Rheumatoid arthritis (RA) a chronic autoimmune disease and Alzheimer’s

By SWA

Diverse environmental fungi are increasingly recognized as causal or contributory factors in a wide range of chronic inflammatory conditions. These include common cutaneous disorders such as atopic dermatitis (eczema) and onychomycosis, as well as mucosal inflammatory diseases such as pharyngitis, laryngitis, esophagitis, asthma, chronic rhinosinusitis, vaginosis, and colitis¹. In immunocompromised individuals, cutaneous candidal infections, manifesting as mucocutaneous candidiasis, often take on a more invasive and destructive course¹,². Beyond these well-characterized associations, emerging evidence also implicates fungi in systemic and neuroinflammatory diseases, including rheumatoid arthritis³ and Alzheimer’s disease (AD), highlighting their broader role in human pathology.

Rheumatoid arthritis (RA), a chronic autoimmune disease primarily affecting the joints, is commonly associated with the development of firm, non-tender subcutaneous nodules near pressure points or joints. These rheumatoid nodules are histologically characterized by a central area of fibrinoid material, a proteinaceous substance resembling fibrin—normally involved in the blood clotting process—surrounded by palisading histiocytes and a peripheral inflammatory zone. Such nodules arise as a consequence of chronic immune dysregulation and persistent inflammation in RA, and while they are typically painless, they can occasionally become symptomatic depending on their size or anatomical location.

Although most commonly observed in the skin and periarticular tissues, rheumatoid nodules can also occur in internal organs, reflecting the systemic nature of the disease. While their presence is strongly associated with RA, similar nodular lesions may rarely appear in other autoimmune conditions such as systemic lupus erythematosus. Importantly, the fibrinoid material within RA nodules reflects ongoing inflammatory tissue injury rather than coagulation abnormalities; however, RA itself confers an increased risk of cardiovascular disease, including atherosclerosis and thrombosis, due to chronic systemic inflammation and immune dysregulation.

Patients presenting with rheumatoid nodules should undergo careful clinical assessment to determine whether intervention is warranted, particularly when nodules impair function or cause discomfort. Understanding the interplay between chronic inflammation, immune dysfunction, and nodule formation remains critical to elucidating the broader pathophysiological consequences of RA.

References: 

Microglia and amyloid precursor protein coordinate control of transient Candida cerebritis with memory deficits
https://www.nature.com/articles/s41467-018-07991-4

In the news: Published:

Host albumin redirects Candida albicans metabolism to engage an alternative pathogenicity pathway
https://www.nature.com/articles/s41467-025-61701-5

© 2000-2025 Sieglinde W. Alexander. All writings by Sieglinde W. Alexander have a fife year copy right. Library of Congress Card Number: LCN 00-192742


 

 

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