Based on the theory that benign prostatic hypertrophy may be induced by androgenic effect of testosterone derivatives, especially 5-alpha - dihydrotestosterone, on prostatic tissue, Chlormadinone acetate(CMA), potent oral synthetic antiandrogen was investigated in the treatment of benign prostatic hypertrophy. Twenty-two patients of prostatic hypertrophy were studied over six months period with a special reference to uroflowmetry and following results were obtained : 1) Chlormadinone acetate induced improvement of obstructive urinary symptoms in terms of uroflowmetric measurement. 2) It is very worthwhile to initiate medical treatment before undergoing any surgical intervention or when surgery is contraindicated.
Chlormadinone Acetate* ; Dihydrotestosterone ; Humans ; Prostatic Hyperplasia* ; Testosterone

The hypertrophied prostate is the most common cause of infravesical obstrcutions, in the male patients with 50 years old or above. Though the cause of benign prostatic. hypertrophy has not clearly identified yet, recently it has been clarified that androgen, especially dihydrotestosterone, may play a great role in the benign prostatic hypertrophy. The author carried out to investigate the effect of Chlormadinone acetate-potent oral synthetic anti-androgen agent on prostatic volume and obstructive urinary symptoms induced by hypertrophied pro. static gland. The following results were obtained; 1. 23 patients were studied :19 patients with benign prostatic hypertrophy and 4 patients with benign prostatic hypertrophy and 4 patients with prostatic cancer. The mean age of patients was 72 years old. 2. The mean prostatic volume was markedly decreased from 58.7+/-2.94cc before treatment to 23.6+/-1.06cc 16 weeks after treatment. 3. Obstructive urinary symptoms, residual urine and nocturnal frequency were improved after treatment. 4. Judging from the fracts mentioned above, it may be believed that Chlormadinone acetate increase the effect of transurethral resection and prevent the rehypertrophied prostate after transurethral resection of prostate.
Aged ; Chlormadinone Acetate* ; Dihydrotestosterone ; Humans ; Hypertrophy ; Male ; Middle Aged ; Prostate ; Prostatic Hyperplasia ; Prostatic Neoplasms ; Transurethral Resection of Prostate

PURPOSE: Chlormadinone acetate (CMA) therapy for benign prostatic hyperplasia (BPH) may lower the serum prostate specific antigen (PSA) level. However, little is known about the effect of CMA on the total or free serum PSA levels of PSA. Such information would be important since PSA testing is useful for prostate cancer screening. Thus, we prospectively studied the effect of CMA therapy on the total and free serum PSA levels. MATERIALS AND METHODS: The patients with lower urinary tract symptoms (LUTS) and BPH who were aged over 50 years were treated with 50mg CMA for 6 months. Men with a PSA level greater than 10ng/ml were excluded to reduce the likelihood of including cases of occult prostate cancer. Those with suspicious findings on the digital rectal examination and serum PSA testing were biopsied to rule out prostate cancer. alpha- blocking agents were permitted to treat the men with LUTS. Serum levels of the total and free PSA were measured at the study baseline and after approximately 3 and 6 months. The prostate volume (PV) was assessed by transrectal ultrasonography. RESULTS: The analysis included 170 patients with a mean age of 67.9 years, a baseline PV of 47.3ml and a baseline total PSA of 4.1ng/ml. The total PSA levels declined from 4.1ng/ml at baseline to 2.0ng/ml after 6 months of treatment (50.7% decrease, p<0.01). The mean percent free PSA (21% to 22% at baseline) was not significantly altered by CMA treatment. The PSA levels and PV at baseline did not affect the rate of decline of PSA. CONCLUSIONS: The total PSA serum levels decreased by an average of 50% during CMA therapy, but the percent free PSA did not change significantly. This information is potentially useful in the interpretation of the PSA data that's used for early detection of prostate cancer in the men receiving CMA.
Chlormadinone Acetate* ; Digital Rectal Examination ; Humans ; Lower Urinary Tract Symptoms ; Male ; Mass Screening ; Prospective Studies ; Prostate* ; Prostate-Specific Antigen* ; Prostatic Hyperplasia* ; Prostatic Neoplasms ; Ultrasonography

Androgens control a broad range of physiological functions. The androgen receptor (AR), a steroid receptor that mediates the diverse biological actions of androgens, is a ligand inducible transcription factor. Abnormalities in the androgen signaling system result in many disturbances ranging from changes in gender determination and sexual development to psychiatric and emotional disorders. Androgen replacement therapy can improve many clinical conditions including hypogonadism and osteoporosis, but is limited by the lack of efficacious and safe therapeutic agents with easy delivery options. Recent progress in the area of gene regulation by steroid receptors and by selective receptor modulators provides an opportunity to examine if selective androgen receptor modulators (SARMs) could address some of the problems associated with current androgen therapy. Since the composition of the transcriptional initiation complex recruited by liganded AR determines the specificity of gene regulation, synthetic ligands aimed at initiating transcription of tissue and promoter specific genes offers hope for developing better androgen therapy. Establishment of assays that predict synthetic ligand activity is critical for SARM development. Advancement in high throughput compound screening and gene fingerprinting technologies, such as microarrays and proteomics, will facilitate and accelerate identification of effective SARMs.
Androgen Antagonists ; pharmacology ; Androgen Receptor Antagonists ; Androgens ; chemistry ; metabolism ; Chlormadinone Acetate ; analogs & derivatives ; pharmacology ; Humans ; Male ; Receptors, Androgen ; physiology ; Receptors, Cytoplasmic and Nuclear ; physiology ; Testosterone Congeners ; pharmacology