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Abnormal cutaneous reactions in dermatitis herpetiformis.

In 94% of the patients with dermatitis herpetiformis, a locally applied ointment with an ester of nicotinic acid (Trafuril) induced an abnormal reaction with erythema, edema, papules, and often vesicles. The appearance of the reaction to Trafuril is similar to DH lesions. It differs markedly from the reactions to iodide where, as a rule, only one large blister results. The reaction is most pronounced 12-24 hours after application of Trafuril. The reactivity is strongest in the predilection areas for dermatitis herpetiformis. Strongly increased reactivity to Trafuril in DH is induced by pretreatment with streptokinase, streptokinase-streptodornase, or urokinase. Diminished reactivity to Trafuril is seen after pretreatment with injections of Compound 48/80, tranexamic acid, cromoglycate, or application of fluocinolone-acetonide, as well as after stroking the skin.

Adult↗

The cutaneous reactions to kallikrein, prostaglandin and thurfyl nicotinate in chronic urticaria and the effect of polyphloretin phosphate.

The erythema and wealing resulting from the application of thurfyl nicotinate ointment (Trafuril) and from the inoculation of kallikrein has been studied in patients with chronic urticaria and normal controls. Polyphloretin phosphate (PPP) suppressed the reaction in controls but in patients with urticaria it increased the reactions to Trafuril and had little effect on the kallikrein reaction. PPP also suppressed the PGE2-induced erythma in normal controls but not in urticaria patients. In a separate study using fibrinolysis autography, prostaglandin (PG) E2 and PGF2alpha depressed fibrinolysis in the skin of two pigs and both kallikrein and Trafuril suppressed fibrinolysis in human skin. It is suggested that the inflammatory reaction induced by thurfyl nicotinate and kallikrein is mediated in part by a prostaglandin-like action. Several anomalies in the action of Trafuril in skin diseases can be explained if such prostaglandin-like activity is mediated in part through inhibition of fibrinolysis.

Chronic Disease↗