Granuloma Annulare: An Updated Review of Epidemiology, Pathogenesis, and Treatment Options

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Abstract

Granuloma annulare (GA) is an inflammatory granulomatous skin disease that can be localized (localized GA) or disseminated (generalized GA), with patch, perforating, and subcutaneous subtypes being less common variants of this benign condition. Recently, new research has emerged that further elucidates GA epidemiology and etiopathogenesis; importantly, new therapeutic options for GA have also been described, although there remains a paucity of randomized controlled studies. In this review, we summarize recent updates on GA epidemiology and etiopathogenesis and offer an updated review of the therapeutic options for GA currently reported in the literature. We hope that the current review galvanizes randomized controlled studies that will in turn help lead to the recommendation of evidence-based treatments for GA.

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Methodological quality and synthesis of case series and case reports

Mohammad Hassan Murad, Shahnaz Sultan, Samir Haffar … (2018)

Case reports and case series are uncontrolled study designs known for increased risk of bias but have profoundly influenced the medical literature and continue to advance our knowledge. In this guide, we present a framework for appraisal, synthesis and application of evidence derived from case reports and case series. We propose a tool to evaluate the methodological quality of case reports and case series based on the domains of selection, ascertainment, causality and reporting and provide signalling questions to aid evidence-based practitioners and systematic reviewers in their assessment. We suggest using evidence derived from case reports and case series to inform decision-making when no other higher level of evidence is available.

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The Role of Inflammation in Diabetes: Current Concepts and Future Perspectives

Sotirios Tsalamandris, Alexios S Antonopoulos, Evangelos Oikonomou … (2019)

Diabetes is a complex metabolic disorder affecting the glucose status of the human body. Chronic hyperglycaemia related to diabetes is associated with end organ failure. The clinical relationship between diabetes and atherosclerotic cardiovascular disease is well established. This makes therapeutic approaches that simultaneously target diabetes and atherosclerotic disease an attractive area for research. The majority of people with diabetes fall into two broad pathogenetic categories, type 1 or type 2 diabetes. The role of obesity, adipose tissue, gut microbiota and pancreatic beta cell function in diabetes are under intensive scrutiny with several clinical trials to have been completed while more are in development. The emerging role of inflammation in both type 1 and type 2 diabetes (T1D and T1D) pathophysiology and associated metabolic disorders, has generated increasing interest in targeting inflammation to improve prevention and control of the disease. After an extensive review of the possible mechanisms that drive the metabolic pattern in T1D and T2D and the inflammatory pathways that are involved, it becomes ever clearer that future research should focus on a model of combined suppression for various inflammatory response pathways.

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Th1 and Th17 cells: adversaries and collaborators.

Jesse M Damsker, Anna M Hansen, Rachel R Caspi (2010)

Autoreactive effector CD4+ T cells have been associated with the pathogenesis of autoimmune disorders. Early studies implicated the interferon (IFN)-gamma-producing T helper (Th)1 subset of CD4+ cells as the causal agents in the pathogenesis of autoimmunity. However, further studies have suggested a more complex story. In models thought to be driven by Th1 cells, mice lacking the hallmark Th1 cytokine IFN-gamma were not protected but tended to have enhanced susceptibility to disease. Identification of the IL-17-producing CD4+ effector cell lineage (Th17) has helped shed light on this issue. Th17 effector cells are induced in parallel to Th1, and, like Th1, polarized Th17 cells have the capacity to cause inflammation and autoimmune disease. This, together with the finding that deficiency of the Th17-related cytokine IL-23 but not the Th1-related cytokine IL-12 causes resistance, led to the notion that Th17 cells are the chief contributors to autoimmune tissue inflammation. Nevertheless, mice lacking IL-17 are not protected from disease and display elevated numbers of IFN-gamma-producing CD4+ T cells, and, in some cases, lack of IFN-gamma does confer resistance. Recent studies report overlapping as well as differential roles of these cells in tissue inflammation, which suggests the existence of a more complex relationship between these two effector T-cell subsets than has hitherto been suspected. This review will attempt to bring together current information regarding interaction, balance, and collaborative potential between the Th1 and Th17 effector lineages.

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Author and article information

Contributors

Tejas P. Joshi:

ORCID: http://orcid.org/0000-0001-7897-2940

tejas.joshi@bcm.edu

Journal

Journal ID (nlm-ta): Am J Clin Dermatol

Journal ID (iso-abbrev): Am J Clin Dermatol

Title: American Journal of Clinical Dermatology

Publisher: Springer International Publishing (Cham )

ISSN (Print): 1175-0561

ISSN (Electronic): 1179-1888

Publication date (Electronic): 8 September 2021

Pages: 1-14

Affiliations

[1 ]GRID grid.39382.33, ISNI 0000 0001 2160 926X, School of Medicine, , Baylor College of Medicine, ; 1 Baylor Plaza, Houston, TX 77030 USA

[2 ]GRID grid.240145.6, ISNI 0000 0001 2291 4776, Department of Dermatology, , MD Anderson Cancer Center, ; Houston, TX USA

Author information

Tejas P. Joshi http://orcid.org/0000-0001-7897-2940

Article

Publisher ID: 636

DOI: 10.1007/s40257-021-00636-1

PMC ID: 8423598

PubMed ID: 34495491

SO-VID: 5f57c1de-7aa3-478b-bd38-371da0d17ae2

License:

This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

History

Date accepted : 25 August 2021

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