written by magic32
Firstly, you should know that correlation between when gyno therapy begins and its level of success is a myth. The appropriate treatments work well regardless of the condition's longevity, as clearly illustrated in numerous cases persistent pubertal gyno resolution.* (SEE BELOW)
Secondly, the amount of time necessary to achieve completely reversed or satisfactorily reduced sustained gyno resolution varies greatly, and is based on a several variables such as: condition type and severity (simple fatty, fatty glandular, nodule/bump, or glandular). It is important to note that one should not discontinue therapy as soon as results are seen, because the ratio imbalance (etiological cause) has not yet been wholly corrected within the affected tissue, thereby making recurrence substantially more likely. Conversely, one should continue therapy for a few weeks (observed as a couple of months w/in clinical trials) after satisfactory results have been attained.* (SEE BELOW)
Thirdly, although some have reported success from A-dex therapy, and I’m not refuting the veracity of these claims, they should indeed be considered within the very subjective light in which they’re presented because of the significant body of clinical research to the contrary. In other words, A-dex may impact some individuals, but when combating gyno one should select a better therapeutic agent, which amounts to the appropriate SERM, DHT, or a stronger AI. Furthermore, even better results have been seen with the concurrent and/or sequential administration of two or more of these agents.
Here are a couple of diverse examples of just how IMPOTENT (even at higher doses) A-dex is in gyno therapy:
Quote:
Evaluation of Tamoxifen and Anastrozole in the Prevention of Gynecomastia and Breast Pain Induced by Bicalutamide Monotherapy of Prostate Cancer
F. Boccardo, A. Rubagotti, M. Battaglia, P. Di Tonno, F.P. Selvaggi, G. Conti, G. Comeri, A. Bertaccini, G. Martorana, P. Galassi, F. Zattoni, A. Macchiarella, A. Siragusa, G. Muscas, F. Durand, D. Potenzoni, A. Manganelli, V. Ferraris, F. Montefiore
Journal of Clinical Oncology, Vol 23, No 4 (February 1), 2005: pp. 808-815
http://jco.ascopubs.org/cgi/content/full/23/4/808
Safety and Efficacy of Anastrozole for the Treatment of Pubertal Gynecomastia: A Randomized, Double-Blind, Placebo-Controlled Trial
Paul V. Plourde, Edward O. Reiter, Hann-Chang Jou, Paul E. Desrochers, Stephen D. Rubin, Barry B. Bercu, Frank B. Diamond, Jr. and Philippe F.
Journal of Clinical Oncology, Vol 23, No 4 (February 1), 2005: pp. 808-815
© 2005 American Society of Clinical Oncology.
http://jcem.endojournals.org/cgi/content/full/89/9/4428
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* THE AFOREMENTIONED PERSISTENT PUBERTAL GYNO RESOLUTION STUDIES & THE SIGNIFICANCE OF TREATMENT DURATION ON SUSTAINED RESULTS:
Quote:
Tamoxifen treatment for pubertal gynecomastia
We evaluated the efficacy of the tamoxifen treatment in 37 patients with pubertal gynecomastia. All had distinct, easily palpable breast swellings with a diameter of over three cm. Pain, tenderness, and swelling associated with gynecomastia were reported by six patients. Eight of the patients were obese. One patient also suffered from varicocele. Pain and size reduction was seen in all patients with tamoxifen treatment. No long-term side effects of tamoxifen were observed. The dose of tamoxifen was increased in three patients due to poor response. Two of the treatment group had recurrence problem at follow-up. We did not need to refer any patient to surgery. Tamoxifen treatment is relatively non-toxic, may be beneficial and we think it should be considered for pubertal gynecomastia.
Derman O, Kanbur NO, Kutluk T.
Section of Adolescent Medicine, Department of Pediatrics,
Hacettepe University Faculty of Medicine, 06100 Ankara-Turkey.
Quote:
Treatment of persistent pubertal gynecomastia with dihydrotestosterone heptanoate.
Four boys with persistent pubertal gynecomastia were given intramuscular dihydrotestosterone heptanoate (DHT-hp) at 2 to 4-week intervals for 16 weeks. By the end of treatment, breast size in all four boys had decreased 67% to 78%. Initial plasma levels of gonadotropins, estradiol, testosterone, and dihydrotestosterone (DHT) were normal. Mean plasma DHT concentration rose with the injections of DHT-hp, and remained elevated throughout the treatment period. Estradiol, LH, FSH, and testosterone decreased during treatment, as did 24-hour urinary LH and FSH. No regrowth of breast tissue was observed 6 to 15 months after treatment, although hormone concentrations had returned to near pretreatment values by 2 months after the last injection. DHT-hp has potential to be an effective medical therapy for persistent pubertal gynecomastia.
Eberle AJ; Sparrow JT; Keenan BS
J Pediatr 1986 Jul;109(1):144-9.
Quote:
Beneficial effects of raloxifene and tamoxifen in the treatment of pubertal gynecomastia.
OBJECTIVES: To assess the efficacy of the anti-estrogens tamoxifen and raloxifen in the medical management of persistent pubertal gynecomastia. STUDY DESIGN: Retrospective chart review of 38 consecutive patients with persistent pubertal gynecomastia who presented to a pediatric endocrinology clinic. Patients received reassurance alone or a 3- to 9-month course of an estrogen receptor modifier (tamoxifen or raloxifene). RESULTS: Mean (SD) age of treated subjects was 14.6 (1.5) years with gynecomastia duration of 28.3 (16.4) months. Mean reduction in breast nodule diameter was 2.1 cm (95% CI 1.7, 2.7, P <.0001) after treatment with tamoxifen and 2.5 cm (95% CI 1.7, 3.3, P <.0001) with raloxifene. Some improvement was seen in 86% of patients receiving tamoxifen and in 91% receiving raloxifene, but a greater proportion had a significant decrease (>50%) with raloxifene (86%) than tamoxifen (41%). No side effects were seen in any patients. CONCLUSION: Inhibition of estrogen receptor action in the breast appears to be safe and effective in reducing persistent pubertal gynecomastia, with a better response to raloxifene than to tamoxifen. Further study is required to determine that this is truly a treatment effect.
Lawrence SE; Faught KA; Vethamuthu J; Lawson ML
J Pediatr. 2004 Jul;145(1):71-6.
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