Does Hormone Replacement Therapy Cause Melasma?

Hormone replacement therapy can contribute to melasma in some women, but the evidence linking HRT directly to new or worsening dark patches is surprisingly thin. Most of what dermatologists know comes from case reports rather than large clinical trials, and at least one controlled study found no significant pigmentation change from low-dose estrogen therapy. The real picture involves a tangle of factors: the type and dose of hormones, individual skin biology, ultraviolet exposure, and even thyroid health.

How Estrogen Drives Pigmentation at the Cellular Level

The biological plausibility for HRT triggering melasma is strong, even if the clinical proof is not. Melanocytes, the cells that produce skin pigment, carry receptors for sex hormones. When estrogen binds to a specific membrane receptor called GPER on melanocytes, it triggers a signaling cascade that ramps up melanin production through the same pathway that sunlight uses. In laboratory experiments, depleting GPER from melanocytes completely eliminated their pigmentation response to estrogen, confirming that this receptor is the key link between the hormone and darkened skin.¹

Estrogen does not act on melanocytes alone. Lab studies show that sex hormones also stimulate keratinocytes, the cells surrounding melanocytes, to produce pro-pigmentary signals. The combined effect amplifies whatever UV damage is already happening. Researchers have described this as estrogen “amplifying the effects of UV on melanogenesis” through both direct effects on melanocytes and indirect effects through neighboring cells.² Progesterone plays a role too, acting through its own membrane receptor, though estrogen appears to be the stronger pigment promoter. Both hormones regulate key enzymes and transcription factors involved in pigment synthesis.³

What the Clinical Evidence Actually Shows

Given the clear laboratory evidence, you might expect large studies documenting melasma outbreaks among HRT users. They don’t exist. A 2025 review of all available evidence concluded that the data linking HRT to melasma is limited and consists largely of case reports.⁴ That is a remarkably weak evidence base for a question that has been around for decades.

One of the few controlled studies directly measuring pigmentation in HRT users found no significant change. Researchers tracked women with pre-existing hyperpigmented lesions who started HRT, measuring pigment levels at three different skin sites over three months. None of the sites showed significant pigment alteration. Neither age, duration of menopause, nor hormone levels correlated with pigmentation changes. The authors concluded that low-dose estrogen replacement therapy does not induce pigmentation changes on its own and that individual susceptibility and multiple additional factors beyond sex hormones are likely responsible for melasma development.⁵

The disconnect between laboratory findings and clinical outcomes is telling. Estrogen clearly can stimulate melanocytes in a dish, but in real patients taking real HRT regimens, the effect is either too small to detect in most women or requires additional triggers to become visible. A dermatology review on menopause and skin disorders put it bluntly: there is no association between menopause and melasma, though cases of melasma developing after starting HRT have been reported.⁶

Dose, Formulation, and Route of Delivery

Not all HRT is equal when it comes to melasma risk. The strongest documented association involves high-dose oral estrogen-only therapy, with case reports describing forearm melasma in women with medium to darker skin tones (Fitzpatrick types III through VI). Case reports also exist for combined oral HRT and transdermal formulations (patches and gels), but they are fewer. Topical and vaginal estrogen preparations have minimal evidence linking them to melasma.⁴

This gradient makes pharmacological sense. Oral estrogen undergoes first-pass metabolism through the liver, producing systemic hormone levels that are generally higher and more variable than those achieved by transdermal routes. A patch delivers estrogen directly into the bloodstream at a steadier, lower concentration. Vaginal estrogen, designed for local tissue effects, produces very little systemic absorption. If estrogen dose is a key variable in triggering melanocyte activity, lower-dose and locally acting formulations would logically carry less pigmentary risk.

The historical connection between hormones and melasma actually predates HRT. The association between melasma and oral contraceptive use was first identified in 1963, when the pill delivered far higher estrogen doses than modern formulations.⁷ Much of what people believe about hormones causing melasma may be based on experiences with those older, higher-dose pills rather than today’s lower-dose HRT regimens.

Ultraviolet Light as the Missing Trigger

Hormones alone rarely seem to be enough. The emerging understanding of melasma treats it as a condition driven by an “exposome,” the full set of environmental and internal factors a person’s skin encounters. Ultraviolet radiation, visible light, air pollution, hormonal levels, oxidative stress, thyroid function, and even psychological stress all interact in melasma’s development.⁸

UV exposure consistently emerges as the most potent trigger. Lab data suggests that estrogen does not so much cause pigmentation as amplify whatever UV-driven melanin production is already underway.² In practical terms, a woman on HRT who is diligent about broad-spectrum sunscreen and sun avoidance may face substantially less melasma risk than one with identical hormone levels who spends hours in direct sunlight. This also helps explain why melasma is more common in sunnier climates and in people with greater baseline melanocyte activity (darker skin types), regardless of whether they are taking hormones.

Visible light is an underappreciated contributor as well. Unlike UV, visible light penetrates standard glass and many sunscreens do not block it effectively. Tinted sunscreens containing iron oxides provide better protection against visible-light-driven pigmentation, which is worth knowing if you are already dealing with melasma or are concerned about developing it on HRT.

What Happens to Melasma at Menopause

If estrogen drives melasma, you might expect it to fade once estrogen levels plummet at menopause. The data says otherwise. A large multicenter study in Brazil found that menopause improved melasma in about 29% of women, worsened it in 38%, and had no effect in roughly 30%.⁹ The fact that menopause worsens melasma more often than it helps is a clue that estrogen is not the whole story.

An intriguing pattern also emerged in that research: postmenopausal women were far more likely to develop melasma in locations beyond the face. About 14% of postmenopausal women with melasma had extra-facial involvement, compared with just 3.5% of premenopausal women. This suggests that the hormonal changes of menopause may shift where melasma appears rather than simply turning it on or off.⁹ The forearm melasma reported in some HRT case reports fits this pattern, since it appears to be more common in postmenopausal women receiving exogenous estrogen.⁴

The Thyroid Connection

Melasma has a well-documented relationship with thyroid problems that many women are unaware of. A study examining women with melasma found that 70% of those who developed it during pregnancy or while using oral contraceptives also had thyroid abnormalities, compared with about 39% of women with melasma that had no obvious hormonal trigger.¹⁰

The researchers proposed that estrogen and progesterone may act as triggering factors for melasma specifically in women who are already predisposed through thyroid autoimmunity. In other words, a woman with an underactive thyroid or Hashimoto’s disease who starts HRT may face a higher melasma risk than a woman with normal thyroid function on the same regimen. This is relevant because thyroid disorders are common in perimenopausal and postmenopausal women, precisely the population most likely to use HRT. If you develop melasma after starting hormone therapy, thyroid screening is worth discussing with your doctor.

Blood Vessels Beneath the Dark Patches

Melasma is often thought of as purely a pigment problem, but the skin beneath those dark patches looks different in other ways too. Studies comparing melasma-affected skin with adjacent normal skin have found significantly more blood vessels, both in number and size, in the melasma zones. The expression of vascular endothelial growth factor (VEGF), a protein that promotes new blood vessel formation, was also elevated. There was a significant relationship between the number of vessels and the degree of pigmentation.¹¹

This vascular component matters for the HRT question because estrogen is a known promoter of blood vessel growth. Both estrogen and angiogenesis have been identified as significant factors in melasma’s development, and at least one research team has proposed treating melasma with a combination anti-estrogen and anti-VEGF topical agent.¹² This dual-pathway thinking helps explain why melasma is so stubborn: even if you address the pigment, the underlying vascular changes can keep feeding new melanin production. It also suggests that HRT’s contribution to melasma, where it exists, may work partly through promoting blood vessel growth in the skin rather than through direct melanocyte stimulation alone.

Who Is Most Susceptible

The case reports linking HRT to melasma cluster in women with Fitzpatrick skin types III through VI, which covers most people of Hispanic, Middle Eastern, South Asian, East Asian, and African descent.⁴ This is consistent with melasma’s overall epidemiology: the condition overwhelmingly affects people with more active melanocytes. If you have lighter skin (types I and II), HRT-related melasma is less likely, though not impossible.

Family history matters too. The Brazilian study on menopausal melasma found that extra-facial melasma was associated with both menopause and a family history of the condition.⁹ If your mother or sisters had melasma, your melanocytes may be more reactive to hormonal shifts, whether those shifts come from pregnancy, oral contraceptives, or HRT. A previous personal history of facial melasma also appears to be a risk factor for developing extra-facial patches later, including on the forearms.

The concept of “individual susceptibility and end organ responsiveness” keeps surfacing in the research.⁵ Some women’s melanocytes simply respond more vigorously to hormonal signals than others, which is why two women on identical HRT regimens can have completely different skin outcomes. This variability is real, and it makes individual risk prediction frustratingly difficult.

Practical Considerations If You Are on HRT

If you are considering or already taking HRT and worried about melasma, a few things are worth knowing. First, stopping HRT solely to prevent melasma is rarely justified, given the limited evidence of a strong causal link and the meaningful benefits HRT provides for vasomotor symptoms, bone health, and quality of life. That said, if you develop new hyperpigmentation after starting HRT, the treatment formulation and dose are reasonable things to discuss with your prescriber.

Broad-spectrum sunscreen is the single most effective melasma prevention measure regardless of whether you take hormones. Because visible light also contributes to pigmentation, a tinted sunscreen with iron oxides provides additional protection that a standard chemical or mineral SPF does not. Reapplication every couple of hours during sun exposure matters more than the SPF number on the bottle.

If melasma does appear, standard treatments like topical retinoids, azelaic acid, vitamin C serums, and prescription lightening agents can all be used alongside HRT. The vascular component of melasma means that treatments targeting blood vessels, including certain laser therapies, may be helpful for resistant cases, though recurrence is common regardless of approach.

Forearm Melasma and Unusual Locations

Most people picture melasma as the butterfly-shaped darkening across the cheeks, forehead, and upper lip. The condition was historically defined this way, with the term “chloasma” originally coined to describe dark facial pigmentation in that characteristic butterfly distribution.⁷ But HRT-associated melasma often shows up in atypical locations, particularly the forearms. This pattern of extra-facial involvement appears more common in postmenopausal women and may catch both patients and clinicians off guard because it does not look like “classic” melasma.

If you are postmenopausal and notice persistent brown patches on your forearms or other sun-exposed areas after starting HRT, melasma is worth considering as a diagnosis. Many women and some physicians may not connect forearm hyperpigmentation with hormones because the condition’s textbook description focuses on the face. Awareness of this atypical presentation can prevent unnecessary biopsies or misdiagnosis as sun damage alone, and it can prompt a conversation about whether a dose or formulation change might help.

1
eLife. Sex steroids regulate skin pigmentation through nonclassical membrane-bound receptors
2
PubMed. How hormones may modulate human skin pigmentation in melasma: An in vitro perspective
3
PubMed Central. Hormonal Crosstalk in Melasma: Unraveling the Dual Roles of Estrogen and Progesterone in Melanogenesis
4
PubMed. Does Hormone Replacement Therapy Influence Melasma Development? A Review of the Evidence and Management Guidelines
5
Maturitas. Hormone replacement therapy in women with pre-existing hyperpigmented lesions
6
PubMed Central. Menopause, skin and common dermatoses. Part 2: skin disorders
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8
PubMed Central. The Exposome in Melasma: A Comprehensive Review of Etiology, Mechanisms, and Implications for Management
9
PubMed Central. Menopause and Common Dermatoses: A Systematic Review
10
PubMed. Association of melasma with thyroid autoimmunity and other thyroidal abnormalities and their relationship to the origin of the melasma
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12
PubMed. Melasma treatment: A novel approach using a topical agent that contains an anti-estrogen and a vascular endothelial growth factor inhibitor