Beriberi heart disease

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

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Overview

Beriberi heart disease is a form of BeriBeri called wet BeriBeri that involves the heart. It is caused by severe thiamine deficiency.[1]

Epidemiology and Demographics

This disease is most prevalent in the Far East, however, in the past decade its prevalence has markedly decreased.

It occurs mainly in individuals whose staple diet consists of polished rice that is deficient in thiamine but high in carbohydrates.

Diets with a high carbohydrate content require a greater intake of thiamine. White bread enriched with thiamine has helped in this respect.

Because alcohol is high in carbohydrate content but deficient in thiamine, some alcoholics become thiamine deficient and weakness of the heart muscle may occur. The disease is also common in fad diet appliers.[2]

Pathophysiology

Pathologically the heart in cardiac beriberi is most often hypertrophied and dilated, with involvement of both the right and left chambers.

Differential Diagnosis

Diagnosis

History and Symptoms

  • The clinical manifestations of beriberi heart disease vary considerably with the severity and rapidity of the onset of the condition.
  • Symptoms of heart failure are more frequently seen. Excessive peripheral edema may occur. Dyspnea, weakness, swelling of the ankles, and a nonproductive nocturnal cough are the most common complaints.

Diagnosis

Laboratory Findings

On laboratory diagnosis for Beriberi heart disease serum pyruvate and lactic acid levels are increased.

Electrocardiogram

The ECG shows low-voltage QRS complex and prolongation of the QT interval.

Chest X-ray

Chest x-ray usually shows congestion of the lungs with pleural effusions.

Treatment

  • Treatment including administration of 100 mg of IV thiamine, then 25 mg daily for about 2 weeks causes dramatic improvement.
  • Disturbance of nerves in the legs often accompanies the heart symptoms and thiamine replacement improves this type of polyneuropathy.

Related Chapters

References

  1. Givertz, M. M., Colucci, W. S., and Braunwald, E. Clinical aspects of heart failure, high output failure; pulmonary edema. In. Heart Disease, sixth edition. E. Braunwald, D. P. Zipes, P. Libby, and R.O. Bonow, eds. W. B. Saunders, Philadelphia, 2005.
  2. Attas M, Hanley HG, Stultz D, Jones MR, McAllister RG. Fulminant beriberi heart disease with lactic acidosis: presentation of a case with evaluation of left ventricular function and review of pathophysiologic mechanisms. Circulation, 1978 Vol 58, 566-572 PMID 679449
  3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:77 ISBN 1591032016
  4. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:68 ISBN 140510368X
  5. Jones RH Jr. Beriberi heart disease. Circulation. 1959 Feb;19 (2): 275-83. PMID 13629790
  6. Gelfand D, Bellet S. Cardiovascular manifestations of beriberi based on a study of ten patients. Med Clin North Am. 1949 Nov; 33: 1643-55. PMID 15391541


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