A narrative review of Catamenial dermatology: A glimpse into the menstrual symphony

The menstrual cycle induces a wide range of physiological changes in the skin and its appendages, often overlooked in dermatologic practice. Catamenial dermatoses, influenced by hormonal fluctuations, present with cyclical skin manifestations. This review explores the underrecognized intersection between menstruation and dermatology, highlighting changes across menstrual phases such as variations in hydration, lipid levels, pigmentation, hair and nail growth, and sweat gland activity. Autoimmune progesterone dermatitis and estrogen dermatitis are key examples of hormone-induced skin responses. These conditions have complex pathogenesis, variable clinical features, and present diagnostic challenges. Treatment options include hormonal suppression and newer therapies such as omalizumab. The review also examines the link between menstruation and increased susceptibility to infections, as well as the flare of preexisting dermatoses. Conditions such as acne, psoriasis, and atopic dermatitis may worsen in relation to hormonal shifts. Understanding the cyclical responses of skin to endogenous hormones can help clinicians better identify and manage hormone-responsive dermatoses, ultimately improving diagnosis and patient care.

Catamenial menstruation progesterone hypersensitivity autoimmune progesterone dermatitis menstrual toxic shock syndrome cutaneous endometriosis.

The menstrual cycle orchestrates a silent symphony within a woman’s body, influencing various physiological systems, including the skin and appendages. The term “catamenial” is derived from the Greek word “katamenia,” which refers to the monthly menstrual flow. Catamenial dermatoses, also known as menstrual-related skin disorders, represent a unique and often under-recognised category of dermatological conditions that are influenced by the hormonal fluctuations of the menstrual cycle. These conditions can significantly impact the quality of life for affected individuals, often presenting with cyclical exacerbations that coincide with specific phases of the menstrual cycle.1-4 Despite their prevalence, catamenial dermatoses are frequently overlooked or misdiagnosed, leading to prolonged patient discomfort and distress. This narrative review aims to provide a comprehensive overview of the current knowledge of catamenial dermatoses, including their pathophysiological mechanisms, clinical manifestations, diagnostic challenges, and management strategies. We conducted a comprehensive English literature search across multiple databases, including PubMed, SCOPUS, EMBASE, MEDLINE, and Cochrane. Using various Boolean operators, we searched with keywords such as ‘menstrual cycle,’ ‘menses,’ ‘skin,’ ‘catamenial dermatoses,’ ‘catamenial dermatology,’ ‘cyclic dermatoses,’ ‘hormone,’ ‘estrogen,’ and ‘progesterone’ individually and in combinations. Our search yielded 68 relevant articles. Additionally, we analysed the references of these articles for further relevant content. Hormonal changes in the menstrual cycle Menstruation marks the start of the cycle (Day 1). During the follicular phase (typically Days 7–14), the ovaries secrete oestrogen, with oestradiol, the most potent form, peaking one day before ovulation. The luteal phase begins after ovulation, around Day 14, and lasts until Day 28. In this phase, the corpus luteum develops, producing progesterone, while oestradiol levels rise again about five days post-ovulation. As the luteal phase concludes, declining levels of oestrogen and progesterone trigger the onset of menstruation.5 Circulating sex hormones, namely, oestrogens, progesterone, and androgens, play a key role in skin homeostasis. Oestrogen receptors are widely distributed in the epidermis and dermis, with Estrogen Receptor-β predominantly present in basal keratinocytes, sebocytes, and eccrine sweat glands and ER-α in the sebocytes. In contrast, progesterone receptors are mainly found in the nuclei of the keratinocytes and sebocytes. Androgen receptors are seen in keratinocytes, about 10% of dermal fibroblasts, sebaceous gland basal cells, sebocytes, and the hair follicle dermal layer, though rare in eccrine sweat glands. This distribution suggests that menstrual cycle–related hormonal changes may significantly influence skin cell activity and contribute to cutaneous disease.6,7 Table 1 outlines the normal effects of various hormones on the skin and its adnexal structures.5-11 | Effect of oestrogen | Stimulation of melanogenesis | Increase mitotic activity in the epidermis | Increase skin thickness | Reduce sebum (high levels) | Decreased collagen breakdown and increased collagen production | Increased water-binding capacity and increased fluid retention | Immunomodulation | Increased vasodilation, increased elasticity | Macrophage polarisation M1 to M2 | Reduction in inflammation and oxidative stress | Reduction of proteolysis in the extracellular matrix | Increase in granulation, angiogenesis, re-epithelialisation, and wound contraction | | Effect of progesterone | Increases sebum production and influences hair follicle sensitivity to androgens. | Stimulates melanin synthesis, leading to increased skin pigmentation. | Induces peripheral vasodilation, contributing to increased skin temperature and vascular permeability in the vulva/vagina. | Reduces epidermal water loss and stimulates vaginal epithelial cell proliferation. | Modulates immune responses by suppressing Th1 and increasing Th2 cytokine production. | Increases production of thick cervical mucus | | Effect of androgens | Increases sebocyte proliferation, boosting sebum production via androgen receptor activation. | Prolongs the anagen phase of hair growth in androgen-sensitive areas, promoting terminal hair development. | Stimulates fibroblast collagen synthesis, increasing dermal thickness. | Enhances angiogenesis, potentially promoting wound re-epithelialization. | Modulates cutaneous cytokine expression, influencing the pathogenesis of inflammatory dermatoses. | May suppress cell-mediated immunity locally in the skin, potentially increasing susceptibility to certain skin infections. | Alters the Th1/Th2 balance in the skin, contributing to the modulation of inflammatory conditions. | Stimulates apocrine gland secretion, contributing to body odour and potentially exacerbating hidradenitis suppurativa. | Induces hair follicle miniaturisation in the scalp via dihydrotestosterone (DHT), leading to androgenetic alopecia. | Modulates the production of antimicrobial peptides by sebaceous glands, influencing skin microbiome dynamics. | Physiological effects on skin and appendages In skin Fluctuating hormone levels cause numerous physiological changes in the skin. Skin thickness, subcutaneous fat, and elasticity vary throughout the menstrual cycle. However, the data is limited, and the mechanisms are unclear.3 Increased transepidermal water loss, surface lipids, and microflora have been reported in the luteal phase. The skin is drier during menses and the early proliferative phase. A study found that women were very susceptible to ultraviolet light during days 20 to 28 of the menstrual cycle.4 Sweat glands Internal body temperature increases in the luteal phase, but conflicting or insufficient data exist on sweat rate and mean skin temperature changes during the menstrual cycle.12 Hair “Bad hair days” (BHD) are when many women complain that their hair is periodically unmanageable. Interestingly, a study found that though BHDs occurred throughout the menstrual cycle, they were more common during menstruation.13 Nails The nails grow faster in the premenstrual phase. Physiological Beau’s lines and transverse leukonychia may be seen with each menstrual cycle.14 Catamenial pigmentary changes Sex steroids can regulate pigmentation, but the mechanisms are not clear. Oestrogen increases the activity of melanogenic enzymes through the melanocyte oestrogen receptors. Androgens also regulate pigmentation through their effects on cyclic Adenosine Monophosphate (cAMP).15 Increased pigmentation has been reported in the luteal phase in small studies, in the peri-ocular region with questionnaires, and in the cheek and under-eye area based on colour reflectance.16,17 Aberrant skin response to hormones Autoimmune progesterone dermatitis Autoimmune Progesterone Dermatitis (APD) was initially described in 1964.18 APD, now proposed to be renamed as progesterone hypersensitivity (PH) is an infrequent, cyclical, immunological disorder that afflicts women during the progesterone surge in the luteal phase.19-21 Although the precise pathogenesis of this condition remains elusive, the primary mechanism involves exposure to endogenous or exogenous progesterone, provoking hypersensitivity reactions that culminate in the clinical manifestation of the disease. Progesterone, widely used in IVF and intracytoplasmic sperm injection cycles to enhance implantation and pregnancy rates, has been increasingly linked to dermatitis due to supraphysiological doses.19 In a prospective study of 200 IVF patients, Sood et al. found dermatological manifestations in 27%, with urticaria (13.5%) being the most common, followed by acneiform eruptions (3%). Notably, 96.3% of urticaria cases occurred in patients on progesterone.22 Pregnancy-associated APD can be triggered by endogenous progesterone from the corpus luteum and placenta. Symptoms may begin intrapartum, persist postpartum, or arise after childbirth. Paradoxically, preexisting APD may improve intrapartum due to auto-desensitisation from rising progesterone levels or a reduced maternal immune response.19 The classification of APD based on inciting factors has been mentioned in Table 2.23 | Classification | Inciting factor | Timing of symptoms | |---|---|---| | Endogenous | Pregnancy | Symptoms onset during pregnancy and may endure into the postpartum period | | Menses | Symptoms preceding menstruation | | | Exogenous | Supplementary progestins for fertility enhancement or contraception | Onset occurs after exposure to exogenous progestins. | | Mixed | Supplementary progestins for fertility enhancement or contraception | It begins after exposure to exogenous progestins but continues alongside premenstrual or pregnancy symptoms. | The disease onset reaches its peak in the third decade, although it can manifest at any point between menarche and menopause.19 The cutaneous lesions due to endogenous APD typically emerge 3-10 days preceding the onset of menstruation, coinciding with a surge in progesterone levels, and resolve a few days after menses begin. The diversity of symptoms is a distinguishing characteristic of APD. There is a noted propensity for symptoms to evolve within a single individual.24,25 Clinically, it manifests as pruritus, eczema, papulovesicular eruption, maculopapular rash, urticaria, angioedema, stomatitis, erythema multiforme, folliculitis, fixed drug eruption, aphthous ulcers, purpura, erythema annular centrifugum, necrolytic migratory erythema, vulvovaginitis, and labial swelling11,26-32 [Figures 1-3]. Systemically, it can induce asthma and severe anaphylaxis.33 A thorough clinical history and physical examination are often sufficient to diagnose APD. Skin prick and intracutaneous tests are deemed unreliable as diagnostic tools for immediate and delayed PH.19,34 [Figure 4] This unreliability stems from the nature of progesterone as a steroid, which necessitates suspension in oil or ethanol as a diluent, thereby limiting the positive predictive value of test outcomes due to potential irritant-induced reactions from these diluents.35 A study reported a staggering 90% rate of false-positive intracutaneous progesterone skin test responses.36 Skin tests may produce late reactions, requiring prolonged surveillance for accurate assessment.34 Since some authors consider APD an autoimmune disease, tests like the autologous serum test, used in autoimmune urticaria, have been applied in select cases.35 Histological characteristics of APD lack specificity and depend on the morphology of the lesion, with superficial perivascular mixed inflammation being the most consistent pathological finding.31 There are no standardised in vivo or in vitro tests for APD diagnosis. Various case reports propose different testing methods for suspected cases.34 Ghosh et al. have recently pioneered the development of an ELISA progesterone assay, marking a significant advancement in this area of research. This assay’s sensitivity, specificity, and positive and negative predictive values were 82%, 100%, 86%, and 100%, respectively, with the basophil mediator release assay results as the gold standard. The impending commercialisation of this assay promises clinicians access to a more dependable diagnostic tool for PH.37 An alternative method proposed for assessing APD and associated T-cell activity in delayed-type hypersensitivity is the IFN-γ-release assay.38 Treatment for APD is tailored to each patient and hinges on factors such as symptom severity and the individual’s fertility preferences.23 For patients who are not pursuing pregnancy, managing or treating APD may involve suppressing ovulation to halt the secretion of endogenous progesterone. Ovulation can be suppressed with oral contraceptives, danazol, tamoxifen, and gonadotropin-releasing hormone agonists such as leuprolide and nafarelin.20,23,32 In persistent symptoms, hysterectomy and bilateral oophorectomy may be considered as a last resort.21 In women who wish to conceive, oral corticosteroids combined with antihistamines can be given.39 Desensitisation can be employed as a safe alternative for symptom control in patients who want to circumvent the potential adverse effects linked with the hormonal agents. 27,33 Omalizumab could serve as a viable treatment option for individuals experiencing recurrent urticaria or anaphylaxis.40,41 A Jamaican woman with recurrent Stevens-Johnson-type reactions, provisionally diagnosed with APD linked to prostaglandin release, showed a positive prick test for 0.01 mL of a PG-F2 analogue. After a hysterectomy for endometriosis-related complications, her symptoms resolved completely.42 Oestrogen dermatitis Oestrogen dermatitis is an uncommon cutaneous reaction to fluctuating endogenous oestrogen levels during the menstrual cycle. Initially, it was proposed by Shelly et al. in 1995 based on premenstrual exacerbations of skin lesions among seven women.43-45 The underlying mechanisms of oestrogen dermatitis have yet to be fully elucidated. Clinically, it can present as generalised pruritus, papulovesicular, bullous, prurigo multiforme, urticarial, or eczematous lesions. The cutaneous lesions typically appear 14 days pre-menstrually and remit shortly after menstruation. A positive immediate or delayed reaction to intradermal oestrogen supports the diagnosis.44,46 Therapeutic options for oestrogen dermatitis include oestrogen desensitisation, tamoxifen, leuprolide, omalizumab, and oophorectomy. Oestrogen-induced dermatitis, even resistant to oophorectomy, has demonstrated a favourable response to treatment with omalizumab.44,46 A comparative overview of APD and oestrogen dermatitis has been mentioned in Table 3.23,29,44,45 The menstrual cycle and the related conditions have been depicted in Figure 5. | Aspect | APD | Oestrogen Dermatitis | |---|---|---| | Aetiology | Autoimmune reaction to endogenous or exogenous progesterone. | Hypersensitivity reaction to oestrogen, often during hormone therapy or changes in hormonal levels. | | Trigger | Progesterone fluctuations, especially during the luteal phase of the menstrual cycle or hormone therapy involving progesterone. | Oestrogen fluctuations, particularly during hormone therapy or phases of the menstrual cycle with increased oestrogen levels. | | Onset | 3 – 10 days before the onset of menses | 14 days prior to the onset of menses | | Clinical presentation | Urticaria, eczema, erythema, papules, vesicles, and sometimes severe anaphylaxis. Lesions often appear in cyclical patterns. | Eczema, erythema, itching, and other dermatitis symptoms are often less cyclic but can be associated with periods of high oestrogen. | | Diagnosis | History of cyclic symptoms, progesterone skin test, and serum progesterone levels. Symptom resolution after suppressing ovulation can confirm the diagnosis. | Clinical history, oestrogen skin test, and serum oestrogen levels. The correlation between symptoms and oestrogen peaks helps in the diagnosis. | | Management | Avoidance of progesterone exposure, use of hormone therapy to suppress ovulation, corticosteroids, and antihistamines. In severe cases, oophorectomy might be considered. | Avoidance of oestrogen exposure, adjusting hormone therapy, corticosteroids, and antihistamines. In some cases, switching to non-estrogenic hormone therapy might be necessary. | | Prognosis | It can be well-managed with appropriate hormonal and symptomatic treatment, though complete resolution can be challenging. | Generally manageable with adjustments to hormone therapy and symptomatic treatment. Prognosis varies with underlying conditions and response to therapy. | Menstruation and sexually transmitted infections Studies show that 50–66% of females have had sex during menstruation, while 4–43% engage in it regularly. Cyclic changes in the vaginal microbiome and immunity may weaken antimicrobial defences, especially in those not using hormonal contraceptives.47 As HIV has been identified in menstrual secretions, intercourse during menses renders the male partner more susceptible to acquiring HIV.48 Decrease in iron and complement function during menstrual flow may facilitate colonisation, invasion, and ascending infection by Neisseria gonorrhoeae.49 The majority of disseminated gonococcal infections develop during or immediately after menstruation.50 A cross-sectional study of 1200 women found an increased risk of bacterial vaginosis in women engaging in sexual intercourse during menses.51 A survey revealed a significant statistical association between intercourse during menses and self-reporting of sexually transmitted infections, such as HIV, Trichomonas vaginalis, bacterial vaginosis, syphilis, chancroid, genital herpes, condyloma acuminata, chlamydia, gonorrhoea, and hepatitis B.52 Herpes simplex may recur during pre-menstrual, menstrual, and immediate post-menstrual periods (‘herpes menstrualis’). Rarely, regular recurrences may be seen during pregnancy or after menopause.53 Dermatoses exacerbated with menstruation Several dermatoses are reported to be exacerbated peri-menstrually [Table 4].7,50,54-77 Perimenstrual exacerbations of dermatological conditions primarily stem from fluctuations in sex hormones, notably oestrogen and progesterone, and their modulation of inflammatory pathways. Pre-menstrual acne flares occur due to multiple factors [Figure 6]. Elevated androgens and oestrogens in the follicular phase and around ovulation increase sebum production and skin lipids, promoting microflora growth. Consequently, low progesterone levels later in the menstrual cycle contribute to acne exacerbation.56,57 Nearly half of atopic eczema patients experience a flare-up in the week before menstruation, which quickly improves once bleeding begins. Increased skin permeability during this time makes the skin more vulnerable to allergens and irritants, contributing to these pre-menstrual flares.58,59 Acne vulgaris | Anogenital pruritus | Aphthous ulceration | Atopic eczema | Autoimmune progesterone dermatitis | Autoimmune oestrogen dermatitis | Beau’s lines | Behcet’s syndrome | Bullous pemphigoid | Contact dermatitis | Cholestatic pruritus | Darier’s disease | Dermographism | Dermatitis herpetiformis | Erosive adenomatosis of nipple secretions | Erythema annular centrifugum | Erythema multiforme | Exercise-induced angioedema | Flushing of face | Gardner-Diamond Syndrome | Glomangiona | Glossodynia | Hand eczema | Hailey-Hailey disease | Hobnail haemangioma | Haemangioma | Hereditary angioedema | Herpes simplex | Hidradenitis suppurativa | Impetigo herpetiformis | Keratolytic winter erythema | Leukonychia | Lichen planus | Lupus erythematosus | Melasma | Neuroticism | Naevus of Ota fluctuation in the intensity of colour | Pemphigoid gestationis | Pompholyx | Psoriasis | Pyoderma gangrenosum | Raynaud phenomenon | Recurrent vulvovaginal candidiasis | Rosacea | Solitary fibrous tumour | Translucent periocular skin | Trichotillomania | Trimethylaminuria odour | TNF Receptor-Associated Periodic Syndrome (TRAPS) | Ulcerative stomatitis | Urticaria | Varicose veins cutaneous symptoms | Hidradenitis suppurativa, though more closely associated with androgens, can experience perimenstrual exacerbations due to fluctuations in androgen sensitivity and progesterone’s impact on apocrine glands and inflammation.60,61 A survey conducted among patients indicated that 204 out of 279 women (approximately 76.7%) observed a deterioration in symptoms related to hidradenitis suppurativa during menstruation.78 Premenstrual hormonal shifts in psoriasis can disrupt immune responses and trigger a rebound of inflammatory cytokines, leading to flare-ups.58,62 Premenstrual aphthous ulcers may stem from oestrogen-induced changes in mucosal immunity.63 The depigmented macules in vitiligo have been reported to become pink or red in some young girls and women during menstruation (Punshi’s sign).79 Exacerbation or recurrence of allergic contact dermatitis during the immediate premenstrual period is common. The follicular phase of the menstrual cycle reduces the sensitised state.80 Hence, false-negative patch test readings are common during this phase.81 Catamenial exacerbations of skin neoplasms such as hobnail haemangioma, arteriovenous haemangioma, and solitary fibrous tumour have been reported.82 Cutaneous endometriosis Cutaneous endometriosis is a rare but well-recognised condition, accounting for 0.5%–1% of all endometriosis cases. Umbilical endometriosis, the most common type, was first described by Villar in 1886. It can be classified as primary or secondary based on surgical history. Primary umbilical endometriosis, or Villar’s nodule, occurs spontaneously in about 30% of cases, with an unclear aetiology. Secondary endometriosis typically follows abdominal or pelvic surgery due to lesion seeding.83 Clinically, it presents as a firm subcutaneous papule or nodule, varying in colour from skin-coloured to blue or violaceous brown. Patients typically experience cyclical pain, swelling, and occasional bleeding corresponding with their menstrual cycle. Although the umbilicus is the most common site, other locations, such as episiotomy wounds, appendectomy scars, caesarean scars, groin, and arm, have also been documented.84-90 Fine needle aspiration cytology should be avoided to prevent the seeding of endometriotic tissue in new areas.89 Surgical excision with a safety margin of at least 1 cm from the skin lesion is diagnostic and therapeutic.90 Hormonal agents that decrease the proliferation of endometrial tissue, such as oral contraceptives, danazol, and gonadotropin-releasing hormone agonists, may be considered. Recurrence following treatment and malignant transformation with histology indicative of endometrioid or clear cell carcinoma are potential complications associated with this condition.83,85 Vicarious menstruation Vicarious menstruation can be defined as extraneous bleeding originating from a location other than the uterine mucous membrane, coinciding with the expected onset of regular menstruation. Vicarious menstruation is a risk factor for haematohidrosis, a rare condition in which a patient sweats blood.91,92 Dermatoses related to the use of menstrual hygiene products Menstrual Toxic Shock Syndrome (mTSS) is a rare, life-threatening disease precipitated by superantigen-producing Staphylococcus aureus. Until the late 1970s, cotton was the primary absorbent material in tampons; however, manufacturers’ introduction of synthetic superabsorbent fibres led to significant Toxic shock syndrome toxin-1 (TSST-1) production.54,93,94 The incidence of Toxic Shock Syndrome (TSS) reached its peak in the early 1980s, after which there was a decrease in menstrual TSS cases attributed to mandatory tampon labelling and enhanced patient education. Overall rates of TSS have remained relatively consistent since the late 1980s, currently ranging from 0.8 to 3.4 per 1,00,000 adults and 0.4 per 1,00,000 in children.94,95-97 According to the US Centres for Disease Control and Prevention, TSS is considered menstrual-associated if onset occurs less than four days before the onset of menses. Table 5 mentions the Centre for Disease Control (CDC) case definition of TSS.97 The development of mTSS involves a complex interplay between the use of intravaginal devices such as tampons, the pathogenicity of S. aureus, host immunity, immunological mechanisms, and alterations in the vaginal ecosystem during menstruation. Instances of TSS in adults unrelated to tampon usage have also been documented, including cases associated with menstrual cups and intrauterine devices.48 Some cases reported in the paediatric literature have raised doubts about the causal relationship between menstrual TSS and tampon usage.98,99 | Clinical criteria | Fever: ≥ 102.F° | Rash: diffuse macular erythroderma | Desquamation: 1–2 weeks following the appearance of the rash | Hypotension: systolic blood pressure ≤ 90 mm Hg for adults or less than the fifth percentile by age for children aged < 16 years old | Multisystem involvement (three or more of the following organ systems): | Gastrointestinal: vomiting or diarrhoea at the onset of illness | Muscular: severe myalgia or creatine phosphokinase level at least twice the upper limit of normal | Mucous membrane: vaginal, oropharyngeal, or conjunctival hyperaemia | Renal: blood urea nitrogen or creatinine at least twice the upper limit of normal for the laboratory, or urinary sediment with pyuria (greater than or equal to 5 leukocytes per high-power field) in the absence of urinary tract infection | Hepatic: total bilirubin, alanine aminotransferase enzyme, or aspartate aminotransferase enzyme levels at least twice the upper limit of normal laboratory | Hematologic: platelets less than 1,00,000/mm3 | Central nervous system: disorientation or alterations in consciousness without focal neurologic signs when fever and hypotension are absent | Laboratory Criteria: Negative results on the following tests, if obtained: | Blood or cerebrospinal fluid cultures: blood culture may be positive for Staphylococcus aureus | Negative serologies for Rocky Mountain spotted fever, leptospirosis, or measles | Probable TSS - Laboratory criteria and four of the five clinical criteria. | Confirmed TSS - Laboratory criteria and all 5 of the clinical criteria, unless the patient dies before desquamation occurs | TSS: Toxic shock syndrome This is corroborated by case studies of adolescents who continued to experience recurring TSS episodes despite discontinuing tampon use.100,101 TSST-1 adheres to human vaginal epithelial cells, potentially through the CD40 receptor, and in conjunction with cytolysins, triggers the generation of pro-inflammatory chemokines, such as IL-8. This cascade of events ultimately results in the infiltration of cells from both the innate and acquired immune systems into the submucosa, leading to the deterioration and increased permeability of mucous membrane barriers.102 Clinically, patients with mTSS typically present with widespread macular erythema that resolves within three days; however, papulopustular and scarlatiniform eruptions are rarely described. Marked oedema of the feet and hands, accompanied by indolent blistering, may also be observed. Generalised erythema of the conjunctiva, oral, oesophageal, bladder, and vaginal mucosa may be present. Later in the second week, most patients develop widespread, pruritic, maculopapular, and sometimes urticarial lesions. Retiform purpura at the peripheries occurs secondary to low platelet count. A highly characteristic finding of mTSS is desquamation, which occurs 10–21 days after the onset of the disease. It may be limited to the fingertips, involve all the plantar and palmar skin.51.102,103 A clinical assessment should be conducted to locate tampons, which should be removed if found. Comprehensive general supportive interventions are crucial, including fluid resuscitation and ventilatory assistance. The initial treatment of choice involves administering intravenous clindamycin at 600–900 mg three times daily for up to 1-2 weeks based on the patient’s clinical response.51 A systematic review on Intravenous Immunoglobulin (IVIG) use highlighted the superior efficacy of polyclonal IVIG in treating TSS, with human-derived poly immunoglobulins offering better neutralisation than synthetic or animal-derived alternatives. IVIG works by neutralising superantigens, effectively treating both staphylococcal and streptococcal TSS.104 Sanitary napkin irritant contact dermatitis occurs secondary to wet local conditions and friction caused by sanitary napkins. It presents as pruritic dermatitis lesions on the vulva and occasionally on the perineal regions.105 Allergenic fragrances were identified in products such as tampons and sanitary napkins. The well-known skin-sensitising chemicals found to leach from menstrual hygiene products include α-isomethyl ionone, hexyl cinnamaldehyde and heliotropine, and benzyl salicylate.106 Colophonium in sanitary napkins can also produce vulvar contact dermatitis.107 Systemic contact dermatitis due to acrylates in the sanitary pads is known to occur.108 Menstrual hygiene products are known to induce symptoms resembling vulvodynia.109 A systematic review on menstrual cup usage identified several adverse effects, including discomfort during insertion and removal, vaginal injuries, irritation of the vagina or cervix, allergic contact dermatitis caused by silicone, and the potential risk of TSS.104 Dermatological disorders associated with menstrual irregularities A study reported that, compared to paucibacillary leprosy, female patients with multibacillary leprosy had higher rates of post-onset menstrual irregularities and elevated gonadotropic hormone levels.110 MB leprosy is also linked to autoimmunity, with autoantibodies like Anti-Neutrophilic Cytoplasmic Antibodies (ANCA), anti-mitochondrial, and anti-phospholipid antibodies, suggesting immune-mediated ovarian failure.111 Systemic lupus erythematosus is associated with a higher prevalence of menstrual irregularities, including amenorrhoea, oligomenorrhoea, and menorrhagia. These disturbances may result from disease activity, systemic inflammation, and the use of immunosuppressive therapies.112,113 Dermatosurgery and menstruation Menstrual irregularities have been reported in some patients, especially associated with liposuction in the lower abdomen and upper thigh areas.114 One study reported that the risk of post-inflammatory hyperpigmentation following CO2 fractionated laser treatment was highest just before or after menstruation, at the end of the luteal phase.115 Drugs and the menstrual cycle The drugs used by dermatologists that can produce menstrual irregularities have been mentioned in Table 6.54,55 | Antiandrogenic effects | Cyproterone acetate | Danazol | Flutamide | Finasteride | Effect on hormones | Tranexamic acid | Oral contraceptives | Immunosuppressants | Systemic corticosteroids | Methotrexate | Cyclophosphamide | Miscellaneous | Griseofulvin | Isotretinoin | Ketoconazole | Spironolactone | Thalidomide |

In conclusion, catamenial dermatoses represent a fascinating and clinically significant area of dermatology that warrants greater attention and understanding. By fostering interdisciplinary collaboration and continuing to explore the hormonal underpinnings of these conditions, we can enhance the quality of care for patients experiencing these challenging and often debilitating skin disorders. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest. Use of artificial intelligence (AI)-assisted technology for manuscript preparation The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

- The effect of menopause on the skin and other connective tissues. Gynecol Endocrinol. 2012;28:273-7. - [CrossRef] [Google Scholar] - Physiological changes associated with the menstrual cycle: A review. Obstet Gynecol Surv. 2009;64:58-72. - [Google Scholar] - Localization of sex steroid receptors in human skin. Histol Histopathol. 2004;19:629-36. - [Google Scholar] - Catamenial dermatoses associated with autoimmune, inflammatory, and systemic diseases: A systematic review. Int J Womens Dermatol. 2019;5:361-7. - [CrossRef] [Google Scholar] - Impact of progesterone on skin and hair in menopause - a comprehensive review. Climacteric. 2021;24:229-35. - [Google Scholar] - Regulatory roles of sex hormones in cutaneous biology and immunology. J Dermatol Sci. 2005;38:1-7. - [CrossRef] [Google Scholar] - Targeting estrogen signaling and biosynthesis for aged skin repair. Front Physiol. 2023;14:1281071. - [CrossRef] [Google Scholar] - The biological actions of estrogens on skin. Exp Dermatol. 2002;11:487-502. - [CrossRef] [Google Scholar] - Menstrual cycle and thermoregulation during exercise in the heat: A systematic review and meta-analysis. J Sci Med Sport. 2020;23:1134-40. - [CrossRef] [Google Scholar] - ‘Bad hair days’, scalp sebum excretion and the menstrual cycle. J Cosmet Dermatol.. 2003;2:190-4. - [Google Scholar] - Human skin pigmentation: Melanocytes modulate skin color in response to stress. FASEB J. 2007;21:976-94. - [CrossRef] [Google Scholar] - Skin pigmentation in relation to the menstrual cycle. J Invest Dermatol. 1966;47:147-55. - [CrossRef] [Google Scholar] - Exogenous progestogen hypersensitivity and its Increasing association with assisted reproductive techniques (ART)/in vitro fertilization (IVF) Indian Dermatol Online J. 2023;15:24-32. - [Google Scholar] - A focused report on progestogen hypersensitivity. Expert Rev Clin Immunol. 2023;19:357-63. - [CrossRef] [Google Scholar] - Dermatological manifestations in patients undergoing in vitro fertilization: A prospective study. J Cutan Med Surg.. 2018;22:280-4. - [Google Scholar] - Presentation and natural history of progestogen hypersensitivity. Ann Allergy Asthma Immunol. 2019;122:156-9. - [CrossRef] [Google Scholar] - Progesterone hypersensitivity: Case report with favorable evolution. Exp Ther Med. 2019;17:1125-7. - [Google Scholar] - Autoimmune progesterone dermatitis: Case report with history of urticaria, petechiae and palpable pinpoint purpura triggered by medical abortion. S Afr Med J. 2016;106:48-50. - [CrossRef] [Google Scholar] - Autoimmune progesterone dermatitis following vaginal progesterone exposure in pregnancy. Obstet Med. 2019;12:100-2. - [CrossRef] [Google Scholar] - Autoimmune progesterone dermatitis: Clinical presentation and management with progesterone desensitization for successful in vitro fertilization. Fertil Steril. 2011;95:e9-13. - [CrossRef] [Google Scholar] - Autoimmune progesterone dermatitis associated with infertility treatment. J Am Acad Dermatol. 2008;58:353-5. - [CrossRef] [Google Scholar] - Autoimmune progesterone dermatitis: Update and insights. Autoimmun Rev. 2016;15:191-7. - [CrossRef] [Google Scholar] - Progesterone hypersensitivity: A challenge for Luteal support. J Hum Reprod Sci. 2018;11:79-81. - [CrossRef] [Google Scholar] - Autoimmune progesterone dermatitis: A systematic review. Dermatitis. 2022;33:249-56. - [CrossRef] [Google Scholar] - Progestogen hypersensitivity in 24 cases: Diagnosis, management, and proposed renaming and classification. J Allergy Clin Immunol Pract. 2016;4:723-9. - [CrossRef] [Google Scholar] - Progesterone autoimmune dermatitis with positive autologous serum skin test result. Obstet Gynecol. 2011;117:495-8. - [Google Scholar] - Intradermal testing for autoimmune progesterone dermatitis: Should we be basing the diagnosis on it? Clin Exp Dermatol. 2021;46:906-9. - [CrossRef] [Google Scholar] - Development of a progesterone-specific IgE assay for diagnosing patients with suspected progestogen hypersensitivity. Ann Allergy Asthma Immunol. 2019;122:616-22. - [CrossRef] [Google Scholar] - Three cases of autoimmune progesterone dermatitis. Ann Dermatol. 2017;29:479-82. - [CrossRef] [Google Scholar] - Autoimmune progesterone dermatitis: A retrospective case series. Int J Womens Dermatol.. 2022;8:e009. - [CrossRef] [Google Scholar] - Anaphylaxis due to progesterone hypersensitivity successfully treated with omalizumab. J Allergy Clin Immunol Pract. 2017;5:852-4. - [CrossRef] [Google Scholar] - Catamenial dermatoses: Has anyone ever considered prostaglandins? Clin Exp Dermatol. 2014;39:509-12. - [CrossRef] [Google Scholar] - Estrogen dermatitis: Case report and examination of estrogen receptor-β in the skin. J Dermatol. 2019;46:263-6. - [Google Scholar] - Treatment of estrogen-induced dermatitis with omalizumab. JAAD Case Rep. 2019;5:481-3. - [CrossRef] [Google Scholar] - Bullous autoimmune estrogen dermatitis. J Am Acad Dermatol. 2003;49:130-2. - [CrossRef] [Google Scholar] - Analyzing the association between menstrual coitus and endometriosis’ pathogenesis: A narrative review. Womens Health (Lond).. 2025;21:17455057241305072. - [Google Scholar] - Sexual transmission of human immunodeficiency virus: Virus entry into the male and female genital tract World Health Organization, global programme on acquired immune deficiency syndrome. Fertil Steril. 1990;54:1-18. - [Google Scholar] - Susceptibility to gonococcal infection during the menstrual cycle. JAMA. 2000;283:1291-2. - [CrossRef] [Google Scholar] - Bolognia JL, Schaffer JV, Cerroni L, eds. Dermatology (4th edition). China: Elsevier; 2018. - Douching in relation to bacterial vaginosis, lactobacilli, and facultative bacteria in the vagina. Obstet Gynecol. 2002;100:765. - [CrossRef] [Google Scholar] - Does intercourse during menses increase the risk for sexually transmitted disease? Arch Gynecol Obstet. 2010;282:627-30. - [CrossRef] [Google Scholar] - Bacterial Infections. In: Griffiths C, Barker J, Bleiker TL, eds. Rook’s Textbook of Dermatology (9th ed). United Kindgdom: Wiley Blackwell; 2016. p. :667-752. - [Google Scholar] - The Skin at Different Ages. In: Sacchidanand S, Oberai S, Inamdar AC, eds. IADVL Textbook of Dermatology (4th ed). Mumbai: Bhalani; 2016. p. :122-8. - [Google Scholar] - The effect of the menstrual cycle on acne. J Am Acad Dermatol. 2001;45:957-60. - [CrossRef] [Google Scholar] - Variations of symptoms of atopic dermatitis and psoriasis in relation to menstrual cycle. J Am Acad Dermatol. 2022;87:892-5. - [CrossRef] [Google Scholar] - The influence of pregnancy and menstruation on the deterioration of atopic dermatitis symptoms. Ann Dermatol. 2010;22:180-5. - [CrossRef] [Google Scholar] - Endocrinologic Aspects of Hidradenitis Suppurativa. Dermatol Clin. 2016;34:45-9. - [CrossRef] [Google Scholar] - Special considerations for women with hidradenitis suppurativa. Int J Womens Dermatol. 2020;6:85-8. - [CrossRef] [Google Scholar] - Psoriasis: Female skin changes in various hormonal stages throughout life--puberty, pregnancy, and menopause. Biomed Res Int. 2013;2013:571912. - [Google Scholar] - Causal associations between estradiol and mouth ulcers: A Mendelian randomization study. Medicine (Baltimore). 2024;103:e37989. - [CrossRef] [Google Scholar] - Gardner-Diamond syndrome: Psychogenic purpura with premenstrual flare. Indian J Dermatol Venereol Leprol 2025:1-3. - [CrossRef] [Google Scholar] - Premenstrual flares of pyoderma gangrenosum controlled with use of a combined oral contraceptive and antiandrogen (ethinyl estradiol/drospirenone) Br J Dermatol. 2016;174:1096-7. - [CrossRef] [Google Scholar] - Recurrent erythema multiforme triggered by progesterone sensitivity. J Cutan Pathol. 2010;37:1164-7. - [CrossRef] [Google Scholar] - The diagnosis and treatment of nail disorders. Dtsch Arztebl Int. 2016;113:509-18. - [CrossRef] [Google Scholar] - Recognizing presentations of pemphigoid gestationis: A case study. Case Rep Obstet Gynecol. 2014;2014:415163. - [CrossRef] [Google Scholar] - Clinical characteristics of rosacea in perimenopausal women. Skin Res Technol. 2024;30:e13542. - [CrossRef] [Google Scholar] - Self-reported flaring varies during the menstrual cycle in systemic lupus erythematosus compared with rheumatoid arthritis and fibromyalgia. Rheumatology (Oxford). 2011;50:703-8. - [CrossRef] [Google Scholar] - Recurrent vulvovaginal candidiasis. Am J Obstet Gynecol. 2016;214:15-21. - [CrossRef] [Google Scholar] - The association of menstrual cycle, pregnancy, and menopause with recurrent oral aphthous stomatitis: A review and critique. Obstet Gynecol. 1992;80:455-8. - [Google Scholar] - Impetigo herpetiformis: Menstrual exacerbations for 7 years postpartum. J Eur Acad Dermatol Venereol. 2005;19:466-9. - [Google Scholar] - Exacerbation of Behçet’s syndrome and familial Mediterranean fever with menstruation. Clin Exp Rheumatol.. 2017;35:95-9. - [Google Scholar] - Hormonally exacerbated hereditary angioedema. Australas J Dermatol. 1992;33:35-8. - [CrossRef] [Google Scholar] - Menses, pregnancy, delivery, and menopause in hidradenitis suppurativa: A patient survey. Int J Womens Dermatol. 2020;6:368-71. - [CrossRef] [Google Scholar] - Nickel contact allergy and menstrual cycle. Contact Dermatitis. 2005;52:309-13. - [CrossRef] [Google Scholar] - Catamenial exacerbations of cutaneous neoplasms. Dermatol Surg. 2020;46:1235-6. - [CrossRef] [Google Scholar] - Endometriosis beyond the Pelvis: A case series of cutaneous endometriosis and literature review. Open J Obstet Gynecol. 2024;14:77-88. - [CrossRef] [Google Scholar] - Extrapelvic endometriosis: A rare entity or an under diagnosed condition? Diagn Pathol. 2013. ;8:194. - [Google Scholar] - Cutaneous endometriosis: a case report and review of the literature. Am J Case Rep. 2021;22:e932493. - [CrossRef] [Google Scholar] - Abdominal scar endometriosis: A case report and review of literature. Indian J Pathol Microbiol. 2023;66:871-3. - [CrossRef] [Google Scholar] - Scar endometriosis: A case report with literature review. Acta Med Iran.. 2015;53:793-5. - [Google Scholar] - Endometriosis node in gynaecologic scars: A study of 17 patients and the diagnostic considerations in clinical experience in tertiary care center. BMC Womens Health.. 2015;15:13. - [Google Scholar] - The clinical characteristics and surgical approach of scar endometriosis: A case series of 14 women. Bosn J Basic Med Sci. 2018;18:275-8. - [Google Scholar] - An interesting case report of hematohidrosis. Indian J Psychol Med. 2017;39:83-5. - [CrossRef] [Google Scholar] - Toxic-shock syndrome associated with phage-group-I staphylococci. Lancet. 1978;2:1116-8. - [CrossRef] [Google Scholar] - Tri-state toxic-shock syndrome study II clinical and laboratory findings. J Infect Dis. 1982;145:441-8. - [Google Scholar] - Toxic shock syndrome in patients younger than 21 years of age, United States, 2006-2018. Pediatr Infect Dis J. 2021;40:e125-8. - [Google Scholar] - Prevalence, comorbidities and mortality of toxic shock syndrome in children and adults in the USA. Microbiol Immunol. 2017;61:463-7. - [CrossRef] [Google Scholar] - Center for disease control. Toxic-shock syndrome: 2011 Case definition. Available at: http://www.cdcgovlibaccesslibmcmasterca/osels/ph_ surveillance/nndss/casedef/toxicsscurrenthtm. Last accessed on 2024 March 24. - Recurrent menstrual toxic shock syndrome with and without tampons in an adolescent. Pediatr Infect Dis J. 2014;33:783-5. - [CrossRef] [Google Scholar] - Toxic shock syndrome of a probable gynecologic source in an adolescent: A case report and review of the literature. J Pediatr Adolesc Gynecol. 2012;25:e133-7. - [CrossRef] [Google Scholar] - A confirmed case of toxic shock syndrome associated with the use of a menstrual cup. Can J Infect Dis Med Microbiol. 2015;26:218-20. - [CrossRef] [Google Scholar] - Fatal toxic shock syndrome from an intrauterine device. Ann Emerg Med. 2009;54:701-3. - [CrossRef] [Google Scholar] - Menstrual toxic shock syndrome: Case report and systematic review of the literature. Lancet Infect Dis. 2019;19:e313-21. - [CrossRef] [Google Scholar] - Toxic shock syndrome: Still a timely diagnosis. Pediatr Emerg Care. 2020;36:e163-5. - [Google Scholar] - Menstrual cup use, leakage, acceptability, safety, and availability: A systematic review and meta-analysis. Lancet Public Health.. 2019;4:e376-e393. - [CrossRef] [Google Scholar] - Sanitary napkin contact dermatitis of the vulva: Location-dependent differences in skin surface conditions may play a role in negative patch test results. J Dermatol. 2007;34:834-7. - [Google Scholar] - Quantitative risk assessment of allergens leaching from menstrual hygiene products. Regul Toxicol Pharmacol. 2022;135:105260. - [CrossRef] [Google Scholar] - Assessment of vulvodynia symptoms in a sample of U.S. women: A follow-up national incidence survey. J Womens Health (Larchmt).. 2008;17:1285-92. - [CrossRef] [Google Scholar] - Menstrual irregularities, fertility status, and ovarian function in female patients with leprosy in India. Int J Dermatol. 2014;53:1114-8. - [Google Scholar] - Menstrual and gonadal function alterations in women with systemic lupus erythematosus. J Assoc Physicians India. 2015;63:38-42. - [Google Scholar] - Menstrual irregularity, pregnancy outcomes, and birth outcomes in patients with systemic lupus erythematosus of childbearing age in China: A multicenter cross-sectional study. Chin Med J (Engl). 2023;136:2886-8. - [CrossRef] [Google Scholar] - Manual Liposuction. In: Venkataram M, ed. ACS(I)Textbook of 2nd ed. New Delhi: Jaypee; 2018. p. :1089-99. - [Google Scholar] - The effect of menstrual cycle on laser induced hyperpigmentation. J Drugs Dermatol. 2013;12:1335-6. - [Google Scholar]