Clinical clues predictive of Stevens-Johnson syndrome as the cause of chronic cicatrising conjunctivitis

Shanbhag, Swapna S; Chanda, Sanjay; Donthineni, Pragnya Rao; Sane, Sayali; Priyadarshini, Smruti Rekha; Basu, Sayan

doi:10.1136/bjophthalmol-2019-314928

Cited by 15 publications

(10 citation statements)

References 23 publications

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“…The clinically diagnosed chronic SJS patients with a history of more than one year of onset of the reaction were recruited in this study. The diagnosis of SJS was confirmed based on the history of acute reaction in the skin and the mucous membrane involvement 23 . The criteria used to define severe dry eye was Schirmer score < 10 mm, OSDI score > 13 and positive corneal staining (> 1 on Oxford Staining Score (OSS)) 24 .…”

Section: Methodsmentioning

confidence: 99%

Differential expression of tear film cytokines in Stevens–Johnson syndrome patients and comparative review of literature

Koduri

Prasad

Upadhyaya

et al. 2021

Sci Rep

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To investigate the differential expression of tear cytokine levels among chronic Stevens–Johnson syndrome (SJS) patients to better understand the role of significantly altered cytokines in disease development. Tear samples were collected using Schirmer strips in 24 eyes of chronic SJS, 24 eyes of age and gender-matched controls, and 14 eyes of aqueous deficiency dry eye disease (DED) patients. The cytokine analysis was performed among 18 analytes which include pro-inflammatory, anti-inflammatory factors, and ELR-negative CXC chemokines. String analysis was performed for the significantly altered cytokines to understand their co-expression and role in the disease development. Additionally, a literature review was conducted to identify the signature cytokines present in chronic SJS tears. The differential expression of IL-6 (p ≤ 0.029), CXCL8/IL-8 (p ≤ 0.009), IL-1β (p ≤ 0.041), IL-2 (p ≤ 0.025), IL-10 (p ≤ 0.053), and CXCL-10 (p ≤ 0.044) were observed in chronic SJS patients and healthy controls. Whereas, IL-6 (p ≤ 0.029), CXCL8/IL-8 (p ≤ 0.058), CCL4 (p ≤ 0.056), GM-CSF (p ≤ 0.0001) IL-10 (p ≤ 0.025), and CXCL-10 (p ≤ 0.010), were differentially expressed in SJS as compared to severe DED patients. String analysis of the significantly altered cytokines revealed the involvement of several biological processes including the chronic inflammatory response, nitric oxide synthesis, angiogenesis, and cellular response to drugs. Among all the cytokines evaluated, the expression of CXCL8/IL-8 and CXCL10 levels were consistently reported in the literature. There was a differential expression of tear cytokines in SJS when compared to DED and healthy controls. The differential expression of CXCL8/IL-8 and CXCL10 was in line with existing literature and their role in chronic SJS pathogenesis merits further evaluation.

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Section: Methodsmentioning

confidence: 99%

Differential expression of tear film cytokines in Stevens–Johnson syndrome patients and comparative review of literature

Koduri

Prasad

Upadhyaya

et al. 2021

Sci Rep

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“…[ 17 ] Bilateral conjunctivitis commonly goes unnoticed during the acute phase and later develops into cicatricial conjunctivitis. [ 13 , 18 ] ADDE in individuals with SJS occurs due to the periductular fibrosis and obstruction of the ductules secondary to subconjunctival fibrosis observed in superotemporal fornix. The palpebral and orbital lobes of the lacrimal glands can have different grades of involvement ranging from distended to apoptotic acini, reduced secretory activity, and ultrastructural changes in myoepithelial cells.…”

Section: Causes Of Addementioning

confidence: 99%

Aqueous-deficient dry eye disease: Preferred practice pattern guidelines on clinical approach, diagnosis, and management

Donthineni¹,

Doctor²,

Shanbhag³

et al. 2023

Indian Journal of Ophthalmology

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Dry eye disease (DED) is a broad term that includes a diverse group of clinical disorders. Aqueous-deficient dry eye (ADDE), a subtype of DED, is characterized by decreased tear production by the lacrimal gland. It can be seen in up to one-third of individuals with DED and can be comorbid with a systemic autoimmune process or occur secondary to an environmental insult. Since ADDE can be a source of long-term suffering and severe visual impairment, early identification and adequate treatment are imperative. Multiple etiologies can underlie ADDE, and it is critical to identify the underlying cause to not only improve the ocular health but also to improve the overall quality of life and well-being of affected individuals. This review discusses the various etiologies of ADDE, highlights a pathophysiology-based approach for evaluating underlying contributors, outlines various diagnostic tests, and reviews treatment options. We present the current standards and discuss ongoing research in this field. Through this review, we propose a treatment algorithm that would be useful for an ophthalmologist in diagnosing and managing individuals with ADDE.

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“…A detailed history should be elicited and a careful ocular examination is warranted. [ 21 ] If a surgical procedure is planned in a case that could potentially be MMP, it may be disastrous if the patient has not been administered systemic immunosuppression first. [ 22 ]…”

Section: Peri-operative Considerations and Surgical Techniquementioning

confidence: 99%

A beginner‘s guide to mucous membrane grafting for lid margin keratinization

Shanbhag

Singh

Koshy

et al. 2021

Indian Journal of Ophthalmology

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The posterior lid margin, where the mucocutaneous junction (MCJ) between the eyelid skin and tarsal conjunctiva is located, plays a critical role in maintaining the homeostasis of the ocular surface. Posterior migration of the MCJ leads to lid-margin keratinization (LMK), which has a domino effect on the delicate balance of the ocular surface microenvironment. This occurs most commonly following Stevens-Johnson syndrome/toxic epidermal necrolysis and is not known to regress spontaneously or with medical therapy. Over time, LMK causes blink-related chronic inflammatory damage to the corneal surface which may have blinding consequences. Lid-margin mucous membrane grafting (MMG) is the only definitive therapy for LMK. Timely MMG can significantly alter the natural course of the disease and not only preserve but even improve vision in affected eyes. Literature searches were conducted on PubMed, using the keywords “mucous membrane grafts,” “lid margin keratinization,” “Stevens-Johnson syndrome,” “toxic epidermal necrolysis,” “lid related keratopathy,” and “lid wiper epitheliopathy”. This review, which is a blend of evidence and experience, attempts to describe the indications, timing, surgical technique, postoperative regimen, and clinical outcomes of MMG for LMK. The review also covers the possible complications and pearls on how they can be effectively managed, including how suboptimal cosmetic outcomes can be avoided. The authors hope that this review will aid ophthalmologists, including cornea and oculoplasty specialists, to learn and perform this vision-saving surgery better, with the aim of helping their patients with chronic ocular surface disorders, relieving their suffering, and improving their quality of life.

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Clinical clues predictive of Stevens-Johnson syndrome as the cause of chronic cicatrising conjunctivitis

Cited by 15 publications

References 23 publications

Differential expression of tear film cytokines in Stevens–Johnson syndrome patients and comparative review of literature

Differential expression of tear film cytokines in Stevens–Johnson syndrome patients and comparative review of literature

Aqueous-deficient dry eye disease: Preferred practice pattern guidelines on clinical approach, diagnosis, and management

A beginner‘s guide to mucous membrane grafting for lid margin keratinization

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