SERUM LEVELS OF TUMOR-NECROSIS-FACTOR-ALPHA AND OTHER CYTOKINES DO NOT CORRELATE WITH WEIGHT-LOSS AND ANOREXIA IN CANCER-PATIENTS

Cancer anorexia-cachexia syndrome (CACS), which is characterized by pr ogressive weight loss (WL) and anorexia (A), is present in 50% of adva nced cancer patients and in 80% of terminally ill cancer patients. One of the most controversial aspects of CACS is its oetiopathogenesis; e xperimental studies have identified certain cytokines [Tumour necrosis factor alpha (TNF-alpha), interleukin 1 (IL-1), interleukin 6 (IL-6), and gamma interferon (gamma-IFN)] as possible cofactors in the onset of the syndrome. The aim of our study was to investigate the correlati on between serum levels of circulating cytokines and severity of CACS. The following series of parameters was indentified in 61 patients wit h advanced and terminal cancer: stage of disease; Karnofsky performanc e status (KPS) and clinical symptoms; biohumoral, anthropometric and i mmunological situation; level of circulating cytokines. All these para meters were evaluated for a possible link with WL/A. Our data do not s how any significant correlation between circulating cytokines and WL/A . A direct correlation was identified between WL/A and nausea (P=0.03 and P<0.001, respectively) whereas inverse correlations were observed for both factors as regards arm circumference (P<0.001 for both), wris t circumference (P<0.001 for both), KPS (P<0.001 and P=0.003, respecti vely) and creatinine (P=0.005 and P=0.03, respectively). Other biochem ical factors, such as haemoglobin, haematocrit, glycaemia, prealbumin, sodium and chlorine were also correlated with at least one of the two clinical parameters in question. Unexpected results were seen in the increases in CD20 and CD4 and in the CD4/CD8 ratio. Serum levels of th ese cytokines do not, therefore, appear to be critical in the onset of CACS. On the contrary, our findings confirmed the clinico-laboratory picture that is characteristic of CACS. If we consider the possibility that CACS is provoked by an aspecific response of the host's defence mechanisms against prolonged neoplastic attack, the increase in CD4 (h elper lymphocytes) could be linked to the persistent response.