This is a very nicely written one-case observational study. The authors attribute the occurrence of CSCR following the cessation of terbinafine treatment. They suggested that the disease appeared with the withdrawal of the drug.
The validity of the presumption is only supported by the appearance of bilateral subretinal fluid, referred to as CSCR, and recent treatment with terbinafine due to onychomycosis. They speculate that a possible depletion of systemic steroids following prolonged terbinafine administration might cause a compensatory up-regulation of mineralocorticoid receptors in the RPE/choriocapillaris, and that cessation of terbinafine treatment might result in a rebound phenomenon, increasing the steroid end-organ effect, and thus might cause CSCR.
We must be careful to avoid a causal relationship from a single observational study validated just with speculation. When we observe an association between two things, it does not mean one thing caused the other thing, even if that association may be strong and consistent.
The study does not reveal any further concrete information about the past relevant ocular or systemic findings. It does not present any data about the presence of CSCR before or during the treatment. We do not know if the patient suffered from Addison-like symptoms. No data is presented about the cortisol levels during and post-treatment.
CSCR is most probably the most appropriate diagnosis in such a setting in a young adult, however, convincing evidence for this diagnosis with fluorescein angiography and autofluorescence examinations would certainly be required.
I fully agree with the authors that the scope of the routine anamnesis should be wide when dealing with this complex and enigmatic condition. I also respect their alert about the probable post-anti-mycotic rebound effect increasing the steroid end-organ effect, and thus causing CSCR.