Purpose The purpose of this paper is to provide a meaningful literature review about the epidemiology, pathogenesis, clinical signs, imaging and treatment of ocular siderosis (OS). Methods A computerized search from inception up to March 2020 of the online electronic database PubMed was performed using the following search strings: “ocular siderosis” and “siderosis bulbi”. The reference list in each article was analysed for additional relevant publications. Results OS is an uncommon cause of visual loss due to a retained ferrous intraocular foreign body (IOFB). It may develop from 18 days to years after a penetrating trauma that usually occurs during hammering. On average, patients are 22–25 years old, and the vast majority are male. The most common cause of OS development is delayed presentation by the patient or missed diagnosis of IOFB after trauma. The pathophysiology is not fully understood; nevertheless, iron deposition causes hydroxyl radical formation, which damages photoreceptors and retinal pigment epithelium. Moreover, iron damages retinal vessels with consequent inner retinal layers degeneration. The most frequent signs are iris heterochromia, pupillary mydriasis, cataract development and retinal arteriolar narrowing with pigmentary retinal degeneration. Electroretinogram signs, in particular, b-wave amplitude reduction, arise earlier than clinical signs. Orbital CT scans and ultrasonography play an essential role in detecting IOFBs. Treatment depends on the IOFB location and OS development. However, it is crucial to remove the IOFB after OS development because visual acuity and clinical signs may improve. Anterior segment IOFBs can be dislodged using an intraocular magnet (IOM) or forceps through limbal paracentesis. In contrast, posterior segment IOFBs require a pars plana vitrectomy and IOM or forceps to be removed through an enlarged sclerotomy or the limbus. Conclusion Recommending the usage of protective glasses and spreading knowledge about OS may further benefit patient care.

In view of contrary reports in the literature on anomalies of taurine concentration in the blood of retinitis pigmentosa patients, taurine clearance has been determined in 19 patients and 17 controls. No significant difference has been found between the average values of the two populations. The taurine content in cataractous crystalline lenses of retinitis pigmentosa patients has been found higher than the taurine content in lenses with senile cataract, but the same behaviour was also shown by five selected proteogenic amino acids. The results are discussed together with related literature data to conclude that taurine can be involved at least in some subtypes of retinitis pigmentosa, but cannot be considered as a marker for the disease.

No abstract