Osteoarthritis more likely in patients with non-alcoholic fatty liver disease
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Key takeaways:
- People with non-alcoholic fatty liver disease had an adjusted OR of 1.72 to develop osteoarthritis, a finding consistent across subgroups.
- Arthritis patients should be screened early and receive intervention.
Non-alcoholic fatty liver disease is an independent risk factor for osteoarthritis, according to data published in Arthritis Research & Therapy.
“Mechanistically, low-grade inflammation and metabolic derangements may at least be involved in the occurrence of [non-alcoholic fatty liver disease (NAFLD)] and OA,” Yu Lu, of the Third Affiliated Hospital of Guangzhou Medical University, in China, and colleagues wrote. “It means that these two diseases have similar causative factors. However, few studies have explored the correlation between NAFLD and OA.”
To examine the link between the two conditions, Lu and colleagues conducted a cross-sectional study of data from the CDC’s National Health and Nutrition Examination Survey from 2017 to 2018. The researchers included 2,262 patients aged older than 20 years (mean age, 48.1 years; 47.8% men), 12.8% of whom had OA (n = 317) and 41.5% of whom had NAFLD (n = 1,140), and used weighted multiple logistic regression models and stratified analyses. Exclusion criteria were “considerable” alcohol consumption and history of hepatitis B or C, the researchers wrote.
According to the researchers, the logistic regression analysis demonstrated that NAFLD was significantly associated with OA, both before and after adjusting for covariates (adjusted OR = 1.72; 95% CI, 1.26-2.34). Subgroup analysis also showed a “significant and consistent association” of NAFLD with OA by age, sex, obesity, metabolic syndrome and high-sensitivity C-reactive protein status (P > .05 for all), they wrote.
“NAFLD is an independent risk marker for OA, suggesting that further evaluation of the underlying mechanism between NAFLD and increased risk is deserved,” Lu and colleagues wrote. “Given the current pandemic of NAFLD and OA, clinicians should screen for NAFLD in arthritis patients and intervene early.”
Perspective
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David A. McLain, MD, MACR, FACP, FRCP
Liver disease stands as one of the primary contributors to global morbidity and mortality, with its prevalence experiencing a notable recent surge. The initial indication of liver impairment manifests as inflammation, often coupled with the buildup of fat known as non-alcoholic fatty liver disease (NAFLD), which inflicts damage upon hepatocytes. At this phase, progression to fibrosis occurs, characterized by the substitution of healthy liver tissue with fibrotic tissue, leading to a decline in liver function.
Subsequently, cirrhosis ensues, representing an advanced stage of fibrosis where a significant portion of liver tissue has been replaced by fibrotic tissue, resulting in substantial impairment of liver function. In chronic inflammatory conditions like rheumatoid arthritis and psoriatic arthritis, which carry a heightened risk of cardiovascular disease (CVD), hepatic changes appear to be more common compared with both the general population and other rheumatic disorders.
The precise mechanisms underlying the development of this comorbidity remain unclear, though chronic inflammation, treatments, autoimmunity and metabolic dysregulation are thought to play significant roles. Although biomechanical overloading due to obesity remains a predominant factor in osteoarthritis, it’s important to acknowledge that inflammatory mediators also play a crucial role in driving the destruction of joint tissues.
The authors of this article suggest three mechanisms linking NAFLD to OA — adenosine 2A receptors, Neuregulin 4 (Nrg4) levels, and endoplasmic reticulum stress. As an illustration, Nrg4 might mitigate the advancement of OA by reducing inflammation (IL-Iβ, IL-6, TNF-α) and safeguarding against chondrocyte apoptosis via the MAPK/JNK signaling pathway.
Conversely, a deficiency in Nrg4 has been observed in individuals with NAFLD. These mechanisms were novel to me, and likely to many rheumatologists as well. Exploring these pathways further could offer insights into the underlying mechanisms of both OA and NAFLD, potentially paving the way for advancements in treatment.
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