CYTOKINE REGULATION OF IRON-METABOLISM - EFFECT OF LOW-DOSE INTERLEUKIN-2 SUBCUTANEOUS THERAPY ON FERRITIN, TRANSFERRIN AND IRON BLOOD-CONCENTRATIONS IN CANCER-PATIENTS

Citation
P. Lissoni et al., CYTOKINE REGULATION OF IRON-METABOLISM - EFFECT OF LOW-DOSE INTERLEUKIN-2 SUBCUTANEOUS THERAPY ON FERRITIN, TRANSFERRIN AND IRON BLOOD-CONCENTRATIONS IN CANCER-PATIENTS, Journal of biological regulators and homeostatic agents, 7(1), 1993, pp. 31-33
Citations number
NO
Categorie Soggetti
Biology,"Medicine, Research & Experimental
ISSN journal
0393974X
Volume
7
Issue
1
Year of publication
1993
Pages
31 - 33
Database
ISI
SICI code
0393-974X(1993)7:1<31:CROI-E>2.0.ZU;2-X
Abstract
It is known that the anemias of chronic diseases, which often occur in neoplastic and in systemic inflammatory disorders, are characterized by high levels of ferritin associated with generally low iron concentr ations, by suggesting an iron transfer defect due to unknown factors. Since both chronic inflammatory diseases and advanced neoplasms are ch aracterized by alterations in the endogenous production of cytokines, a possible involvement of interleukins in chronic disease-related anom alies of iron metabolism cannot at present be excluded The present stu dy was carried out to investigate the effect of low-dose IL-2 subcutan eous immunotherapy (3 million IU/day for 6 days/week for 4 weeks) on f erritin, transferring and iron serum levels in cancer patients. Six pa tients with metastatic gastrointestinal carcinomas were evaluated. Fer ritin mean levels significantly decreased during IL-2 treatment, and t his finding was associated with a significant increase in transferrin values. Iron mean levels increased in response to IL-2, without, howev er, significant differences in respect to the pretreatment concentrati ons. These preliminary data, by showing changes in ferritin, transferr in and iron in cancer patients during the immunotherapy with IL-2, wou ld suggest the existence of a cytokine regulation of iron transfer fro m tissues to blood, perhaps by modulating the macrophage function.