Reactive infectious mucocutaneous eruption:
            <i>Mycoplasma pneumoniae</i>
            ‐induced rash and mucositis and other parainfectious eruptions

Ramien, Michele

doi:10.1111/ced.14404

Cited by 36 publications

(59 citation statements)

References 71 publications

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“…RIME requires identification and treatment of the underlying infection, supportive care, and potential antimicrobial and immunosuppressive therapies. In fact, the use of antibiotics to treat community acquired pneumonia in patients with RIME has been emphasized [ 69 , 70 ]. One study examined the role of etanercept treatment in RIME and showed that this therapy led to improvement in physical findings within 2 days of drug administration [ 71 ].…”

Section: Clinical Updatesmentioning

confidence: 99%

Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis: A Review of Diagnosis and Management

et al. 2021

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Stevens–Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) are rare diseases that are characterized by widespread epidermal necrosis and sloughing of skin. They are associated with significant morbidity and mortality, and early diagnosis and treatment is critical in achieving favorable outcomes for patients. In this scoping review, Excerpta Medica dataBASE and PubMed were searched for publications that addressed recent advances in the diagnosis and management of the disease. Multiple proteins (galectin 7 and RIP3) were identified that are promising potential biomarkers for SJS/TEN, although both are still in early phases of research. Regarding treatment, cyclosporine is the most effective therapy for the treatment of SJS, and a combination of intravenous immunoglobulin (IVIg) and corticosteroids is most effective for SJS/TEN overlap and TEN. Due to the rare nature of the disease, there is a lack of prospective, randomized controlled trials and conducting these in the future would provide valuable insights into the management of this disease.

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Section: Clinical Updatesmentioning

confidence: 99%

Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis: A Review of Diagnosis and Management

et al. 2021

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“…Typical target lesions which are raised are only found in patients with EM ( 34 ). Additionally, MP-induced rash and mucositis (MIRM) emerged as an entity in 2015, which mostly affects mucous membranes and has minimal or even absent cutaneous involvement ( 35 , 36 ). MIRM has a milder disease course than EMM and SJS/TEN ( 8 ).…”

Section: Discussionmentioning

confidence: 99%

Erythema Multiforme Major Associated With Community-Acquired Pneumonia: Lessons From a Case Report

Fan

Luo

et al. 2021

Front. Pediatr.

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Background: Erythema multiforme (EM) is an acute immune-mediated inflammatory mucinous skin disorder. The etiology of pediatric EM involves infections, medications, autoimmune diseases, and genetic factors.Case Report: An 8-year-old girl with Mycoplasma pneumoniae (MP) associated community-acquired pneumonia developed erythema target-like symptoms 1 week after azithromycin administration. The erythema quickly spread throughout the body involving the oral and ocular mucous membranes, the trunk, and the extremities, and eventually developed into erythema multiform major (EMM). Through drug withdrawal and specific treatment including systemic corticosteroids and supportive care, her clinical symptoms were improved. After 31 days, most of the mucocutaneous symptoms were relieved, except pigmentation. Human leukocyte antigen (HLA) gene sequencing was performed and 20 HLA genotypes were identified. The patient follow-up lasted for 18 months. Rashes appeared on her trunk when receiving azithromycin orally after discharge and then disappeared after azithromycin withdrawal.Conclusions: Pediatric EM is a rare disease and recognition of its etiology is important for EM management. In this case, azithromycin and HLA-DQB1*03:01 genotype may contribute to EMM.Lesson: For drug-induced EM, rapid identification and withdrawal of the causative drugs is critical. Re-exposure to the same drug or exposure to drugs with similar chemical structures should also be avoided. Patient education and rational use of medicines are essential for pediatric patients.

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“…At present, immunological pathology has garnered much attention ( 18 ). There are common antigenic components in cell membranes of the body and the cell membrane glycolipid antigen of MP ( 19 ). After MP infection, the inflammatory response produced by macrophages, neutrophils and lymphocytes infiltrating around the alveolar and bronchial vessels is the pathological feature of MPP autoimmunity ( 20 ).…”

Section: Introductionmentioning

confidence: 99%

Baicalin relievesMycoplasma pneumoniaeinfection‑induced lung injury through regulating microRNA‑221 to inhibit the TLR4/NF‑κB signaling pathway

Zhang

Wang

et al. 2021

Mol Med Rep

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Mycoplasma pneumoniae (MP) is a common pathogen that can cause respiratory infections. MP pneumonia (MPP) leads to numerous complications, including lung injury and even death. The present study aimed to investigate the protective effects of Baicalin treatment on MP infection-induced lung injury and the molecular mechanism underlying these effects. Briefly, after mice were infected intranasally by MP and treated with Baicalin (80 mg/kg), serum levels of MP-immunoglobulin M (IgM) were detected by ELISA. The expression levels of C-reactive protein (CRP) in lung tissue were detected by immunohistochemistry and the bronchoalveolar lavage fluid (BALF) was examined by ELISA. Inflammatory factors and inflammatory cells in the BALF were assessed. The expression levels of microRNA (miR)-221 in lung tissue were examined by reverse transcription-quantitative PCR and pathological changes in lung tissue were detected by H&E staining. Cell apoptosis was evaluated by TUNEL assay and the protein expression levels of TLR4, MyD88 and NF-κB were detected by western blotting. Baicalin treatment significantly reduced serum levels of MP-IgM and CRP expression in lung tissue during MP infection. In addition, Baicalin decreased the levels of IL-1β, IL-6, IL-18 and TNF-α in the BALF, and the number of inflammatory cells. Baicalin also reduced the inflammatory infiltration in lung tissue induced by MP infection, improved the pathological changes detected in lung tissue, reduced apoptosis, and downregulated the protein expression levels of TLR4, MyD88 and NF-κB. Furthermore, Baicalin treatment downregulated the expression of miR-221 and the protective effects of Baicalin were attenuated by miR-221 overexpression. In conclusion, Baicalin has a therapeutic effect on mice with MP infection-induced lung injury, which may be related to inhibition of miR-221 expression and regulation of the TLR4/NF-κB signaling pathway.

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Reactive infectious mucocutaneous eruption: Mycoplasma pneumoniae ‐induced rash and mucositis and other parainfectious eruptions

Cited by 36 publications

References 71 publications

Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis: A Review of Diagnosis and Management

Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis: A Review of Diagnosis and Management

Erythema Multiforme Major Associated With Community-Acquired Pneumonia: Lessons From a Case Report

Baicalin relievesMycoplasma pneumoniaeinfection‑induced lung injury through regulating microRNA‑221 to inhibit the TLR4/NF‑κB signaling pathway

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