CACS - Cancer anorexia/cachexia syndrome - weight loss and loss of lean body mass.
50% of patients with cancer lose some body weight with one-third losin more than 5% of their original body weight and as many as 20% of cancer deaths resulting from cachexia.
Reduction in oral intake does not solely explain why cachexia occurs - may occur in patients that appear to take in sufficient calories. Nutrition support does not successfully restore the loss of lean body mass with CACS.
Known factors contributing to development of CACS:
- Early satiety
- Taste Changes
Imbalance between pro-inflammatory and anti-inflammatory cytokines.
Pro-inflammatory (thought to be primary mediators assoc with development of CACS):
- Tumor necrosis factor (TNF)
- Interleukins 1 and 6 (IL-1, IL-6)
- Interferon Gamma (IFN-Y)
In animal studies, the infusion of pro-inflammatory cytokines found to produce anorexia, weight loss, proteolysis, lypolysis, and elevation sin cortisol and glucagon levels. Also increase energy expenditure.
Hormones that affect appetite:
- Leptin - reduces appetite - down regulation of leptin production and expression of leptin receptors in the hypothalamus by tumor necrosis factor
- Grehlin - increases appetite - reductions in gstric production of ghrelin synthesis by various cytokines.
Proteolysis-inducing factor: a glycoprotein isolated from the urine of weight-losing cancer patients but not from weight loss from other sources.