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Changes in BMI were positively correlated with changes in IL-23 and significant positive correlations were observed between BMI and DAS28-CRP, CRP, IL-13, IL-17, leptin, and TNF-α.
Weight loss was linked to decreased levels of leptin and cytokines, particularly serum interleukin-23 (IL-23), which may partially explain the anti-inflammatory effect of weight loss in patients in psoriatic arthritis (PsA), according to a study published in Arthritis Research and Therapy.1
“Patients with PsA are frequently obese,” Anton Jonatan Landgren, MD, associated with the Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden, and colleagues. “We have previously shown decreased disease activity in patients with PsA with a body mass index (BMI) ≥ 33 kg/m2 following weight loss treatment with Very Low Energy Diet (VLED), resulting in a median weight loss of 18.6% at six months after baseline.”
Patients with PsA have an increased risk of cardiovascular risk because of chronic inflammation and an increased risk of cardiovascular disease due to chronic inflammation coupled with an increased prevalence of obesity (defined as a BMI of ≥ 30 kg/m2), diabetes, and hypertension, when compared with those without PsA. Obesity is also linked to an increased risk of PsA, poorer treatment outcomes, and more severe disease activity.2
Investigators evaluated the effects of VLED (640 kcal per day) during 12 or 16 weeks, depending on baseline BMI of < 40 or ≥ 40 kg/m2, on cytokines and adipokines at 6 months in previously assessed patients with PsA as well as age-, sex-, and weight-matched controls. After this follow-up period, food was gradually reintroduced after 12 weeks and each study participant received individualized energy-restricted dietary advice by dietitians. The cytokine and adipokine levels were measured using Magnetic Luminex Assays.
Eligible patients were adults between 25 and 75 years of age, met the classification criteria for PsA (CASPAR), and had a BMI of ≥ 33 kg/m2. Patients were recruited from hospitals in Western Sweden and controls were recruited from the Regional Obesity Center at Sahlgrenska University Hospital. Patients with PsA were followed up at baseline, month 3, and month 6. All participants were followed for a total of 12 months in accordance to the routines for structured weight loss treatment at the Regional Obesity Center and were seen by a physiotherapist at baseline, 6 months, and 12 months.
In total, 41 patients (median age 54 [interquartile range] (IQR) 49 – 62) years; 63% women) were matched with 39 controls (median age 55 (IQR 46–60) years; 74% women). In patients with PsA, IL-23 (median IQR .40 [.17 – .54] ng/mL vs .18 (.10 – .30) ng/mL, P <.001) and leptin (26.28 (14.35 – 48.73) ng/mL vs. 9.25 (4.40 – 16.24) ng/mL, P <.001) were significantly reduced.
The serum total (tot)-adiponectin and high molecular weight (HMW) adiponectin significantly increased. Comparable results were reported in controls. Additionally, changes in BMI were positively correlated with changes in IL-23 (P <.001) and significant positive correlations between BMI and Disease Activity Score based on 28 joints using C-reactive protein (DAS28-CRP), CRP, IL-13, IL-17, leptin, and tumor necrosis factor (TNF)-α. Negative correlations were observed between BMI and tot-adiponectin.
Investigators noted the lack of a control group with PsA that did not receive a dietary intervention as a limitation of the study. However, they did include a control group that underwent the same VLED treatment. Additionally, the effects on cytokines and adipokines may have been influenced by temporary starvation and the impact of physical activity on these levels was not evaluated. The strengths of the study included the follow-up design, successful weight loss intervention, and low attrition rate.
“The study supports important links between obesity both in general and in PsA through IL-23,” investigators concluded.
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