Sclera Less Involved in Steroid-Induced CSCR Than Idiopathic Pathology

The exact pathogenesis of central serous chorioretinopathy (CSCR) is not fully known, although researchers suspect a relationship with stress, especially for men, patients aged between 30 to 60 years, patients who smoke, those with short axial length, or patients who’ve had corticosteroid exposure. A research group in Japan demonstrated a thicker sclera in patients with idiopathic CSCR (iCSCR) compared with normal eyes, and posited that choroidal circulation may be disrupted by scleral thickening.

This team has now conducted the first investigation comparing scleral thickness of patients with iCSCR with those exhibiting signs of steroid-induced CSCR (sCSCR), as reported in Ophthalmology Science. The study shows ​​scleral thicknesses are significantly thinner in patients with sCSCR than in those with iCSCR, suggesting less scleral involvement in disease pathogenesis for the former group. 

The researchers examined medical records for 110 eyes of 110 patients with CSCR from October 2018 to October 2020. Participants included 96 eyes with iCSCR, and 14 with sCSCR. For those with sCSCR, exposure to steroids comprised dermal, inhalation, intranasal, oral, and topical medications.

CSCR diagnoses were based on imaging with optical coherence tomography (OCT), fluorescein angiography, as well as indocyanine green angiography (ICGA) which illustrated changed choroidal circulatory patterns including early filling delay, and middle or later vessel dilation and vascular hyperpermeability. Scleral thickness was measured 6 mm posterior to the scleral spur, vertically from anterior to posterior scleral border. Mean scleral thickness was significantly thinner in the sCSCR cohort than in the iCSCR group at points measured superiorly (P <.001), inferiorly (P =.002), nasally (P =.001), and temporally (P =.018).

More patients in the sCSCR set were women (P =.015), which agrees with prior studies showing female patients with sCSCR are more affected by corticosteroid use than men. In multivariable analysis, significant factors influencing onset of sCSCR proved to be mean scleral thickness at the four directional points (P =.002), and female sex (P =.046). The investigation speculates that female and male differences in sex hormone regulation may create unique conditions influencing the role steroids play in prompting CSCR.

This investigation found that mean subfoveal choroidal thickness (SCT) did not significantly differ between cohorts. Also, an investigator discovered 2 key structural proportional differences in the sCSCR group compared with the iCSCR group: decreased ratio of large choroidal vascular layer thickness to SCT, and reduced luminal to total choroidal area. Therefore, eyes with sCSCR may differ from iCSCR in intrachoroidal structures, with steroid-induced CSCR possibly occurring without features related to scleral thickening — thick choroid or choroidal vasodilation — seen in eyes with iCSCR.

Previous research has shown a connection between heightened sympathetic nerve activity and onset of acute CSCR, and that raised activity may create vascular resistance, altering blood flow patterns in the choroid. “In fact, steroids reportedly inhibit norepinephrine uptake by non-neuronal cells, thereby increasing norepinephrine concentration at the sympathetic nerve ending and lead to sympathetic nervous system dominance,” according to the study.

Limitations of this investigation include differing lengths of steroid exposure for participants, and various dose-based effects that could not be scrutinized. Also, AS-OCT was performed manually rather than with a more objective, automated system. Researchers suggest the new data reveals less importance of scleral thickness in the development of sCSCR than in iCSCR.

Reference

Sawaguchi S, Terao N, Imanaga N, et al. Scleral thickness in steroid-induced central serous chorioretinopathy. Ophthalmol Sci. Published online February 7, 2022. doi:10.1016/j.xops.2022.100124