Spironolactone and Topical Retinoids in Adult Female Cyclical Acne
February 2014 | Volume 13 | Issue 2 | Original Article | 126 | Copyright © 2014
Erin Lessner MD,a Samantha Fisher MD,b Katherina Kobraei MD,b Michael Osleber MD,b Rebecca Lessner BS,c Lauren Elliott MD,d and Stanton Wesson MDb
aDepartment of Ophthalmology, University of South Carolina, Columbia, SC
bDepartment of Dermatology, University of Florida, Gainesville, FL
cLincoln Memorial University, DeBusk School of Medicine, Harrogate, TN
dDepartment of Emergency Medicine, University of California San Diego, San Diego, CA
PURPOSE: To access the efficacy of spironolactone and topical retinoids in the treatment of female cyclical acne.
METHODS: A retrospective chart review on 41 female patients age 19-57 years old with cyclical acne was performed. Patients were examined over the course of 2 to 102 months while taking 50 to 200mg of spironolactone and topical tretinoin 0.025% or adapalene 0.1% cream. All were diagnosed with acne rated mild to severe, prior to treatment, and were started on an initial dose of 50mg po daily. If significant improvement was not seen within the first 3-6 months, the dose was either held or increased in 25mg increments every 3 months. Patients on oral and topical antibiotics, as well as patients on photodynamic therapy were excluded from the study. The response to treatment was rated on a 0-4 scale with 0 being no response and 4 corresponding to clear skin.
RESULTS: One patient (2.4%) had no response to treatment. This patient was only on 50mg po daily for only 2 months. Only 5 (12.2%) patients had minimal response to treatment and 9 (22.0%), 12 (29.3%), and 14 (34.1%) had a good, excellent, or clear response respectively. The study showed 26 (63.4%) women on treatment with spironolactone and topical retinoids had an excellent or clear outcome, and 35 (85.4%) were considered to have a good, excellent, or clear response.
CONCLUSION: The addition of spironolactone to topical retinoid treatment suggests a superior response to retinoids alone in clearance of female adult cyclical acne.
J Drugs Dermatol. 2014;13(2):126-129.
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Spironolactone was developed as a mineralocorticoid receptor antagonist following the observation that spirolactones block the effect of mineralocorticoids in the late 1950’s. The resulting increase in salt and water excretion led to spironolactone’s approval by the US Food and Drug Administration for management of congestive heart failure, cirrhosis of the liver, nephrotic syndrome, essential hypertension, hypokalemia, and primary hyperaldosteronism.1 Additionally, over the past three decades, spironolactone’s effects outside the distal renal tubule have led to dermatologic uses in treatment of androgen mediated conditions, including acne, hirsutism, and alopecia.
Spironolactone is formulated as a tablet without a readily available intravenous form because of the drug’s poor aqueous solubility.2 Spironolactone is partially absorbed, with oral bioavailability estimated to be in the 65-90% range.2,3 Food increases the bioavailability of the drug, however the therapeutic impact of this effect remains unknown.2 Spironolactone undergoes rapid hepatic metabolism, and more than 90% of available drug is protein bound.1 Multiple metabolites, including 7α-methylspironolactone, 6β-hydroxy-7-α- methylspironolactone, and canrenone, are formed and also have therapeutic effects. The half-life of spironolactone is estimated to be 1.4 hours, however, the half-lives of its metabolites are much longer. Canrenone, for instance, has a half-life of 16.5 hours, which may prolong the therapeutic effects of the drug. The half-lives of spironolactone and its metabolites are significantly increased in the setting of hepatic dysfunction and cirrhosis, with t1/2 of spironolactone increased to approximately 9 hours.2 Additionally, dosing adjustments must be made in the setting of renal dysfunction or end stage renal disease, as spironolactone and its metabolites are primarily excreted via the urine, with secondary excretion in bile.1
Mechanism of Action
Spironolactone acts primarily through competitive inhibition of aldosterone receptors, and its main site of action is the blockade of the sodium potassium pump in the distal renal tubule.1 The resulting increase in water and sodium excretion is largely responsible for the diuretic and antihypertensive effects that are beneficial in its approved indications. This inhibition also results in retention of potassium.1 It also has direct inhibitory effects on the cardiovascular system’s reactivity to the adrenergic and the renin-angiotensin-aldosterone systems.4
In addition, spironolactone produces anti-androgenic effects by targeting a variety of other mechanisms. Spironolactone has been shown to competitively inhibit binding of