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June 1993

Hyperamylasemia in Toxic Epidermal Necrolysis

Author Affiliations

Department of Dermatology Hôpital Henri Mondor 94010 Créteil, France; Biochemistry Laboratory Hôpital Albert Chenevier 94010 Créteil, France; Biochemistry Laboratory Hôpital Cochin 75006 Paris, France; Department of Dermatology Hôpital Henri Mondor 94010 Créteil, France

Arch Dermatol. 1993;129(6):792-793. doi:10.1001/archderm.1993.01680270136027

To the Editor.—  Mucous membranes and systemic manifestations of toxic epidermal necrolysis (TEN) (also known as Lyell's syndrome) include oropharyngeal, ocular, genital, pulmonary, and intestinal involvement.1,2 Hyperamylasemia was reported in only a few cases and its origin, ie, salivary and/or pancreatic, remained controversial.3,4 The purpose of this study was to investigate the incidence and the origin of hyperamylasemia in TEN.

Materials and Methods.—  We reviewed retrospectively cases from 1985 through 1990 that fulfilled the criteria of TEN.1 Sixty-four patients with at least two determinations of amylase were included in the study. Amylase was assayed using the colorimetric method (α-amylase, Merck-Clevenot, Chelles, France) (normal, 50 to 220 U/L). Patients with hyperamylasemia (at least twice normal) were age and sex matched with patients without hyperamylasemia. These two groups of patients with TEN were compared for involvement of body surface area and mucous membranes, biological parameters (glycemia, serum aminotransferases levels,

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