Abstract
Five to 6000 cases of beriberi among Americans in a Japanese prison camp in the Philippine Islands are reported. Dependent edema responded to protein feedings but did not respond to the admn. of thiamine chloride. The "wet beriberi" was due to a hypoproteinemia and not vit. B1 deficiency. Beriberi heart disease was manifested in 3 ways: (1) tachycardia, arrhythemia, poor exercise tolerance and normal size heart; (2) chronic congestive failure with right and left ventricular enlargement; (3) acute cardiac dilatation and failure and sudden death. Thiamine chloride, if given early and in adequate dosage, corrected the cardiac disease. Digitalis had no effect. The typical lesions of dry beriberi were ascending, symmetrical peripheral neuritis of arms and legs, optic neuritis, degeneration of posterolateral tracts of spinal cord, and "beriberi spots", a skin lesion resembling erythema nodosum. Sensory disturbances were predominant. Motor manifestations were minimal or absent except in a few showing ankle or wrist drop. An irreversible optic atrophy was a frequent sequela. Thiamine chloride first corrected the anorexia, nervous manifestations, tachycardia, and arrhythemia and improved exercise tolerance. The neuritis responded sooner to the entire B complex than to thiamine alone. There was no advantage of the intrathecal over the subcutaneous route. There may be nutritional causes of poly-neuritis other than the lack of thiamine.

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