The rheumatism induced by anticonvulsants has been described in literature mostly because of phenobarbital therapy. The possible onset of this clinical picture due to other antiepileptic drugs is unusual and not well defined. We report the case of a 87-year-old female, affected by partial seizures treated with carbamazepine for 20 years, who came to our observation for the onset of disturbances that clearly resemble the classic syndrome of rheumatism induced by barbiturates: the diagnostic hypothesis of a drug side effect was confirmed by the marked clinical improvement of the patient after carbamazepine was stopped and substituted by gabapentin.
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J Cardiothorac Surg
January 2025
Department of General Internal Medicine, Hangzhou Xixi Hospital, Hangzhou Sixth People's Hospital, Hangzhou Xixi Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, 310023, China.
Background: Gout is a metabolic disease caused by decreased blood uric acid excretion and purine metabolism disorders. Long-term and persistent metabolic dysfunction gradually affects other organ functions and is the main factor inducing Myocardial Infarction (MI) and Heart Failure (HF), seriously affecting the health of patients. This study adopts a meta-analysis to analyze the risk of MI and HF in gout patients.
View Article and Find Full Text PDFPLoS One
January 2025
Faculty of Medicine Dentistry and Health Sciences, Department of Medicine, Royal Melbourne Hospital, Melbourne Medical School, University of Melbourne, Parkville, Victoria, Australia.
Objectives: We previously reported that CCL17 gene-deficient mice are protected from developing pain-like behaviour and exhibit less disease in destabilization of medial meniscus (DMM)-induced OA, as well as in high-fat diet (HFD)-exacerbated DMM-induced OA. Here, we explored if therapeutic neutralization of CCL17, using increasing doses of a neutralizing monoclonal antibody (mAb), would lead to a dose-dependent benefit in these two models.
Design: DMM-induced OA was initiated in male mice either fed with a control diet (7% fat) or 8 weeks of a 60% HFD, followed by therapeutic intraperitoneal administration (i.
Nan Fang Yi Ke Da Xue Xue Bao
January 2025
First Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei 230031, China.
Objectives: To investigate the mechanism mediating the regulatory effect of miR-155-5p on proliferation of human submandibular gland epithelial cells (HSGECs) in primary Sjogren's syndrome (pSS).
Methods: Dual luciferase reporter assay was used to verify the targeting relationship between miR-155-5p and the PI3K/AKT pathway. In a HSGEC model of pSS induced by simulation with TRAIL and INF-γ, the effects of miR-155-inhibitor-NC or miR-155 inhibitor on cell viability, cell cycle, apoptosis and proliferation were evaluated using CKK8 assay, flow cytometry and colony formation assay.
Nan Fang Yi Ke Da Xue Xue Bao
January 2025
Department of Rheumatology, Henan Provincial Hospital of Traditional Chinese Medicine// Second Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou 450002, China.
Objectives: To investigate the role of the BNIP3-PI3K/Akt signaling pathway in mediating the inhibitory effect of Decoction (BYHWT) on mitochondrial autophagy in human synovial fibroblasts from rheumatoid arthritis patients (FLS-RA) cultured under a hypoxic condition.
Methods: Forty normal Wistar rats were randomized into two groups (=20) for daily gavage of BYHWT or distilled water for 7 days to prepare BYHWT-medicated or control sera. FLS-RA were cultured in routine condition or exposed to hypoxia (10% O) for 24 h wigh subsequent treatment with IL-1β, followed by treatment with diluted BYHWT-medicated serum (5%, 10% and 20%) or control serum.
J Clin Invest
January 2025
Division of Rheumatology, Center of Excellence for Intestinal and Immunology Research, University of Alberta, Edmonton, Alberta, Canada.
Superantigen-induced (Sag-induced) autoimmunity has been proposed as a mechanism for many human disorders, without a clear understanding of the potential triggers. In this issue of the JCI, McCarthy and colleagues used the SKG mouse model of rheumatoid arthritis to characterize the role of Sag activity in inflammatory arthritis by profiling arthritogenic naive CD4+ T cells. Within the diseased joints, they found a marked enrichment of T cell receptor-variable β (TCR-Vβ) subsets that were reactive to the endogenously encoded mouse mammary tumor virus (MMTV) Sag.
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