J. Garcia-suarez et al., HCV-associated thrombocytopenia: clinical characteristics and platelet response after recombinant alpha 2b-interferon therapy, BR J HAEM, 110(1), 2000, pp. 98-103
Hepatitis C virus (HCV) has been proposed as a possible causative agent of
chronic thrombocytopenia. We investigated HCV infection in a series of 51 u
nselected Spanish patients with chronic acquired thrombocytopenia, Anti-HCV
and HCV viraemia were detected in 13/51 (22.5%) of cases; this prevalence
was particularly significant when compared with HCV seropositivity in age-m
atched controls (0.4%). Anti-HCV-positive patients, four men and nine women
with a median age of 59.3 years (range 36-72), had a mean platelet count o
f 55.8 x 10(9)/1 (range 12-96). Only one of our HCV-positive thrombocytopen
ic patients had hypersplenism. Platelet-associated IgG (PAIgG) was negative
, as measured by immunofluorescent now cytometric analysis in 11/13 HCV-pos
itive thrombocytopenic patients. Thus, thrombocytopenia in our HCV-positive
patients appeared to be non-autoimmune mediated. In six patients, a trial
of recombinant alpha 2b-interferon (IFN-alpha) given at a dose of 3 MU thre
e times per week. for 6-24 months gave a durable (> 1 year) and significant
increase in platelet count in all six patients. The maximum increase occur
red after 6 months of IFN-alpha therapy. In conclusion, the ability of IFN-
alpha to increase platelet counts in HCV-positive thrombocytopenic patients
supports mechanisms involving a direct role for HCV inhibiting platelet pr
oduction.