Project description:Female pattern hair loss (FPHL) is nonscarring progressive thinning of hair with gradual decrease in the number of hair, especially in the frontal, central, and parietal scalp, due to a process known as follicular miniaturization. The etiopathogenesis of FPHL is complex with multiple factors such as genetics, inflammation, hormones, and environment playing role in it. It usually manifests as slowly progressive hair thinning, mainly over the vertex and upper parietal scalp, the frontal hairline is often spared and the miniaturization is also not as severe as in men. A thorough history, clinical examination, hair loss evaluation tests, dermoscopy, and scalp biopsy can help in establishing the diagnosis. Various biochemical tests may be needed in patients with hyperandrogenism. The treatment includes medical and surgical modalities. Topical minoxidil is still considered the first line of treatment. Along with medical therapy, cosmetic camouflage may also be needed in some cases.
Project description:Female Pattern Hair Loss or female androgenetic alopecia is the main cause of hair loss in adult women and has a major impact on patients' quality of life. It evolves from the progressive miniaturization of follicles that lead to a subsequent decrease of the hair density, leading to a non-scarring diffuse alopecia, with characteristic clinical, dermoscopic and histological patterns. In spite of the high frequency of the disease and the relevance of its psychological impact, its pathogenesis is not yet fully understood, being influenced by genetic, hormonal and environmental factors. In addition, response to treatment is variable. In this article, authors discuss the main clinical, epidemiological and pathophysiological aspects of female pattern hair loss.
Project description:Female pattern hair loss (FPHL) is the most common form of alopecia in women. Affected women may experience psychological distress and impaired social functioning. Early diagnosis and initiation of treatment are desirable because treatments are more effective to avoid the progression of hair loss than stimulating regrowth. Typically, a diagnosis of FPHL can be confirmed by review of a patient's medical history and a physical examination alone. Testing a scalp biopsy is diagnostic but usually not required. In women with signs of hyperandrogenism, an investigation for ovarian or adrenal disorders should be performed. Treatment for FPHL is obscured by myths. The aim of FPHL treatment could be two-fold: Reverse or stabilize the process of hair follicle miniaturization. Mild-to-moderate FPHL in women can be treated with oral antiandrogen therapies (cyproterone acetate and spironolactone) and/or topical minoxidil with good results in many cases. If used correctly, available medical treatments arrest the progression of the disease and reverse miniaturization in most patients with mild-to-moderate FPHL. Hair systems and surgery may be considered for selected cases of severe FPHL.
Project description:BackgroundAlopecia, a benign dermatologic condition affecting both genders, particularly harms female patients due to psychosocial effects. Female pattern hair loss (FPHL), the primary cause of hair loss in women, lacks sufficient Korean epidemiological studies examining its psychosocial aspects.ObjectiveThis study aimed to explore FPHL's psychosocial impacts, including quality of life (QoL), depression, anxiety, medical consumption, and hair loss factors in Korean women.MethodsA total of 202 patients with FPHL were interviewed using a validated questionnaire to assess the QoL, psychological impact, and pattern of medical consumption. The severity of hair loss was evaluated using the "basic and specific (BASP) classification" by dermatologists. The Hair-Specific Skindex-29 (HSS29) was used to assess the QoL and Beck depression inventory (BDI), Beck anxiety inventory (BAI) to evaluate psychological aspects, and medical expenses and the number of clinic visits to determine medical consumption.ResultsThe global HSS29 score of FPHL was 40.97±18.92, indicating a notable impact on QoL. The mean BDI and BAI scores were 14.47 and 10.06, respectively. In multivariable regression analysis, HSS29, BDI, and BAI scores were most affected by the severity of hair loss (p<0.001).ConclusionFPHL damages the psychosocial aspects of patients, such as QoL, depression, and medical consumption, according to the severity of hair loss.
Project description:Studies on androgenetic alopecia (AGA or patterned hair loss (PHL)) have suggested different underlying pathological mechanisms between males and females. While many genetic factors for male hair loss have been identified through genome-wide association studies (GWASs), the genetic determinants of female hair loss remain unclear. In this study, we analyzed approximately 1000 individuals (436 males and 568 females) to identify sex-specific genetic factors. We conducted three independent GWASs for the total, male-only, and female-only groups, identifying three novel loci (rs7814359, rs2163085, and rs4793158 of the TSNARE1, FZD1, and GJC1 genes, respectively). rs7814359 showed a significant genome-wide association with AGA in the combined sex group and a weak association in both the male-only and female-only groups. The single nucleotide polymorphism (SNP) rs2163085 showed a significant genome-wide association with AGA in the combined group and notable significance in females. The rs4793158 SNP showed a suggestive association with AGA in both the combined and female-only groups. TSNARE1, related to rs7814359, is involved in vesicle transport. FZD1 is a key regulator of the Wnt signaling pathway. GJC1 is a gap junction protein. The associations of FZD1 and GJC1 with female-specific AGA suggest that sex hormones, such as estrogen, may influence FPHL through these genes. These findings will contribute to our understanding of the sex-specific pathophysiology of AGA.
Project description:Background:Female pattern hair loss (FPHL) is an important cause of hair loss in adult women and has a major impact on patient's quality of life. It evolves from the progressive miniaturization of follicles that leads to a subsequent decrease of hair density, leading to non-scarring diffuse alopecia, with characteristic clinical, dermoscopic, and histological patterns. Vitamin D receptor (VDR) is expressed in follicular keratinocytes and dermal papilla cells and is shown to have important role in hair growth and regulation of hair cycle. VDR polymorphism was not extensively investigated in hair disorders including FPHL. Aim:To investigate the association between VDR gene polymorphism (Cdx-1 and Taq-1) and FPHL to explore if these polymorphisms affect the disease occurrence or influence its clinical presentation. Methods:A case-control study was conducted on 30 female patients with FPHL and 30 age-matched female healthy subjects, as a control group. Degree of hair loss was assessed by Ludwig grading. VDR gene polymorphisms, Taq-1 and Cdx-1 were investigated by real time polymerase chain reaction. Results:CC genotype, TC genotype, and T allele of Taq-1 were more prevalent in FPHL patients than in control group. They increased disease risk by 12.6, 2.1, and 2.9 folds, respectively. AA genotype, GA genotype, and G allele of Cdx-1 were significantly more prevalent among FPHL patients than in control group. They increased disease risk by 7.5, 5.2, and 5.5 folds, respectively. Conclusion:Taq-1 and Cdx-1 can be considered as risk factors for FPHL. They may play role in disease persistence rather than disease initiation. This association may be explained by failure of new anagen growth and decreased proliferation of hair follicle stem cells. Further studies are recommended to confirm current findings.
Project description:Female pattern hair loss (FPHL) is a non-scarring alopecia resulting from the progressive conversion of the terminal (t) scalp hair follicles (HFs) into intermediate/miniaturized (i/m) HFs. Although data supporting nutrient deficiency in FPHL HFs are lacking, therapeutic strategies are often associated with nutritional supplementation. Here, we show by metabolic analysis that selected nutrients important for hair growth such as essential amino acids and vitamins are indeed decreased in affected iHFs compared to tHFs in FPHL scalp skin, confirming nutrient insufficiency. iHFs also displayed a more quiescent metabolic phenotype, as indicated by altered metabolite abundance in freshly collected HFs and release/consumption during organ culture of products/substrates of TCA cycle, aerobic glycolysis, and glutaminolysis. Yet, as assessed by exogenous nutrient supplementation ex vivo, nutrient uptake mechanisms are not impaired in affected FPHL iHFs. Moreover, blood vessel density is not diminished in iHFs versus tHFs, despite differences in tHFs from different FPHL scalp locations or versus healthy scalp or changes in the expression of angiogenesis-associated growth factors. Thus, our data reveal that affected iHFs in FPHL display a relative nutrient insufficiency and dormant metabolism, but are still capable of absorbing nutrients, supporting the potential of nutritional supplementation as an adjunct therapy for FPHL.