Lichen Planus; An Inboen Error of Metabolism

Abstract

Summary.— The Km of the enzyme glucose‐6‐phosphate dehydrogenase for its substrate glucose‐6‐phosphate has been determined in normal human skin and skin from lichen planus patients. There was a clear difference between the 2 groups comparable to that found in congenital erythrocyte glucose‐6‐phosphate dehydrogenase deficiency. The results are discussed in relation to the aetiology and clinical picture of lichen planus.

What is going on in lichen planus?

“…Cotton and his colleagues (1972) have approached the problem differently and compared glucose-6-phosphate dehydrogenase (G-6-PDH) enzyme activity in biopsies from patients with lichen planus and from the skin of normal controls. Cotton et al (1972) found a clear difference between the two groups and concluded that lichen planus is associated with a congenital abnormality in the G-6-PDH in the skin. This interesting finding has still to be confirmed by other workers, and Jarrett et al (1975) have challenged their results indicating that the difference could be accounted for by the fact that the lymphocytes in the heavy dermal infiltrate also contain this enzyme and that this may well be different from that occurring in epidermal cells.…”

Deficiency of circulating IgA and IgM in adult patients with lichen planus

“…Despite much recent investigation the cause of lichen planus remains unknown (Black, 1972). The development of a lichen planus papule has been attributed to a viral infection (Swanbeck & Thyresson, 1964;Depaoli, 1953), to an inborn error of metabolism (Cotton, van den Hurk & van der Staak, 1972) or to continuous minute damage of unknown origin to the cells in the basal layer of the epidermis (Marks, Black & Wilson Jones, 1973;Presbury & Marks, 1974). Black (1972) stated that there is very little evidence for an autoimmune cause for lichen planus, but Sarkany & Gaylarde (1972), in a preliminary investigation, reported in vitro lymphocyte transformation in two of six patients with lichen planus when their lymphocytes were cultured in the presence of a homogenate made from a lesion taken from the patient's own skin; and Lachapelle & De la Brassine (1973) used autoradiographic and cytochemical techniques on lichen planus lesions and found the cells in the dermal infiltrate to be proliferating lymphoblasts.…”

Immunologically mediated epidermal cell injury

“…There has been much speculation about the etiology of this pattern of cutaneous injury (recently reviewed by Lowe [34]). Both infectious [8,61] and metabolic [15] etiologies have been proposed but there is little good data to support these mechanisms. The finding of immunoglobulin deposits in some lesions of both the cell-rich lichenoid disease prototype, lichen planus (LP), and the cell-poor prototype, cutaneous lupus erythematosus (LE), has suggested a humoral immune mechanism in the LTR.…”