Central serous retinopathy associated with adrenocorticotrophic hormone therapy. A case report and a hypothesis

Central serous retinopathy (CSR) has been linked by several authors to the therapeutic use of adrenocorticotrophic hormone (ACTH) or corticosteroids or to endogenous ACTH hypersecretion. Various pathogenic mechanisms have been suggested to explain this phenomenon; all relate to the steroids as the causative agents.

A simultaneous, bilateral central serous retinopathy developed in a woman treated by intramuscular injections of a synthetic ACTH analog for arthritis. The condition resolved 2 months after stopping the use of this drug.

Many investigators consider CSR to be either a disorder of the retinal pigment epithelium (RPE) ion-pump function or a result of choroidal vascular hyperpermeability. ACTH has a melanotrophic part, melanocyte-stimulating hormone (MSH), that may affect RPE cells, which are melanin-pigmented cells of neuroectoderm origin, and alter their ionic pumping properties. This is supported by evidence in the literature for the effect of MSH on animal RPE cells, as well as on other secreting epithelia. MSH is known to act through increasing intracellular cAMP levels. Based on the current concepts regarding the pathogenesis of CSR, two possible mechanisms for ACTH/MSH-associated CSR are suggested. In the first, MSH increases intracellular cAMP levels in RPE cells, thereby inducing pump dysfunction and a reversal of ionic current direction, leading to subretinal fluid accumulation. An alternative mechanism is based on the known ability of MSH to increase the permeability of blood-aqueous and blood-brain barriers. It is hypothesized that MSH disrupts the outer blood-retinal barrier or causes leakage from choroidal vessels.