Correction of a suppressor cell deficiency in four patients with familial mediterranean fever by in vitro or in vivo colchicine

We have previously reported that three patients with familial Mediterranean fever (FMF) had deficient concanavalin A (Con A) activated suppressor cell inhibition of the proliferation of healthy volunteers' phytohaemagglutinin stimulated responder cells. When these three FMF patients were treated with long term oral colchicine (2 mg/day), their Con A activated suppressor cell deficiency was corrected and FMF attacks prevented. In the present report, the effect of in vitro as well as in vivo colchicine treatment on the suppressor cell function of these three FMF patients as well as one more FMF patient was tested to determine whether colchicine can directly increase suppressor cell function rather than colchicine's preventing FMF attacks by unknown mechanisms which only indirectly results in a correction of the suppressor cell deficiency. Long term oral colchicine treatment corrected the suppressor cell deficiency in the four FMF patients (5±2%, 35±5%, and 46±4% for mean ±s.e.m.% suppression for 0, 1 and 2 mg/day of oral colchicine, respectively). Oral colchicine treatment corrected their suppressor cell deficiency within one week of commencing treatment and even corrected one of the FMF patient's suppressor cell deficiency while he still had some FMF attacks on 1 mg/day of colchicine. Suppressor cells from two of the in vivo untreated FMF patients cultured with 10^-5 M colchicine plus Con A significantly (P<0·01) suppressed proliferation (36±5%) as compared to their suppressor cells cultured only with Con A (4±7%). Furthermore, these in vivo untreated FMF patients' suppressor cells cultured with 10^-5 M colchicine (without Con A) often suppressed as compared to their suppressor cells cultured in medium. Thus colchicine appears to directly correct these FMF patients' suppressor cell deficiency. These observations raise the possibility that colchicine may be therapeutically useful in treating patients with other diseases associated with an absolute or relative deficiency of suppressor cell function.