Sir,

Central serous chorioretinopathy (CSR) is characterised by serous elevation of neurosensory retina at the posterior pole. It typically affects young and middle aged men. Type A personality, male gender, emotional stress, pregnancy, increased levels of endogenous cortisol1 and treatment with corticosteroids2 have been associated with central serous chorioretinopathy. We report a case of CSR in a patient on regular testosterone therapy because of hypogonadotropic hypogonadism.

Case report

A 52-year-old man presented to eye clinic with a 1-week history of grey patch in front of his right eye. He never had any significant ocular problem in the past. He was diagnosed with acromegaly 24 years ago and subsequently had trans-sphenoidal surgery 7 years later, and radiotherapy 13 years later. Four years ago, he developed hypogonadotropic hypogonadism and he was started on testosterone replacement regime of injection testosterone 500 mg every four weekly. At 1 month prior to his presentation, testosterone dose was increased to 500 mg every three weekly as he was losing early morning erection. At 2 weeks before presentation, his serum hormone profile was carried out, which showed peak testosterone levels of more than 69 mmol/l (normal: 10–35 mmol/l). The serum cortisol levels and growth hormone levels were normal. He was not taking any other medication although he had been on bromocriptine in the past.

On examination his visual acuity in right eye was 6/18 and 6/6 in left eye. The anterior segment examination of both eyes was unremarkable. Dilated fundus examination of the right eye with slit-lamp biomicroscopy showed neurosensory serous detachment of about 2-disc diameter centred at fovea. These finding were consistent with central serous chorioretinopathy. The patient underwent fundus fluorescein angiography to rule out choroidal neovascular membrane, which revealed typical CSR (Figure 1). At 4 week follow-up appointment his visual symptoms were slightly better, and dilated fundus examination of right eye showed resolving CSR. At this stage, his blood peak testosterone levels were 34 mmol/l. In 6 weeks time his central serous retinopathy resolved completely with no sequels. The testosterone trough levels at this stage were normal at 14.9 mmol/l and so were the growth hormone and cortisol levels.

Figure 1
figure 1

Late frame of fundus fluorescein angiogram of right eye showing typical CSR.

Full size image

After 6 months, his visual acuity remained 6/6 with no ocular symptoms. He was still on 500 mg testosterone injection every third week and his hormone levels were in normal range.

Comments

Central serous chorioretinopathy typically affects males from 20 to 45 years old, however, there are case reports of CSR occurring in patients of 60 years or older.3 The aetiology and pathogenesis of CSR remain obscure although several hypothesis have been advanced. These include abnormal choroidal vascular hyperpermeability, physical defect in Bruch's membrane and localised retinal pigment epithelium (RPE) dysfunction. Corticosteroids have long been implicated in the pathogenesis of CSR. Gass and Little4 postulated that a major breakdown occurs in the permeability of the choriocapillaris, thus enabling large protein molecules and fluid to enter into subretinal space. By inhibiting fibroblastic proliferation and enhancing capillary fragility, corticosteroids are assumed to impair the eye ability to repair the focal damage to choriocapillaris. Corticosteroids also interfere with ion transport across RPE according to this hypothesis. Glucocorticoids also cause structural alteration of the Bruch's membrane by inhibiting collagen synthesis.1 Further evidence comes from the fact that elevated plasma cortisol levels are found during normal pregnancy5 and in patients with type A personality,6 conditions that are associated with CSR.

Androgens or testosterone have never been implicated as a factor involved in the pathogenesis of CSR, however, there is clinical and experimental evidence that associates testosterone with CSR. The fact that incidence of CSR is much higher in males as compared to females and it decreases as the age advances correlates with the levels of plasma testosterone. There is a gradual decline in total plasma testosterone levels with advancing age in older men.7 Furthermore, plasma testosterone levels are higher in people with type A behaviour8 and in normal pregnancy.9 Testosterone is known to promote atherosclerosis, retain sodium and experimental studies have shown that it affects the vascular tone. Human RPE cells are found to have androgen receptors.10

Intramuscular testosterone therapy is known to cause fluctuation of plasma testosterone levels. Our patient developed an acute rise of plasma testosterone levels after his testosterone dose was increased, which was followed by the development of CSR. The temporal relation of serum testosterone levels and development of CSR in this case shows an association between the two, which needs to be further investigated.

In summary, this is a first reported case of central serous chorioretinopathy associated with systemic testosterone therapy.