasize that HDF is a useful and prompt treatment for LA to get over the critical phase of neurological and cardiological damage.
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5/35. Severe metabolic acidosis and heart failure due to thiamine deficiency.

    We report the case of a male patient with severe metabolic acidosis and heart failure caused by thiamine deficiency. He was admitted in August 1998 to the Tokai University Oiso Hospital because of severe dyspnea. The patient was diagnosed with heart failure and metabolic acidosis of unknown causes based on arterial blood gas analysis, chest x ray, and ultrasonic echocardiographic examinations. Our previous experience in treating a patient with thiamine deficiency caused by total parenteral nutrition without thiamine supplementation suggested that this patient was deficient in thiamine. The serum thiamine level was low and the lactate level was high. After intravenous administration of thiamine, the acidosis and heart failure disappeared. Dietary analysis showed that thiamine intake was low (0.32 mg/1000 kcal/d). thiamine deficiency should be included in the differential diagnosis when encountering cases of heart failure with severe metabolic acidosis, even in developed countries.
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6/35. role of cofactors in the treatment of malnutrition as examplified by magnesium.

    In the absence of appropriate amounts of metabolically important cofactors such as magnesium, replenishment of malnourished patients with protein and carbohydrate will exaggerate the underlying abnormality even though the primary deficiency is corrected. The malnourished patients cannot utilize the food substances provided unless they have within their cells commensurate amounts of all the necessary cofactors required for the metabolism of the food supplied. This therapeutic problem in malnutrition is illustrated by three different examples of clinical deterioration when caloric and vitamin replenishment have been undertaken in the face of magnesium deificiency.
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7/35. 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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8/35. Lactic acidosis from thiamine deficiency during parenteral nutrition in a two-year-old boy.

    This is a case report of a two-year-old boy who was operated electively for a blind-loop syndrome of the proximal jejunum. Because of the appearance of chylous ascites, parenteral nutrition was carried out postoperatively. The boy developed a severe uncompensated acidosis and paralytic ileus. Relaparotomy on suspicion of ischemic bowel did not explain the cause of the acidosis and ileus. Postoperatively, the child's condition worsened, requiring intensive care. The drastically elevated lactate levels corroborated the eventually suspected diagnosis of a vitamin B1 deficiency syndrome. The administration of thiamine within two hours produced correction of the acidosis without further bicarbonate therapy. In 24 hours circulation was stabilized. Two months post-operatively the boy had completely recovered from the sequelae of his shock event.
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9/35. Haemorrhagic thiamine deficient encephalopathy following prolonged parenteral nutrition.

    Neuropathological examination of three patients who were maintained on parenteral nutrition without substitution of thiamine demonstrated an acute haemorrhagic encephalopathy. The lesions differed substantially from the classic features of thiamine deficient encephalopathy regarding the histopathological alterations and the topographical distribution. The extreme rapidity of thiamine deprivation may have been responsible for the abrupt clinical onset of the disease and the intensity of the morphological alterations.
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10/35. Severe lactic acidosis due to thiamine deficiency in a patient with B-cell leukemia/lymphoma on total parenteral nutrition during high-dose methotrexate therapy.

    An 11-month-old girl with B-cell leukemia/lymphoma developed profound lethargy due to severe lactic acidosis during chemotherapy and total parenteral nutrition (TPN). Initial treatment with NaHCO3 was ineffective. Treatment with a vitamin cocktail (OH-cobalamin, pyridoxine, thiamine, riboflavine, biotin, carnitine) at pharmacologic doses rapidly improved the child's clinical and laboratory status. Lactic acidosis was caused by an impairment of pyruvate dehydrogenase complex, which was due to lack of its necessary cofactor thiamine in the TPN. This case report indicates that lactic acidosis may be a front-line diagnosis in patients on TPN with lethargy and outlines the need for monitoring thiamine supply in TPN.
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