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Golimumab-induced lichen planus pigmentosus in a patient with ulcerative colitis.
An Bras Dermatol
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Department of Dermatology, Faculty of Medicine, Universidad de los Andes, Santiago, Chile.
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Children's Hospital, Capital Institute of Pediatrics, Beijing 100020, China. Electronic address:
Ulcerative colitis (UC) is a chronic relapsing inflammatory bowel disease for which current therapeutic approaches still face many dilemmas, and targeting macrophage polarization and metabolism for the treatment of this disease is a potentially effective strategy. The gut microbial metabolite indole-3-propionic acid (IPA) has favorable anti-inflammatory and antioxidant effects and plays a role in a variety of disease models. IPA is effective in the treatment of UC, but the underlying mechanisms have not been well explored.
View Article and Find Full Text PDFApplicability of colon capsule endoscopy for monitoring ulcerative colitis: a systematic review.
Scand J Gastroenterol
March 2025
Department of Surgery, Odense University Hospital, Svendborg, Denmark.
Background: As the target of therapy in Ulcerative colitis (UC) has changed from symptomatic relief to mucosal healing, endoscopic visualization is mandatory. Colon capsule endoscopy (CCE) may serve as a less invasive and more tolerable alternative to standard colonoscopy (SC) for the monitoring of UC.
Objectives: To evaluate the diagnostic accuracy, adverse events and tolerability for CCE compared to SC.
Platelet activation stimulates macrophages to enhance ulcerative colitis through PF4/CXCR3 signaling.
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Graduate School, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
Platelets are involved in hemostasis and immune regulation, but little is currently known regarding their role in inflammatory bowel disease. In the present study, the mechanism by which platelet activation affects macrophage C‑X‑C motif chemokine receptor 3 (CXCR3) by releasing platelet factor 4 (PF4), thus aggravating ulcerative colitis (UC) disease progression, was investigated. A dextran sulfate sodium‑induced mouse model showed co‑localization of the platelet marker PF4 with the macrophage M1 marker inducible nitric oxide synthase.
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Division of Gastroenterology and Hepatology, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
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