title: Systemic vasculitis in patients with hepatitis C.
abstract: OBJECTIVE
  To analyze the main characteristics of patients infected with hepatitis C virus (HCV) presenting with different types of vasculitis syndrome.
  
  
  METHODS
  We retrospectively compared 2 groups of patients with HCV presenting with systemic vasculitis: 10 with biopsy proven polyarteritis nodosa-type systemic vasculitis (PAN, Group 1) and 7 with mixed cryoglobulinemia syndrome (MC, Group 2).
  
  
  RESULTS
  Patients of Group 1 presented with different features than Group 2: life threatening systemic vasculitis (10 vs 0; p < 0.01), severe multifocal sensorimotor mononeuropathies versus distal moderate sensory polyneuropathies, malignant hypertension (5 vs 0; p = 0.04), cerebral angiitis (2 vs 0), ischemic abdominal pain (2 vs 0), kidney and liver microaneurisms (2 vs 0), increased erythrocyte sedimentation rate and C-reactive protein (7 vs 0; p < 0.01), renal insufficiency (5 vs 0; p = 0.04), HCV genotype 1b (3 vs 6; p = 0.06), and lower activity of chronic hepatitis (p = 0.02). Neuromuscular biopsies showed lesions of vasculitis in all patients, but the type of vasculitis was different in Group 1 compared to Group 2: medium size artery involvement (7 vs 0; p < 0.01), necrotizing vasculitis (10 vs 0; p < 0.01), and mononuclear cell infiltrate in perivascular areas (0 vs 7; p < 0.01). Using prednisone, plasma exchanges, and interferon-alpha, complete recovery was obtained in all PAN-type patients except one. In Group 2 patients, interferon-alpha did not have any effect on the peripheral neuropathy.
  
  
  CONCLUSIONS
  HCV infection may be associated with different types of systemic vasculitis, i.e., polyarteritis nodosa or mixed cryoglobulinemia. Because of differences in clinical and pathological features and therapeutic strategy, PAN-type vasculitis should be distinguished from MC-type vasculitis in HCV patients.
authors.affiliation: Department of Internal Medicine, H pital La Pitié-Salpêtrière, Paris, France. patrice.cacoub@psl.ap-hop-paris.fr
authors.forename: P
authors.initials: P
authors.lastname: Cacoub
authors.forename: T
authors.initials: T
authors.lastname: Maisonobe
authors.forename: V
authors.initials: V
authors.lastname: Thibault
authors.forename: A
authors.initials: A
authors.lastname: Gatel
authors.forename: J
authors.initials: J
authors.lastname: Servan
authors.forename: L
authors.initials: L
authors.lastname: Musset
authors.forename: J C
authors.initials: JC
authors.lastname: Piette
mesh_terms: D000328:Adult; D000368:Aged; D000792:Angiography; D003449:Cryoglobulinemia / Q000150:complications / Q000473:pathology* / Q000503:physiopathology / Q000628:therapy; D003450:Cryoglobulins / Q000032:analysis / Q000145:classification; D004594:Electrophysiology; D005260:Female; D016174:Hepacivirus / Q000276:immunology / Q000302:isolation & purification; D019698:Hepatitis C, Chronic / Q000150:complications / Q000473:pathology*; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use; D007668:Kidney / Q000098:blood supply / Q000000981:diagnostic imaging; D008297:Male; D008643:Mesentery / Q000098:blood supply / Q000000981:diagnostic imaging; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000473:pathology / Q000502:physiology; D010543:Peroneal Nerve / Q000473:pathology / Q000502:physiology; D020427:Peroneal Neuropathies / Q000150:complications / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D010951:Plasma Exchange; D010488:Polyarteritis Nodosa / Q000150:complications / Q000473:pathology* / Q000503:physiopathology / Q000628:therapy; D011241:Prednisone / Q000627:therapeutic use; D012189:Retrospective Studies
chemical_list: D003450:Cryoglobulins; D016898:Interferon-alpha; D011241:Prednisone