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Beriberi heart disease should be considered in all patients with cardiac failure and a history of alcohol abuse or dietary deficiency. We studied the haemodynamic changes which took place immediately after intravenous administration of thiamine to a patient with high-output beriberi. Cardiac output and stroke volume fell rapidly, but not below normal levels, and systemic vascular resistance rose.

Six patients with gross thiamine deficiency found during normal psychiatric practice in England are described. Two surveys of newly admitted psychiatric patients are recounted. A major degree of biochemical deficiency, with or without minimal clinical manifestations, was found. Only three (1%) of 326 patients surveyed had gross clinical deficiency. It is thought that severe thiamine deficiency, though rare in the Western countries, has not been eradicated. Deficiency may cause psychiatric conditions like Wernicke's encephalopathy or may be a secondary feature in mental illness due to anorexia, in reduced food intake, and in poor nutrition. The importance of being aware of the possibility for correct diagnosis is emphasised.

Adults who had been drinking alcohol were admitted to hospital with severe lacticacidosis and died within two days. Empirical treatment with thiamine proved to be a cure for the disorder, for it was acute pernicious or fulminating beriberi. Thiamine deficiency is neglected as a cause of lacticacidosis.

In one case of fulminant hepatic failure by acute alcoholic hepatitis, renal failure seemed to be related to active renal vasoconstriction by systemic endotoxemia due to impaired hepatic clearance of toxins, associated with or complicated by a located intravascular coagulation with acute tubular necrosis. The associated thiamin deficiency may have accentuated this renal vasoconstriction.

A case of Shoshin beriberi found in a patient with severe metabolic acidosis and shock was presented. We believe the metabolic acidosis in this case is ascribable to overproduction of pyruvate and lactate resulting from lack of thiamine due to preferential intake of sake, precooked food, and rice, and also to shock. The hemodynamic studies done after recovery from shock revealed that the cardiac output, which was initially high, decreased to a slightly low level and then increased to a normal level, concomitant with an increase in the peripheral vascular resistance after introductory administration of thiamine. After treatment with thiamine, all abnormalities disappeared.

A case of beriberi heart failure in a chronic hemodialyzed patient is described. The etiology and the diagnostical criteria are discussed. The possibility of this complication in chronic hemodialyzed patients is considered.

Cardiac beriberi is considered a rare disease in western society. A patient with fulminant Shoshin-type beriberi was studied in the acute phase and found to have severe metabolic acidosis, high output biventricular failure, and markedly low systemic vascular resistance. Red blood cell transketolase activity was abnormally low. Following treatment with thiamine, diuretics, digitalis and oxygen, all abnormalities disappeared. The historical background of the disease is reviewed along with a discussion of pathophysiologic mechanisms responsible for the hemodynamic profile and lactic acidosis. Angiographic and hemodynamic data on the patient presented suggest relative depression of left ventricular function in the acute phase of beriberi. Since beriberi is uncommonly encountered, emphasis is placed on diagnostic and therapeutic implications of the disease which may not be widely appreciated.

Of 898 former Far East prisoners of war, assessed between 1968 and 1981, 49 (5.5%) had evidence of persisting symptomatic neurological disease dating back to their periods of malnutrition in captivity. The commonest syndromes were peripheral neuropathy (often of "burning foot" type), optic atrophy, and sensori-neural deafness. Though nutritional neuropathies disappeared soon after release in most ex-Far East prisoners of war, in some they have persisted up to 36 years since exposure to the nutritional insult.

The AA. report a case of thymine acute deficiency in a 35 year old chronic alcoholic and malnourished male, who was admitted to the hospital because of high-output heart failure, peripheral polyneuropathy, cortico-cerebellar atrophy (associated with RMN), ataxia and peripheral edema. The diagnosis of wet Beri-beri combined with Wernicke-Korsakoff syndrome was made and appropriate therapy with pulse daily dose of parenteral thymine instituted. At the fifth day of therapy the cardio-circulatory hyperkinetic syndrome was markedly improved and after three weeks neurological damage was also alleviated. The AA. outline the importance of early diagnosis and treatment for this form of high-output heart failure, which has a poor prognosis and, if left untreated, can determine the death of the patient in a few days.

Haemodynamic measurements before and after treatment are described in two patients with beriberi heart disease. The first patient had severe disease with a cardiac output of 17.3 litres per minute, which had returned to normal a month later. The second patient had moderate disease with a cardiac output of 7.4 litres per minute; a fall in this and a rise in systemic vascular resistance was found one and two hours after the intravenous injection of aneurine hydrochloride. The plasma pyruvate concentration was raised in the first patient but only slightly so in the second, in whom the pyruvate metabolism test was abnormal. The haemodynamic studies in both cases were of considerable help in making the diagnosis. The diagnosis of beriberi should be considered in any patient with heart disease who has a history of alcoholism, especially as prompt vitamin treatment is curative.