ABSTRACT
Twenty-four previously untreated patients with a diagnosis of prostatic cancer were treated with chlormadinone acetate (CMA) alone (100 mg/day) for 4 weeks, and luteinizing hormone-releasing hormone analogue (LH-RHa) was added for the next 24 weeks. Marked decreases in blood LH, testosterone (T), prostate specific antigen (PSA), gamma-seminoprotein (gamma-Sm), and prostatic acid phosphatase (PAP) were observed after a single dose of CMA. T levels were significantly increased 3 days after the initial dose of LH-RHa, and did not return to the pretreatment level. There were no significant increases in any of the markers, nor were there any flare-up cases. Triglyceride levels, which were slightly elevated before the start of treatment, were significantly decreased 24 weeks after the completion of combined therapy. PSA was evaluated as partial response (PR) or better in 86.7% of the patients. Overall evaluation showed PR or better in 75.0% of the patients. These findings suggest that prior administration of CMA followed by combined administration with LH-RHa is useful in the treatment of prostatic cancer. No negative effects on lipid metabolism were observed at any time during the treatment period.
Subject(s)
Antineoplastic Agents, Hormonal/administration & dosage , Chlormadinone Acetate/administration & dosage , Leuprolide/administration & dosage , Lipid Metabolism , Progesterone Congeners/administration & dosage , Prostatic Neoplasms/drug therapy , Aged , Aged, 80 and over , Apolipoproteins/blood , Cholesterol/blood , Drug Administration Schedule , Drug Therapy, Combination , Humans , Male , Middle Aged , Prostate-Specific Antigen/blood , Prostatic Neoplasms/blood , Testosterone/blood , Triglycerides/bloodABSTRACT
We measured prostatic acid phosphatase (PAP), gamma-seminoprotein (gamma-Sm) and prostatic specific antigen (PSA) levels simultaneously in the serum of 52 patients with untreated prostatic cancer and 44 patients with benign prostatic hypertrophy to assess the clinical usefulness of these tumor markers. PAP and PSA were measured by radioimmunoassay and gamma-Sm by enzyme immunoassay. The positive rates of PAP, gamma-Sm and PSA in patients with prostatic cancer were 50.0, 61.5 and 69.2%, respectively, and those in patients with benign prostatic hypertrophy were 11.4, 13.6 and 13.6%, respectively. In patients with early stage prostatic cancer (stage A and B), the positive rates of PAP, gamma-Sm and PSA were 20.8, 41.7 and 54.2%. The efficiency of PSA was the highest among the three markers. The positive rate of the combination assay of PAP and PSA, that of gamma-Sm and PSA and that of PAP, gamma-Sm and PSA were slightly higher than that of the PSA assay alone. However, the efficiency of the PSA assay alone was higher than that of any combination. No significant correlation was found between histopathological grade and the level of each tumor marker. A significant correlation was found between PAP and gamma-Sm (r = 0.68, P less than 0.001), and between PAP and PSA (r = 0.61, P less than 0.001), but there was no correlation between gamma-Sm and PSA. These results suggest that PSA is the most useful marker and the combination assay of multiple markers is not so advantageous, at least for screening of prostatic cancer.
