May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
Serum Levels of Antibodies to Carbonic Anhydrase II in Patients With Retinitis Pigmentosa
Author Affiliations & Notes
  • Y. Lu
    Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, Ann Arbor, Michigan
  • E. Filippova
    Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, Ann Arbor, Michigan
  • J. Heckenlively
    Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, Ann Arbor, Michigan
  • Footnotes
    Commercial Relationships Y. Lu, None; E. Filippova, None; J. Heckenlively, None.
  • Footnotes
    Support Foundation Fighting Blindness
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 3747. doi:
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      Y. Lu, E. Filippova, J. Heckenlively; Serum Levels of Antibodies to Carbonic Anhydrase II in Patients With Retinitis Pigmentosa. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3747.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose:: Autoimmune anti-retinal antibodies (ARAs) are postulated to play an important role in Cancer Associated Retinopathy (CAR), Melanoma Associated Retinopathy (MAR), and CAR-like syndrome, which includes retinitis pigmentosa (RP) patients with an autoimmune exacerbation of their retinopathy from anti-retinal antibodies. Carbonic anhydrase II (CAII) has been implicated as a causative antigen in our and other investigators’ work. We have initiated investigations of CAII as reported below.

Methods:: Serum samples from 59 patients diagnosed with RP were screened for antiretinal proteins activity by western blotting. Enzyme linked immunosorbent assay (ELISA) were performed to evaluate the titer of anti-CAII antibodies. Patient records were reviewed to ascertain if there was a specific clinical association with CAII antibodies.

Results:: We found ~30 kDa band in 23 (39%) out of 59 patients’ sera. As compared with normal controls (0.08±0.06), there was no significant difference in the CA II antibody titer in RP patients (0.11±0.15) (p=0.52). However, 9 (39%) out of these 23 patients show high titers (A405 > 0.110) of antibodies to CAII (0.24±0.13). No clear associated was seen between antibodies to CAII and electroretinographic dysfunction, presence of cystoid edema, retinal wrinkling, or unique visual field alterations in these 9 patients.

Conclusions:: ARAs at 30 kDa are relatively common when testing for antibody activity in the group of RP patients who have circulating ARAs. We found that 9 out of 23 (39%) patients with high titer CAII antibody but no specific clinical association. This suggests that CA II antibody in RP patients may be less significant diagnostically. The pathogenetic role of anti-CA II antibody remains uncertain.

Keywords: retinal degenerations: hereditary 
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