Hair loss (alopecia) is a common presentation in both primary care and dermatology. It often signals underlying inflammation or abnormalities in hair cycling or hair shaft structure, requiring a thorough and systematic evaluation. Clinical guidelines emphasize pattern recognition, trigger identification, and targeted interventions. This article equips physician associates (PAs) with an evidence-based approach to assessing patient history, conducting physical examinations, selecting appropriate diagnostics, and implementing treatment strategies for alopecia. History and scalp inspection guide diagnosis, with the differential including such conditions as telogen effluvium (diffuse), alopecia areata (focal), and androgenetic alopecia (patterned). Recommended laboratory tests include thyroid-stimulating hormone, complete blood cell count, and iron studies, while scalp biopsy is used to confirm scarring. Treatments address causes, with avoidance of triggers central to effluvium, intralesional steroids or baricitinib for alopecia areata, minoxidil-based therapy for androgenetic alopecia, and antifungals for tinea capitis. By integrating trichoscopy, selective testing, and etiology-specific care, PAs can enhance diagnostic accuracy and optimize outcomes for patients with hair loss.

Background and objective Alopecia encompasses a heterogeneous group of scarring and non-scarring disorders that often have overlapping clinical features, complicating diagnosis when scalp biopsy is unavailable. The real-world diagnostic yield of trichoscopy in rural Indian populations remains incompletely characterised. The objective of this study is to evaluate the diagnostic yield of trichoscopy, quantify its capacity to alter or refine provisional clinical diagnoses, and assess its role in reducing invasive investigations. Methods A hospital-based cross-sectional study enrolled 200 consecutive alopecia patients at a rural tertiary care centre over 18 months (April 1, 2024, to October 1, 2025). Trichoscopy was performed with a handheld dermatoscope (Illuco IDS-1100; ILLUCO Co., Ltd., Gyeonggi-do, Republic of Korea). A provisional diagnosis was recorded prior to trichoscopy; outcome was classified as confirmed, refined, or inconclusive against the final composite diagnosis. Discriminatory features were analysed by chi-square and Fisher's exact tests. Results Trichoscopy was diagnostically contributory in 195/200 (97.5%): confirming the diagnosis in 190/200 (95.0%), refining it in 5/200 (2.5%), and being inconclusive in 5/200 (2.5%). Two cases (2/200, 1.0%) of presumed alopecia areata were re-diagnosed as tinea capitis on identification of comma hairs, averting inappropriate corticosteroid therapy; three cases (3/200, 1.5%) of presumed telogen effluvium were re-diagnosed as female pattern hair loss based on hair diameter diversity >20%. Comma hairs demonstrated 78.6% sensitivity (11/14) and 100% specificity (186/186) for tinea capitis (p < 0.001), directed targeted KOH testing (12/14, 85.7% positive yield), and limited the diagnosis-deciding scalp biopsy rate to 2/200 (1.0%). Conclusions Trichoscopy shows strong potential as a first-line, non-invasive triage tool in routine dermatology practice, particularly in resource-limited settings where it may help confirm diagnoses, avert mismanagement, and reduce the need for invasive investigations; multi-centre validation against an independent reference standard is needed before this can be firmly established.

Dear Editor, Calcitonin gene-related peptide (CGRP) is a neuropeptide with potent vasodilatory effects and a key role in trigeminovascular signaling, underlying the pathogenesis of migraine. Consequently, the inhibition of CGRP activity has been demonstrated to reduce the incidence of acute migraine attacks. Based on this evidence, monoclonal antibodies against CGRP or its receptor have been approved by the European Medicines Agency for prevention of both episodic and chronic migraine. Among CGRP inhibitors, galcanezumab has also been authorized for the treatment of episodic cluster headache. Since the advent of CGRP inhibitors, several cases of drug-induced telogen effluvium have been reported, with incidence rates ranging from 1.10% to 7.23%. However, to the best of our knowledge, alopecia areata (AA) associated with CGRP inhibition remains undescribed in the literature. [...].

The face of Leonardo da Vinci's Mona Lisa (ca. 1503-1519) has attracted several medical presentations, most recently the hypothesis of frontal fibrosing alopecia (FFA) masquerading as Renaissance fashion. I present a systematic retrospective iconodiagnosis grounded in an explicit methodological framework, in the technical literature on the painting - including thirteen-band multispectral imaging - and in the documented biography of the sitter, Lisa Gherardini (1479-ca. 1542). Four reproducible findings are legible on the panel: complete bilateral absence of the eyebrows; complete bilateral absence of the eyelashes; a frontal hairline without a transition zone; and intact, non-scarred periocular and frontal skin. Tested against these findings, Renaissance cosmetic depilation, FFA, secondary syphilis, lepromatous leprosy, telogen effluvium, and trichotillomania each fail on at least one cardinal sign, whereas alopecia areata universalis accounts for all four without exception. The single supraciliary hair detected by multispectral analysis, previously read as the relic of a vanished painted eyebrow, is reinterpreted as a faithfully depicted solitary surviving terminal hair - a recognized expression of incomplete, asynchronous follicular involvement in alopecia areata, illustrated here by a clinical photograph of an eight-year-old patient with an identical finding. The sitter's documented age (24 years in 1503) and biographic stressors are congruent with the early-onset epidemiology of extensive alopecia areata. Limitations of retrospective diagnosis are addressed and explicit criteria for disproof are also stated. The most contemplated face in Western art is reframed as a dignified Renaissance document of alopecia areata universalis.

Alopecia areata (AA) is a common autoimmune condition that affects approximately 2% of the global population. Although it most commonly presents with the abrupt onset of well-circumscribed, non-scarring alopecic patches on the scalp, the nails and other hair-bearing areas are also frequently affected. Clinical evaluation should document disease extent and employ trichoscopy to identify characteristic signs of the condition (e.g., black-dot hairs, exclamation point hairs). The Severity of Alopecia Tool (SALT) is standard for quantifying severity, and newer instruments like the Alopecia Areata Severity Scale (AASc) incorporate extra-scalp involvement and psychosocial burden. Moreover, machine learning approaches and validated patient-reported outcome measures, such as the Alopecia Areata Patient Priority Outcomes (AAPPO), have emerged that can standardize assessment and longitudinal tracking. AA prognosis is influenced by several factors, including age, disease subtype, extent and duration of hair loss, and family history. Pathogenesis is heterogeneous, multifactorial, and includes the collapse of immune privilege with cytotoxic CD8+ T cell inflammation. Genetic and pharmacologic data support a key role for the JAK/STAT pathway and demonstrate that Th2-related inflammation is involved in select patients. The quality-of-life impact of AA and associated comorbidities are substantial.

Diffuse unpatterned alopecia (DUPA) is an uncommon and incompletely characterized variant of androgenetic alopecia (AGA) marked by diffuse follicular miniaturization across the entire scalp, including the occipital region, which distinguishes it from classic patterned AGA and often precludes hair transplantation.

Chronic stress commonly precipitates telogen effluvium (TE), but sustained stress can further induce follicular miniaturization and fibrosis. Thus, stress-induced alopecia may be considered a pathological continuum that progresses from TE to fibrotic follicular degeneration. Stress-induced alopecia involves multiple pathological mechanisms including follicular fibrosis, miniaturization and hair thinning. Currently, there is a lack of systematic therapeutic approaches targeting its multi-target pathological processes. This study proposes a novel combination strategy (EBP: EGCG, Biotin and Pal-GHK) designed to synergistically modulate the TGF-β/Smad and BMP signaling pathways to target key pathological processes in stress-induced alopecia. Through molecular docking, cell co-culture experiments, animal models and microbial interaction analysis, the EBP combination was systematically evaluated for its effects in inhibiting follicular fibrosis, promoting follicular regeneration and enhancing keratin synthesis. The results demonstrated that EBP effectively inhibited TGF-β/Smad pathway and activated BMP pathway. In the stress-induced fibrotic alopecia mouse model, compared to the Model group, the High EBP group significantly upregulated BMP2 by 2.77-fold, while downregulating TGF-β1 and P-Smad2 expression levels to 35.7% and 65.9%, respectively. These molecular changes were accompanied by substantial improvements in hair follicle morphology, hair shaft quality and hair regrowth. Furthermore, microbial biotransformation of EBP components may contribute to prolonged biological activity and sustained therapeutic efficacy. This study provides novel theoretical and experimental evidence for multi-target combined therapy in stress-induced alopecia.

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have rapidly expanded beyond the treatment of type 2 diabetes mellitus (T2DM) and obesity, with increasing relevance to dermatologic practice as more patients present while receiving these therapies. This medication class now includes oral formulations including oral semaglutide and the first non-peptide oral GLP-1RA, orforglipron as well as next-generation triple agonists such as retatrutide, which demonstrated up to 24.2% body weight reduction in phase 2 trials and a favorable body composition profile, with preferential fat over lean mass loss. Although GLP-1 RAs provide substantial metabolic and weight reduction benefits, their growing use has introduced a broad spectrum of systemic and cutaneous adverse effects that dermatologists must recognize and monitor. This review summarizes the current evidence regarding the safety profile of GLP-1RAs with emphasis on dermatologic implications and interdisciplinary monitoring considerations. Common adverse effects include gastrointestinal (GI) intolerance, nutritional deficiencies, gallbladder disease, pancreatitis, and loss of lean body mass. Other rarer potential side effects include anemia, neuropsychiatric, and sexual health effects. Emerging data also suggest associations with ophthalmologic complications, skeletal fragility in older adults, and alterations in body composition that may influence cosmetic and procedural outcomes. Dermatologic adverse events include alopecia, eczematous and hypersensitivity eruptions, bullous and pustular dermatoses, acneiform eruptions, hyperhidrosis, and significant facial volume loss ("Ozempic face"). Current evidence regarding GLP-1RA use in pregnancy remains limited and evolving, with recommendations generally advising discontinuation prior to conception. Given the increasing overlap between metabolic disease management and dermatologic care, dermatologists should understand contraindications, screening strategies, nutritional monitoring, and counseling considerations associated with GLP-1RA therapy. A multidisciplinary approach involving primary care physicians, endocrinologists, ophthalmologists, dietitians, and dermatologists is essential to optimize patient safety while maintaining the substantial therapeutic benefits of these medications.