HS and Hormones: Understanding the Connection
Hormonal fluctuations are among the most well-documented triggers for HS flares. Understanding how androgens, estrogen, and progesterone influence HS can help patients and clinicians develop more targeted management strategies.
Medical Disclaimer: This article is for educational purposes only. Hormonal treatments for HS require evaluation and prescription by a qualified physician. Read full disclaimer.
If you have hidradenitis suppurativa and notice that your flares follow a predictable pattern - worsening before your period, improving during pregnancy, or changing after starting or stopping hormonal contraceptives - you are not imagining it. Hormonal influences on HS are real, well-documented, and clinically significant. Women planning a family should also read our guide on HS and pregnancy.
HS predominantly affects women (approximately 3:1 female to male ratio), typically begins after puberty, and often improves after menopause - all patterns that point to hormonal involvement. Understanding these connections opens the door to hormonal management strategies that can meaningfully reduce flare frequency and severity. Men with HS have a distinct hormonal profile - see our article on HS in men.
The Role of Androgens in HS
Androgens - the class of hormones that includes testosterone, DHEA, and dihydrotestosterone (DHT) - are the most studied hormonal factor in HS pathogenesis. While HS patients do not necessarily have elevated androgen levels in their blood, the hair follicles and sebaceous glands in HS-affected areas appear to be hypersensitive to androgenic stimulation.[4]
Follicular Hyperkeratosis
Androgens stimulate keratinocyte proliferation in hair follicles, contributing to the follicular plugging that initiates HS lesion formation.
Sebaceous Gland Stimulation
Androgens increase sebum production in affected areas, creating an environment that promotes bacterial colonization and inflammation.
Apocrine Gland Activity
Apocrine sweat glands, which are concentrated in HS-affected areas, are androgen-sensitive. Increased apocrine activity may contribute to the inflammatory cascade.
This androgenic hypersensitivity explains why anti-androgen treatments such as spironolactone can be effective in some HS patients, even when serum androgen levels appear normal.[1]
HS and the Menstrual Cycle
Many women with HS report predictable flares in the 1-2 weeks before their period, a pattern known as perimenstrual HS. This corresponds to the luteal phase of the menstrual cycle, when progesterone levels are high and estrogen levels fall. Several mechanisms may explain this pattern:
Track Your Cycle and Flares
Keeping a flare diary alongside a menstrual cycle tracker for 2-3 months can help establish whether your HS has a hormonal pattern. This information is valuable for your dermatologist and gynecologist when considering hormonal management options.
Hormonal Management Options for HS
Several hormonal interventions have evidence for HS management. These are typically considered as adjunctive therapy alongside standard HS treatments, not as replacements. Always discuss these options with both your dermatologist and gynecologist or endocrinologist.
Spironolactone
Anti-androgenAn aldosterone antagonist with anti-androgenic properties, spironolactone is one of the most commonly used hormonal treatments for HS in women. It blocks androgen receptors in hair follicles and sebaceous glands, reducing androgenic stimulation. Typical doses range from 50-200mg/day. Not appropriate for men due to feminizing side effects.
Available by prescription. Requires monitoring of potassium levels.
Combined Oral Contraceptives
Estrogen + ProgestinCombined oral contraceptives (COCs) may help HS by stabilizing hormonal fluctuations and, with the right progestin, reducing androgenic stimulation. Not all COCs are equal - progestins with low androgenic activity (such as desogestrel, norgestimate, or drospirenone) are preferred. Progestin-only pills or implants with androgenic progestins may worsen HS in some patients.
Discuss progestin type with your gynecologist. Not appropriate for all patients.
Finasteride
5-alpha reductase inhibitorFinasteride blocks the conversion of testosterone to the more potent DHT. Case reports and small series suggest benefit in some HS patients, particularly men. More research is needed to establish its role in HS management.
Teratogenic - must not be used during pregnancy or by women who may become pregnant.
Metformin
Insulin sensitizer / indirect anti-androgenMetformin reduces insulin resistance and indirectly lowers androgen levels by reducing insulin-stimulated androgen production. Particularly relevant for HS patients with PCOS, metabolic syndrome, or diabetes. Some small studies show modest benefit in HS.
Primarily used for diabetes and metabolic conditions. Discuss with your physician.
HS Across Hormonal Life Events
Puberty
HS typically begins after puberty, when androgens surge. The mean age of onset is 21-23 years. Early-onset HS (before age 18) is associated with more severe disease.
Pregnancy
HS behavior during pregnancy is unpredictable. Some women improve (possibly due to immune modulation), while others worsen. See our dedicated HS and Pregnancy guide for detailed information.
Read the HS and Pregnancy GuidePostpartum
Many women experience HS flares in the weeks after delivery, corresponding to the rapid hormonal shift and return of menstrual cycling.
Perimenopause
The hormonal fluctuations of perimenopause can trigger or worsen HS in some women. The transition period may be more problematic than established menopause.
Menopause
Most women with HS report improvement or remission after menopause, consistent with the role of cyclical hormonal fluctuations in disease activity. This is one of the strongest pieces of evidence for hormonal involvement in HS.
PCOS
Polycystic ovary syndrome (PCOS), a condition characterized by androgen excess and insulin resistance, is significantly more common in women with HS. Women with both conditions may benefit particularly from anti-androgen treatments.