ABSTRACT
The quantity and quality of the adipose tissue is altered in obesity: hypertrophy of adipocytes, decrease in expandability, fibrosis, production of pro-inflammatory cytokines and adipokines, inflammatory infiltration by pro-inflammatory M1 macrophages and T lymphocytes. Excess adipose tissue and obesity are associated with low-grade inflammation that can aggravate chronic inflammatory diseases, decrease treatment efficacy, contribute to the development of comorbidities, and of the disease in its preclinical phase. Obesity increases the incidence of rheumatoid arthritis (RA), psoriasis, psoriatic arthritis with a weight-dose effect. It is also a predictor of worse response to treatment, in particular TNF inhibitors. Weight loss induced by bariatric surgery decreases the risk of psoriasis and psoriatic arthritis and improves disease activity and remission in RA. A 5% weight loss through a low-calorie diet improves the response to TNF inhibitors in psoriatic arthritis, losing even more weight improves the response even more. In RA, the beneficial effect of weight loss from a low-calorie diet on disease activity has been reported in a few observational studies but has not been demonstrated in a randomized controlled trial. Screening and management of obesity are part of the dietary recommendations of the French Society for Rheumatology in patients with chronic inflammatory rheumatic diseases. Of course, this should be combined with other lifestyle modifications such as smoking cessation, higher food quality, increased physical activity and reduced sedentary behavior.
ABSTRACT
It is clear that there is an increased cardiovascular (CV) risk in rheumatoid arthritis (RA) as a result of systemic inflammation. Hand osteoarthritis (HOA) patients, also have an increased CV risk, but the causes are still debated. Our objective was to compare CV risk factors and risk scores between HOA and RA patients. Thirty-five HOA patients were matched by age (< 3 years) and sex to 35 RA patients in a case-control study. We compared their CV risk profiles and their risk of occurrence of CV events at 10 years using the risk equations SCORE1, SCORE2, and QRISK3. There was a significant increase in SCORE1, SCORE2, but not in QRISK3 in the RA group compared to the HOA group, provided that the multiplication coefficient for RA was applied. This increase was found to no longer be significant for SCORE1 when RA patients have low disease activity (DAS28 ≤ 3.2; n = 8). There was no difference between groups in the frequency of metabolic syndrome, blood pressure, abdominal circumference, body mass index, uricemia, triglyceridemia, HDL cholesterolemia, or pain intensity. Conversely, HOA patients had higher LDL cholesterol and fasting blood glucose levels, in the main analysis and in the subgroup of moderate/high RA activity patients (DAS28 > 3.2; n = 26). We found a higher CV risk in RA compared to HOA patients with moderate/high disease activity. The increased CV risk reported in OA remains to be confirmed in HOA, but these patients appear to have a pro-atherogenic lipid and glycemic profile.
