Presentation: Cryofibrinogen in Patients with Hepatitis C Virus (HCV)-Mixed Cryoglobulinemia (MC) Vasculitis (2007)

2002 Cryofibrinogen in Patients with Hepatitis C Virus (HCV)-Mixed Cryoglobulinemia (MC) Vasculitis

Background: Mixed cryoglobulin (CG) is usually associated with hepatitis C virus (HCV) infection and may cause a systemic vasculitis. The presence of a cryofibrinogen (CF), another cryoprotein, in the serum of HCV infected patients has not been evaluated.
Aim: to study the prevalence, clinical and therapeutic impacts of CF status in HCV infected patients, with or without HCV-related vasculitis.
Patients and methods: from January, 2000 to December, 2006, 139 consecutive HCV infected (HCV RNA+) patients have been screened for CF and CG (positive if > 0.05 g/L for both). Fifty four patients presented with an HCV-related vasculitis involving the skin (38), the nerve (37), the joints (22), and the kidneys (13). Immunologic, virological and clinical characteristics and their evolution during follow-up period were evaluated according to the CF/CG status at baseline. For treated patients, a sustained virological response (SVR) was defined by persistent HCV RNA negativity 6 months after ending antiviral therapy.
Results: At baseline, 51/139 (37%) patients were CF+, most of whom [45/51 (88%)] were also CG+. Among 88 CF- patients, only 36 (41%) patients were CG+ (p<0.001). In HCV-related vasculitis patients, 26/54 (48%) were CF+ compared to 25/85 (29%) of non-vasculitis patients (p=0.03). In patients with non symptomatic cryoglobulin, 20/32 (63%) were CF+. Main clinical manifestations of HCV-related vasculitis were not different in the 25 patients CF+CG+ compared to the 24 CF-CG+: skin (76%/75%), nerve (72%/63%), kidney (12%/38%), joints (40%/50%), non-Hodgkin lymphoma (12%/8%) (p=NS). Ninety-six patients had a sufficient follow-up (mean 28.7 months) and were more deeply analyzed. Among patients CF+ at baseline (n=40), 11/24 (46%) of those who received an HCV treatment were CF- at the end of follow-up (EOF) compared to only 4/16 (25%) of those who did not receive antiviral drugs (p=NS). Most of CF+ patients were CG+ (90-95%) and those who became CF- became also CG-. Respective rates for CF- patients at baseline (n=56) were 22/28 (79%) and 19/28 (68%) (p=NS). For treated patients who showed a SVR (n=31), 8/18 (44%) CF+ patients at baseline were CF- at the EOF, whereas 11/13 (85%) CF- at baseline remained CF- at EOF (p=0.03). In the non-SVR patients (n=21), respective rates were 3/6 (50%) vs. 11/15 (73%) (p=0.35). The cryoprotein profile at baseline (CF/CG) had no significant impact on the response to HCV treatment, either clinical response of the vasculitis or SVR.
Conclusions: In HCV-infected patients, CF is more frequently present in patients with MC related vasculitis. Antiviral therapy decreased the rate of CF+ patients, when the CG disappeared. The presence of CF had no impact on clinical presentation of the vasculitis, and on clinical and virological response to antiviral therapy.

 A. delluc, None; D. Saadoun, None; P. ghillani, None; D. sene, None; Z. amoura, None; J. piette, None; P. cacoub, None.