Drveejay, good post, thanks.
GreasyGreek said:
I didn't know finasteride was harsh on the liver. Can anyone dig up some info on this? I'm really curious, because I have run it with orals before... I normally split proscar tabs into 4 and take 1.25 mgs per day.
According to the studies I've seen it seems to be quite safe.
Urology 2001 Apr;57(4 Suppl 1):64-7 Related Articles, Links
Androgen antagonists: Potential role in prostate cancer prevention.
Trump DL, Waldstreicher JA, Kolvenbag G, Wissel PS, Neubauer BL.
University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA.
This article summarizes discussions of the importance of androgens and androgen antagonists in the genesis of prostate cancer. These discussions occurred at a recent symposium on prostate cancer chemoprevention sponsored by the National Cancer Institute. Considerable information exists indicating the importance of androgens in the development of prostate cancer. Trials in breast cancer indicate that estrogen antagonists prevent breast cancer-suggesting, by analogy, that the blockade of androgen action might prevent the emergence of prostate cancer. The 5alpha-reductase inhibitors block the intracellular metabolism of testosterone and inhibit the growth of the prostate. Limited data suggest that 5alpha-reductase inhibitors reduces prostate-specific antigen in men with localized and advanced, primary or recurrent prostate cancer. An ongoing national trial of 18,000 men over 50 years of age has completed accrual and will evaluate whether a standard dose of finasteride will prevent the development of prostate cancer.
The toxicity profile of finasteride (Proscar, Merck & Co., West Point, PA), the only approved 5alpha-reductase inhibitor, is favorable leading to its evaluation as a potential chemopreventive agent for prostate cancer. Anti-androgens such as bicalutamide (Casodex, AstraZeneca, Wilmington, DE) are active in the treatment of prostate cancer and comparable, in some trials, to testicular androgen suppression. These data suggest that antiandrogens may be active in the prevention of prostate cancer; however, the toxicity of antiandrogens (gynecomastia, gastrointestinal toxicity) poses concerns for application in prevention studies. Opportunities for study of factors predictive or associated with the development of prostate cancer and new agents that may interrupt this process offer numerous leads that may reduce the incidence of prostate cancer.
Hinyokika Kiyo 1996 Apr;42(4):323-31 Related Articles, Links
Effect of long-term administration of finasteride (MK-906), an inhibitor of 5 alpha-reductase, in patients with benign prostatic hyperplasia.
Yoshida O, Oishi K, Okada Y, Mizutani Y, Itokawa Y, Tomoyoshi T, Okada K, Komatz Y, Matsuda T, Takeuchi H.
Department of Urology, Faculty of Medicine, Kyoto University, Japan.
We evaluated the effect of long-term administration of finasteride (MK-906), a potent inhibitor of 5 alpha-reductase in patients with benign prostatic hyperplasia (BPH). The effect of an increase in dose was also assessed. Finasteride was administered to 61 patients with BPH at the dose of 1 mg/day for 48 weeks. Thirty three of these patients subsequently received finasteride at the dose of 5 mg/day for further 24 weeks in an open extension study. Urinary symptoms, urinary flow rate, residual urinary volume, prostatic volume and serum concentrations of dihydrotestosterone and prostate-specific antigen were examined periodically during the treatment. The size of the prostate and total urinary symptom scores decreased progressively during the first 16 weeks of treatment. The patients who received finasteride had a significant increase in the maximal urinary flow rate and a significant decrease in residual urinary volume. After 72 weeks of treatment, finasteride at an increased dose of 5 mg did not provide additional benefit to patients, although the effects of the drug at a dose of 1 mg were well maintained. Treatment with finasteride was well tolerated at both doses.
In conclusion, the treatment of BPH with 1 mg of finasteride per day for 48 weeks results in a significant increase in maximal urinary flow rate, and a decrease in prostatic volume, symptoms of obstruction and residual urinary volume, with minimal toxicity.
Kaohsiung J Med Sci 2002 Aug;18(8):379-85 Related Articles, Links
Finasteride in the treatment of Taiwanese men with androgenetic alopecia: a 12-month open-label study.
Lin JH, Chen WC.
Department of Dermatology, College of Medicine, National Cheng Kung University, 138 Sheng-Li Road, Tainan 704, Taiwan.
Finasteride 1 mg/day is effective in the treatment of androgenetic alopecia (AGA). Our open-label study assessed the efficacy and safety of finasteride for the treatment of Taiwanese men with AGA. We enrolled 34 Taiwanese men (aged 18-40 yr) with AGA of modified Norwood/Hamilton scale (MNHS) grade II-V. In investigator assessments at 12 months, five of 21 subjects (23.8%) had two-grade improvement in MNHS grade and 12 of 21 subjects (57.1%) had one-grade improvement; the others remained at the same grade. In global photographic evaluation, five of 31 subjects (15.1%) had observable hair growth at 6 months and 11 of 21 subjects (52.4%) had observable hair growth at 12 months. Patient self-assessment of hair growth was favorable across all questions in the treatment course, more significantly at 12 months than at 6 months; nine of 21 subjects (42.9%) were satisfied with their overall appearance at 12 months. Serum prostate specific antigen levels had decreased by 23.4% at 12 months.
Adverse effects, including abnormal liver function (5/34), were minimal, and the causal relationship with finasteride could not be established. Thus, in Taiwanese men with AGA, finasteride 1 mg/day for 1 year slowed the progression of hair loss and increased hair growth.
The effet on HDL/La
Atherosclerosis 2000 Sep;152(1):159-66 Related Articles, Links
Changes in HDL-cholesterol and lipoprotein Lp(a) after 6-month treatment with finasteride in males affected by benign prostatic hyperplasia (BPH).
Denti L, Pasolini G, Cortellini P, Sanfelici L, Benedetti R, Cecchetti A, Ferretti S, Bruschieri L, Ablondi F, Valenti G.
Department of Geriatrics, Cattedra di Gerontologia e Geriatria, Universita di Parma, Via Don Bosco 2, 43100, Parma, Italy.
Androgen effects on lipoproteins, mainly high density lipoprotein (HDL), could be exerted by a direct interaction of testosterone (T) or dihydrotestosterone (DHT) with liver androgen receptors. To assess if T needs to be converted into DHT to affect lipid metabolism, 13 patients were studied, affected with benign prostatic hyperplasia (BPH) and treated with an inhibitor of 5 alpha-reductase (finasteride). They were compared with 15 untreated controls. At baseline and after 3 and 6 months of therapy, each patient was evaluated as for lipoprotein and hormone concentrations, as well as for nutritional status. Body composition was assessed by anthropometry and bio-impedance analysis (BIA). Treatment was associated with a significant increase of HDL-cholesterol (HDL-C), mainly HDL3 subclass, and lipoprotein(a) (Lp(a)), as well as a decline of DHT, whereas no significant changes were apparent for T, estradiol (E2), sex hormone binding hormone (SHBG) and body composition indexes. However, no significant associations between DHT and lipid relative changes were apparent at bivariate correlation analysis. This finding was confirmed by comparing patient subsets identified by cluster analysis, according to HDL subclass individual responses. Rather, a slight association with E2 for HDL2 (positive) and HDL3 (negative) was found. In conclusion, finasteride can modify HDL and Lp(a) concentrations. However, by the data, these effects cannot be definitively attributed to the changes in DHT synthesis induced by finasteride, since a direct and non-specific interference of the drug on liver metabolism cannot be excluded.
