Abstract
Delayed cutaneous hypersensitivity and inflammatory responses were evaluated in patients with various types and stages of genitourinary cancer. The study was designed to evaluate the influence of tumor type, tumor stage, surgery, radiation therapy, and the course of the malignancy upon the skin test responses. Renal, prostate and bladder cancer patients had significant depressions in their response to recall antigens, DNCB, and croton oil. Impairment of primary delayed hypersensitivity (DNCB response) correlated with tumor stage in bladder but not renal and prostate cancer. Recall antigen response failed to correlate well with stage of disease and was of less value in assessing host immunocompetance. Differences in the effect of cancer on the immune system were found between bladder cancer and renal and prostate cancer patients. These may be explained by variation in cell origin, differences in host response or other characteristics of each type of cancer. The frequency of impaired inflammatory reactions (to croton oil) indicate that defects exist in both the inflammatory and immune mechanisms. The skin test responsiveness following radiation therapy was markedly depressed in a group of bladder cancer patients. However, skin test response in the entire cancer population (renal, prostate and bladder) was not affected by radiation. No significant differences in response could be attributed to the dose of radiation. Changes in response noted after surgery and anesthesia varied depending upon the time interval that elapsed between the skin test and surgery. Patients tested within 10 days of surgery demonstrated depression of skin test responsiveness, whereas those tested 4 to 12 months later demonstrated a significant increase in DNCB responsiveness, presumably due to tumor removal. Tumor removal permitted return of primary and secondary delayed hypersensitivity and inflammatory reactions over a period of many months. Prognostic value was greater for DNCB tests. Survival was poorer in those patients initially unresponsive to DNCB.
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