J. Musial et al., GAMMA-INTERFERON ADMINISTRATION TO PATIENTS WITH ATOPIC-DERMATITIS INHIBITS FIBRINOLYSIS AND ELEVATES C1 INHIBITOR, Thrombosis research, 89(6), 1998, pp. 253-261
Recombinant human gamma interferon was used to treat 10 atopic dermati
tis patients. Recombinant gamma interferon was administered weekly for
three consecutive days at 50 mu g/M-2 SQ for four weeks. All patients
' dermatitis improved with recombinant gamma interferon therapy and pl
asma tumor necrosis factor-alpha levels rose with treatment. Recombina
nt gamma interferon treatment positively correlated with reduced total
plasma fibrinolysis as measured by the fibrin lysis plate, plasmin-al
pha(2)antiplasmin complexes, and tissue type plasminogen activator lev
els. Accordingly, plasminogen activator inhibitor levels increased. Tr
eatment also was associated with a transient increase in thrombin-anti
thrombin III complexes. Recombinant gamma interferon resulted in a sig
nificant increase in C1 inhibitor antigen but not activity. Plasma pre
kallikrein, high molecular weight kininogen, and factor XII levels wer
e not decreased. However, 5 of the 10 atopic dermatitis patients befor
e therapy had circulating cleaved plasma high molecular weight kininog
en detected on immunoblot, indicating prior kallikrein formation. The
cleaved, circulating plasma high molecular weight kininogen disappeare
d in four out of the five original patients who were reexamined at one
year after treatment. These combined data indicated that recombinant
gamma interferon treatment reduced total plasma fibrinolysis. In untre
ated atopic dermatitis, circulating cleaved high molecular weight kini
nogen also may be a presenting manifestation. (C) 1998 Elsevier Scienc
e Ltd.