The candidacidal activity and the production of oxygen radicals by monocytes were investigated in untreated and long-term remission patients with Hodgkin's disease (HD). Both groups showed a decreased candidacidal function of monocytes with a chemiluminescence (CL) response significantly lower and delayed, with respect to normal controls. Indomethacin at 1 pg/ml corrected the monocyte deficiency increasing the CL response to normal values and normalizing the kinetics in the untreated patients. However, in patients in remission, the peak was delayed and followed by a significant increase in the production of oxygen radicals compared with untreated patients. A direct linear correlation was found between the percentages of lysed Cundidu and maximum CL peak of stimulated monocytes. When prostaglandin E2 (PGE-2) levels, measured in supernatants of cultured mononuclear cells, were plotted against the per- centages of killed Cundidu, an inverse linear correlation was found. Therefore, monocytes from HD patients have a dysfunction in the generation of oxygen radicals and a decreased candidacidal activity associated with excessive production of PGE-2. Indomethacin can correct the oxidative metabolism in the untreated patients while in apparently "cured" patients the disorder persists.
Cancer 62:2 1 28-2 133,1988.
MPAIRMENT OF CELLMEDIATED IMMUNITY in patients I with Hodgkin's disease (HD) is well do~umented.'-~
Although some of the immunologic abnormalities can be resolved with successful HD treatment, there are others that persist for many years after apparent cure.2,375-7 The mechanisms that lead to the depressed cellular immunity in HD are not well defined.
Recent studies have suggested that alterations in immunoregulation by cells of monocyte-macrophage and/ or T-cell lineages, mainly through their cell products can explain the persistent immunosuppression in this dise a ~e , ~, * -' ~
In previous studies, we found that peripheral blood monocytes from patients with untreated HD fail to lyse ingested Candida. l6 Inhibitors of prostaglandin synthesis can correct the lytic deficiency both in vitro and in vivo.I7 These data suggest that prostaglandins could be one of the biologic factors responsible for the macrophage