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PubMed2002

[Hirsutism and hypertrichosis in adults: investigations and treatment].

Hypertrichosis, characterized by increased hair growth located in non-androgen-dependent areas, does not justify the monitoring of hormone levels, conversely to hirsutism, with increased hair growth in androgen-dependent areas of the female genitals. Adult hypertrichosis is iatrogenic (minoxidil, ciclosporine, diazoxide or glucocorticosteroids), of metabolic origin (porphyria), nutritional (anorexia) or paraneoplastic (hypertrichosis lanuoginosa). Metabolic or general assessment can help clinical diagnosis. In non-iatrogenic hirsutism the following must be eliminated: 1) a virilizing tumor (ovarian, adrenal) when confronted with rapid progression or recent hirsutism, plasma testosterone (T)>1.5ng/ml and/or (adrenal tumor) DHEA-sulfate (DHEAS)>700 microgram/dl and associated with hypertension; 2) when confronted with characteristic signs of hirsutism, Cushing's syndrome (post-dexamethasone cortisol), hyperprolactinemia (pooled PRL), or acromegalia (IGF1). Measurement of 17-OH-progesterone at 8 am on the 4th day of the cycle detects the late manifestation homozygous forms of a 21-hydroxylase (21OHD) block. The more frequent forms are: 1) ovarian polymicrocystic or hirsutism-anovulation syndromes without other causes (LH/FSH, T, hyperinsulinemia, sonography); 2) functional adrenal hyperandrogenia (increased DHEAS without organic cause); 3) idiopathic hirsutism. Treatment can be local (discoloration, depilation, diathermo-coagulation, laser). Treatment of hirsutism of organic origin is etiologic. The inhibitory effects of glucocorticosteroids are mediated by 21OHD. The most effective treatments are anti-androgenic: cyproterone acetate, progesterone-like and anti-gonadotropic (contraceptive) agents; and the only product in France officially indicated in hirsutism , spironolactone (anti-mineralocorticosteroid); and flutamide, pure anti-androgen (probably hepatoxic). Finasteride (type II 5 alpha-reductase inhibitor) appears less effective. Estrogen-progestagen-like agents can be associated with anti-androgens. We should also mention the GnRH-agonists, and finally, dietetics and metformine (in cases of insulin-resistance).

Adult↗
PubMed2002

Gateways to Clinical Trials.

Gateways to Clinical Trials is a guide to the most recent clinical trials in current literature and congresses. The data in the following tables has been retrieved from the Clinical Studies knowledge area of Prous Science Integrity, the drug discovery and development portal, http://integrity.prous.com. This issue focuses on the following selection of drugs: Adalimumab, aeroDose insulin inhaler, agomelatine, alendronic acid sodium salt, aliskiren fumarate, alteplase, amlodipine, aspirin, atazanavir; Bacillus Calmette-Guérin, basiliximab, BQ-788, bupropion hydrochloride; Cabergoline, caffeine citrate, carbamazepine, carvedilol, celecoxib, cyclosporine, clopidogrel hydrogensulfate, colestyramine; Dexamethasone, diclofenac sodium, digoxin, dipyridamole, docetaxel, dutasteride; Eletriptan, enfuvirtidie, eplerenone, ergotamine tartrate, esomeprazole magnesium, estramustine phosphate sodium; Finasteride, fluticasone propionate, fosinopril sodium; Ganciclovir, GBE-761-ONC, glatiramer acetate, gliclazide, granulocyte-CSF; Heparin sodium, human isophane insulin (pyr), Hydrochlorothiazide; Ibuprofen, inhaled insulin, interferon alfa, interferon beta-1a; Laminvudine, lansoprazole, lisinopril, lonafarnib, losartan potassium, lumiracoxib; MAb G250, meloxicam methotrexate, methylprednisolone aceponate, mitomycin, mycophenolate mofetil; Naproxen sodium, natalizumab, nelfinavir mesilate, nemifitide ditriflutate, nimesulide; Omalizumab, omapatrilat, omeprazole, oxybutynin chloride; Pantoprazole sodium, paracetamol, paroxetine, pentoxifylline, pergolide mesylate, permixon, phVEGF-A165, pramipexole hydrochloride, prasterone, prednisone, probucol, propiverine hydrochloride; Rabeprazole sodium, resiniferatoxin, risedronate sodium, risperidone, rofecoxib rosiglitazone maleate, ruboxistaurin mesilate hydrate; Selegiline transdermal system, sertraline, sildenafil citrate, streptokinase; Tadalafil, tamsulosin hydrochloride, technosphere/Insulin, tegaserod maleate, tenofovir disoproxil fumarate, testosterone heptanoate, testosterone undecanoate, tipifarnib, tolterodine tartrate, topiramate, troglitazone; Ursodeoxycholic acid; Valdecoxib, valsartan, vardenafil, venlafaxine hydrochloride, VX-745.

Clinical Trials as Topic↗
PubMed2002

Gateways to clinical trials.

Gateways to Clinical Trials is a guide to the most recent clinical trials in current literature and congresses. The data in the following tables has been retrieved from the Clinical Studies knowledge area of Prous Science Integrity, the drug discovery and development portal, http://integrity.prous.com. This issue focuses on the following selection of drugs: Abacavir sulfate, abciximab, acetylcysteine, adefovir dipivoxil, alfuzosin hydrochloride, aliskiren fumarate, alosetron hydrochloride, amlodipine besilate, apomorphine hydrochloride, atazanavir, atorvastatin, atorvastatin calcium, atrasentan; Basiliximab, beraprost sodium, bevacizumab, bivalirudin, botulinum toxin type A, botulinum toxin type B; Celecoxib, cetuximab, cilansetron, cilomilast; Daclizumab, darbepoetin alfa, docetaxel, duloxetine hydrochloride; Efalizumab, efavirenz, eletriptan,, entecavir, eplerenone, epoetin alfa, eptifibatide, esomeprazole magnesium. ezetimibe; Filgrastim, finasteride, fluvastatin sodium, follitropin alfa; Gemcitabine, gemeprost, ghrelin (human); HE-2000; Infliximab, 111In-Pentetreotide, interferon alfa-2 alpha, interferon alfa-2 beta, interferon beta-1 alpha, irbesartan, irinotecan hydrochloride; Ketamine hydrochloride; L-778123, lafutidine, lamivudine, lamivudine/zidovudine, latanoprost, letrozole, licofelone, lopinavir, losartan potassium, loxiglumide, lubeluzole; Magnesium sulfate, MeGLA, meloxicam, mycophenolate mofetil; NBI-6024, nelfinavir mesilate, nesiritide, nevirapine, niacin, NN-2211; Octreotide, orlistat; PC-515, peginterferon alfa-2 alpha, peginterferon alfa-2b, pemetrexed disodium, pibrozelesin hydrochloride, pimagedine, pirfenidone, pitavastatin calcium, premarin/trimegestone, prucalopride; Rabeprazole sodium; reboxetine, risedronate sodium, ritonavir, rituximab, rofecoxib, roflumilast, rosuvastatin calcium; Sertraline, sibutramine hydrochloride monohydrate, sildenafil citrate, spironolactone, stavudine; Tacrolimus, tadalafil, tamsulosin hydrochloride, tenecteplase, thalidomide, travoprost; Valsartan; Zoledronic acid monohydrate.

Clinical Trials as Topic↗
PubMed2002

[Enzyme inhibition in the drug therapy of benign prostatic hyperplasia].

Enzyme inhibition belongs to common mechanisms of drug action and enzymes of hormone metabolism belong to targets in the treatment of benign prostatic hyperplasia. Transformation of testosterone to 5 alpha-dihydrotestosterone is catalyzed by cholestenone-5 alpha-reductase (EC 1.3.1.22, 5 alpha-reductase). Different effects of dihydrotestosterone and testosterone represent a rational basis for pharmacotherapy by 5 alpha-reductase inhibition. The enzyme is active in the prostate and other organs and tissues, with different distribution of at least two 5 alpha-reductase isoenzymes. Beside this, progesterone-5 alpha-reductase (EC 1.3.1.30) as another enzyme with 5 alpha-reductase activity is present in human tissues including the prostate. The existence of several 5 alpha-reductase activities gives bright possibilities of 5 alpha-reductase inhibition. Basic 5 alpha-reductase inhibitors are synthetic steroid (e.g. finasteride--Proscar). Various mechanisms of their effect (classical reversible competitive inhibition, mechanism-based "suicide" inhibitors, tightly bound irreversible inhibitors...) represent different pharmacokinetic patterns, too. Non-steroidal 5 alpha-reductase inhibitors (e.g. polyunsaturated fatty acids) are effective components of several phytopharmaceuticals. They receive attention due to their complexity and low hazards. Extracts of Serenoa repens seeds (Permixon, Capistan in the Czech Republic), of Pygeum africanum, of Urtica radicis roots (Urtica, Urtiron) or catequine structures from the green tea belong to this group. Beside androgens, participation of estrogens in the origin and development of benign prostatic hyperplasia is probable. Inhibition of the "aromatase" complex, which catalyzes transformation of androgens to estrogens, may contribute to the complexity of phytotherapeutic effects.

Cholestenone 5 alpha-Reductase↗
PubMed2002

Gateways to clinical trials.

Gateways to Clinical Trials is a guide to the most recent clinical trials in current literature and congresses. The data in the following tables has been retrieved from the Clinical Studies knowledge area of Prous Science Integrity, the drug discovery and development portal, http://integrity.prous.com. This issue focuses on the following selection of drugs: Abacavir sulfate, adalimumab, AERx morphine sulphate, alefacept, alemtuzumab, alendronic acid sodium salt, alicaforsen sodium, almotriptan, amprenavir, aripiprazole, atenolol, atorvastatin calcium; BSYX-A110; Cantuzumab mertansine, capravirine, CDP-571, CDP-870, celecoxib; Delavirdine mesilate, docetaxel, dofetilide, donepezil hydrochloride, duloxetine hydrochloride, dutasteride, dydrogesterone; Efavirenz, emtricitabine, enjuvia, enteryx, epristeride, erlotinib hydrochloride, escitalopram oxalate, etanercept, etonogestrel, etoricoxib; Fesoterodine, finasteride, flt3ligand; Galantamine hydrobromide, gemtuzumab ozogamicin, genistein, gepirone hydrochloride; Indinavir sulfate, infliximab; Lamivudine, lamivudine/zidovudine/abacavir sulfate, leteprinim potassium, levetiracetam, liposomal doxorubicin, lopinavir, lopinavir/ritonavir, losartan potassium; MCC-465, MRA; Nebivolol, nesiritide, nevirapine; Olanzapine, OROS(R)-Methylphenidate hydrochloride; Peginterferon alfa-2a, peginterferon alfa-2b, Pimecrolimus, polyethylene glycol 3350, pramlintide acetate, pregabalin, PRO-2000; Risedronate sodium, risperidone, ritonavir, rituximab, rivastigmine tartrate, rofecoxib, rosuvastatin calcium; Saquinavir mesilate, Stavudine; Tacrolimus, tadalafil, tamsulosin hydrochloride, telmisartan, tomoxetine hydrochloride, treprostinil sodium, trimegestone, trimetrexate; Valdecoxib, venlafaxine hydrochloride; Zoledronic acid monohydrate.

Clinical Trials as Topic↗
PubMed2003

Saw palmetto for prostate disorders.

Saw palmetto is an herbal product used in the treatment of symptoms related to benign prostatic hyperplasia. The active component is found in the fruit of the American dwarf palm tree. Studies have demonstrated the effectiveness of saw palmetto in reducing symptoms associated with benign prostatic hyperplasia. Saw palmetto appears to have efficacy similar to that of medications like finasteride, but it is better tolerated and less expensive. There are no known drug interactions with saw palmetto, and reported side effects are minor and rare. No data on its long-term usage are available. The herbal product also has been used to treat chronic prostatitis, but currently there is no evidence of its efficacy.

Adult↗
PubMed2003

[Relation between hypertension and clinical cases of benign prostatic hyperplasia].

OBJECTIVES: To confirm the relationship between hypertension and lower urinary tract symptoms (LUTS) in our environment, and to evaluate the association between hypertension and LUTS secondary to benign prostatic hypertrophy (BPH). METHODS: We prospectively studied during 3 months all male patients older than 50 years (163 patients) analysing previous medical history, IPSS, digital rectal examination, urine sediment, basic biochemical profile, PSA, uroflowmetry, and urinary tract ultrasound. Patients with neurological diseases, previous pelvic trauma, diabetes mellitus, suspicious digital rectal examination, abnormal PSA, or under treatment with alpha blockers, antidepressants, finasteride or antipsychotic drugs were excluded. RESULTS: From a total of 163 patients 113 were classified as suffering clinical BPH (LUTS, prostate greater than 30 gm, and uroflowmetry < 15 ml/sec), and 75 as hypertensive. Among 75 hypertensive patients 31 presented IPSS greater than 7 (41.3%) in comparison to 20 out of 88 non hypertensive patients (22.7%), being the difference statistically significant. CONCLUSIONS: Our study confirms what has been previously reported by other authors, that there is a statistically significant relationship between hypertension and LUTS secondary to BPH.

Aged↗
PubMed2003

Common hair loss disorders.

Hair loss (alopecia) affects men and women of all ages and often significantly affects social and psychologic well-being. Although alopecia has several causes, a careful history, dose attention to the appearance of the hair loss, and a few simple studies can quickly narrow the potential diagnoses. Androgenetic alopecia, one of the most common forms of hair loss, usually has a specific pattern of temporal-frontal loss in men and central thinning in women. The U.S. Food and Drug Administration has approved topical minoxidil to treat men and women, with the addition of finasteride for men. Telogen effluvium is characterized by the loss of "handfuls" of hair, often following emotional or physical stressors. Alopecia areata, trichotillomania, traction alopecia, and tinea capitis have unique features on examination that aid in diagnosis. Treatment for these disorders and telogen effluvium focuses on resolution of the underlying cause.

Alopecia↗
PubMed2003

Enzyme induction and dietary chemicals as approaches to cancer chemoprevention: the Seventh DeWitt S. Goodman Lecture.

Research on cancer chemoprevention is an important approach for decreasing both the incidence and number of deaths from cancer. The use of tamoxifen to prevent breast cancer, finasteride to prevent prostate cancer, and aspirin to prevent colon cancer are recent examples of cancer chemoprevention. This article describes research from my laboratory and related research from other laboratories on the effects of enzyme induction on chemical carcinogenesis as an approach to cancer chemoprevention, as well as studies on the inhibitory effects of curcumin, caffeine, (-)-epigallocatechin gallate (EGCG), and tea in animal models of carcinogenesis. The later substances appear to work, at least in part, by enhancing apoptosis in DNA-damaged cells or in tumors. The results of our studies and those of others provide a rationale for clinical trials on the potential chemopreventive effects of curcumin, caffeine, EGCG, and tea on the formation of cancer of the skin, mouth, esophagus, stomach, and colon in people with precancerous lesions and a high risk of developing these cancers. It was pointed out that several compounds that are effective cancer chemopreventive agents in one experimental setting can enhance carcinogenesis in another experimental setting. These results suggest that it may be necessary to tailor the cancer chemopreventive regimen to individual subjects with known carcinogen exposures or to high cancer risk individuals with mechanistically understood pathways of carcinogenesis so that chemopreventive agents with known mechanisms of action can be better customized to the individual and selected on a more rational basis.

Animals↗
PubMed2004

Patients with bladder outlet obstruction who refuse treatment show no clinical and urodynamic change after long-term follow-up.

OBJECTIVE: To evaluate in patients with mild bladder outlet obstruction (BOO) who refused the proposed treatment and were on watchful waiting (WW), the symptomatic and urodynamic changes after 1-5 years of follow-up. METHODS: 102 patients with lower urinary tract symptoms (LUTS) and BOO (Schafer class: 2-6, median 3) were clinically and urodinamically re-evaluated after 1-5 years of follow-up. Of these, 82 were submitted to medical (alfuzosin or finasteride) or surgical treatment (prostatectomy or TUIP) and 20, who refused the proposed treatment, were on WW. A retrospective study was made on these 20 patients who underwent a second International Prostatic Symptom Score and pressure-flow evaluation after 1-5 years (median: 22 months) of watchful waiting. Wilcoxon matched-pairs signed-ranks test and Kruskal Wallis as appropriate were used for statistical analysis. RESULTS: In the group of patients who refused the proposed treatment, no statistically significant differences between the two evaluations were observed for any of the parameters investigated: International Prostatic Symptom Score (15.1 +/- 6.8; 14.7 +/- 7.5); maximum flow (11.5 +/- 4.2; 12.1 +/- 4.3); residual urine (90.2 +/- 154.5; 113.3 +/- 158.4); Schäfer class (2.9 +/- 0.9; 2.8 +/- 1.2); Urethral Resistance Algorithm (37.1 +/- 14.4; 37.3 +/- 16.3); Projected Isometric Pressure (113.7 +/- 26.5; 112.7 +/- 21.8). CONCLUSIONS: Patients with mild BOO may remain clinically and urodynamically stable for a long time.

Aged↗
PubMed2004

[Androgenetic alopecia].

The physiopathology of androgenetic alopecia is linked to the action of the androgens of the bulbs pilairs of the scalp. The action of these androgens can be associated with the level of hormones in circulation and with the genetic predisposition which will influence the activity of these androgens at the periphery. The classifications of the evolution of alopecia will be done following Norwood for the male and following Ludwig for the female. Hormonal investigation will be effectuated on the female only in the case of research on or the identification of hyperandrogenia; this is essential in order to direct the therapy. The diagnose and the therapeutic follow-up are essentially clinical but can be assisted by a trichogram which will show-up the miniaturisation process of androgenetic alopecia and the telogen effluvium of the affected areas. The treatment of alopecia can be local or general. The local treatment will use a lotion of minoxidil 2 to 5% whether the patient is male of female. On males, an inhibitor of the 5 alpha reductase 2, finasteride, has shown its efficiency at a dose of 1 mg/day. On females oestroprogestatives will be used, if they are not counter-advised, associated with an anti-androgen: either cyproterone acetate or spironolactone. A therapeutic evaluation will be made after 6 months of treatment.

Alopecia↗
PubMed2004

[System review of the Chinese medicine bushenhuoxue for treating benign prostatic hyperplasia].

OBJECTIVE: To make a system review of the effects of Bushenhuoxue (kidney-tonifying and blood-activating prescription), a category of compound Chinese medicines, on benign prostatic hyperplasia (BPH) and its side effects. METHODS: All the research articles about Chinese medicines treating BPH from January 1978 to February 2003 were retrieved using the methods of international evidence-based medicine (EBM), and their qualities were evaluated based on JADAD standard and concealment of research allocation. Then the included articles went through META-analysis with Revman 4.2 software. RESULTS: The efficacy of Bushenhuoxue on BPH was better than Qianliekang but not statistically different from finasteride. The combined use of Bushenhuoxue with surgery had no statistical difference from mere surgical treatment. Four articles reported the side effects of this compound Chinese medicine including upset and pain in the abdomen, nausea, diarrhea and dryness of the nose. CONCLUSION: Massive, multi-center and randomized controlled clinical trials should be conducted to find out more effective methods for treating BPH with Chinese medicines based on the improvement of measurable symptom evaluation method and for evaluating their side effects.

Drugs, Chinese Herbal↗
PubMedDate not supplied

[Diagnostic and prognostic value of serum prostate specific antigen in prostate carcinoma].

The upper normal limit of serum prostate specific antigen (PSA) of 4 ng/ml is positively evaluated since it discriminates a large percentage of patients having prostate cancer. The PSA limit of 2.5 ng/ml may be used accordingly for patients younger than 50 years of age. The PSA range of 3.3-4 ng/ml may indicate a percentage of patients positive for prostate carcinoma. The PSA above 10 ng/ml indicates that patients have prostate carcinoma by more than 50 %, which is more than double as compared to patients having PSA limits between 4.1-10 ng/ml. It is important to repeat doubtful PSA tests after 3-4 months. If within a year an increase in PSA of more than 2 ng/ml is detected, a high risk of death from prostate cancer is expected. The time for doubling PSA values within a year is described as "velocity index". As for free PSA, this test is not often applied in many nuclear medicine centers. According to the Mayo Clinic, USA, instructions, when total PSA is 2-3.9 ng/ml and free PSA above 18% of these values, the possibility of prostate cancer is less than 10%. On the contrary, for the above total PSA values, if free PSA is less than 10% of these values, the possibility of prostate cancer increases to more than 30%. It is suggested that PSA values be expressed per g of prostate tissue in order to relate to prostate volume. However, one should have in mind that prostate carcinomas have less PSA per g than hyperthophic glands and their volume is usually larger. There are cases where treatment of prostate hypertrophy with finasteride or treatment of prostate cancer with anticancer drugs, may induce a false low PSA. More information about the practical importance of PSA values is expected after 2 or 3 years when a study by the National Cancer Institute of USA on 74,000 men will be completed.

Editorial↗
PubMed2005

Prostate cancer: chemoprevention update 2005.

INTRODUCTION: If an agent can slow the growth of existing prostate cancer cells, it remains plausible that it may be effective as an adjunct to surgery, radiation or chemotherapy. DISCUSSION: Level-1 evidence will be needed in order to definitively prove the efficacy of agents as chemoprevention strategies for prostate cancer. Currently, only finasteride fulfills this criterion. Two major trials are underway that will assess the role of soy, vitamin E and selenium in prostate cancer prevention. CONCLUSION: Tantalizing prospects for effective chemoprevention of prostate cancer exist. Fortunately, well-conducted randomized trials will allow us to answer many of these questions within the next 2 to 8 years.

Antineoplastic Agents↗
PubMed1999

Marketing lifestyle drugs==>to consumers = increased market share. 7-8 September 1999, London, UK.

This conference focused on 'lifestyle' drugs, the kind of medicines treating conditions not considered as diseases, such as erectile dysfunction, male baldness, stress, etc, to improve quality of life and well-being. The lifestyle area is the fastest growing area in pharmaceuticals, driven by drugs such as Viagra (sildenafil; Pfizer Inc), Propecia (finasteride; Merck & Co Inc), Xenical (orlistat; F Hoffmann-La Roche Ltd) and others. The aging population in developed countries has a new perception of health, which is an improvement of wellness. Patients are more informed and conscious about their own health and the higher involvement in copayment and decision-making are changing pharmaceutical markets and, consequently, pharmaceutical industry's business and R&D strategies. Successful marketing of lifestyle drugs requires taking into account the above scenario, using new communication tools and being able to re-think the conventional marketing strategies adopted so far.

Journal Article↗
PubMed2005

[Novel therapeutics strategies in benign hypertrophy of prostate management].

The benign hypertrophy of prostate (BPH) is a progressive disease which can assign all the men to various degrees, involving an unquestionable repercussion on the quality of life. The two types of drugs commonly used for the treatment of the symptomatic BPH are the inhibitors of 5-alpha-reductase and the alpha-blockers. They last one relatively long action, making it possible to prevent occurred of complications like the acute urinary retention or the prostatic recourse to the surgery. A risk of progression and development of urinary complications can require an association of these two therapeutic agents in order to obtain a faster and durable improvement of symptomatology. The results of various studies are reported which highlight the interest of this therapeutic combination and underline the contribution of an inhibitor of 5-alpha-reductase among patients presenting a significant prostatic volume and a high PSA. Taking into account the risk of bad compliance and side effects with the long course, after a treatment combined for six months by tamsulosine and dutasteride, the stop of the alpha-blocker allows a maintenance of the situation obtained. Lastly, several clinical studies made it possible to draw the attention to the potentially preventive action of the inhibitors of 5-alpha-reductase in the development of the prostate cancer by its action to the DHT. These observational studies left the place to the PCPT study which made it possible to confirm a reduction in the prevalence of the cancer of prostate in a group of patients treated by finasteride compared with a placebo group. Currently, the preventive potential role of the dutasteride is also the subject of a study (REDUCE). These results are necessary in order to better define the interest and the role of the inhibition of 5-alpha-reductase in a strategic attitude of prostate cancer prevention.

5-alpha Reductase Inhibitors↗
PubMed2006

[Nutrition and pharmacological treatment for prevention of prostate cancer].

Prostate cancer is the most common neoplasm and the second cause of cancer death. It is an excellent target for primary chemopreventive strategies for the following reasons: it is highly prevalent and has a long latency period, there are identifiable risk factors and a precursor lesion and it produces a biochemical marker (serum PSA) which can serve as an intermediate end point in chemoprevention studies. The goal of primary prevention strategies is to prevent development of clinical life-threatening neoplasms in asymptomatic patients with no evidence of clinical disease. Identification of populations at risk for developing cancer is the cornerstone of chemoprevention. Well-established risk factors for prostate cancer include African-American race, older age and family history. Data on diet and obesity are less clearly defined. Since high grade prostatic intraepithelial neoplasia (PIN) is an early predictor of prostate cancer, preventive strategies focusing on men with high grade PIN are being explored. It was demonstrated that finasteride could significantly reduce prostate cancer in asymptomatic men with normal PSA and no abnormalities on rectal examination. Elevated prostaglandin levels, and upregulation of cyclooxygenase-2 (COX-2) are found in prostate cancer cell lines. There is some epidemiologic evidence that regular use of NSAIDs, which inhibit COX-2, may be associated with a lower risk of prostate cancer. In the field of nutrition, data from prospective large-scale studies demonstrated that increased consumption of lycopene-rich tomato-based foods referred to a reduction in the risk for prostate cancer. Vitamin E was also found to reduce prostate cancer risk. Prospective data showed that vitamin D has an inhibitory effect on prostate cancer development while increased calcium consumption, independent from dietary intake, might increase the risk. Dietary fat intake, particularly from animal sources, may also increase the risk for prostate cancer. Whether this effect is strictly due to the already identified compounds or to other compounds, remains to be explored. Further study will hopefully help to establish a core set of nutritional and dietary factors that can positively or negatively affect prostate cancer development, as well as a set of pharmacologic agents that can reduce the risk of prostate cancer development and/or progression in selected patients.

Anticarcinogenic Agents↗
PubMed2006

BPH: epidemiology and comorbidities.

Recently published data suggest that clinical benign prostatic hyperplasia (BPH), which is hallmarked by the occurrence of moderate-to-severe lower urinary tract symptoms (LUTS), occurs in about one quarter of men in their 50s, one third of men in their 60s, and about half of all men 80 years or older. Although effective treatments for LUTS/BPH are available, this condition often occurs in the context of common, age-related comorbidities such as cardiovascular disease, hypertension, and erectile dysfunction. Alpha1-selective adrenergic receptor (a1-AR) antagonists (eg, alfuzosin, doxazosin, tamsulosin, terazosin) remain the cornerstone of therapy for LUTS/BPH. In addition, 5-alpha-reductase inhibitors (ie, dutasteride, finasteride) have been associated with improvements in LUTS/BPH in men with larger prostates, especially when used in combination with a1-AR antagonists. Although all these drugs have been shown to be beneficial for the treatment of BPH, there are differences in side-effect profiles. When selecting an appropriate course of therapy, these side effects and any impact they may have on existing comorbid conditions must be considered.

5-alpha Reductase Inhibitors↗