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Bettina Hohberger, Ursula Schlotzer-Schrehardt, Robert Lämmer, Ulrich-Christoph Welge-Lüßen, Friedrich E Kruse; Agonistic β2-adrenergic receptor autoantibody positivity in progressive glaucoma suspects. Invest. Ophthalmol. Vis. Sci. 2017;58(8):4607.
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© ARVO (1962-2015); The Authors (2016-present)
Agonistic autoantibodies (AAB) against G protein-coupled receptors (GPCR) have been found in several diseases including asthma and arterial hypertension. β2-adrenergic receptors (ß2-AR) are expressed in trabecular meshwork and ciliary body, being potentially involved in the regulation of aqueous humor dynamics. Agonistic β2-adrenergic receptor autoantibodies (β2-AABs) have been detected in ocular hypertension (OHT) and glaucoma patients, yet not in healthy controls. The aim of this study was to compare the rate of perimetric progression in glaucoma suspects in the presence and absence of β2-AAB.
43 glaucoma suspects were included in the study. All patients showed an increased intraocular pressure and in part a glaucomatous optic disc alteration without any perimetric defects. Annually, all patients underwent complete ophthalmological examinations including visual field testing (Octopus G1). Serum samples were analyzed for the presence of β2-AAB.1 Longitudinal perimetric analyses were performed over a follow-up period of 18 years. Perimetric progression was defined as a MD>2.8 and ≥3 adjacent test points on the pattern deviation map with a probability of <5% or ≥2 adjacent test points on the pattern deviation map with a probability of <1%, confirmed at least once. The protocol was approved by the local Ethics Committee (no. 3457) and the study was registered.2
β2-AAB were detected in 31 of 43 glaucoma suspects (72%), whereas 12 patients showed no β2-AAB (28%). A perimetric progression was seen in 6 of 62 eyes of the β2-AAB positive patients (10%). However a perimetric progression was only seen in 1 of 24 eyes of patients without β2-AAB (4%). β2-AAB positivity was found in 86% of all glaucoma suspects, which showed a progressive visual field.
In this pilot study β2-AAB were detected in a large number of glaucoma suspects. In addition the presence of β2-AAB seemed to be associated with the development of visual field defects. First we plan to confirm this relationship in a larger cohort. Secondly we wish to investigate the potential mechanism, by which β2-AAB impair optic nerve head function.1 Dragun D et al. (2005) Angiotensin II type 1-receptor activating antibodies in renal-allograft rejection. N Engl J Med 352: 558-5692 Erlangen Glaucoma Registry, ISSN 2191-5008, CS-2011; NTC00494923
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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