Central serous chorioretinopathy (CSC or CSCR), also known as central serous retinopathy (CSR), is an eye disease that causes visual impairment, often temporary, usually in one eye. When the disorder is active it is characterized by leakage of fluid under the retina that has a propensity to accumulate under the central macula. This results in blurred or distorted vision (metamorphopsia). A blurred or gray spot in the central visual field is common when the retina is detached. Reduced visual acuity may persist after the fluid has disappeared.The disease is considered of unknown cause. It mostly affects white males in the age group 20 to 50 (male:female ratio 6:1) and occasionally other groups. The condition is believed to be exacerbated by stress or corticosteroid use. Pathophysiology
Recently, central serous chorioretinopathy has been understood to be part of the pachychoroid spectrum. In pachychoroid spectrum disorders, of which CSR represents stage II, the choroid, the highly vascularized layer below the retina, is thickened and congested with increased blood vessel diameter, especially in the deep choroid (the so-called Hallers layer). This results in increased pressure from the deep choroid against the superficial choroid close to the retina, damaging the fine blood vessels (capillaries) needed to supply oxygen and nutrients to the retinal pigment epithelium and retina. Additionally, fluid can leak from these damaged vessels and accumulate under the retina. Different stages of the pachychoroid are defined depending on the amount of cumulative damage.
This allows sucroferric oxyhydroxide to bind phosphate as intended and be excreted without coming into contact with medications in the gut that it might interact with. According to the US prescribing information, Velphoro should not be prescribed with oral levothyroxine. The combination of sucroferric oxyhydroxide and levothyroxine is contraindicated because sucroferric oxyhydroxide contains iron, which may cause levothyroxine to become insoluble in the gut, thereby preventing the intestinal absorption of levothyroxine. Hyperphosphatemia
In a healthy person, normal serum phosphate levels are maintained by the regulation of dietary absorption, bone formation and resorption, equilibration with intracellular stores, and renal excretion. When kidney function is impaired, phosphate excretion declines. Without specific treatment, hyperphosphataemia occurs almost universally, despite dietary phosphate restriction and conventional dialysis treatment. In patients on dialysis, hyperphosphataemia is an independent risk factor for fractures, cardiovascular disease and mortality. Abnormalities in phosphate metabolism such as hyperphosphatemia are included in the definition of the new chronic kidney disease–mineral and bone disorder (CKD-MBD). Structure and mechanism of action
Sucroferric oxyhydroxide comprises a polynuclear iron(III)-oxyhydroxide core that is stabilised with a carbohydrate shell composed of sucrose and starch. The carbohydrate shell stabilises the iron(III)-oxyhydroxide core to preserve the phosphate adsorption capacity. Dietary phosphate binds strongly to sucroferric oxyhydroxide in the gastrointestinal (GI) tract. The bound phosphate is eliminated in the faeces and thereby prevented from absorption into the blood. As a consequence of the decreased dietary phosphate absorption, serum phosphorus concentrations are reduced.