[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 34.204.194.190. Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Article
July 1932

INFLUENCE ON CARBOHYDRATE METABOLISM OF EXPERIMENTALLY INDUCED HEPATIC CHANGES: II. PHOSPHORUS POISONING

Author Affiliations

SAN FRANCISCO; LEIPZIG, GERMANY

From the Medizinische Universitätsklinik, Professor Dr. Morawitz, Director, Leipzig.

Arch Intern Med (Chic). 1932;50(1):58-75. doi:10.1001/archinte.1932.00150140065005
Abstract

In order to produce a diffuse injury of the hepatic parenchyma with as little damage as possible to other organs, the two classic poisons phosphorus and chloroform were used. Anatomically, phosphorus, according to Mosiman and Whipple,1 attacks chiefly the cell protoplasm. The lesions produced by moderate phosphorus poisoning consist of fatty degeneration, which is described by Opie and Alford2 as usually appearing in the early stages in the center of the lobules, while later it is most conspicuous near the portal spaces. Severe poisoning by phosphours produces coagulative necrosis, which has a tendency to be at the periphery of the lobules.

Phosphorus may produce fatty degeneration of a moderate degree also in other organs. However, to quote from an article on the hepatic factor in chloroform and phosphorus poisoning by Williamson and Mann,3 "The liver is the most seriously damaged organ histologically and physiologically." Opie and Alford,

×