(recurrent polyserositis)
5,902 results
  • LLM-supported self-diagnosis and self-treatment of familial Mediterranean fever: a case report. [Case Reports]
    EULAR Rheumatol Open. 2026 Dec; 2(4):100244.Pauz J, Kremer P, … Krusche MER
  • Large language models (LLMs) are increasingly being used by patients to seek explanations for persistent or unexplained symptoms. However, their impact on real-world diagnostic pathways and patient behavior remains poorly understood. We report the case of a 34-year-old male of Egyptian origin with recurrent episodes of fever, severe migratory abdominal pain, arthralgia, myalgia, and intermittent …
  • Triggering Factors in Pediatric Familial Mediterranean Fever: A New Perspective on Colchicine Resistance. [Journal Article]
    Mod Rheumatol. 2026 Oct 05. [Online ahead of print]Zora HK, Donmez O, … Kilic SSMR
  • CONCLUSIONS: Although triggering factors were more frequently reported in patients with colchicine-resistant pediatric FMF, disease severity and disease duration were independently associated with their presence. IL-1 antagonist therapy substantially reduced both trigger-associated attacks and triggering factors. Recognition of modifiable triggers and their genetic associations may support personalized management and improved disease control.
  • Real-world safety of concomitant colchicine and statin therapy. [Journal Article]
    Arthritis Care Res (Hoboken). 2026 Sep 28. [Online ahead of print]Meidan R, Loutati R, … Eviatar TAC
  • CONCLUSIONS: Although colchicine-statin concomitant therapy was associated with higher rates of laboratory and clinical adverse events, the additional risk beyond statin monotherapy was small, supporting their use when clinically indicated.
  • A Novel Dominantly Segregating PSMB10 Splice-Site Variant in Familial Autoinflammatory Disease with Immunoproteasome and Interferon-Related Dysregulation. [Journal Article]
    Genes (Basel). 2026 Aug 25; 17(9).Onat UI, Bülbül A, … Tahir Turanli EG
  • CONCLUSIONS: We report a novel PSMB10 splice-site variant as a strong potential contributor to an unclassified autoinflammatory disease, with a predicted disruption of canonical splicing and loss of protein function. Our findings expand the clinical spectrum of immunoproteasome-associated disorders and suggest that immunoproteasome-related dysregulation and variable interferon responses may contribute to disease severity. The intrafamilial variability observed in this family suggests that additional genetic or immunogenetic factors may modify disease expression, even in autoinflammatory disorders that appear to follow a monogenic inheritance pattern.