Comment on “Surgically induced necrotizing scleritis (SINS): Is it a standalone condition or a variant of necrotizing scleritis?”

Dear Editor, We read the article “Surgically induced necrotizing scleritis (SINS): Is it a standalone condition or a variant of necrotizing scleritis?” with great interest. The article compares the clinical characteristics of 15 SINS patients (15 eyes) with nine age-matched patients (11 eyes) with idiopathic necrotizing scleritis. The authors found no significant differences between the groups, concluding that “SINS is part of the spectrum of necrotizing scleritis rather than an independent entity.”[1] There is a significant debate regarding the terminology used to describe scleral necrosis after ocular surgery, with SINS being the most popular term.[2] Necrotizing scleritis is characterized by granulomatous inflammation, composed of plasma cells, histiocytes, and multinucleated giant cells, with fibrinoid necrosis within the sclera.[2] We have proposed that surgically-induced scleral necrosis (SISN), rather than SINS, is a more appropriate term from the pathogenic point of view.[2] Resected scleral analysis of nine SISN patients with systemic autoimmune disease reported immune complex deposition, increased T-helper lymphocytes, and HLA-DR overexpression. Moreover, vasculitis with fibrinoid necrosis and neutrophil vessel wall invasion was present in 75% of specimens.[3] Similar histopathologic findings were found in rheumatoid arthritis necrotizing scleritis unrelated to ocular surgery.[4] In contrast, tissue analysis from idiopathic scleritis revealed diffuse lymphocytic infiltration, few plasma cells, and polymorphonuclear cells, but non-granulomatous inflammation or vasculitis.[4] Furthermore, iodine I-125 brachytherapy-induced scleral necrosis showed a thickened sclera containing neutrophils and foamy histiocytes but no granulomatous inflammation, giant cells, or epithelioid histiocytes.[5] Such histopathologic evidence, along with the different pathogenic mechanisms (trauma, infection, ischemia, toxicity, and autoimmune) associated with SISN strongly suggest that not all cases are driven by the same pathogenic mechanism.[2] In a recently published study, we compared the outcomes of SISN patients with confirmed associated autoimmune disease versus those with other SISN pathogenic mechanisms, mainly, trauma, ischemia, and toxicity (non-autoimmune SISN).[6] All 31 eyes within the autoimmune disease group required systemic corticosteroids and IMT (n = 29) or biologics (n = 2). Remission was achieved in 87%, with only 13% requiring a surgical procedure. Contrariwise, 60% of eyes with non-autoimmune SISN achieved remission with non-steroidal anti-inflammatory drugs alone, 25% with combined systemic steroids, and only 8% of eyes required IMT.[6] Patients with autoimmune SISN had more severe scleral inflammation at baseline and a higher incidence of ocular complications during follow-up.[6] These findings strikingly differ from those reported by Magesan et al.,[1] in which, despite the absence of an underlying autoimmune disease, systemic steroids alone or combined with IMT were required in 47% and 53% of patients, respectively. Furthermore, 44% of patients in the idiopathic necrotizing scleritis group required IMT, with no significant differences in ocular complications between groups.[1] Based on their findings, Magesan et al.[1] concluded that SISN is part of the same spectrum of idiopathic necrotizing scleritis and not a different group of scleral necrosis disorders. However, the reported histopathological evidence and the clinical and surgical risk factors involved in cases of SISN suggest that such entities differ in their pathogenic mechanisms based on the type of surgical insult, perioperative adjunctive therapy, and underlying systemic autoimmune diseases.[2-6] Financial support and sponsorship: Nil. Conflicts of interest: There are no conflicts of interest.