β thalassemia is a hereditary hemolytic disease caused by the defect of β globin gene. Transfusion-dependent β thalassemia patients need long-term blood transfusion to survive, and a series of systemic and ocular complications will occur in the disease itself and long-term blood transfusion. Retinal blood vessel density decreases, retinal thickness thinned and elastic pseudoxanthoxanoma syndrome are found in fundus due to long-term anemia and side effects of iron chelating agent. At present, there are few reports about eye changes in thalassemia patients, and the cognition is relatively scarce. Therefore, it is necessary to be vigilant for physicians, deeply explore the cause and symptomatic treatment, combined with individual disease characteristics, to provide a more scientific and accurate plan for clinical treatment.
Hydroxychloroquine retinopathy is an ocular lesions that develops following long-term or excessive use of hydroxychloroquine. The early clinical presentation of this lesion is nonspecific and is often detected when severe central vision impairment occurs in late stage. It currently mainly includes hydroxychloroquine binding to melanin, inducing degeneration of the retinal pigment epithelium, increasing the pH of lysosomes in the retinal pigment epithelium and interfering with the visual cycle. In recent years, with the development of retinal imaging technology and the in-depth study of hydroxychloroquine retinopathy, characteristic fundus structural changes such as retinal and choroidal thickness and blood vessels may occur in the early stage. This not only provides an important basis for the early diagnosis of hydroxychloroquine retinopathy, but also provides important clues for investigating its pathogenesis. Clinicians' proficiency in relevant fundus changes and pathogenesis will facilitate early diagnosis and treatment, while also minimizing irreversible central vision impairment in patients.