Lornoxicam induced Toxic Epidermal Necrolysis (TEN) in a 54 years old female: A case report and its systematic literature review with respect to its causes and treatment overview

Background: Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are uncommon but life-threatening diseases mostly caused by drugs. Although various systemic immunomodulating agents have been used, their therapeutic efficacy has been inconsistent. Introduction: Toxic epidermal necrolysis is a severe dermatological condition that can be life-threatening as it damages the mucosa and epidermis layers of the skin with widespread necrosis, erythema, and the formation of bullae on various mucosal surfaces of the genitourinary, gastrointestinal, respiratory tracts, ocular and surrounding areas can also be affected, potentially leading to sepsis and death and is often triggered by drugs such as Amoxicillin, medications used for respiratory tract infections, hereditary noncompliance to certain drugs, Sulpha drugs (e.g., allopurinol), anti-epileptic drugs (e.g., phenytoin, Lamotrigine, carbamazepine, phenobarbital), NSAIDs (e.g., ibuprofen, Piroxicam, Paracetamol, Mefenamic acid, Diclofenac sodium, Tolmetin, Oxybutazone), Quinolones (e.g., ciprofloxacin, Trovafloxacin). Methodology: In this research article we have explained our case report, as well as we have described the systematic literature review of TEN, We did a literature search using electronic bibliographic databases and Journals : such as ELSEVIER ,British Medical Journals ,MEDLINE (Ovid SP and PubMed), EMBASE, The Cochrane Library (Cochrane Database of Systematic Reviews (CDSR), and Cochrane Central Register of Controlled Trials (CENTRAL), as well as annual meetings abstracts from inception till Oct 2021. The literature search has focused mainly on randomized clinical trials, meta-analysis, phase II/III, and retrospective studies. Objectives · Explained the case report in view of NSAID in old people can cause SJS/TEN. · To explain the treatment options of SJS/TEN. Results and conclusions: Despite the rarity of her lornoxicam-induced TEN, this case highlights the urgent need to recognize and detect drug-induced skin reactions early. The patient's complex presentation, including thrombotic microangiopathy and suspected disseminated intravascular coagulation, required a multidisciplinary approach including nephrology, dermatology, and hematology. A comprehensive management plan that includes hemodialysis, corticosteroids, antibiotics, and symptomatic treatment highlights the importance of individualized treatment strategies in managing such complex clinical scenarios. Research shows that the basic mechanism behind JS/TEN Fas-Fas ligand mediated apoptosis but the recent research studies suggested that the reactive oxygen species (ROS) as the initiating factor for keratinocyte damage and that it precedes the activation of the aforementioned apoptotic systems. Treatment includes steroids, immunoglobulins, TNF alpha inhibitors (Infliximab, adalimumab, gulimumab and Etanercept), plasma paresis, immune suppressive therapies such as cyclosporine. In symptomatic management patients can have dialysis for renal failure.