[Serous central chorioretinopathy and endogenous hypercortisolemia].

BACKGROUND

The exact pathogenic mechanism of the accumulation of subretinal fluid at the posterior pole of the fundus in cases of central serous chorioretinopathy (CSC) is not well established. Recently, it was reported that CSC is more frequent among patients with endogenous Cushing's syndrome. Thus, it has been suggested that glucocorticoids might be involved in the pathogenesis of CSC. Subsequently, additional observations, have confirmed the relationship between glucocorticoids and CSC. We present preliminary data on the endogenous cortisol secretion in patients with CSC.

PATIENTS AND METHOD

Sixteen patients (14 men and 2 women, 35-65 years of age) suffering from CSC, not exposed to exogenous glucocorticoids and without clinical and/or biological stigmata of endogenous Cushing's syndrome, have been examined. Twenty four hour urinary free cortisol (24 h-UFC) secretion was measured within one week of their CSC episode. Twenty four hour urinary free cortisol of age and sex matched controls were also measured.

RESULTS

Twenty four hour urinary free cortisol was 188.20 nmol/l +/- 34.1 for the patients suffering from CSC and 115.3 nmol/l +/- 63.4 for the control group (p < 0.05).

CONCLUSION

These results give additional evidence that glucocorticoids may play a role in the pathogenesis of CSC. However, given the substantial variability of urinary free cortisol levels, as indicated by the increased SD, additional number of patients should be examined.