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Abstract Number: 176

Prevalence and Associations of Hepatitis C Arthritis in Chronic Hepatitis C Virus Infection

Elizabeth D. Ferucci1, Holly S. Ryan2, Tammy L. Choromanski1, Lisa J. Townshend-Bulson2, Stephen E. Livingston2, Brian J. McMahon2 and Mark H. Wener3, 1Division of Community Health Services, Alaska Native Tribal Health Consortium, Anchorage, AK, 2Alaska Native Tribal Health Consortium, Anchorage, AK, 3Rheumatology & Lab Med, University of Washington, Seattle, WA

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: autoantibodies, hepatitis and inflammatory arthritis

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Session Information

Title: Infection-related Rheumatic Disease

Session Type: Abstract Submissions (ACR)

Background/Purpose: Chronic infection with hepatitis C virus (HCV) has been reported to cause inflammatory arthritis and/or fibromyalgia.  Case series of patients with HCV-associated arthritis have been described, but population-based studies of individuals with chronic HCV including systematic interview and evaluation by a rheumatologist have been limited.

Methods: Study participants were recruited from a population-based cohort with chronic HCV.  Any individual in the cohort who had not been treated with anti-viral therapy was invited to participate.  The study visit included an interview for  joint symptoms and fatigue, including the London Fibromyalgia Epidemiology Study Screening Questionnaire; assessment of functional status with the Health Assessment Questionnaire disability index (HAQ-DI); examination by a rheumatologist including joint count and tender point count; and a blood draw.  Sera were tested for the following autoantibodies: cyclic citrullinated peptide (CCP), rheumatoid factor (RF) by nephelometry, RF isotypes (IgG, IgM, and IgA) by ELISA, and ANA by immunofluorescence.  After the study visit and medical record review, participants were categorized as follows: 1) HCV-associated arthritis; 2) RA; and 3) no inflammatory arthritis.

Results: To date, 71 study participants have been recruited, of whom 6 (8.5%) were classified as HCV-associated arthritis, 4 (5.6%) as RA, and 61 (85.9%) as no inflammatory arthritis.  CCP and RF were more common in those with RA, when compared to HCV arthritis and no inflammatory arthritis groups (CCP 67%, 0%, and 2%, respectively, p =0.006; RF 100%, 20%, and 40%, p=0.03).   Of the RF isotypes, only RF IgG prevalence differed by group (75%, 0%, and 27%, p=0.04).  ANA prevalence did not differ by group (50%, 80%, and 35%, p=0.09).  The mean HAQ-DI was similar across groups (0.41, 0.52, and 0.29, p=0.29), and the prevalence of fatigue interfering with activities was also similar (50%, 83%, 48%, p=0.29).  There was a difference between groups in screening positive for fibromyalgia on the questionnaire (25%, 67%, and 15%, p=0.01), but no difference in mean number of tender points on examination (10.5, 8.2, 4.6, p=0.06) or in the proportion with 11 or more tender points present (50%, 33%, and 16%, p=0.09).

Conclusion: In chronic HCV infection, CCP, RF, and RF IgG differ in the groups with HCV arthritis, RA, and no inflammatory arthritis.  Positive fibromyalgia screen by questionnaire is more common among those with HCV arthritis, but disability, fatigue, and the number of tender points on exam are similar.  Future studies are ongoing with a goal to expand our ability to characterize HCV associated arthritis.


Disclosure:

E. D. Ferucci,
None;

H. S. Ryan,
None;

T. L. Choromanski,
None;

L. J. Townshend-Bulson,
None;

S. E. Livingston,
None;

B. J. McMahon,
None;

M. H. Wener,

BioRad Laboratories,

2,

Inova Diagnostics, Inc.,

.

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