الفهرس 
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Abstract
Psoriatic arthritis (PsA), which is a chronic inflammatory arthritis that affects 20–30 percent of psoriasis (PsO) patients, is significantly linked to obesity, especially excess visceral adiposity. Patients who have PsA may have skin and nail disease with joint inflammation and may also have other manifestations like enthesitis, uveitis, dactylitis, axial inflammatory arthritis, metabolic syndrome and constitutional manifestations related to long term inflammation, such as fatigue.
Chronic low-grade inflammation is a common pathophysiological mechanism that links obesity with psoriasis. Adipocytes have an imbalance, which leads to an overproduction of inflammatory mediators known as adipokines. Leptin, TNF-a, plasminogen activator inhibitor-1 (PAI-1), and interleukin-6 are examples of adipokines (IL-6). There is also a reduction in the release of preventive adipokines such adiponectin. Obese people have a pro-inflammatory state as a result of this imbalance.
Obesity is defined by the World Health Organization as a body mass index (BMI) of greater than or equal to 30 kg/m2. Overweight is defined as a BMI of 25 to 29.99. Another type of obesity is abdominal obesity, also known as central obesity, which develops when excessive abdominal fat has grown up to the point where it appears to be harmful to one’s health. It has been associated to cardiovascular disease, metabolic syndrome, and vascular disease. It is diagnosed by measuring waist circumference and waist to hip ratio. BMI measures overall body fatness, whereas waist circumference measures visceral fat and the risk of obesity-related disease.
It is noted that there is a direct relationship between obesity and the risk of psoriasis or PsA in genetically predisposed individual, as the higher a patient’s BMI and the longer he or she has been obese, the higher the risk of disease.
Behavioral factors, on the other hand, can be a link between PsA and obesity, as pain and inflammation in arthritis patients can lead to a vicious cycle of reduced physical activity and overeating, making them more prone to obesity, sedentary lifestyles, and further reductions in mobility and physical activity.
The aim of this work was to study the relationship between PsA and obesity as regard clinical and laboratory study.
This study comprised fifty patients with PsA diagnosed using the CASPAR criteria and sixty healthy controls.
Patients with other skin diseases, chronic inflammatory or autoimmune diseases other than PsA, with history or current use of steroids therapy were excluded.
All of the patients had their musculoskeletal systems clinically evaluated. DAPSA, BASDAI, and VAS were used to assess disease activity, while HAQ-DI was used to assess impairment. Laboratory investigation as: CRP and leptin hormone were measured in patients and control subjects.
Obesity assessment was done by measuring BMI, WC, WHR and PBF using Inbody 220 apparatus- Body composition analyzer in patient and control subjects.
As regarding the central obesity, there was a statistically significant difference between patients group and control group, while there was no statistically significant difference between both groups as regarding the other parameters of obesity.
There is a strong positive association between PBF and DAPSA as well as PBF and VAS in the patient group, but there is no significant correlation between other obesity markers and clinical PSA assessment.
There was also statistically significant difference between two studied groups regarding leptin hormone and CRP level.