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Updated: Aug 24, 2026
Measuring Psoriasis Severity at Home
Published on: March 1, 2024
Sex Hormones in Psoriatic Disease: A Systematic Review
Yueqiao Cai1,2,3, Hui Xiao1,2,3,4, Yinli Zhou1,2,3
1Department of Dermatology, Hunan Key Laboratory of Skin Cancer and Psoriasis, Hunan Engineering Research Center of Skin Health and Disease, Xiangya Clinical Research Center for Cancer Immunotherapy, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, 410008, Hunan, China.
Background:
Psoriasis (PsO) and psoriatic arthritis (PsA) are closely related inflammatory diseases with marked sex differences. Disease activity often fluctuates during major endocrine transitions such as pregnancy and menopause. However, the impact of sex hormones on PsO and PsA remains incompletely understood.
Objective:
To summarize clinical associations and immunomodulatory roles of sex hormones in PsO and PsA.
Methods:
Following PRISMA guidelines, we systematically searched PubMed, Embase, Web of Science, Scopus, and the Cochrane Library from inception to 10 December 2025. Eligible studies included clinical and supportive preclinical evidence on estrogens, progesterone, androgens, prolactin, and related hormonal factors in PsO and PsA. Clinical study quality was assessed using Joanna Briggs Institute tools.
Results:
A total of 72 studies were included. High-estrogen states (e.g., pregnancy) are associated with improvement or low disease activity in PsO, whereas postpartum and menopause are high-risk periods for relapse. Evidence for PsA is limited and inconsistent, although postpartum may be a higher-risk window for worsening. Evidence on menopausal hormone therapy remained inconclusive and appeared to vary by formulation, timing, and population; experimental lesion-targeted hormonal approaches are being explored. In male patients, circulating testosterone levels are frequently reduced and may be associated with disease severity, metabolic comorbidities, and reproductive dysfunction. Prolactin may also contribute to psoriatic inflammation, particularly through stress-related and local tissue pathways.
Conclusions:
Fluctuations in estrogen and progesterone associated with female life stages, as well as reduced androgen levels in males, may influence disease activity. PsO often improves during pregnancy but may worsen postpartum or around menopause, while altered prolactin signaling may also be involved. Evidence for PsA and hormone-based interventions remains limited and inconsistent. Clinicians should consider closer monitoring during major hormonal transitions, while further mechanistic and clinical validation is needed to clarify the role of sex hormones in psoriatic disease.
