[Keratoacanthoma and its clinical variants. Review of the literature and histopathologic analysis of 90 cases].

Current knowledge about the etiology and histogenesis of keratoacanthoma (KA) is first reviewed, after which the various clinical and histological patterns of this tumor are presented. The differential diagnosis, particularly against spinocellular carcinoma (SCC), and possible forms of therapy are discussed. A series of 90 KAs seen in the period 1976-1986 were investigated histopathologically with reference to the overall architecture, the epithelial differentiation, the behavior towards the adjacent tissue, and the extent and composition of the cellular infiltrate. In addition to routine staining with hematoxylin-eosin and Giemsa, several files have been subjected to immunohistological analysis by means of the peroxidase-antiperoxidase method (PAP) (keratin, lysozyme, epithelial membrane antigen, tissue polypeptide antigen). In 79 cases (88%) the overall architecture found was that of an endo-exophytic, dome-shaped structure with a central crater filled with a plug and with epithelial "lips" at the margins. In 3 KA (3%) a more endophytic picture was seen though no ulceration was observed. In 2 tumors in the very early stages (2%), there was no formation of horn crater and no epithelial lips. Similarly, 5 flat, plaque-like KA (6%) also showed no horn crater. With the exception of 3 aggregated (and/or multicentric) KA (3%), no solitary or multiple types were found. In 88 cases (98%), proliferation of the epidermis was observed mainly in the lateral and basal parts. In 86 KA (96%) there was a relatively well-demarcated, sharp border to the basal tumor portions. In 4 cases (4%) a less precise definition of the outer tumor margins was observed, because of a considerable pseudocarcinomatous, though not truly infiltrative, growth pattern. In 24 KA (27%) there was a strong tendency to formation of one or more sequesters. In the majority of cases, maturation of the epithelial cells was normal. Abnormal multipolar mitoses (7 cases; 8%) and relatively pronounced cellular atypies (8 cases; 9%) were occasionally observed. There was a clear correlation between the composition and extent of the inflammatory infiltrate and the tumor growth stage. In 78 KA (87%) large numbers of intraepithelial neutrophilic microabscesses were shown. In only 13 cases (14%) were substantial numbers of eosinophilic leukocytes observed, and 3 of these tumors (3%) later developed eosinophilic microabscesses.(ABSTRACT TRUNCATED AT 400 WORDS)