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Interferon-gamma-mediated JAK-STAT activation and tyrosine kinase 2 (TYK2) signaling through IL-12, IL-23, and type I interferons are implicated in GA pathogenesis. Deucravacitinib, a selective allosteric TYK2 inhibitor, was used in a 59-year-old woman with biopsy-confirmed interstitial-type GA refractory to topical corticosteroids. Deucravacitinib 6 mg daily produced complete lesion clearance within one month, with early, self-resolving aphthous ulcers as the only reported adverse effects.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/rapid-and-successful-treatment-of-generalized-granuloma-annulare-with-deucravacitinib-case-report/457946/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/rapid-and-successful-treatment-of-generalized-granuloma-annulare-with-deucravacitinib-case-report/457946.png","ImageObject",300,407,{"name":92,"@type":93},"Himbo","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-27","2026-09-30",true,{"@type":102,"interactionType":103,"userInteractionCount":29},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What condition is discussed and why is it difficult to treat?","Question",{"text":112,"@type":113},"The article focuses on granuloma annulare (GA), a chronic granulomatous skin condition that is often resistant to standard therapies such as corticosteroids and other systemic treatments.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How does deucravacitinib relate to GA pathogenesis?",{"text":117,"@type":113},"The treatment targets TYK2, which mediates signaling through IL-12, IL-23, and type I interferons that support interferon-gamma-driven JAK-STAT activation implicated in GA.",{"name":119,"@type":110,"acceptedAnswer":120},"What were the patient’s outcomes and main side effects after treatment started?",{"text":121,"@type":113},"After initiating deucravacitinib 6 mg daily, the patient achieved complete clearance of lesions within one month. Adverse effects were limited to brief aphthous ulcers during the first two weeks, which resolved spontaneously.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},457946,1791128077,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":29,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":24,"language":139,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":140,"faqs":141,"seo_title":142,"seo_description":67,"update_tm":143,"read_time":144,"preview_page_count":4},687197100911,"https://ap-avatar.wpscdn.com/avatar/a000239b6f1da00475?x-image-process=image/resize,m_fixed,w_180,h_180&k=1785132997149421697","Review began 10/26/2025  \nReview ended 12/04/2025  \nPublished 12/08/2025  \n© Copyright 2025  \nLee et al. This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 4.0. , which permits unrestricted use , distribution , and reproduction in any medium , provided the original author and source are credited.  \nDOI: 10.7759/cureus.98761  \nOpen Access Case Report  \nRapid and Successful Treatment of Generalized Granuloma Annulare With Deucravacitinib  \nMichael J. Lee 1, Maria Isabelle P. Avenido 1, Emily Ames 1 , David G. Cotter 2  \n1. Medicine, University of Nevada Las Vegas School of Medicine, Las Vegas, USA 2. Dermatology, University of Nevada Las Vegas School of Medicine, Las Vegas, USA  \nCorresponding author: Michael J. Lee, [leem72@unlv.nevada.edu](leem72@unlv.nevada.edu)  \nAbstract  \nGranuloma annulare (GA) is a chronic granulomatous dermatosis that often proves resistant to conventional therapies. Increasing evidence implicates interferon-gamma-mediated JAK-STAT activation in GA pathogenesis, with tyrosine kinase 2 (TYK2) playing a central role through IL-12, IL-23, and type I interferon signaling. Deucravacitinib, a selective allosteric TYK2 inhibitor, has emerged as a potential therapy by targeting these pathways. We present the case of a 59-year-old woman with biopsy-confirmed interstitialtype GA that was unresponsive to topical corticosteroids. Initiation of deucravacitinib 6 mg daily led to complete clearance of lesions within one month. Reported adverse effects were limited to brief episodes of aphthous ulcers during the first two weeks of therapy, which resolved spontaneously. Laboratory testing two weeks after treatment initiation showed mild elevations in lipids and glucose and slightly decreased calcium, though baseline labs were not available for comparison and no serious adverse events occurred. This case highlights the potential of deucravacitinib as a novel therapeutic option for refractory GA and adds to emerging evidence that TYK2 inhibition may represent a targeted and effective approach for this condition.  \nCategories: Dermatology  \nKeywords: aphthous ulcers, deucravacitinib, granuloma annulare, immuno-modulator, interstitial granuloma annulare, selective tyk2 inhibitor  \nIntroduction  \nGranuloma annulare (GA) is a chronic, granulomatous skin condition that presents with annular papules or plaques, often resistant to standard treatments, with an incidence of 0 .04% and a prevalence of 0 .06% in the United States [1-3]. While its etiology remains uncertain, recent evidence points to a dysregulated immune response involving Th1-mediated interferon-gamma (IFN-γ) signaling and downstream JAK-STAT pathway activation [1] . Histologically, GA shows palisading or interstitial histiocytes surrounding collagen with mucin deposition [2] . Although spontaneous remission can occur, many patients experience persistent or generalized disease that proves resistant to conventional therapies such as corticosteroids, retinoids, or systemic immunosuppressants [1,4] . Granuloma annulare has also been associated with metabolic comorbidities, particularly dyslipidemia and diabetes mellitus, most frequently in generalized forms of the disease [2,5] .  \nAdvances in immunology have reshaped the understanding of GA pathogenesis. Lesional tissue demonstrates enrichment of Th1 cytokine pathways, particularly IFN-γ, with downstream JAK-STAT activation [1,4] . This framework has driven interest in targeted inhibition of cytokine signaling. Recent clinical reports show improvement of GA with JAK inhibitors, delivered both systemically and topically, highlighting this pathway as a promising therapeutic target [6-8]  \nTyrosine kinase 2 (TYK2), a member of the JAK family, selectively mediates signaling through IL-12, IL-23, and type I interferons [9] . Genetic data in humans show that TYK2 deficiency impairs IL-23-dependent IFN-γ responses, underscoring its central role in granulomatous immun","cbCaiv80uvCh9Wu5","https://ap.wps.com/l/cbCaiv80uvCh9Wu5","pdf",2624981,"English","# Abstract\n# Introduction\n# Case Presentation\n## Clinical findings\n## Treatment course and outcomes\n## Adverse effects and laboratory findings","[{\"question\":\"What condition is discussed and why is it difficult to treat?\",\"answer\":\"The article focuses on granuloma annulare (GA), a chronic granulomatous skin condition that is often resistant to standard therapies such as corticosteroids and other systemic treatments.\"},{\"question\":\"How does deucravacitinib relate to GA pathogenesis?\",\"answer\":\"The treatment targets TYK2, which mediates signaling through IL-12, IL-23, and type I interferons that support interferon-gamma-driven JAK-STAT activation implicated in GA.\"},{\"question\":\"What were the patient’s outcomes and main side effects after treatment started?\",\"answer\":\"After initiating deucravacitinib 6 mg daily, the patient achieved complete clearance of lesions within one month. Adverse effects were limited to brief aphthous ulcers during the first two weeks, which resolved spontaneously.\"}]","Rapid and Successful Treatment of Generalized Granuloma Annulare With Deucravacitinib - Case Report | PDF",1790750933,13]