Arthritis & Rheumatism, Volume 60,
October 2009 Abstract Supplement
The 2009 ACR/ARHP Annual Scientific Meeting
Philadelphia October 16-21, 2009.
Investigation of Possible Etiological Link Between Parainfluenza-1 and Giant Cell Arteritis
Davis1, Trevor E., Battaglioli2, Gino, Pinheiro1, Joaquim, Carlson3, J. Andrew, Lamson2, Daryl M., St. George2, Kirsten
Albany Medical Center, Albany, NY
New York State Dept of Health, Slingerlands, NY
Albany Medical Colleg, Albany, NY
Purpose:
An infectious etiological trigger of Giant Cell Arteritis (GCA) is suggested by initial symptoms resembling a viral prodrome and by epidemiology which reveals both temporal and geographical clusters of GCA. The histologic hallmark of GCA is multinucleated giant cells found in temporal artery biopsies. Only a small number of human viruses are known to induce multinucleated giant cells, including respiratory syncytial virus (RSV), human parainfluenza virus (HPIV), measles virus, Epstein Barr Virus, and herpes simplex virus. Serological testing for HPIV-1 antibodies, revealed a correlation between recent infection and GCA, but this has not yet been clearly confirmed or refuted by biopsy studies. We hypothesized HPIV-1 would be detected more frequently in GCA-positive temporal artery biopsies than in GCA-negative biopsies. Furthermore there would be no difference in frequency of detection for other common respiratory viruses including influenza A and B, RSV (1, 2, and 3), HPIV (2, 3, and 4), human metapneumovirus, enterovirus, and rhinovirus.
Method:
After IRB approval, we obtained archived temporal artery biopsy samples from 80 consecutive symptomatic patients referred to Albany Medical Center for pathological examination in 2003–2007. An a priori power analysis indicated that the specimens available were sufficient to detect an increase in the proportion of HPIV-1 by 30% in GCA-positive biopsies, compared with negative biopsies, with a power of 80%, and alpha of 0.05. Pathologic examination was accomplished previously by established techniques. Samples were formalin fixed and paraffin embedded. For molecular analysis, paraffin was removed using xylene and sample nucleic acid was extracted using a WaxFree extraction kit in accordance with the manufacturer's protocol. The samples were then prepared for reverse transcription polymerase chain reaction using the ResPlex II and run per protocol developed at the Wadsworth Center in collaboration with Genaco.
Results:
In the 68 temporal artery biopsy samples adequate for PCR studies, 12 were previously classified, by a pathologist, as positive for GCA, and 56 were negative. No viral nucleic acid (including HPIV-1) was detected in any of the specimens, including the 12 GCA positives (proportion = 0.00, 1 sided 95% CI, 0.00–0.28). The observed number of HPIV-1 positives, 0 in 12 GCA (+) temporal artery biopsies, is significantly less (p<0.05 by 1-sided Fisher's exact test) than the minimum we expected a priori, if HPIV-1 were etiologically related to GCA.
Conclusion:
Our findings do not support the role of HPIV-1 as an etiologic agent for GCA. However, it is possible that the current methodology is insufficient to confirm this relationship. For instance, if the virus is not infecting the temporal arteries directly but rather causing the pathologic changes of GCA indirectly such as through immune complex deposition or if the virus infected the tissue but is no longer present. Further investigation into a possible causative agent of GCA is necessary.
To cite this abstract, please use the following information:
Davis, Trevor E., Battaglioli, Gino, Pinheiro, Joaquim, Carlson, J. Andrew, Lamson, Daryl M., St. George, Kirsten; Investigation of Possible Etiological Link Between Parainfluenza-1 and Giant Cell Arteritis [abstract]. Arthritis Rheum 2009;60 Suppl 10 :131
DOI: 10.1002/art.25214
