5-alpha Reductase Inhibitors
Azasteroids
Finasteride
Prostatic Hyperplasia
3-Oxo-5-alpha-Steroid 4-Dehydrogenase
Cholestenone 5 alpha-Reductase
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Oxidoreductases Acting on CH-CH Group Donors
Aldehyde Reductase
Simvastatin
Lovastatin
Pravastatin
Hydroxymethylglutaryl CoA Reductases
Sorbitol
Sugar Alcohol Dehydrogenases
Glutathione Reductase
Cytochrome-B(5) Reductase
Nitrite Reductases
Oxidoreductases
FMN Reductase
Thioredoxin-Disulfide Reductase
Mutagenicity tests on epristeride in vitro and in vivo. (1/197)
AIM: To evaluate the genetic effects of epristeride (Epr), a new prospective drug for treating benign prostatic hyperplasia. METHODS: 1) Assaying reverse mutation in histidine nutritional deficiency strain of Salmonella typhimurium 2) detecting chromosome aberrations in Chinese hamster lung cells (CHL); 3) micronucleus assays of mouse bone marrow; 4) counting sperm shape abnormalities 35 d after first ig Epr. RESULTS: 1) The reverse mutation happened at almost the same rate of the negative control. Epr did not induce bacterial mutation. 2) In vitro, the rates of aberration were all below 3%, thus Epr did not induce chromosome damage in CHL. 3) Micronucleated polychromatic erythroblasts (PCE) were not apparently more than those of sovent control, Epr did not induce the formation of micronuclei in PCE. 4) With Epr 818, 682, and 341 mg.kg-1, the head abnormalities of sperms were 5.3% +/- 2.7%, 5.3% +/- 1.9%, and 5.2% +/- 1.2%, respectively. CONCLUSION: No genetic toxicity of Epr was detected. (+info)Z-350, a novel compound with alpha 1-adrenoceptor antagonistic and steroid 5 alpha-reductase inhibitory actions: pharmacological properties in vivo. (2/197)
The alpha(1)-adrenoceptor-antagonistic and steroid 5alpha-reductase-inhibitory actions of Z-350 [(S)-4-{3-{4-{1-(4-methylphenyl)-3-[4-(2-methoxyphenyl)piperazine-1-y l]propoxy}benzoyl}indole-1-yl}butyric acid hydrochloride] were investigated in rabbits and rats in vivo. Z-350 (1-30 mg/kg), administered intraduodenally, dose-dependently inhibited phenylephrine-induced increases in prostatic urethral pressure with an ED(50) value of 3.8 mg/kg in anesthetized male rabbits, whereas the effects on mean blood pressure and orthostatic hypotensive response were weaker when compared with other alpha(1)-adrenoceptor antagonists, tamsulosin and prazosin. Z-350 (1-10 mg/kg p.o.) dose-dependently inhibited the prostatic steroid 5alpha-reductase activity in rats with an ED(50) value of 2.8 mg/kg. The daily oral administration of Z-350, at >==10 mg/kg for 7 days, significantly reduced the prostatic growth induced by testosterone in castrated rats, with no effect on dihydrotestosterone-induced prostatic growth. These results indicate that Z-350 exhibited alpha(1)-adrenoceptor-antagonistic and 5alpha-reductase inhibitory actions at almost equal doses in vivo, and was expected to improve the bladder outlet obstruction associated with benign prostatic hyperplasia with smaller cardiovascular adverse effect. (+info)Evaluation of the EDSTAC female pubertal assay in CD rats using 17beta-estradiol, steroid biosynthesis inhibitors, and a thyroid inhibitor. (3/197)
The Endocrine Disrupter Screening and Testing Advisory Committee has recommended the female pubertal onset assay as a Tier I test to detect potential endocrine-disrupting chemicals (EDs). We evaluated this assay's ability to detect EDs acting through various mechanisms. In two similar experiments, weanling female rats were dosed for 20 days by gavage with vehicle (0.5% methocel) or the following test compounds (mg/kg/day): 17beta-estradiol (E2; 0.1, 2, or 4), ketoconazole (KETO; 24, 50, or 100), finasteride (FIN; 20), testolactone (TL; 220), fadrozole (FAD; 0.6, 1.2, or 6.0) or 6-propylthiouracil (PTU; 240). In vehicle-treated females, mean age at pubertal onset, as evidenced by vaginal opening (VO), varied interexperimentally from 32.3+/-1.6 days to 33.5+/-1.8 days. At 0.1 mg/kg E2, age at VO was reduced slightly to 31.0+/-1.6 days, but not significantly (alpha=0.05). Higher E2 doses (2.0 and 4.0) reduced age at VO to 28 days. KETO delayed VO, but this delay was significant only at 100 mg/kg (39.7+/-2.4 days). FIN and TL had no effect on age at pubertal onset; however, FAD significantly delayed VO. PTU delayed VO to 34.2+/-1.1 days and altered thyroid weight, histology, and hormone levels. With each compound, significant changes in age at VO were accompanied by decreased uterine or ovarian weights. Thus, although this assay did not detect TL or lower doses of E2 (0.1 mg/kg) or KETO (< or = 50 mg/kg), it was capable of detecting EDs operating through a variety of mechanisms. (+info)Steroid 5alpha-reductase inhibitory activity and hair regrowth effects of an extract from Boehmeria nipononivea. (4/197)
The acetone extract of Boehmeria nipononivea showed both potent 5alpha-reductase inhibitory activity and hair regrowth promotion effects on mice. 5alpha-Reductase inhibitory activity-guided fractionation led to six active fatty acids: alpha-linolenic, linoleic, palmitic, elaidic, oleic and stearic acids. The extract of B. nipononivea, and alphalinolenic, elaidic and stearic acids exhibited a hair regrowth effect. (+info)Anti-tumour effects and pharmacokinetic profile of 17-(5'-isoxazolyl)androsta-4,16-dien-3-one (L-39) in mice: an inhibitor of androgen synthesis. (5/197)
17-(5'-Isoxazolyl)androsta-4,16-dien-3-one (L-39), a novel androstene derivative, was synthesized and evaluated in vitro and in vivo. L-39 showed potent and non-competitive inhibition of human testicular microsomal 17alpha-hydroxylase/C(17,20)-lyase with an IC50 value of 59 nM and Ki of 22 nM. L-39 also showed potent and competitive inhibition of 5alpha-reductase in human prostatic microsomes with IC50 and Ki values of 33 and 28 nM respectively. L-39 (5 microM) has also been shown to manifest anti-androgenic activity in cultures of human prostate cancer cell lines (LNCaP) by preventing the labelled synthetic androgen R1881 (5 nM) from binding to the androgen receptors. Androgen-dependent human prostate cancer xenografts (PC-82) were grown in nude mice and the effects of L-39 (50 mg kg(-1) day(-1)) on tumour growth and prostate-specific antigen (PSA) levels were determined after 28 days. L-39 significantly (P < 0.01) diminished tumour growth and wet weights to a similar extent as castration or flutamide treatment. L-39 also significantly (P < 0.01) reduced serum PSA levels by more than 80% in the mice bearing human prostate cancer xenografts. Pharmacokinetic studies were also conducted in male Balb/c mice. After subcutaneous administration of a single bolus dose, L-39 was rapidly absorbed into the systemic circulation. Peak plasma levels occurred at 0.75 h and then declined with a t(1/2) of 1.51 h. The bioavailability of L-39 after subcutaneous administration was 28.5%. These results demonstrate that L-39 is a potent inhibitor of androgen synthesis and is effective in reducing the growth of human prostate cancer xenografts in nude mice. Although improvements in the bioavailability are necessary, L-39 is a potential lead compound with this profile as an inhibitor of prostate cancer growth. (+info)Effects of a new steroidal aromatase inhibitor, TZA-2237, and/or chlormadinone acetate on hormone-induced and spontaneous canine benign prostatic hyperplasia. (6/197)
OBJECTIVE: It has been known for many years that human benign prostatic hyperplasia (BPH) is composed predominantly of hyperplastic stromal cells rather than epithelial cells. In the present study the effects of a new steroidal aromatase inhibitor on hormone-induced and spontaneous canine BPH were investigated. METHODS: (1) Effects of TZA-2237 on hormone-induced canine BPH. Ten castrated beagles were administered testosterone and androstenedione 6 days/week for 8 months, and divided randomly into three groups after 2 months of treatment as follows. Group I served as controls, Group II was given 0.5 and Group III was given 2.5 mg/kg/day TZA-2237 5 days/week for 6 months. (2) Effects of TZA-2237 on spontaneous canine BPH. Twenty aged beagles with BPH were divided into five groups, Group IV was untreated, Group V was treated with 1 and Group VI with 5mg/kg/day TZA-2237 5 days/week for 31 weeks. Group VII was treated with 5mg/kg/day Atamestane and Group VIII was treated with 0.3 mg/kg/day chlormadinone acetate (CMA) 5 days/week. (3) Effects of TZA-2237 combined with CMA on spontaneous canine BPH. Three aged beagles with BPH were treated with 1mg/kg/day TZA-2237 and 0.03 mg/kg/day CMA 5 days/week for 20 weeks (Group IX) and a further three aged beagles with BPH were treated with 0.3 mg/kg/day CMA alone 5 days/week (Group X). RESULTS: Hormone-induced prostatic growth was significantly suppressed in group III compared with that in other groups. In Group III, the intraprostatic aromatase activity, estradiol level and androgen receptor content decreased significantly in comparison with the values in Group I. The prostatic weights in Groups V, VI and VII increased significantly in comparison with the weight in Group IV. Serum LH and testosterone levels in Groups V, VI, and VII increased significantly in comparison with the level in Group IV. The prostatic weight in Group IX was decreased only slightly, but the smooth muscle component was decreased significantly. CONCLUSIONS: TZA-2237 is a new, unique and effective aromatase inhibitor that causes inhibition of both epithelial and stromal compartments in hormone-induced canine BPH. Dual inhibition of androgen and estrogen resulted in inhibition of smooth muscle growth, and should prove effective as a new method of treatment given the atrophic effects on not only the epithelium but also the stroma in human BPH. (+info)Increased levels of clusterin (SGP-2) mRNA and protein accompany rat ventral prostate involution following finasteride treatment. (7/197)
Finasteride is a well-known inhibitor of the prostatic enzyme 5 alpha-reductase type 2 which prevents conversion of testosterone into 5 alpha-dihydrotestosterone, the active intraprostatic androgen, which causes prostate involution through a combination of cell atrophy and cell death. The drug is widely used to improve symptoms of benign prostatic hyperplasia in man. Clusterin, a glycoprotein which is generally up-regulated under conditions inducing cell atrophy or organ involution, is produced at a high level in the regressing rat ventral prostate following androgen ablation. According to several authors, clusterin does not respond to finasteride treatment, suggesting a different action of testosterone and 5 alpha-dihydrotestosterone. We show here that, under our conditions, finasteride was capable of inducing production of both clusterin mRNA and protein in the rat ventral prostate. In fact, by using different and converging techniques, such as Northern hybridization, in situ hybridization histochemistry and immunohistochemistry, we were able to show a strong induction of the clusterin gene in the epithelial cell population of the gland. The response to finasteride, which was similar to that seen with castration, occurred with a delay of a few days. In situ and immunohistochemistry experiments indicated that both orchidectomy and finasteride administration resulted in increased transition of the epithelial cells from the columnar to the cuboidal (atrophic) shape, and this was accompanied by an increased intensity of the signal for clusterin. Thus, it appears that induction of clusterin is part of the molecular process leading to prostate involution caused by either orchidectomy or finasteride administration. (+info)Antiandrogenic effects of novel androgen synthesis inhibitors on hormone-dependent prostate cancer. (8/197)
We have found that in addition to being potent inhibitors of 17alpha-hydroxylase/C17,20-lyase and/or 5alpha-reductase, some of our novel androgen synthesis inhibitors also interact with the mutated androgen receptor (AR) expressed in LNCaP prostate cancer cells and the wild-type AR expressed in hormone-dependent prostatic carcinomas. The effects of these compounds on the proliferation of hormone-dependent human prostatic cancer cells were determined in vitro and in vivo. L-2 and L-10 are delta4-3-one-pregnane derivatives. L-35 and L-37 are delta5-3beta-ol-androstane derivatives, and L-36 and L-39 are delta4-3-one-androstane-derived compounds. L-2, L-10, and L-36 (L-36 at low concentrations) stimulated the growth of LNCaP cells, indicating that they were interacting agonistically with the mutated AR expressed in LNCaP cells. L-35, L-37, and L-39 acted as LNCaP AR antagonists. To determine whether the growth modulatory effects of our novel compounds were specific for the mutated LNCaP AR, competitive binding studies were performed with LNCaP cells and PC-3 cells stably transfected with the wild-type AR (designated PC-3AR). Regardless of AR receptor type, all of our novel compounds were effective at preventing binding of the synthetic androgen methyl-trienolone[17alpha-methyl-(3H)-R1881 to both the LNCaP AR and the wildtype AR. L-36, L-37, and L-39 (5.0 microM) prevented binding by >90%, whereas L-35 inhibited binding by 30%. To determine whether the compounds were acting as agonists or antagonists, LNCaP cells and PC-3AR cells were transfected with the pMAMneoLUC reporter gene. When luciferase activity was induced by dihydrotestosterone, all of the compounds were found to be potent inhibitors of transcriptional activity, and the pattern of inhibition was similar for both receptor types. However, L-2, L-10, and L-36 were determined to be AR agonists, and L-35, L-37, and L-39 were wild-type AR antagonists. When tested in vivo, L-39 was the only AR antagonist that proved to be effective at inhibiting the growth of LNCaP prostate tumor growth. L-39 slowed tumor growth rate in LNCaP tumors grown in male SCID mice to the same level as orchidectomy, significantly reduced tumor weights (P < 0.05), significantly lowered serum levels of prostate-specific antigen (P < 0.02), and significanty lowered serum levels of testosterone (P < 0.05). L-39 also proved to be effective when tested against the PC-82 prostate cancer xenograft that expresses wild-type AR. These results show that some of our compounds initially developed to be inhibitors of androgen synthesis also interact with the human AR and modulate the proliferation of hormone-dependent prostatic cancer cells. Therefore, compounds such as L-39, which have multifunctional activities, hold promise for the treatment of androgen-dependent prostate tumors. (+info)1. Benign Prostatic Hyperplasia (BPH): The enlargement of the prostate gland can put pressure on the urethra and bladder, making it difficult to urinate.
2. Prostatitis: Inflammation of the prostate gland can cause urinary retention.
3. Bladder Outlet Obstruction: A blockage in the muscles of the bladder neck or urethra can prevent urine from flowing freely.
4. Neurological Disorders: Conditions such as multiple sclerosis, Parkinson's disease, and spinal cord injuries can disrupt the nerve signals that control urination, leading to urinary retention.
5. Medications: Certain medications, such as antidepressants, antipsychotics, and anesthetics, can cause urinary retention as a side effect.
6. Urinary Tract Infections (UTIs): UTIs can cause inflammation and scarring in the bladder or urethra, leading to urinary retention.
7. Impacted Stone: Kidney stones that are too large to pass can cause urinary retention if they become lodged in the ureter or bladder.
8. Bladder Cancer: Tumors in the bladder can grow and block the flow of urine, leading to urinary retention.
9. Urethral Stricture: A narrowing of the urethra can cause urinary retention by restricting the flow of urine.
Symptoms of urinary retention may include:
1. Difficulty starting to urinate
2. Weak or interrupted urine stream
3. Painful urination
4. Inability to fully empty the bladder
5. Frequent urination
6. Leaking of urine (incontinence)
7. Blood in the urine
Treatment for urinary retention depends on the underlying cause and may include medications, catheterization, or surgery. It is important to seek medical attention if symptoms persist or worsen over time, as untreated urinary retention can lead to complications such as kidney damage or sepsis.
Treatment options include medications such as alpha-blockers and 5-alpha-reductase inhibitors, minimally invasive therapies such as transurethral microwave therapy or laser therapy, and surgical intervention such as a transurethral resection of the prostate (TURP) or robotic-assisted laparoscopic surgery.
There are also lifestyle changes that can help manage Prostatic Hyperplasia, including limiting fluid intake before bedtime, avoiding caffeine and alcohol, and following a healthy diet. It is important to consult with a healthcare professional for proper diagnosis and treatment of this condition.
In simpler terms, Prostatic Hyperplasia is an enlargement of the prostate gland which can cause urinary problems and discomfort. Treatment options include medication, minimally invasive therapies, and surgery, and lifestyle changes can also help manage the condition.
List of 5α-reductase inhibitors
5α-Reductase inhibitor
Minamestane
MK-434
Prostate cancer
5α-Reductase
Pharmacology of cyproterone acetate
Effects of hormones on sexual motivation
Polycystic ovary syndrome
Torilis japonica
Antiandrogen
Benign prostatic hyperplasia
Prostatic artery embolization
Pattern hair loss
Turosteride
SRD5A1
FCE 28260
Cancer
Cancer prevention
Testosterone enanthate
Discovery and development of 5α-reductase inhibitors
Aqueous humour
Transurethral resection of the prostate
MK-386
Management of hair loss
Dutasteride
Izonsteride
Medication
Urinary retention
Pre-ejaculate
Metabolism
Isocitrate dehydrogenase
Enzyme inhibitor
Peripheral neuropathy
SRD5A2
Mupirocin
Chromosome 6
Pharmacology of bicalutamide
Dyslipidemia
Ketoconazole
Nucleoside triphosphate
Alpha-1 blocker
Azurin
List of OMIM disorder codes
High-density lipoprotein
Glossary of diabetes
Gestonorone caproate
Coagulation
Methylprednisolone
Bifluranol
Cholera
Oxymetholone
Drug class
List of MeSH codes (D12.776)
Finasteride
DailyMed - Search Results for 5-alpha Reductase Inhibitors
Alpha Reductase Inhibitors - PubMed
Alpha Reductase Inhibitors - PubMed
5-alpha reductase inhibitors - Definition - NIDDK
Finasteride - brand name list from Drugs.com
Preventive Oncology: Overview, Risk Assessment, Modifiable Risk Factors
Сыромоноедение | Best Natural 5 Alpha Reductase Inhibitors - Сыромоноедение
Biomarkers Search
NIH Clinical Center Search the Studies: Study Number, Study Title
CanMED: HCPCS
Dutasteride: MedlinePlus Drug Information
BMC Urol Volume 23; 2023 - PMC
Prostate, Acinus - Atrophy - Nonneoplastic Lesion Atlas
NIH Guide: TREATMENT OF BENIGN PROSTATIC HYPERPLASIA: PILOT STUDY
Council Minutes - September 2013 | National Institute on Aging
Parallel Phase III Randomized Trials for High Risk Prostate Cancer Evaluating De-Intensification for Lower Genomic Risk and...
MeSH Browser
Prostate cancer - Symptoms and causes - Mayo Clinic
Common BPH medications raise cardiac failure risk
Trial of Rucaparib in Patients With Metastatic Hormone-Sensitive Prostate Cancer Harboring Germline DNA Repair Gene Mutations -...
Physiochemical Activity|N0000000065
BPH Medications May Increase Heart Failure Risk - Renal and Urology News
DailyMed - Search Results for 5-alpha Reductase Inhibitors
Dermatologic Manifestations of Hirsutism Medication: Antihypertensives, Antiandrogens, Dermatologic agents, Glucocorticoids,...
Grant Abstract: Clinical Evaluation & Treatment Center for BPH
Overtreatment of Prostate Cancer Common - ProgressiveHealth.com
Benign Prostate Hyperplasia - Prostate Imaging | UCLA Health
FINASTERIDE16
- The 5-alpha reductase inhibitors in clinical use in the United States include two agents of similar chemical structure (azasteroids) and activity: finasteride (Proscar: 1992) and dutasteride (Avodart: 2001). (nih.gov)
- 5-alpha reductase inhibitors include finasteride which primarily blocks the type II form of the enzyme and dutasteride which blocks both type I and II forms). (nih.gov)
- Amazingly this is a method that's far more effective at inhibiting alpha 5 reductase from creating DHT in the scalp, than any synthetic drug like finasteride . (syromonoed.com)
- Finasteride is a 5-alpha-reductase inhibitor, which is applied in the treatment of BHP and male baldness. (nih.gov)
- In the doses used finasteride acts mainly by inhibiting the 5-alpha-reductase type 2, thereby reducing the serum level of DHT by approximately 70% and by about 85-90% in the prostate. (nih.gov)
- 14. Comparative study of human steroid 5alpha-reductase isoforms in prostate and female breast skin tissues: sensitivity to inhibition by finasteride and epristeride. (nih.gov)
- 16. Finasteride, an inhibitor of 5 alpha-reductase, suppresses prostatic dihydrotestosterone in men with benign prostatic hyperplasia. (nih.gov)
- 20. Pharmacokinetic parameters and mechanisms of inhibition of rat type 1 and 2 steroid 5alpha-reductases: determinants for different in vivo activities of GI198745 and finasteride in the rat. (nih.gov)
- Inhibitors of 5α-reductases, enzymes involved in intraprostatic conversion of testosterone to its biologically active form dihydrotestosterone, such as finasteride and epristeride, are known to induce atrophy of prostate. (nih.gov)
- 2004. Comparison of the pharmacological effects of a novel selective androgen receptor modulator, the 5α-reductase inhibitor finasteride, and the antiandrogen hydroxyflutamide in intact rats: New approach for benign prostate hyperplasia. (nih.gov)
- Evidence for atrophy and apoptosis in the ventral prostate of rats given the 5alpha-reductase inhibitor finasteride. (nih.gov)
- Men with mild BPH symptoms are often treated with medications including 5-alpha-reductase inhibitors such as finasteride (Proscar) and/or alpha-adrenergic blockers such as tamsulosin (Flomax). (uclahealth.org)
- Other medications like 5- alpha reductase inhibitor (eg: Finasteride or Dutasteride) can also be used in combination with alpha- blocker or alone. (ndtv.com)
- Like finasteride (the active ingredient in Propecia), dutasteride is an inhibitor of the enzyme 5 alpha-reductase which converts testosterone to DHT (dihydrotestosterone), the hormone responsible for genetic hair loss. (bernsteinmedical.com)
- As important, the half-life of dutasteride is significantly longer than finasteride (5-6 weeks vs. 6-8 hours). (bernsteinmedical.com)
- You may be familiar with finasteride (Proscar) and dutasteride (Avodart) as drugs used to treat benign prostatic hyperplasia (BPH), but studies have also looked at whether these two 5-alpha-reductase inhibitors could help prevent prostate cancer. (prostate.net)
Benign Prostatic H10
- Dihydrotestosterone and the concept of 5alpha-reductase inhibition in human benign prostatic hyperplasia. (nih.gov)
- Adherence to 5-alpha reductase inhibitor therapy for benign prostatic hyperplasia: clinical and economic outcomes. (bvsalud.org)
- Our goal was to quantify relationships between adherence to 5-alpha reductase inhibitors (5-ARIs), the risk of acute urinary retention (AUR) and prostate surgery , and medical costs related to patients with benign prostatic hyperplasia (BPH). (bvsalud.org)
- 3. [Dihydrotestosterone and the role of 5 alpha-reductase inhibitors in benign prostatic hyperplasia]. (nih.gov)
- 4. Marked suppression of dihydrotestosterone in men with benign prostatic hyperplasia by dutasteride, a dual 5alpha-reductase inhibitor. (nih.gov)
- 5. Dihydrotestosterone and the prostate: the scientific rationale for 5alpha-reductase inhibitors in the treatment of benign prostatic hyperplasia. (nih.gov)
- 7. Dutasteride: a potent dual inhibitor of 5-alpha-reductase for benign prostatic hyperplasia. (nih.gov)
- 11. Dutasteride: a novel dual inhibitor of 5alpha-reductase for benign prostatic hyperplasia. (nih.gov)
- 15. 5alpha-reductase inhibitors in benign prostatic hyperplasia and prostate cancer risk reduction. (nih.gov)
- 18. A review on steroidal 5α-reductase inhibitors for treatment of benign prostatic hyperplasia. (nih.gov)
Testosterone5
- They act by inhibiting the steroid 5-alpha reductase which catalyzes the conversion of testosterone to dihydrotestosterone. (nih.gov)
- 5 alpha reductase is an enzyme in the body that converts testosterone into DHT which then goes on to cause hair loss in men affected with androgenic alopecia. (syromonoed.com)
- Type 2 alpha 5 reductase is an enzyme that converts testosterone to dihydroxytestosterone. (syromonoed.com)
- DHT is formed by the reduction of testosterone by the enzyme 5-alpha-reductase, which has two isoenzymes. (nih.gov)
- Potential mechanisms for the associations between cardiac failure and [5-alpha reductase inhibitors] include the deleterious impact on metabolic disorders and cardiac function through their antiandrogen effect and blockage of serum testosterone conversion to dihydrotestosterone," wrote the authors of the current study. (urologytimes.com)
Tamsulosin2
- In some clinical studies, patients taking dutasteride with another drug called alpha-blocker (such as tamsulosin) were more likely to have heart failure than patients taking only dutasteride or an alpha-blocker. (thefamilyrx.com)
- If you have significant voiding symptoms which are bothersome then you may need medications like alpha-blockers (eg: Tamsulosin). (ndtv.com)
Prostate Cancer3
- 8. The rationale for inhibiting 5alpha-reductase isoenzymes in the prevention and treatment of prostate cancer. (nih.gov)
- 19. New steroidal 17β-carboxy derivatives present anti-5α-reductase activity and anti-proliferative effects in a human androgen-responsive prostate cancer cell line. (nih.gov)
- Abiraterone (Zytiga), a hormone therapy drug approved for treatment of metastatic prostate cancer, may also help eliminate localized high-risk prostate cancer, according to researchers who will present their findings at the American Society of Clinical Oncology meeting in Chicago June 1-5, 2012. (prostate.net)
Dutasteride3
- Dutasteride is in a class of medications called 5-alpha reductase inhibitors. (medlineplus.gov)
- Dutasteride (Avodart) is a prescribed medicine classified under the group of drugs known as 5-alpha reductase inhibitors. (thefamilyrx.com)
- Dutasteride, a new 5-α-reductase inhibitor, has shown a specific action in medical research by decreasing the volume of the transition zone in contact with the prostatic urethra. (thefamilyrx.com)
Enzyme1
- It is important to note that compared to the Type II form of the 5 alpha-reductase enzyme, the Type I variety is present in many different organs of the body, including the brain, which accounts for the increased potential side effects. (bernsteinmedical.com)
TURP1
- The mechanisms usually evoked to explain the effect of "5-ARI" on hematuria related to BPH and on TURP hemorrhage are related to the reduction of microvasculature density of prostatic epithelium and regulating the activity of growth factors of androgen-controlled angiogenesis. (thefamilyrx.com)
20231
- Published online 2023 Mar 5. (nih.gov)
Patients6
- In patients with BPH who received 5-ARI therapy , greater adherence and persistence were associated with significantly reduced risks of AUR and prostate surgery and with significantly lower medical costs . (bvsalud.org)
- 20 ng/mL prior to starting ADT Note: Patients receiving a 5-alpha reductase inhibitor (ex. (urotoday.com)
- The highest risk was observed in patients exposed to alpha blocker therapy alone. (urologytimes.com)
- The highest risk for cardiac failure was among BPH patients taking alpha blockers alone or in combination, according to the study published in The Journal of Urology . (urologytimes.com)
- The data set Siemens and colleagues studied included 8339 BPH patients exposed to 5-alpha reductase inhibitors, 55,383 exposed to alpha blockers, and 41,491 who had taken a combination. (urologytimes.com)
- Consider 5-alpha-reductase inhibitors, which shrink the prostate, for patients who have predominantly irritative symptoms (urgency and frequency). (consultant360.com)
Blockers10
- The era of medical therapy for BPH dawned in the mid 1970s with the use of nonselective alpha-blockers such as phenoxybenzamine. (medscape.com)
- The medical therapeutic options for BPH have evolved significantly since then, with the development of receptor-specific alpha-blockers that comprise current first-line therapy, as well as the approval of 5-alpha-reductase inhibitors. (medscape.com)
- An approximately 4- to 6-point improvement is expected in IPSS/AUA-SI scores when alpha-blockers are used. (medscape.com)
- Selective long-acting alpha-1 blockers - Terazosin, doxazosin, slow-release (SR) alfuzosin. (medscape.com)
- Investigators studied data on more than 175,200 men with BPH treated with 5-alpha reductase inhibitors, alpha blockers, or a combination. (urologytimes.com)
- Secondly, the alpha blockers (maybe specifically nonselective alpha blockers) have a higher association with new cardiac failure. (urologytimes.com)
- The issue of cardiac failure and alpha blockers arose almost 20 years ago in the ALLHAT trial (NCT00000542), among the first studies to highlight a possible link between alpha blockers and hypertension. (urologytimes.com)
- Although it hasn't changed my practice that much-I still of course use alpha blockers-it has made me more diligent in assessing cardiovascular health," Siemens said. (urologytimes.com)
- The evidence also makes Siemens discuss the choice of his primary care colleagues' use of nonselective alpha blockers when they are being prescribed for lower urinary tract symptoms. (urologytimes.com)
- Over the last decade significant advances have been made in characterizing this abnormality and treating it with medical therapy (such as alpha blockers and 5 alpha reductase inhibitors) and minimally invasive surgical techniques (such as stents, lasers, hyperthermia and others). (nih.gov)
Medications1
- Medical treatment of benign prostatic hypertrophy can use three types of medications: plant extracts, alphablockers which have an essentially symptomatic effect, and inhibitors of 5-α-reductase ("5-ARI") which, through their hormonal action, reduces the volume of the prostate gland, and therefore, can improve clinical symptomatology and reduce the risk of long-term complications. (thefamilyrx.com)
Serotonin2
- Isotretinoin is both a serotonin reuptake inhibitor and a 5-alpha reductase inhibitor (5ARI), so it could give rise to PSSD or PFS, or all three conditions may have something else in common. (rxisk.org)
- While serotonin and 5-alpha reductase may be where these problems start, they seem to go beyond this. (rxisk.org)
Therapy3
- Interestingly, alpha-blocker therapy has not been shown to reduce the overall long-term risk for acute urinary retention (AUR) or need for BPH-related surgery. (medscape.com)
- and 9% higher among men exposed to 5-alpha reductase inhibitor therapy alone. (urologytimes.com)
- Nonselective alpha blocker treatment had an 8% higher risk of cardiac failure than selective alpha blocker therapy, according to the paper. (urologytimes.com)
Compounds2
- Here's the top 4 natural compounds that inhibit 5 alpha reductase. (syromonoed.com)
- Green tea contains two important compounds for inhibiting 5 alpha reductase scientists found. (syromonoed.com)
Inhibition1
- 17. Potency of a novel saw palmetto ethanol extract, SPET-085, for inhibition of 5alpha-reductase II. (nih.gov)
Therapeutic1
- The first line of treatment for mild to moderate symptoms usually consists of alpha-blocking agents because of the rapid onset of their therapeutic effect. (consultant360.com)
Appendix1
- This portion of the meeting was closed to the public, in accordance with the determination that it concerned matters exempt from mandatory disclosure under Sections 552(b)(c)(4) and 552(b)(c)(6), Title 5, U.S. Code and Section 10(d) of the Federal Advisory Committee Act, as amended (5 U.S.C. Appendix). (nih.gov)
Treatment2
- Because of the availability of more alpha-1-receptor-specific agents, phenoxybenzamine is no longer often used for the treatment of BPH. (medscape.com)
- However, the circulating and intraprostatic DHT could be further reduced by a more effective dual 5-alpha-reductase inhibitor, which would be efficacious in the treatment of benign prostate hyperplasia and other DHT-related disorders. (nih.gov)
Trials1
- It's not as well known yet but initial trials are promising as a 5 alpha reductase inhibitor. (syromonoed.com)
Medication1
- The baseline PSA value should be doubled for PSAs taken while on 5-alpha reductase inhibitors and the medication should be discontinued prior to randomization but a washout period is not required. (urotoday.com)
Significantly1
- Alklaizing the bloodstream by consuming foods that have a net alkaline effect on the body can significantly reduce the amount of type 2 alpha 5 reductase in the scalp. (syromonoed.com)
Treatments2
- Participants will have 5 radiation treatments. (nih.gov)
- A past study from 2005 indicated that a stronger single dose of radiation (8 Gy) is as effective as 20 Gy for 5 treatments or 30Gy over 10 treatments. (progressivehealth.com)
Type2
- Type 2 alpha 5 reductase operates below neutral in our scalps. (syromonoed.com)
- The 5-alpha-reductase type 2 is the predominant isoenzyme in genital tissue and thus also in the prostate. (nih.gov)
Adverse1
- It is nonselective, antagonizing both the alpha 1- and alpha 2-adrenergic receptors, which results in a higher incidence of adverse effects. (medscape.com)
Effective2
- Oral ingestion is the least effective way you can benefit from saw palmettos inhibiting effect on 5-alpha-reductase because it's diluted throughout the entire body. (syromonoed.com)
- Alkalizing the bloodstream is in my experience the most effective and long term solution for inhibiting 5 alpha reductase and can have a dramatic effect on preventing further hair loss. (syromonoed.com)
Agents2
- therefore, alpha-adrenergic receptor-blocking agents should theoretically decrease resistance along the bladder neck, prostate, and urethra by relaxing the smooth muscle, thus allowing easier passage of urine. (medscape.com)
- The 5-alpha reductase inhibitors are a family of agents used to treat benign prostatic hypertrophy. (nih.gov)
Review1
- In accordance with the provisions of Public Law 92-463, the meeting was closed to the public on Tuesday, September 17, from 3 to 5 p.m. for the review, discussion, and evaluation of grant applications in accordance with the provisions set forth in Sections 552(b)(c)(4) and 552(b)(c)(6), Title 5, U.S. Code and Section 10(d) of the Public Law 92-463. (nih.gov)
Term1
- Even advanced forms of the cancer have a long-term survival rate that lasts 5 years or more. (progressivehealth.com)
Effects2
- Saw palmetto is probably the most well-known and also controversial 5 alpha reductase inhibitor, due to the variation in results and side effects associated with high oral dosages. (syromonoed.com)
- Alpha blocker] association with cardiac failure, on the other hand, may be linked to their vasodilatory effects and blood pressure variability. (urologytimes.com)
Current1
- Neither of the 5-alpha reductase inhibitors in current use has been linked to clinically apparent acute liver injury. (nih.gov)
Years1
- 5 years. (nih.gov)
Section1
- The 5-alpha reductase inhibitors used for benign prostatic hypertrophy are discussed individually, with references on their hepatotoxicity given together at the end of this introductory section. (nih.gov)