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Cryoglobulinaemia vasculitis in patients coinfected with HIV and hepatitis C virus
David Saadoun1, Laurent Aaron, Mathieu Resche-Rigon
1Service de Médecine Interne, Hôpital La Pitié-Salpêtrière, Paris, France.
Insights
Hepatitis C virus (HCV) and human immunodeficiency virus (HIV) coinfection can cause mixed cryoglobulinemia (MC) vasculitis. Anti-HCV therapy showed a beneficial effect in these patients.
Area of Science:
- Immunology
- Infectious Diseases
- Rheumatology
Background:
- Mixed cryoglobulinemia (MC) vasculitis is a rare condition often associated with hepatitis C virus (HCV) infection.
- The interplay between HCV and human immunodeficiency virus (HIV) coinfection in the context of MC vasculitis requires further elucidation.
Purpose of the Study:
- To characterize mixed cryoglobulinemia (MC) vasculitis in patients coinfected with HCV and HIV.
- To compare the clinical features and outcomes of MC vasculitis in HIV/HCV-coinfected patients versus HCV-monoinfected patients.
Main Methods:
- A retrospective multicenter study was conducted using the GERMIVIC Database, analyzing 4005 HIV/HCV-coinfected patients.
- The characteristics and outcomes of 11 HIV/HCV-coinfected patients with MC vasculitis were compared to 118 HCV-monoinfected patients with MC vasculitis.
Main Results:
- HIV/HCV-coinfected patients with MC vasculitis were younger, more frequently male, and had a history of intravenous drug use compared to HCV-monoinfected patients.
- Common clinical manifestations included polyneuropathy, purpura, arthralgia, and kidney involvement. Anti-HCV therapy (interferon-alfa and ribavirin) demonstrated a beneficial effect, leading to sustained virological response and clinical improvement in some patients.
- Antiretroviral therapy did not significantly improve MC vasculitis, irrespective of HIV virological response.
Conclusions:
- Anti-HCV therapy offers a beneficial treatment strategy for patients coinfected with HIV and HCV presenting with MC vasculitis.
- Understanding the specific characteristics of MC vasculitis in the context of HIV/HCV coinfection is crucial for effective management.
Objective:
To describe mixed cryoglobulinaemia (MC) vasculitis in patients coinfected with hepatitis C virus (HCV) and HIV.
Design:
Retrospective multicentre study through the GERMIVIC Database of 4005 HIV/HCV-coinfected patients.
Methods:
The characteristics and outcome of 11 HIV/HCV-coinfected patients with MC vasculitis were analysed and compared with those of 118 HCV-infected patients with MC vasculitis.
Results:
The mean age was 46 years (SD, 14), with 82% male. The median initial CD4 cell count was 367 cells/microl (range, 252-846). After a mean follow-up of 44.4 months, two deaths (18%) were noted. Clinical manifestations of MC included polyneuropathy in seven (64%), purpura in four (36%), arthralgia in four (36%), and kidney involvement in three (27%). Six patients received combination treatment with interferon-alfa and ribavirin, three of whom had sustained HCV virological response and were complete clinical responders. Four patients received corticosteroids and two showed a partial clinical response. Regardless of the HIV virological response, antiretroviral therapy did not improve MC vasculitis. Compared with patients with HCV monoinfection, coinfected patients were younger (P < 0.001), more frequently male (P = 0.03), more frequently intravenous drug users (P < 0.001), had higher HCV viraemia (P = 0.004), higher liver necroinflammation (P = 0.03), higher gammaglobulinaemia (P < 0.001) and lower cryoglobulin level (P = 0.03). The clinical manifestations of MC vasculitis did not differ significantly between the two groups.
Conclusion:
There was a beneficial effect of anti-HCV therapy for HIV/HCV-coinfected patients with MC vasculitis.
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