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Article
March 1974

Hepatic Coma in Cirrhosis, Portal Hypertension, and Following Portacaval ShuntIts Etiologies and the Current Status of Its Treatment

Author Affiliations

Boston
From the Department of Surgery, Harvard Medical School; and the Surgical Physiology Laboratory, Massachusetts General Hospital, Boston.

Arch Surg. 1974;108(3):325-336. doi:10.1001/archsurg.1974.01350270055010
Abstract

This article considers the pathogenesis of hepatic coma. Molecular mechanisms involving possible disorders in cerebral transmitters are related to the most salient fact about hepatic coma: the liver-brain axis. Various competing, but not necessarily mutually exclusive, theories are examined for relevance and compatibility with clinical and experimental information. Evidence is presented against the role of ammonia as the sole factor in the pathogenesis of coma. Known amino acid imbalances in hepatic coma are related to possible disturbances in neurotransmitters in the brain and the role of false neurotransmitters examined. Therapy is related to biochemical mechanisms.

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