Cases reported "Thiamine Deficiency"

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1/21. 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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ranking = 1
keywords = lactic acidosis, acidosis
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2/21. 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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ranking = 0.51893948129263
keywords = acidosis
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3/21. 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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ranking = 0.91268933715979
keywords = lactic acidosis, acidosis
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4/21. 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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ranking = 0.41515158503411
keywords = acidosis
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5/21. 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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ranking = 0.36325763690484
keywords = acidosis
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6/21. Shoshin beriberi in an infant of a thiamine-deficient mother.

    The classical form of thiamine deficiency in children is comprised of peripheral neuropathy, encephalopathy and high-output cardiac failure, predominantly right-sided. "Shoshin beriberi" cardiac failure has a different presentation, with vasoconstriction, hypotension and severe metabolic acidosis. A three-month breast-fed infant developed these features (biochemical tests confirmed the diagnosis). His mother, although non-symptomatic, had biochemical evidence of thiamine deficiency.
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ranking = 0.051893948129263
keywords = acidosis
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7/21. 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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ranking = 1.0848484149659
keywords = lactic acidosis, acidosis
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8/21. Severe lactic acidosis and thiamine deficiency during total parenteral nutrition--case report.

    We encountered a case of total parenteral nutrition-associated lactic acidosis that did not respond to sodium bicarbonate or other conventional emergency treatments. He was characterized by minimal food intake before surgery, delayed gastric emptying after pylorus-preserving pancreatoduodenectomy due to pancreas head cancer and long-term total parenteral nutrition without food intake and vitamin supplements after surgery. After thiamine administration, the patient very quickly recovered with dramatic reestablishment of the acid-base balance. We emphasize the need to supplement total parenteral nutrition with thiamine-containing vitamins for the patients whose food intake does not meet nutritional requirements and to intravenously replenish using high-dose thiamine simultaneously with the manifestation of signs and symptoms of severe lactic acidosis with unknown cause. In conclusion, thiamine deficiency should be included in the differential diagnosis of lactic acidosis for the patients who received total parenteral nutrition without food intake and vitamin supplements.
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ranking = 1.2051135446427
keywords = lactic acidosis, acidosis
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9/21. 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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ranking = 0.53541671471095
keywords = lactic acidosis, acidosis
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10/21. thiamine deficiency as a cause of metabolic acidosis.

    Since its introduction in the 1970s, total parenteral nutrition (TPN) has gained popularity as a means of nutritional support for patients who cannot orally ingest sufficient calories and nutrients to promote wound healing or recovery from debilitating illness. As this treatment modality is employed among heterogenous groups of patients, a number of potential problems have been identified. Fortunately, most of these difficulties can be eliminated or minimized by understanding the metabolic goals of TPN and by employing proper catheter management. One of the unusual complications, a high anion gap metabolic acidosis refractory to bicarbonate therapy, occurred in one of our patients who was receiving TPN without adequate thiamine supplementation. The casual relationship between thiamine deficiency and metabolic acidosis has been well described in the literature, but remains under-recognized by many physicians.
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ranking = 0.31136368877558
keywords = acidosis
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