Fighting steroids with steroids: a case of bilateral central retinal vein occlusion in an anabolic steroid user

Central retinal vein occlusion (CRVO) is a common cause of painless monocular vision loss, typically occurring in adults over 50 years old with hypertension, hyperlipidaemia and diabetes mellitus.^1–4 It rarely occurs in younger individuals without traditional cardiovascular risk factors.^4,5 CRVO is thought to be caused by a thrombotic event occurring in the central retinal vein, posterior to the lamina cribrosa.^1,2 Contributing factors include compression, venous endothelial damage and thrombophilia.^1,2 Ophthalmic examination of CRVO reveals dilated and tortuous retinal veins with intraretinal haemorrhages in all quadrants.¹ Management includes metabolic optimisation for secondary prevention and treatment of sequelae such as ocular neovascularisation and cystoid macular oedema (CMO) with intravitreal anti-vascular endothelial growth factor (anti-VEGF) agents, corticosteroids and laser photocoagulation.¹

This report highlights a unique case of a 47-year-old male with sequential bilateral CRVOs associated with anabolic steroid use. Anabolic steroids are becoming increasingly recognised for their prothrombotic effects, yet their role in retinal vascular occlusions remains largely unexplored. This case provides insights into the potential pathophysiological mechanisms linking anabolic steroid use to retinal vascular disease and underscores the importance of identifying non-traditional risk factors in younger patients presenting with vascular disease. Understanding these associations is critical as anabolic steroid use becomes more prevalent, particularly among athletes and bodybuilders. Additionally, this report discusses the challenges in managing refractory CMO and optimising visual outcomes in atypical CRVO presentations.

Case presentation

A 47-year-old male presented with a 2-day history of painless monocular vision loss in his left eye. He had a history of recreational anabolic androgenic steroid use consisting of weekly intramuscular injections of 500mg testosterone enanthate and occasional nandrolone decanoate (DECA) use. His typical regime included 1 month off anabolic steroids every 2–3 months. He had no significant medical history and was not on any other regular medications. On examination, the left eye visual acuity (VA) was 6/60+2 (pinhole [PH] no improvement), with an intraocular pressure (IOP) of 40mmHg. There was no relative afferent pupillary defect (RAPD). On gonioscopy, his left eye’s anterior chamber angles were closed without neovascularisation. Fundoscopy showed CRVO, and optical coherence tomography (OCT) revealed CMO. Workup included blood pressure (114/71mmHg), full blood count (within normal limits), renal function (estimated glomerular filtration rate [eGFR] >90mL/min/1.73m²), lipids (total cholesterol 5.7mmol/L, high-density lipoprotein [HDL] 0.94mmol/L, low-density lipoprotein [LDL] 3.4mmol/L), HbA_1c (34mmol/mol) and coagulation studies (international normalised ratio [INR] and activated partial thromboplastin time [APTT] within normal limits).

Treatment with a single intravitreal bevacizumab injection resolved the CMO, improving VA to 6/12 (PH no improvement). Bilateral peripheral iridotomies were performed, after which both eyes’ IOP remained 9–10mmHg and his angles remained open without plateau iris configuration or peripheral anterior synechiae. Despite being encouraged to stop, the patient continued to use anabolic steroids.

Fifteen months later, the patient developed right CRVO with CMO (Figure 1). Initial treatment with three monthly intravitreal bevacizumab injections improved but did not resolve the CMO. Subsequent intravitreal triamcinolone resolved his CMO, improving the right eye VA from 6/120 (PH 6/76-1) to 6/12 (PH 6/9.5).

View Figure 1.

Discussion

While CRVO primarily affects older patients with hypertension, hyperlipidaemia and/or diabetes, younger patients often have non-traditional cardiovascular disease risk factors.^4,5 Rothman et al. found traditional risk factors were present in all patients older than 50 with CRVO, but only 53% of those younger than 50.⁴ Of the remaining 47%, a non-traditional risk factor was identified in 71% of cases, most commonly thrombophilia.⁴

Anabolic steroids are associated with coronary, cerebral, retinal and limb thrombosis.^6,7 They promote thrombosis through several mechanisms, including stimulating thrombopoiesis, erythropoiesis and coagulation factor production.⁷ Additionally, anabolic steroids enhance platelet aggregation by increasing platelet-activating factor (PAF), elevating intracellular calcium levels and promoting both the production and sensitivity of thromboxane A2 (TxA2).⁷ Moreover, these agents impair vascular endothelial function by reducing nitric oxide (NO) production and suppressing prostaglandin I2 (PgI2) synthesis, exacerbating the prothrombotic state.⁷ Finally, anabolic steroids contribute to hyperlipidaemia, accelerating atherosclerosis and increasing the risk of cardiovascular disease.⁸

CMO, a common complication of CRVO, results from raised venous pressure, blood-retinal barrier disruption, inflammatory cytokines and elevated VEGF levels.⁹ Intravitreal anti-VEGF therapy is first-line therapy; however, corticosteroids offer the theoretical benefit of reducing inflammation in addition to disrupting the VEGF pathway.^9,10 Prior literature suggests that intravitreal therapy is more effective in younger patients, resulting in fewer injections required.⁵ In this case, the multifaceted prothrombotic effects of anabolic steroids may have contributed to the refractory nature of his right eye’s CMO. Perhaps the pathways described above are more responsive to anti-inflammatory agents. Despite the resolution of CMO, the patient’s final VA remained limited to 6/12 bilaterally. Studies have shown that final VA outcomes in CRVO are strongly influenced by initial VA and the degree of retinal ischaemia.¹ Before the advent of intravitreal anti-VEGF therapy, patients presenting with a VA of 6/15–6/60 only improved to better than 6/15 in 19% of cases.¹¹ Additionally, photoreceptor damage due to subclinical retinal ischaemia and prolonged CMO likely contributed to the incomplete visual recovery, despite resolution of the oedema.

This report is the first to associate anabolic steroid use with CRVO. Previous cases of branch retinal vein occlusions (BRVOs) have been documented in young bodybuilders using anabolic steroids.⁶ Given the increasing prevalence of anabolic steroid use, with a lifetime prevalence of 6.4% among males, clinicians must maintain a high index of suspicion when assessing young patients with vascular disease.^12,13 Identifying anabolic steroid use as a contributing risk factor may help to explain vascular disease in atypical cohorts and aid in forming treatment strategies.

Conclusion

This case highlights the importance of recognising androgenic anabolic steroid use as a potential risk factor for retinal vascular disease in younger patients. It emphasises the need for a thorough history to identify non-traditional cardiovascular risk factors. As anabolic steroid use becomes increasingly prevalent, clinicians must remain vigilant for identifying its complications and tailor treatments accordingly.