Immunological and clinical follow up of hepatitis C virus associated cryoglobulinaemic vasculitis.
OBJECTIVE
To study immunological markers and compare these markers with standard measures for the clinical and immunological follow up of vasculitis activity in hepatitis C virus (HCV) associated cryoglobulinaemic vasculitis (CV).


METHODS
Serial serum samples from eight patients with newly diagnosed HCV associated CV were followed during interferon alpha treatment induced remission of the CV. Vasculitis activity and disease extent were evaluated with the Birmingham vasculitis activity score (BVAS) and disease extent index (DEI). Cryoglobulinaemia, complement levels (C3c, C4, and CH50), rheumatoid factor (RF), autoantibodies such as antinuclear antibodies, soluble interleukin 2 receptor (sIL2r), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble CD30 (sCD30) were determined.


RESULTS
All patients achieved either complete or partial remission of their CV during interferon alpha treatment. There was a significant reduction in vasculitis activity and disease extent (BVAS, DEI), cryoglobulinaemia, RF, sIL2r, sICAM-1, and sCD30. Complement C3c levels increased significantly during this period. Erythrocyte sedimentation rate and levels of complement C4 and CH50 did not change significantly. Both clinical measures (BVAS and DEI) correlated significantly only with C3c and sCD30.


CONCLUSIONS
Although this study was of only a small group of patients, it shows that BVAS and DEI as clinical measures and C3c and sCD30 as immunological markers may be useful in the follow up of disease activity of HCV associated CV. The data indicate that activity of the humoral (cryoglobulinaemia, RF, autoantibodies) and cellular (sIL2r, sICAM-1, sCD30) immune response and endothelial damage (sICAM-1) are found in HCV associated CV.
Department of Rheumatology, University of Lübeck, and Rheumaklinik Bad Bramstedt, Oskar-Alexander-Str. 26, 24576 Bad Bramstedt, Germany.
P
P
Lamprecht
F
F
Moosig
A
A
Gause
K
K
Herlyn
E
E
Csernok
H
H
Hansen
W L
WL
Gross
D000974:Antibodies, Antinuclear / Q000097:blood; D015415:Biomarkers; D001799:Blood Sedimentation; D015932:Complement C3c / Q000032:analysis; D003181:Complement C4 / Q000032:analysis; D015941:Complement Hemolytic Activity Assay; D003449:Cryoglobulinemia / Q000097:blood / Q000188:drug therapy / Q000209:etiology*; D005260:Female; D019698:Hepatitis C, Chronic / Q000097:blood / Q000150:complications* / Q000188:drug therapy; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D016898:Interferon-alpha / Q000627:therapeutic use; D017730:Ki-1 Antigen / Q000097:blood; D008297:Male; D008875:Middle Aged; D015375:Receptors, Interleukin-2 / Q000097:blood; D012217:Rheumatoid Factor / Q000097:blood; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric; D016896:Treatment Outcome; D014657:Vasculitis / Q000097:blood / Q000188:drug therapy / Q000209:etiology*
D000974:Antibodies, Antinuclear; D015415:Biomarkers; D003181:Complement C4; D016898:Interferon-alpha; D017730:Ki-1 Antigen; D015375:Receptors, Interleukin-2; D018799:Intercellular Adhesion Molecule-1; D015932:Complement C3c; D012217:Rheumatoid Factor