Chronic inflammation in psoriasis and obesity: implications for therapy

Med Hypotheses. 2006;67(4):768-73. doi: 10.1016/j.mehy.2005.11.050. Epub 2006 Jun 15.


A recent study has shown an indisputable relationship between psoriasis and obesity. Obesity leads to a higher risk in developing psoriasis and a poorer long-term clinical outcome of psoriasis. Furthermore, loosing weight may improve the psoriasis. A network of pro-inflammatory cytokines (especially tumour necrosis factor alpha (TNF-alpha)) is believed to play an important role in the pathophysiology of both obesity and psoriasis. The chronic low-level inflammation- as seen in obesity--may contribute to the extent of psoriatic lesions in obese patients. TNF-alpha in obesity is presumed to be derived from inflammatory cells (macrophages) in the adipose tissue and in psoriasis from activated T cells. Several drugs, such as peroxisome proliferator activated receptor (PPAR)-gamma agonists and TNF-alpha blocking agents, that target the pro-inflammatory pathways involved in both psoriasis and obesity have proven their benefit in the treatment of these entities. Furthermore, changes in levels of metabolic hormones as ghrelin and leptin in obesity may also play a role in the pathogenesis of deterioration of psoriasis by their potency to release pro-inflammatory mediators (e.g. interleukin (IL) 6 and TNF-alpha). We hypothesize that the treatment of obese psoriasis patient could be focused on reducing the obesity-induced inflammation. Reducing this obesity-induced inflammation may finally lead to a better clinical outcome. Weight loss could lead to a less inflammatory state by reducing concentrations of TNF-alpha, IL-6, leptin and improving insulin sensitivity.

MeSH terms

  • Chronic Disease
  • Humans
  • Inflammation / complications
  • Inflammation / immunology
  • Models, Biological
  • Obesity / complications*
  • Obesity / immunology
  • Obesity / physiopathology
  • Psoriasis* / drug therapy
  • Psoriasis* / etiology
  • Psoriasis* / immunology
  • Psoriasis* / physiopathology
  • Tumor Necrosis Factor-alpha / immunology
  • Tumor Necrosis Factor-alpha / metabolism
  • Tumor Necrosis Factor-alpha / physiology


  • Tumor Necrosis Factor-alpha