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February 1962

Enzymes, Acantholysis, and Pemphigus

Author Affiliations


From The Department of Dermatology, College of Physicians and Surgeons, Columbia University, and The Dermatology Service, The Presbyterian Hospital.

Present address of Dr. Weakley: The Subdepartment of Dermatology, Department of Medicine, and the Department of Physiological Chemistry, The Johns Hopkins School of Medicine and Hospital, Baltimore.

Arch Dermatol. 1962;85(2):190-194. doi:10.1001/archderm.1962.01590020030004

The mechanical basis of acantholysis is the loss of both structure and function of the intercellular bridges (desmosomes) which connect certain epithelial cells. Using electron microscopy, Wilgram, Caulfield, and Lever1 have recently provided evidence that this is a result of intracellular damage in epithelial cells. It is thought that cell necrosis also plays a primary role in acantholysis produced by the virus of herpes zoster2 and by cantharidin.3 On the contrary, epithelial-cell separation produced by salts such as LiBr appears to be due to mechanical forces exerted upon the desmosomes,4,5 even though it occurs only in viable tissue.4,6

Histologically, cantharidin acantholysis closely resembles that of pemphigus vulgaris.7 This fact has led several investigators to use it as an experimental model for investigation of the biochemical mechanism of acantholysis. The early experiments of Haas et al.8 showing inhibition of respiration in mouse liver slices