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Continuing Education Activity ‘Stevens:Johnson syndrome and toni epidermal neerolysis are ncuterarejand potentially fatal skin'revtions involving {asso skitrundyn'some eases; veosal membranes accompanied by systemic symproms, Medications are causative in ‘over 80 percent of cases. Stevens-Johnson syndrome and toxi epidermal necrolysis are distinguished based on the extent of the detached skin surface area. Tis activity illustrates the evaluation and treatment of Stevens-Johnson symdrome and of toxic epidermal necrolysis and reviews the role of the interprfessional team in managing those with ‘these conditions. Objectives: + Describe the difference between Stevens-Johnson syndrome and toxic epidermal necrolysis. + Summarize differential diagnoses of Stevens-lobnson syndrome and of toxic epidermal necrolysis. ‘+ Review the treatment options for Stevens-lobnson syadcome and toxic epidermal necrolysis. ‘+ Explain the role of interprofessional team members in optimizing collaboration and communication to ensure patients with Stevens-Johnson syndrome o toxic epidermal necrolysis receive high-quality care, which will lead toenhanced outcomes. ‘Access fee multiple choice questions on this topic. Introduction Previously known as Lyell syndrome, Stevens-Johnson syndrome (SIS), and toxic epidermal necrolysis (TEN) are variants ofthe same condition and are distinct from erythema muliforme major staphylococcal sealded skin syndrome, and other drug eruptions1](213] Stevens-Johnson syndrome'toxic epidermal necrolysis i a are, acute, serious, and potentially fatal skin reaction in ‘hich there are sheet-Hke skin and mucosal loss accompanied by systemic symptoms. Medications are causative in lover 80% of cases, ‘Stevens-Johnson syndrome'toxi epidermal necrolysis is classified by the extent ofthe detached skin surface ara, ‘+ Stevens-Johnson syndrome: less than 10% body surface area ‘+ Overlap Stevens-Johnson syndromeltoric epidermal nerolysis: 10% to 30% body surface area ‘+ Toxic epidermal necrolysis more than 30% body surface area Etiology ‘Exocylosis arid tumor nccrosis factor-alfa (TNE=alpha death receptor pathway. [4)[5] ‘Current theories address the following mechanisms, among others.sv 312 Fat Stevens Johnson Syndrome -SistPeats “NCBI Bookshet + Granulysin, found inthe cytotoxic granules, isthe main cause of keratinocyte apoptosis. + Fas-FasL, expressed on the activated cytotoxi T cells ean also destroy keratinocytes va the production of intracellular caspases. Cytotoxic T cells exocytose perforin and granzyme B, which eveate channels in the target cell membrane activating the easposes ‘TNF-alpha may eause apoptosis or protect from it. vous oxide (NO) induced by TNF-alpha and interferon (IFN}-alpha may stimulate caspases Epidemiology ‘Stevens Johnson syndromeltoxie epidermal necrolysis is estimated to aeet wo to'seven per millon people each Year ‘i ect anyone witha genetic predisposition: any age either sex, and all races, although itis more common in older people and women. It is muck more likely to occur in people infected ‘with the buman immunodeficiency vius (HIV), with an estimated incidence of 1/1000 [6]7(8] + Numerous medications have been reported to trigger Stevens-Johnson syndromeftoxic epidermal necrolys + Stevens-Johnson syndrome!toxic epidermal ncerolysis are rarely associated with vaccination and ifeetions such ‘as mycoplasma, cytomegalovirus, and dengue. “The drugs that most commonly cause Stevens-Johnson syndromertoxie epidermal necro “© Contrast media Genetic factors inelude human leukocyte antigen (HLA) sllotypes that lead to an increased risk of Stevens-Johnson syndromeftoxic epidermal necrolysis when exposed to aromatic anticonvulsants and allopurinal, Family members of patient with Stovens- Johnson syndromeftoxie epidermal necrolysis should be advised that they are at sk of developing the disease and should be cautious about taking any medication associated with the dscase (9) ‘To date findings have included te risk of Stevens-Johnson syndrome/toxic epidermal necrolysis in: «+ Han Chinese, Thai, Malaysian, and South Indian people if they carry /7L4-B*/502 and take aromatic anticoavalsans. 1 Han Chinese ifthey cary H1L4-B*5801 and take allopurinol «+ Europeans if they cary FILA-BS701 and take abacavir, o if they carry HLA-A*3101 and take carbamazepine. Pathophysiology “The initial step for Stevens-Johason syndrome/toxic epidermal necrolysis may be interaction binding of a drug associated antigen o metabolite withthe major histocompatbilty complex (MHC) type 1 of cellular peptide o form an immunogenic compound, The exact mechanism is speculative{10] Stevens-Johason syndrome/toxic epidermal necrolysis is T40 tahun, denyut jantung >120/menit, terdapat kanker atau keganasan hematologik, epidermolisis. >10% LPB, kadar urea serum >10mMIL (>28mg! dL), kadar bikarbonat serum <20mEqj/L, kadar ula darah sewaktu > 14mM/L (>252mgi/dL). Nilai SCORTEN ini dianjurkan untuk dievaluasi pada hari ket dan ke, PEMERIKSAAN PENUNJANG Tidak ada pemeriksaan laboratori peentng untuk menunjang aayrens Pomeroy hislopalologis Kull dapat menvinnienen diagnosis banding, dan umumnya oe untuk kepentingan medicolegal” pemerukan laboratorum peru dlakukan unt emeriksaan eparahan penyakit dan untuk ta luk evaluasi se na pasien