Mycoplasma‐Associated Stevens–Johnson Syndrome in Children: Retrospective Review of Patients Managed With or Without Intravenous Immunoglobulin, Systemic Corticosteroids, or a Combination of Therapies

Abstract

Administration of intravenous immunoglobulin (IVIG) to patients with Stevens-Johnson syndrome (SJS) has been controversial. The objective of this study was to evaluate the effectiveness of IVIG, systemic corticosteroids, or both in treating Mycoplasma pneumoniae-associated SJS (mpSJS). Retrospective series of 10 pediatric mpSJS cases were stratified into four treatment groups: IVIG alone, IVIG and systemic corticosteroids together, systemic corticosteroids alone, and supportive care. The efficacy of therapy was evaluated on the basis of several proxies of disease severity, including hospital length of stay (LOSt ) and number of febrile days (Febt ) after initiation of therapy. Patients treated with IVIG alone had a longer LOSt and more Febt , despite different baseline characteristics, than patients treated with supportive therapy. Of patients who received IVIG, 50% were treated with corticosteroids concurrently and had similar characteristics of disease severity but showed a non-statistically significant trend toward shorter LOSt and fewer Febt than those who received IVIG alone. A patient treated with corticosteroids alone had the shortest LOSt in this series. Therefore treatment with IVIG alone was associated with a more severe disease course than supportive therapy, although causality cannot be inferred given possible confounding by indication. When systemic corticosteroids were used alone or in conjunction with IVIG, hospital LOSt and Febt trended lower than with the use of IVIG alone, although disease severity at baseline was similar between those treated with IVIG and corticosteroids concurrently and those treated with IVIG alone. It was thus concluded that treatment with systemic corticosteroids as monotherapy or in combination with IVIG may be preferable to IVIG alone. Further large-scale studies are warranted to evaluate this hypothesis.

The Effect of Intravenous Immunoglobulin Combined with Corticosteroid on the Progression of Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: A Meta-Analysis

“…Total 15 studies observed either cessation time or hospitalization length[9, 25–27, 31, 32, 36–44]. Of these, 3 studies recruited patients with SJS only[9, 36, 37], 5 studies chose TEN patients only[26, 31, 38–40] and 7 studies imposed no restrictions about patients recruitment[25, 27, 32, 41–44].…”

“…Two common variables, the time to arrest progression and the hospitalization length, were utilized to measure the improvements of patients. A small part of studies that reported the time of progression arrest by describing when fever control[9], skin healing[31] and re-epithelialization[32] occurred were also included, because these descriptions were supposed to reflect to what magnitude did IVIG treatment accelerate the improvement.…”

“…Since this system is proven to be reliable and applicable for estimating risk for death among both SJS and TEN patients[6–8], doctors routinely calculate the score after the admission. Meanwhile, numerous studies set SCORTEN-derived expected mortality as internal control to evaluate the effects of immunomodulatory therapy on death prevention[9–12]. …”

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“…Report by Stevens Johnson Syndrome foundation (SJSF), has shown that commonly used over-the-counter medications like paracetamol, amoxicillin, and ibuprofen, and herbal products with Ginseng can trigger SJS and TEN [23,24]. SJS has been tailored to viral and Mycoplasma pneumonia without previous sensitization [19,[25][26][27][28][29][30]. Studies in immunicompromized patients show that they are more susceptible to SJS [18,[30][31][32][33][34][35].…”

Anatomy, Physiology and Drugs Triangular Dynamics in Steven Johnsons Syndrome

“…23,24 SJS has been tailored to viral and Mycoplasma pneumonia without previous sensitization. 19,[25][26][27][28][29][30] Studies in immunicompromized patients show that they are more susceptible to SJS. 18,[30][31][32][33][34][35] This suggests genetic inclination to the varying manifestations of SJS.…”