Stevens‐Johnson syndrome: Pathogenesis, diagnosis, and management

Abstract

Cutaneous drug reactions are the most common type of adverse drug reaction. These reactions, ranging from simple pruritic eruptions to potentially life-threatening events, are a significant cause of iatrogenic morbidity and mortality. Stevens-Johnson syndrome (SJS) is a serious and potentially life-threatening cutaneous drug reaction. Although progress has been made in the management of SJS through early detection, prompt hospitalization, and immediate cessation of offending agents, the prevalence of permanent disabilities associated with SJS remains unchanged. Nevertheless, despite being a problem that is global in scope, government and health care agencies worldwide have yet to find a consensus on either diagnostic criteria or therapy for this disorder. Here, we provide the internist and emergency room physician with a brief review the SJS literature and summarize the latest recommended interventions with the hope of improving early recognition of this disease and prevention of permanent sequelae and mortality that frequently complicate SJS.

Stevens-Johnson syndrome caused by combined use of lamotrigine and fluoxetine and review of the literature

“…It has been postulated that patients with slow intrinsic acetylation rates and those taking medications such as azoles, protease inhibitors, SSRIs, and quinolones are at increased risk of developing SJS [13]. Slow acetylation may be a factor in the development of a number of adverse cutaneous drug reactions, as the reduced rate of acetylation causes the accumulation of reactive metabolites that induce cell-mediated cytotoxic reactions directed against the epidermis, thereby resulting in keratinocyte apoptosis [8,14]. In the light of these findings, we think that LTG and fluoxetine exert a synergistic effect in developing SJS.…”

“…Since medications are the most common cause of SJS, a thorough drug history must be obtained, and all potential offending agents must be immediately discontinued [8]. In this study, the patient's psychotropic medications were discontinued.…”

“…In immunological mechanisms, LTG metabolites have been claimed to assume the role of hapten and lead to immunological reactions, particularly to T-celloriginated reactions and cell-associated cytotoxicity [4]. On the other hand, genetic factors may play a role in the development of SJS in non-immunological mechanisms [8]. It has been postulated that patients with slow intrinsic acetylation rates and those taking medications such as azoles, protease inhibitors, SSRIs, and quinolones are at increased risk of developing SJS [13].…”

“…Various theories have implicated both immunological and non-immunological mechanisms, with the prevailing evidence suggesting primary involvement of the immunologic response [8]. In immunological mechanisms, LTG metabolites have been claimed to assume the role of hapten and lead to immunological reactions, particularly to T-celloriginated reactions and cell-associated cytotoxicity [4].…”

“…Although a variety of etiologies, such as infections and underlying malignancies, have been implicated as potential causes of SJS, drugs remain the predominant inciting agent [8]. The drugs most reported in inciting SJS are antibiotics (40%), antiepileptics (11%) and analgesics (5-23%) [4].…”