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There has been an abundance of threads related to gynecomastia. The answers for the questions have been very broad and often wrong. Please recognize that for gyno, nolvadex(tamoxifen) is the best choice of the drugs that are readily available. Raloxifene may be better but the availability is low. .
Remember, estrogen is the real culprit in relation to gyno; blocking the receptors, which nolvadex does, is the goal.
Studies in support:
* Nolvadex to treat/reduce gyno *
Management of physiological gynaecomastia with tamoxifen.
Khan HN, Rampaul R, Blamey RW.
Professorial Unit of Surgery, Department of Surgery, Nottingham City Hospital, Nottingham NG5 1PB, UK.
AIMS: We aimed to confirm suggestions that tamoxifen therapy alone may resolve physiological gynaecomastia. METHODS: A prospective audit of the outcome of tamoxifen routinely given to men with physiological gynaecomastia was carried out at Nottingham. Men referred with gynaecomastia had clinical signs recorded, e.g., type (diffuse 'fatty' or retro-areolar 'lump'), size and possible aetiology. They were offered oral tamoxifen 20mg once daily for 6-12 weeks. On follow-up patients were assessed for complete resolution (CR), partial resolution where patient is satisfied with outcome (PR) or no resolution (NR). Success was either CR or PR. RESULTS: Thirty-six men accepted tamoxifen for physiological gynaecomastia. Median age was 31 (range 18-64). Tenderness was present in 25 (71%) cases. Sixteen men (45%) had 'fatty' gynaecomastia and 20 had 'lump' gynaecomastia. Tamoxifen resolved the mass in 30 patients (83.3%; CR=22, PR=8) and tenderness in 21 cases (84%; CR=0, PR=0). Lump gynaecomastia was more responsive to tamoxifen than the fatty type (100% vs. 62.5%; P=0.0041). CONCLUSIONS: Oral tamoxifen is an effective treatment for physiological gynaecomastia, especially for the lump type.
Prevention and management of bicalutamide-induced gynecomastia and breast pain: randomized endocrinologic and clinical studies with tamoxifen and anastrozole.
Saltzstein D, Sieber P, Morris T, Gallo J.
Urology San Antonio Research PA, Pasteur Medical Plaza, San Antonio, Texas, USA.
A randomized, double-blind, placebo-controlled multicenter trial involving 107 men receiving bicalutamide ('Casodex') 150 mg/day therapy following radical therapy for prostate cancer assessed tamoxifen ('Nolvadex') 20 mg/day and anastrozole ('Arimidex') 1 mg/day for the prophylaxis and treatment of gynecomastia/breast pain. Tamoxifen, but not anastrozole, significantly reduced the incidence of gynecomastia/breast pain when used prophylactically and therapeutically. Serum testosterone levels increased with tamoxifen relative to placebo but prostate-specific antigen levels declined in all treatment groups. Further studies are needed to define the optimum tamoxifen dose and to assess any impact on cancer control. The use of tamoxifen in this setting remains to be investigated.
Treatment of gynecomastia with tamoxifen: a double-blind crossover study.
Parker LN, Gray DR, Lai MK, Levin ER.
Benign asymptomatic or painful enlargement of the male breast is a common problem, postulated to be due to an increased estrogen/testosterone ration or due to increased estrogenic or decreased androgenic stimulation via estrogen or androgen receptor interactions. Treatment at present consists of analgesic medication or surgery. However, treatment directed against the preponderance of estrogenic stimulation would seem to represent a more specific form of therapy. In the present double-blind crossover study, one-month courses of a placebo or the antiestrogen tamoxifen (10 mg given orally bid) were compared in random order. Seven of ten patients experienced a decrease in the size of their gynecomastia due to tamoxifen (P less than 0.005). Overall, the decrease for gynecomastia for the whole group was significant (P less than 0.01). There was no beneficial effect of placebo (P greater than 0.1). Additionally, all four patients with painful gynecomastia experienced symptomatic relief. There was no toxicity. The reduction of breast size was partial and may indicate the need for a longer course of therapy. A followup examination was performed in eight out of ten patients nine months to one year after discontinuing placebo and tamoxifen. There were no significant changes from the end of the initial study period except for one tamoxifen responder who developed a recurrence of breast tenderness after six months, and one nonresponder who demonstrated an increase in breast size and a new onset of tenderness after ten months. Therefore, antiestrogenic treatment with tamoxifen may represent a safe and effective mode of treatment for selected cases of cosmetically disturbing or painful gynecomastia.
---Prolactin concerns
Tamoxifen inhibits prolactin signal transduction in ER - NOG-8 mammary epithelial cells.
Das R, Vonderhaar BK.
Laboratory of Tumor Immunology and Biology, National Cancer Institute
Tamoxifen (TAM), an antiestrogen, also acts as an antilactogen in mammary cells. In the present study we analyze the effect of TAM on the signal transduction pathway for prolactin (Prl). TAM bound specifically to NOG-8, an estrogen receptor-negative mammary cell line. Within 5 min of Prl treatment, raf-1, MEK and MAP kinase were induced 2-3-fold over the control level. TAM completely inhibited this Prl-induced activation of kinases as well as Prl binding and cell growth. These results indicate the potential role of TAM as an antilactogen in Prl responsive systems.
Antiestrogenic properties of raloxifene.
Draper MW, Flowers DE, Neild JA, Huster WJ, Zerbe RL.
Lilly Research Laboratories, Eli Lilly and Company
This 21-day, open-label study evaluated the effects of raloxifene and tamoxifen on estrogen-induced changes in serum levels of anterior pituitary hormones (prolactin, luteinizing hormone, and follicle-stimulating hormone), sex steroids (testosterone, estradiol), and binding globulins [thyroid binding globulin (T3 resin uptake), transcortin, sex steroid binding globulin]. Seventeen healthy male volunteers completed the study after being randomized to one of three treatments: raloxifene, tamoxifen, or placebo. Six subjects received raloxifene (200 mg daily) for 10 days, 6 subjects received tamoxifen [20 mg twice a day (b.i.d.)] for 10 days, and 5 subjects received placebo for 10 days. All subjects received ethinyl estradiol (20 micrograms b.i.d.) for 7 days starting 3 days after initiation of study drug or placebo treatment. Results of the primary analysis of this study indicate that for six of the seven analyzable parameters of estrogen action (excluding luteinizing hormone) raloxifene blunted the estrogen response; this effect was significant only for T3 resin uptake. Tamoxifen administration significantly blunted or reversed the estrogen effect in all six of these parameters.
Remember, estrogen is the real culprit in relation to gyno; blocking the receptors, which nolvadex does, is the goal.
Studies in support:
* Nolvadex to treat/reduce gyno *
Management of physiological gynaecomastia with tamoxifen.
Khan HN, Rampaul R, Blamey RW.
Professorial Unit of Surgery, Department of Surgery, Nottingham City Hospital, Nottingham NG5 1PB, UK.
AIMS: We aimed to confirm suggestions that tamoxifen therapy alone may resolve physiological gynaecomastia. METHODS: A prospective audit of the outcome of tamoxifen routinely given to men with physiological gynaecomastia was carried out at Nottingham. Men referred with gynaecomastia had clinical signs recorded, e.g., type (diffuse 'fatty' or retro-areolar 'lump'), size and possible aetiology. They were offered oral tamoxifen 20mg once daily for 6-12 weeks. On follow-up patients were assessed for complete resolution (CR), partial resolution where patient is satisfied with outcome (PR) or no resolution (NR). Success was either CR or PR. RESULTS: Thirty-six men accepted tamoxifen for physiological gynaecomastia. Median age was 31 (range 18-64). Tenderness was present in 25 (71%) cases. Sixteen men (45%) had 'fatty' gynaecomastia and 20 had 'lump' gynaecomastia. Tamoxifen resolved the mass in 30 patients (83.3%; CR=22, PR=8) and tenderness in 21 cases (84%; CR=0, PR=0). Lump gynaecomastia was more responsive to tamoxifen than the fatty type (100% vs. 62.5%; P=0.0041). CONCLUSIONS: Oral tamoxifen is an effective treatment for physiological gynaecomastia, especially for the lump type.
Prevention and management of bicalutamide-induced gynecomastia and breast pain: randomized endocrinologic and clinical studies with tamoxifen and anastrozole.
Saltzstein D, Sieber P, Morris T, Gallo J.
Urology San Antonio Research PA, Pasteur Medical Plaza, San Antonio, Texas, USA.
A randomized, double-blind, placebo-controlled multicenter trial involving 107 men receiving bicalutamide ('Casodex') 150 mg/day therapy following radical therapy for prostate cancer assessed tamoxifen ('Nolvadex') 20 mg/day and anastrozole ('Arimidex') 1 mg/day for the prophylaxis and treatment of gynecomastia/breast pain. Tamoxifen, but not anastrozole, significantly reduced the incidence of gynecomastia/breast pain when used prophylactically and therapeutically. Serum testosterone levels increased with tamoxifen relative to placebo but prostate-specific antigen levels declined in all treatment groups. Further studies are needed to define the optimum tamoxifen dose and to assess any impact on cancer control. The use of tamoxifen in this setting remains to be investigated.
Treatment of gynecomastia with tamoxifen: a double-blind crossover study.
Parker LN, Gray DR, Lai MK, Levin ER.
Benign asymptomatic or painful enlargement of the male breast is a common problem, postulated to be due to an increased estrogen/testosterone ration or due to increased estrogenic or decreased androgenic stimulation via estrogen or androgen receptor interactions. Treatment at present consists of analgesic medication or surgery. However, treatment directed against the preponderance of estrogenic stimulation would seem to represent a more specific form of therapy. In the present double-blind crossover study, one-month courses of a placebo or the antiestrogen tamoxifen (10 mg given orally bid) were compared in random order. Seven of ten patients experienced a decrease in the size of their gynecomastia due to tamoxifen (P less than 0.005). Overall, the decrease for gynecomastia for the whole group was significant (P less than 0.01). There was no beneficial effect of placebo (P greater than 0.1). Additionally, all four patients with painful gynecomastia experienced symptomatic relief. There was no toxicity. The reduction of breast size was partial and may indicate the need for a longer course of therapy. A followup examination was performed in eight out of ten patients nine months to one year after discontinuing placebo and tamoxifen. There were no significant changes from the end of the initial study period except for one tamoxifen responder who developed a recurrence of breast tenderness after six months, and one nonresponder who demonstrated an increase in breast size and a new onset of tenderness after ten months. Therefore, antiestrogenic treatment with tamoxifen may represent a safe and effective mode of treatment for selected cases of cosmetically disturbing or painful gynecomastia.
---Prolactin concerns
Tamoxifen inhibits prolactin signal transduction in ER - NOG-8 mammary epithelial cells.
Das R, Vonderhaar BK.
Laboratory of Tumor Immunology and Biology, National Cancer Institute
Tamoxifen (TAM), an antiestrogen, also acts as an antilactogen in mammary cells. In the present study we analyze the effect of TAM on the signal transduction pathway for prolactin (Prl). TAM bound specifically to NOG-8, an estrogen receptor-negative mammary cell line. Within 5 min of Prl treatment, raf-1, MEK and MAP kinase were induced 2-3-fold over the control level. TAM completely inhibited this Prl-induced activation of kinases as well as Prl binding and cell growth. These results indicate the potential role of TAM as an antilactogen in Prl responsive systems.
Antiestrogenic properties of raloxifene.
Draper MW, Flowers DE, Neild JA, Huster WJ, Zerbe RL.
Lilly Research Laboratories, Eli Lilly and Company
This 21-day, open-label study evaluated the effects of raloxifene and tamoxifen on estrogen-induced changes in serum levels of anterior pituitary hormones (prolactin, luteinizing hormone, and follicle-stimulating hormone), sex steroids (testosterone, estradiol), and binding globulins [thyroid binding globulin (T3 resin uptake), transcortin, sex steroid binding globulin]. Seventeen healthy male volunteers completed the study after being randomized to one of three treatments: raloxifene, tamoxifen, or placebo. Six subjects received raloxifene (200 mg daily) for 10 days, 6 subjects received tamoxifen [20 mg twice a day (b.i.d.)] for 10 days, and 5 subjects received placebo for 10 days. All subjects received ethinyl estradiol (20 micrograms b.i.d.) for 7 days starting 3 days after initiation of study drug or placebo treatment. Results of the primary analysis of this study indicate that for six of the seven analyzable parameters of estrogen action (excluding luteinizing hormone) raloxifene blunted the estrogen response; this effect was significant only for T3 resin uptake. Tamoxifen administration significantly blunted or reversed the estrogen effect in all six of these parameters.
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