buy tamoxifen

Gynecomastia (GM) is a condition of increased breast volume in men that can recognize a variety of clinical conditions 1:

  • – situations dependent on glandular hyperplasia (so-called true GM);
  • – situations where the increase in volume depends on the accumulation of adipose tissue (false GM or lipomastia);
  • – Mixed hyperplasia, with an increase in various proportions of both glandular and fatty components.

The most common situation is pubertal or postpubertal GM, when – usually without identifiable hormonal abnormalities – we observe the development of GM, which tends to regress to acceptable levels within 2 to 3 years after puberty . These situations, also defined as physiological GM, are explained by the hypersensitivity of the mammary gland tissue to stimulation by hormones produced during puberty.

In clinical practice, there are situations (28 to 40%, depending on the series) where the problem is temporally related to the medication intake (See. table). For this reason – especially in adults with a recent problem – a recent pharmacologic history is especially important 2.

Situations due to systemic hormonal changes are in the minority, but initial clinical evaluation should not neglect examination of estradiol, total testosterone, LH, FSH, prolactin and hCG levels to detect hypogonadism, hyperprolactinemia or very rare cases of secretory estrogenic neoplasms or paraneoplastic hCG syndromes.

In most cases where there are no significant hormonal changes and no drug can be traced, the idiopathic condition of GM is due to an increased sensitivity of the breast tissue to circulating estrogens. In these cases, it can lead to persistent situations, sometimes – especially in adolescents – with strong emotional impact: it is usually an aesthetic problem or, less commonly, a painful disorder for which there are few alternatives to surgical resolution 3. Nevertheless, the demand for a nonsurgical approach to achieve the most lasting results with well tolerated and comfortable medications is common.

Because the pathogenesis is explained by an overreaction of estrogen receptors, attention was focused on drugs with anti-estrogenic effects, while dopamine agonist drugs were effective only in cases (a minority) with documented hyperprolactinemia 4 – 5. Experiments with synthetic anti-estrogens used in the 70s (clomiphene and cyclofenil) 6 through 9 have yielded inconsistent results, for which experiments have focused mainly on tamoxifen, a very widely used molecule in hormonal therapy for breast cancer.

Website Tamoxifen is a synthetic non-steroidal molecule belonging to the so-called SERMs (Selective Estrogen Receptor Modulators), drugs that can behave as receptor antagonists in some tissues and agonists in other organs. Tam plays an antagonist role at the breast and bone tissue agonist receptors, whereas at the endometrium it is a partial agonist 10. This drug, because of its anti-estrogenic effect on breast tissue, has been evaluated in numerous studies performed in patients with puberal GM, as well as in patients with GM secondary to medication, especially in cases resulting from treatment with anti-androgens in androgen block in prostate adenocarcinoma.

Overall, published studies present data on 869 patients treated with Tam: most results are from studies in which the drug was used – in idiopathic HM, in men without proven systemic hormonal disease; – in anti-androgen therapy in patients with prostate carcinoma.

In idiopathic GM, the most evaluated dose was 20 mg/day in one or two doses of 11 to 15. Non-significant data – 10 or 40 mg. The duration of the studies varied: with a therapy duration of 3 to 6 months, the result, evaluated clinically or by ultrasound, was found to be favorable in 70 to 80% of cases. Treatment effects are inevitably transient, and in clinical practice, therapy is usually discontinued after 6-8 months, followed by a waiting period to monitor the development of the problem. In cases of relapse, an additional period of treatment is often suggested, but data on this issue from randomized clinical trials are completely lacking. Tamoxifen was generally well tolerated, even at a mongi duration of 16 to 17; side effects noted were mild and only in 6 cases resulted in discontinuation of treatment. No serious adverse events, particularly liver damage or thrombotic episodes, have been reported. Tamoxifen use caused predictable hormonal responses according to its receptor action profile and did not result in changes in hemocoagulation parameters or other risk factors 18 – 19. Efficacy was superior to that of danazol, compared to which Tam is also better tolerated 20. The efficacy of tamoxifen was slightly lower than that of raloxifene in the only comparative study 21.

The efficacy of tamoxifen is clinically more evident and more prolonged in cases of GM secondary to medication 22. The 20 mg/day dose administered to patients with adenocarcinoma of the prostate, operated or unoperated, was effective in both therapy and prevention of GM with bicalutamide 23 – 24. At the same dose, anastrozole 25 – 26 and breast radiotherapy 27 – 28 were also more effective. Tamoxifen treatment was ineffective at a weekly dose of 20 mg after a prior dose of 20 mg/day 29. One study compared prophylactic administration of 10 mg of tamoxifen for one year vs. therapeutic administration of 20 mg with better symptom outcomes in previously treated patients. Treatment with 10 or 20 mg had no significant effect on the course of prostate disease 30. Overall, despite concerns 31 about the overall quality of the studies being very modest (lack of data from randomized and controlled trials, small number of samples studied), the effectiveness of therapy with tamoxifen, appears to derive from the results of all the studies. Several reviews support its use in all types of GM for 3 to 6 months 32 – 34. Given the mechanism of action, it is still important to take a cautious stance in patients still in the growth phase, as the drug may affect long bone maturation.

There is no indication for gynecomastia for any of the treatments described, which is therefore an off-label condition to be prescribed and treated according to the procedures set forth in the Legislative Decree of February 17, 1998, n. 23 when prescribed in group C, except in cases documented and submitted to individual local boards (if any) that may determine grantless dispensing of the drug.

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