Cataract steroid-induced

Figure 3 Mechanism of steroid-induced cataract according to the most prominent hypothesis. It involves first the formation of Schiff bases between the steroid C-20 ketone group and nucleophilic groups such as e-amino groups of lysine residues of proteins and then a Heyns rearrangement involving the adjacent C-21 hydroxyl group that results in stable amine-linked adducts.

The pathogenesis of steroid-induced cataract is likely multi-fectorial, including bonding of certain chemicals, water accumulation, protein agglutination, and various biochemical consequences of abnormal glucose metabolism. 

Timing of follow-up examinations depends on doses and duration of treatment, required every 6 months for cataract formation, but sooner for lOP and retinal/nerve concerns. Those with any visual disturbance must be advised to seek care. Surgical removal of steroid-induced PSC is similar to conventional PSC. 

In addition to the suppression of the hypophysial-pituitary axis and adrenal atrophy, these drugs can cause a variety of adverse effects, including osteoporosis, pancreatitis, steroid-induced diabetes mellitus, cataracts, glaucoma, psychosis, oral candidiasis and other opportunistic infections, immunosuppression, infertility, weight gain, and skin atrophy. Severe edema may also be produced, particularly in the face, depending on the degree of mineralocorticoid activity. 

In order to understand the mechanisms of steroid induced cataract, the route of the administered steroid into the crystalline lens should be clarified. Although intralenticular corticosteroid penetration studies have been performed the methodologies applied were different from those of the authors. This study aimed to investigate topographic lenticular dmg distribution together with the route of dmg penetration into the ocular tissues by using a convenient HPLC technique combined with a newly applied microsectioning method. 

Our study reveals that adult patients with IBD who are treated with corticosteroids have a high incidence (56%) of PSC, raised lOP, or both. These patients, therefore, are at risk for continued opacification of their lenses and the development of steroid-induced glaucoma. Upon lowering the dose of steroids, raised lOP is reversible in the majority of patients and PSC, in its early stages, is reversible in some. To avoid ocular and other systemic complications of therapy, acute and chronic doses of steroids should be minimized. Because of individual susceptibility for glaucoma and cataract and their time-and dose-dependent nature, each patient receiving corticosteroids for IBD or any other condition must be carefully followed by an experienced ophthalmologist. 

Difluprednate is an effective agent for both control of anterior segment inflammation and reduction of CME in paediatric patients with uveitis when used as an adjuvant to systemic immunomodulatory therapy. A high rate of steroid-induced lOP elevation and cataract formation is seen in this population. Close monitoring of paediatric patients receiving difluprednate is recommended. 

Complications associated with anterior uveitis may include cataracts, glaucoma, band keratopathy, and CME. Posterior subcapsular cataracts are the most commonly encountered lenticular change associated with chronic uveitis. Additionally, it is well known that long-term topical steroid use can induce or accelerate posterior subcapsular cataract development. 

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