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The in vitro effect of hydroxychloroquine on skin morphology and transglutaminase *
Author(s) -
Wolf Ronni,
Schiavo Ada Lo,
Lombardi Maria Luisa,
Esposito Carla,
Ruocco Vincenzo
Publication year - 1997
Publication title -
international journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.677
H-Index - 93
eISSN - 1365-4632
pISSN - 0011-9059
DOI - 10.1046/j.1365-4362.1997.00227.x
Subject(s) - psoriasis , epidermis (zoology) , keratinocyte , in vitro , tissue transglutaminase , barrier function , medicine , hydroxychloroquine , dermatology , immunology , pathology , microbiology and biotechnology , biology , enzyme , biochemistry , anatomy , disease , covid-19 , infectious disease (medical specialty)
Background Antimalarials are some of the most notorious drugs which may induce psoriasis, with 25% of all reported cases being associated with them. Antimalarials do not induce psoriasis de novo , but trigger subclinical psoriasis. In a previous report, we suggested that antimalarials exert their effect by interfering with the epidermal transglutaminase (TGase) activity. Objective on verify this hypothesis by examining the effect of hydroxychloroquine sulfate (HCQS) on cultured human skin and on TGase activity in vitro.Materials and methods Skin samples from normal donors were cultured in the presence of HCQS for 4 days, and then processed for microscopic examination. TGase activity was assayed in the presence of HCQS and compared with blanks. Results Significant changes in epidermal morphology were seen in all explants cultured in the presence of HCQS at all concentrations employed. Areas of enhanced and irregular keratinization were observed in the upper epidermis, while a loss of cell polarity, with keratinocyte crowding and disarray, was seen in the lower epidermis. In addition, we observed intraepidermal splitting at different levels and dermo‐epidermal detachments. HCQS showed a concentration‐dependent inhibition of TGase activity. Conclusions We suggest that HCQS causes an initial break in the barrier function of the epidermis by inhibiting TGase activity; this is followed by a physiologic response of the epidermis aimed at barrier restoration. This rather nonspecific stimulus to epidermal proliferation is probably sufficient to trigger psoriasis in predisposed individuals or aggravate it in psoriatic patients.