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1.
J Drugs Dermatol ; 20(2): 134-142, 2021 02 01.
Article in English | MEDLINE | ID: mdl-33538559

ABSTRACT

BACKGROUND: Impetigo, a highly contagious bacterial skin infection commonly occurring in young children, but adults may also be affected. The superficial skin infection is mainly caused by Staphylococcus aureus (S. aureus) and less frequently by Streptococcus pyogenes (S. pyogenes). Antimicrobial resistance has become a worldwide concern and needs to be addressed when selecting treatment for impetigo patients. An evidence-based impetigo treatment algorithm was developed to address the treatment of impetigo for pediatric and adult populations. METHODS: An international panel of pediatric dermatologists, dermatologists, pediatricians, and pediatric infectious disease specialists employed a modified Delphi technique to develop the impetigo treatment algorithm. Treatment recommendations were evidence-based, taking into account antimicrobial stewardship and the increasing resistance to oral and topical antibiotics. RESULTS: The algorithm includes education and prevention of impetigo, diagnosis and classification, treatment measures, and follow-up and distinguishes between localized and widespread or epidemic outbreaks of impetigo. The panel adopted the definition of localized impetigo of fewer than ten lesions and smaller than 36 cm2 area affected in patients of two months and up with no compromised immune status. Resistance to oral and topical antibiotics prescribed for the treatment of impetigo such as mupirocin, retapamulin, fusidic acid, have been widely reported. CONCLUSIONS: When prescribing antibiotics, it is essential to know the local trends in antibiotic resistance. Ozenoxacin cream 1% is highly effective against S. pyogenes and S. aureus, including methycyllin-susceptible and resistant strains (MRSA), and may be a suitable option for localized impetigo.J Drugs Dermatol. 2021;20(2):134-142. doi:10.36849/JDD.5475 THIS ARTICLE HAD BEEN MADE AVAILABLE FREE OF CHARGE. PLEASE SCROLL DOWN TO ACCESS THE FULL TEXT OF THIS ARTICLE WITHOUT LOGGING IN. NO PURCHASE NECESSARY. PLEASE CONTACT THE PUBLISHER WITH ANY QUESTIONS.


Subject(s)
Anti-Bacterial Agents/therapeutic use , Critical Pathways/standards , Impetigo/drug therapy , Staphylococcus aureus/drug effects , Streptococcus pyogenes/drug effects , Aminopyridines/pharmacology , Aminopyridines/therapeutic use , Anti-Bacterial Agents/pharmacology , Antimicrobial Stewardship/standards , Bridged Bicyclo Compounds, Heterocyclic/pharmacology , Bridged Bicyclo Compounds, Heterocyclic/therapeutic use , Delphi Technique , Diterpenes/pharmacology , Diterpenes/therapeutic use , Drug Resistance, Bacterial , Evidence-Based Medicine/standards , Fusidic Acid/pharmacology , Fusidic Acid/therapeutic use , Humans , Impetigo/diagnosis , Impetigo/microbiology , Microbial Sensitivity Tests/standards , Mupirocin/pharmacology , Mupirocin/therapeutic use , Practice Guidelines as Topic , Quinolones/pharmacology , Quinolones/therapeutic use , Skin Cream/pharmacology , Skin Cream/therapeutic use , Staphylococcus aureus/isolation & purification , Streptococcus pyogenes/isolation & purification , Systematic Reviews as Topic
2.
JCI Insight ; 3(6)2018 03 22.
Article in English | MEDLINE | ID: mdl-29563329

ABSTRACT

A defect in indoleamine 2,3-dioxygenase 1 (IDO1), which is responsible for immunoregulatory tryptophan catabolism, impairs development of immune tolerance to autoantigens in NOD mice, a model for human autoimmune type 1 diabetes (T1D). Whether IDO1 function is also defective in T1D is still unknown. We investigated IDO1 function in sera and peripheral blood mononuclear cells (PBMCs) from children with T1D and matched controls. These children were further included in a discovery study to identify SNPs in IDO1 that might modify the risk of T1D. T1D in children was characterized by a remarkable defect in IDO1 function. A common haplotype, associated with dysfunctional IDO1, increased the risk of developing T1D in the discovery and also confirmation studies. In T1D patients sharing such a common IDO1 haplotype, incubation of PBMCs in vitro with tocilizumab (TCZ) - an IL-6 receptor blocker - would, however, rescue IDO1 activity. In an experimental setting with diabetic NOD mice, TCZ was found to restore normoglycemia via IDO1-dependent mechanisms. Thus, functional SNPs of IDO1 are associated with defective tryptophan catabolism in human T1D, and maneuvers aimed at restoring IDO1 function would be therapeutically effective in at least a subgroup of T1D pediatric patients.


Subject(s)
Diabetes Mellitus, Type 1/immunology , Diabetes Mellitus, Type 1/metabolism , Indoleamine-Pyrrole 2,3,-Dioxygenase/immunology , Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism , Tryptophan/metabolism , Animals , Antibodies, Monoclonal, Humanized/pharmacology , Child , Cytokines/metabolism , Diabetes Mellitus, Type 1/pathology , Disease Models, Animal , Female , Gene Expression Regulation, Enzymologic , Genetic Association Studies , Humans , Immune Tolerance , Immunotherapy , Indoleamine-Pyrrole 2,3,-Dioxygenase/genetics , Leukocytes, Mononuclear/metabolism , Mice , Mice, Inbred C57BL , Mice, Inbred NOD , Multivariate Analysis , Polymorphism, Single Nucleotide , Receptors, Interleukin-6/drug effects
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