An updated clinico-investigative approach to diagnosis of cutaneous hyperandrogenism in relation to adult female acne, female pattern alopecia & hirsutism a primer for dermatologists.

INTRODUCTION: Hyperandrogenism is a clinical state consequent to excess androgen production by the ovary, adrenals, or increased peripheral conversion of androgens. The varied manifestations of hyperandrogenism include seborrhea, acne, infertility, hirsutism, or overt virilization of which adult female acne, hirsutism, and female pattern hair loss are of clinical relevance to dermatologists. AREAS COVERED: We limited our narrative review to literature published during period from 1 January 1985 to Dec 2022 and searched PubMed/MEDLINE, Web of Science (WOS), Scopus, and Embase databases with main search keywords were 'Hyperandrogenism,' 'Female,' 'Biochemical,' 'Dermatological', and 'Dermatology.' We detail the common etiological causes, nuances in interpretation of biochemical tests and imaging tools, followed by an algorithmic approach which can help avoid extensive tests and diagnose the common causes of hyperandrogenism. EXPERT OPINION: Based on current data, total testosterone, sex hormone binding globulin, DHEAS, prolactin, free androgen index, and peripheral androgenic metabolites like 3-alpha diol and androsterone glucuronide are ideal tests though not all are required in all patients. Abnormalities in these biochemical investigations may require radiological examination for further clarification. Total testosterone levels can help delineate broadly the varied causes of hyperandrogenism. Serum AMH could be used for defining PCOM in adults.

Traumatic Anserine Folliculosis and Comedones: The Role of Dermoscopy in Differentiation.

Traumatic anserine folliculosis (TAF) is an under-recognized and under-reported entity that is commonly mistaken as comedonal acne. It is seen in children and young adults and friction has been implicated as a probable factor in its causation. As face is the commonest site, biopsy may not be a feasible diagnostic option. Dermoscopy proves to be a reliable non-invasive diagnostic tool to differentiate these two disorders. In this article, we describe the dermoscopic features of TAF in three patients and also attempt to highlight the clinical and dermoscopic distinction between TAF and comedonal acne.

A prospective study examining isolated acne and acne with hyperandrogenic signs in adult females.

BACKGROUND: Adult female acne (AFA) occurs beyond 25 years of age and can present either as isolated acne or with hyperandrogenic signs. METHODS: 120 females aged ≥ 25 years were evaluated for acne, hirsutism and androgenetic alopecia. Hormonal assessment included total testosterone (TT), sex hormone binding globulin (SHBG), free androgen index (FAI), Anti Mullerian Hormone (AMH), 17-hydroxyprogesterone (17-OHP), dehydroepiandrosterone sulfate (DHEAS), follicle stimulating hormone (FSH), luteinizing hormone (LH), thyroid stimulating hormone (TSH) and prolactin. Polycystic ovary syndrome (PCOS) was diagnosed using Rotterdam's criteria. RESULTS: The mean GAGS score was 15.57 ± 4.04.71.66% females had acne with hyperandrogenic signs (hirsutism, 55.81%; hyperseborrhoea, 65.12%; irregular menses, 36.05%) and 18.33% had increased androgen levels. The group with hyperandrogenic signs had longer duration of disease, truncal acne, significant adolescent acne history, stress, inappropriate diet and PCOS compared to the isolated acne group. The mean androgen levels were higher in the former but the difference was statistically insignificant. CONCLUSIONS: Adult female acne can be associated with hyperandrogenic features though routine hormonal tests may not reveal an underlying abnormality except PCOS. End-organ hypersensitivity is the most plausible explanation and thus justifies the use of antiandrogens in its management.

A prospective study of anti-mullerian hormone and other ovarian and adrenal hormones in adult female acne.

Polycystic ovarian syndrome (PCOS) diagnosis in adult female acne (AFA) is tough owing to unreliable ultrasonography in virgins or obese females and inconsistent hyperandrogenemia. We analyzed hormones in AFA and established a diagnostic cut-off value of anti-mullerian hormone (AMH) for PCOS. Female acne patients aged ≥25 years were assessed with total testosterone (TT), sex hormone binding globulin (SHBG), free androgen index (FAI), AMH, 17-hydroxyprogesterone (17-OHP), dehydroepiandrosterone sulfate (DHEAS), follicle stimulating hormone (FSH), and luteinizing hormone (LH). Rotterdam's criteria defined PCOS. AMH was measured (Access AMH assay) to calculate the diagnostic cut off value using receiver operating characteristic (ROC) curve. Of 120 cases, 25.83% had PCOS. This group had significant clinical hyperandrogenism, truncal and adolescent acne, polycystic ovarian morphology (PCOM), and raised hormones (AMH, TT, FAI, LH, and LH/FSH). AMH levels were significantly higher in the PCOS group (6.91 ± 3.85 ng/mL) and positively correlated with TT, FAI, 17OHP, LH, and LH/FSH ratio. AMH at >5.1 ng/mL (sensitivity-70.97% and specificity-82.02%) predicted PCOS and correlated with PCOM. AMH (>5.1 ng/mL) is useful for diagnosing PCOS and surrogate for hyperandrogenemia and PCOM. Its correlation with hormones in non PCOS AFA highlights its sensitivity to diagnose endocrinological derangements.

A Prospective Study Examining Trigger Factors and Hormonal Abnormalities in Adult Female Acne.

BACKGROUND: Numerous triggers have been implicated in adult female acne including endogenous (hormonal dysfunction and genetic predisposition) and exogenous causes (drugs, cosmetics, sunscreens, stress, and smoking). AIMS: To evaluate the role of various trigger factors in adult female acne and to analyze the androgenic hormone pattern including anti-Mullerian hormone (AMH) in these patients. MATERIALS AND METHODS: Patients having acne of age ≥25 years were analyzed using a pre devised proforma to elicit trigger factors while the severity was graded using the Global Acne Grading System (GAGS). A detailed hormonal assessment was undertaken that assessed total testosterone (TT), sex hormone-binding globulin (SHBG), free androgen index (FAI), AMH, 17-hydroxyprogesterone (17-OHP), dehydroepiandrosterone sulfate (DHEAS), follicle-stimulating hormone (FSH), luteinizing hormone (LH), thyroid-stimulating hormone (TSH), and prolactin. RESULTS: Out of the 165 cases seen and sub-analyzed for triggers, premenstrual flare, diet, cosmetics, and stress were the most commonly implicated causes. Among cosmetics, fairness creams and foundations were implicated. The hormonal analysis revealed deranged values of all hormones with the most common being 17-OHP and AMH. Almost 42.8% patients with DHEAS derangement and 58.75% females with raised 17-OHP suffered from moderate to severe stress. LIMITATIONS: A prospective cohort correlation study of the implicated triggers is needed to confirm the association with adult female acne. CONCLUSIONS: Adult female acne may be triggered by diet, stress, and cosmetics and there is a distinct hormonal milieu that accounts for hyperandrogenemia. We noted high levels of adrenal androgens which have been known to be associated with stress and sleep deprivation. Our study shows the value of counseling adult female acne patients about various acne triggers.

Late leprosy reaction presenting as erythema multiforme-like erythema nodosum leprosum with underlying rifampicin resistance and its potential implications.

Erythema multiforme (EM)-like erythema nodosum leprosum (ENL) is a rare atypical presentation, and its late appearance after the completion of multidrug therapy (MDT) is unusual. We describe the case of a lepromatous leprosy patient who after the completion of MDT presented to us with late EM-like ENL and was found to be resistant to rifampicin. We discuss the implications of this finding and the potential role of resistant bacilli in causing reactions with atypical presentations.

A study comparing the clinical and hormonal profile of late onset and persistent acne in adult females.

BACKGROUND: Adult acne has been classified into two major subtypes: "persistent acne" and "late onset acne". A surrogate marker of hyperandrogenism (HA) in adult female acne is the presence of clinical signs of HA and biochemical hyperandrogenemia. We compared the clinical and hormonal profiles of the two acne subtypes and evaluated the likely source of androgen excess - ovarian or adrenal. METHODS: Female acne patients 25 years of age and older were evaluated for clinical HA. Hormonal assessment included total testosterone (TT), sex hormone binding globulin (SHBG), free androgen index (FAI), anti-Mullerian hormone (AMH), 17-hydroxyprogesterone (17-OHP), dehydroepiandrosterone sulfate (DHEAS), follicle stimulating hormone (FSH), luteinizing hormone (LH), thyroid stimulating hormone (TSH), and prolactin. DHEAS and 17-OHP represented adrenal androgens and AMH indicated ovarian reserve. RESULTS: Of 120 cases, clinical HA was seen in 71.67% while biochemical hyperandrogenemia was detected in only 18.33% of patients. Though late onset was more common in adult acne patients (56.6%), the persistent acne subgroup (43.33%) had a younger age at onset, a past history of adolescent acne (51.92%), truncal predilection (44.23%), polycystic ovary syndrome (PCOS) (44.23%), significant presence of irregular menses (40.38%) and hirsutism (57.69%), and increased TT (13.46%), 17-OHP (76.92%), AMH (44.23%), and increased LH/FSH (15.38%) ratio. PCOS was seen more in the persistent acne patients with clinical HA and increased 17-OHP levels. CONCLUSION: Persistent acne patients had marked clinical HA, PCOS, and hormonal abnormalities necessitating an endocrinological evaluation. As a corollary, this subgroup would benefit from antiandrogen therapy.