Spironolactone is in a class of medications called androgen receptor antagonists. It binds to androgen receptors
preventing testostorone from binding. Spironolactone is typically used to treat high blood pressure as
it causes the kidneys to eliminate unneeded water and sodium from the body into the urine. It acts as a
competitive antagonist at aldosterone receptors. The most important of these receptors are situated in
the distal portion of the renal tubules.
Men are noramlly not prescribed Spironolactone. Exceptional results for many men but at a high cost of side effects. Severe Gynecomastia being the most common side effect.
25mg-200mg per day.
|Significant Side Effects
Spironolactone causes gynecomastia by several mechanisms. It can block androgen production by inhibiting enzymes in the testosterone synthetic pathway (i.e. 17a hydroxylase and 17-20-desmolase), but it can also block receptor-binding of testosterone and dihydrotestosterone. In addition to decreasing testosterone levels and biologic effects, spironolactone also displaces estradiol from SHBG, increasing free estrogen levels.
Mechanism Of Action: Spironolactone is a specific pharmacologic antagonist of aldosterone, acting primarily through competitive binding of receptors at the aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule. Spironolactone causes increased amounts of sodium and water to be excreted, while potassium is retained. Spironolactone acts both as a diuretic and as an antihypertensive drug by this mechanism. It may be given alone or with other diuretic agents which act more proximally in the renal tubule.
Aldosterone Antagonist Activity: Increased levels of the mineralocorticoid, aldosterone, are present in primary and secondary hyperaldosteronism. Edematous states in which secondary aldosteronism is usually involved include congestive heart failure, hepatic cirrhosis, and the nephrotic syndrome. By competing with aldosterone for receptor sites, spironolactone provides effective therapy for the edema and ascites in those conditions. Spironolactone counteracts secondary aldosteronism induced by the volume depletion and associated sodium loss caused by active diuretic therapy.
Spironolactone is effective in lowering the systolic and diastolic blood pressure in patients with primary hyperaldosteronism. It is also effective in most cases of essential hypertension, despite the fact that aldosterone secretion may be within normal limits in benign essential hypertension.
Through its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
Spironolactone has not been demonstrated to elevate serum uric acid, to precipitate gout, or to alter carbohydrate metabolism.
The effect of food on spironolactone absorption (two 100 mg spironolactone tablets) was assessed in a single dose study of 9 healthy, drug-free volunteers. Food increased the bioavailability of unmetabolized spironolactone by almost 100%. The clinical importance of this finding is not known.
Reversal of andro-genetic alopecia in a male. A spironolactone effect?
This 73-year-old white male has been bald since the age of 28. He developed nonA-nonB-induced liver cirrhosis and had been treated with spironolactone for the last 6 years. For the last 3 months, his hair had started to regrow over the scalp. This might be related to the antiandrogenic effect of spironolactone.
Treatment of female pattern hair loss with oral antiandrogens.
It has not been conclusively established that female pattern hair loss (FPHL) is either due to androgens or responsive to oral antiandrogen therapy.
To evaluate the efficacy of oral antiandrogen therapy in the management of women with FPHL using standardized photographic techniques (Canfield Scientific), and to identify clinical and histological parameters predictive of clinical response.
For this single-centre, before-after, open intervention study, 80 women aged between 12 and 79 years, with FPHL and biopsy-confirmed hair follicle miniaturization [terminal/vellus (T/V) hair ratio < or = 4 : 1] were photographed at baseline and again after receiving a minimum of 12 months of oral antiandrogen therapy. Forty women received spironolactone 200 mg daily and 40 women received cyproterone acetate, either 50 mg daily or 100 mg for 10 days per month if premenopausal. Women using topical minoxidil were excluded. Standardized photographs of the midfrontal and vertex scalp were taken with the head positioned in a stereotactic device. Images were evaluated by a panel of three clinicians experienced in the assessment of FPHL, blinded to patient details and treatment and using a three-point scale.
As there was no significant difference in the results or the trend between spironolactone and cyproterone acetate the results were combined. Thirty-five (44%) women had hair regrowth, 35 (44%) had no clear change in hair density before and after treatment, and 10 (12%) experienced continuing hair loss during the treatment period. Ordinal logistic regression analysis to identify predictors of response revealed no influence of patient age, menopause status, serum ferritin, serum hormone levels, clinical stage (Ludwig) or histological parameters such as T/V ratio or fibrosis. The only significant predictor was midscalp clinical grade, with higher-scale values associated with a greater response (P = 0.013).
Eighty-eight percent of women receiving oral antiandrogens could expect to see no progression of their FPHL or improvement. High midscalp clinical grade was the only predictor of response identified. A placebo-controlled study is required to compare this outcome to the natural history of FPHL.
Lack of endocrine systemic side effects after topical application of spironolactone in man.
In six healthy male volunteers, the percutaneous absorption of spironolactone was compared with placebo in a double-blind crossover study. The subjects were randomly given either a cream containing 5% spironolactone or placebo to be applied in a randomized sequential way to a well defined skin area equivalent to 55% of body area. During the 72 h following the application of the ointment, blood levels of canrenone, the major metabolite of spironolactone, have been determined. In order to estimate the systemic antiandrogenic effect of spironolactone, plasma levels of 17-alpha-Hydroxy progesterone (17 alpha-OH-P), Testosterone (pT) and non-conjugated 3 alpha-Androstanediol (3 alpha-diol, metabolite of the active androgen 5 alpha-Dihydrotestosterone or DHT) as well as salivary Testosterone (sT) which relate to the free and active plasma testosterone fraction have also been measured. Urinary levels of canrenone have been determined 48 hours after cream application. No changes in any levels of these hormones have been detected and plasma canrenone levels were undetectable during the 72 hours of topical treatment. Topically administered, spironolactone appears to have only a local skin impregnation.
Topical spironolactone inhibits dihydrotestosterone receptors in human sebaceous glands: an autoradiographic study in subjects with acne vulgaris.
The interaction between spironolactone and dihydrotestosterone (DHT) receptors was evaluated with an autoradiographic technique. The inhibition of DHT receptors by spironolactone was found to be related to the decrease of tritiated DHT granules in the sebaceous glands of the treated site. 6 male patients affected by acne vulgaris entered the study. The acute study was performed by applying to 25 cm2 of the back a cream containing 5% spironolactone under occlusive dressing. The dosage of spironolactone applied was 4 mg/cm2 for 48 h. The long-term study was performed by applying the same amount to the entire back, without occlusion, twice daily for 1 month. Skin biopsies were taken at the end of the treatment, incubated with tritiated DHT and processed for autoradiography. Both the acute and the long-term study revealed a decrease of the autoradiographic granules in the treated site. This effect is related to the binding of spironolactone with dihydrotestosterone receptors in the sebaceous glands. Our study demonstrates that 5% topical spironolactone cream acts as an antiandrogen in human sebaceous glands, competing with DHT receptors and producing a decrease of labelled DHT. At the concentrations used the effect has been only local. No side-effects were recorded during both studies.
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