[Initial manifestation of eruptive exanthematous psoriasis vulgaris caused by captopril medication]

Angiotensin-converting enzyme (ACE) is identical to the dipeptidyl carboxypeptidase kininase II, which inactivates bradykinin. That is why captopril, an orally active ACE inhibitor, alters the kallikrein-kinin-arachidonic acid system. It is suggested that this mechanism could be responsible for the dosage-dependent incidence of polymorph cutaneous eruptions during therapy with captopril. A 42-year-old female patient with no previous personal or family history of psoriasis developed an eruptive-exanthematous type of psoriasis vulgaris 1-2 weeks after the beginning of captopril therapy. It is suggested that the onset of the dermatosis was produced by a blockade of bradykinin inactivation. This might have increased the production of arachidonic acid and led to elevated concentrations of inflammatory mediators.