June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Influence of Agonistic β2-Adrenergic Receptor Autoantibodies on Retinal Capillary Flow in Ocular Hypertension and Open-Angle Glaucoma
Author Affiliations & Notes
  • Bettina Hohberger
    Ophthalmology, University Erlangen-Nuremberg, Erlangen, Germany
  • Joanna Harazny
    Department of Human Physiology, University of Warmia and Masuria, Olsztyn, Poland
  • Robert Laemmer
    Ophthalmology, University Erlangen-Nuremberg, Erlangen, Germany
  • Georg Michelson
    Ophthalmology, University Erlangen-Nuremberg, Erlangen, Germany
  • Anselm Juenemann
    Department of Ophthalmology, University of Rostock, Rostock, Germany
  • Footnotes
    Commercial Relationships Bettina Hohberger, None; Joanna Harazny, None; Robert Laemmer, None; Georg Michelson, None; Anselm Juenemann, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 2748. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Bettina Hohberger, Joanna Harazny, Robert Laemmer, Georg Michelson, Anselm Juenemann; Influence of Agonistic β2-Adrenergic Receptor Autoantibodies on Retinal Capillary Flow in Ocular Hypertension and Open-Angle Glaucoma. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2748.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: Agonistic Autoantibodies (AABs) against G protein coupled receptors (GPCR) are found in several human diseases (e. g. Asthma, arterial hypertension). β2-adrenergic receptors (ß2-AR) are involved in the regulation of aqueous humor dynamics and were found on retinal blood vessels. Agonistic β2-adrenergic receptor autoantibodies (β2-AABs) were found in glaucoma suspects and glaucoma patients, yet not in normals. The aim of this study was to investigate retinal capillary flow and its potential correlation with β2-AAB activity in these groups.

Methods: 74 probands were included (25 normals, 21 OHTs, 10 pre-perimetric POAGs, 18 POAGs; Erlangen Glaucoma Registry, ISSN 2191-5008, CS-2011; NTC00494923). All patients underwent complete ophthalmological examinations including examinations with Octopus G1 program and measurements of retinal capillary flow by Heidelberg Retina Flowmetry. Serum probes of all patients were analyzed of β2-AABs using a bioassay (1). In this assay the alteration of the beating rate of spontaneously beating cultured neonatal rat cardiomyocytes, expressing GPCR, due to the applied serum level of AABs, is counted. Statistical analysis was done using non-parametric U-Test. The protocol was approved by the local Ethics Committee (3457).<br /> (1) Dragun D et al. (2005) Angiotensin II type 1-receptor activating antibodies in renal-allograft rejection. N Engl J Med 352: 558-569

Results: (1) Retinal capillary flow was reduced in OHTs (246±59 [AU]) and glaucoma patients (pre-POAG: 238±49 [AU]; POAG: 247±62 [AU]). (2) Correlation analysis for all patients with β2-AAB positivity showed a significant correlation of retinal capillary flow with β2-AAB (p=0.014; R=0.349). (3) Subgroup analysis for patients with OHT, glaucoma patients with and without perimetric defects revealed no correlation of retinal capillary flow in patients with OHT (p=0.298). However a tendency could be observed in pre-POAG (p=0.144; R=0.497) up to a statistically significant correlation between retinal capillary flow and β2-AAB in POAG (p=0.012; R=0.578).

Conclusions: The high percentage of β2-AAB positivity in glaucoma patients and glaucoma suspects suggests a potentially primary role for β2-AAB in glaucoma disease. The strong correlation of β2-AABs with retinal capillary flow in POAG as well as the trend in pre-POAG, suggest a potential influence of β2-AABs on retinal microcirculation.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×