Normalization of monocyte candidacidal deficiency by cyclooxygenase inhibitors in Hodgkin's disease

In a previous work, the authors found that the peripheral blood monocytes from patients with Hodgkin's disease (HD) had depressed lytic capability to kill Candida pseudotropicalis and depressed phagocytic function. The aim of this study was to evaluate if cyclooxygenase inhibitors could correct the defective macrophage functions. Fifteen untreated patients with HD and 10 normal subjects were studied. The incubation of the cells from the patients with HD with indomethacin (IM) at 1, 3, and 10 micrograms/ml and with acetylsalicylic acid (ASA) at 20 micrograms/ml increased their previously deficient ability to kill C. pseudotropicalis, reaching values close to those of normal subjects. The oral administration of ASA during 1 week also corrected the monocyte lytic deficiency in the patients' group. Neither the in vitro nor the in vivo treatment with these cyclooxygenase inhibitors had any significant effect on normal subjects' monocytes' lytic function. The drugs did not improve the impaired phagocytic function in patients with HD. These results indicate that the failure of the lytic activity of the monocytes in HD could be associated to an excessive production of PGE2, and the oral administration of inhibitors of the cyclooxygenase activity can correct such abnormality whereas the phagocytic dysfunction is not reverted by them.