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Prospective assessment of body weight and body composition changes in patients with psoriasis receiving anti‐TNF‐α treatment
Author(s) -
RENZO LAURA DI,
SARACENO ROSITA,
SCHIPANI CATERINA,
RIZZO MARIAGIOVANNA,
BIANCHI ALESSIA,
NOCE ANNALISA,
ESPOSITO MARIA,
TIBERTI SERGIO,
CHIMENTI SERGIO,
DE LORENZO ANTONINO
Publication year - 2011
Publication title -
dermatologic therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.595
H-Index - 68
eISSN - 1529-8019
pISSN - 1396-0296
DOI - 10.1111/j.1529-8019.2011.01439.x
Subject(s) - medicine , psoriasis , psoriatic arthritis , tumor necrosis factor alpha , lean body mass , adipose tissue , pathogenesis , weight gain , cytokine , body mass index , prospective cohort study , gastroenterology , immunology , endocrinology , body weight
Tumor necrosis factor (TNF)‐α is a pro‐inflammatory cytokine associated with psoriasis pathogenesis. Anti‐TNF‐α therapies are effective in psoriasis. A significant weight gain has been reported in patients treated with anti‐TNF‐α agents. The aim of the present study was to evaluate the body composition changes in psoriatic patients receiving anti‐TNF‐α therapies according with disease phenotype. Forty patients affected with psoriasis were followed up for 24 weeks and divided into two groups: psoriasis vulgaris (PsO) and psoriatic arthritis (PsA). Anthropometric, blood biochemical, body composition parameters, resting metabolic rate, and disease activity indexes were measured at baseline and at week 24. After 24 weeks of anti‐TNF‐α administration, the disease activity indexes and concentration of inflammatory markers were significantly decreased. Seventy‐five percent of PsO and 60% of PsA patients had an increase in body weight. Weight changes correlated with fat mass gain in the PsO group, and with fat and lean mass gain in the PsA group. In the present study, we demonstrated that a blockage of TNF‐α bioactivity is related with fat and lean mass gain in both PsO and PsA subjects. The anti‐TNF‐α therapies could play a key role in the cross talk between adipose tissue and skeletal muscle, mediated by the reduction of TNF‐α and interleukin‐6 production.