Female Fekinina 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 alopecla. It andrpgenetica 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 aalopecia, authors discuss the main clinical, epidemiological and pathophysiological aspects of female pattern hair loss. It is an allusion to the constant hair loss suffered by these animals during life. The term is also registered this way among the health femininw descriptors DECS for scientific indexing in Brazil. The description of the classical clinical pattern of baldness in men is known since antiquity.
As an example, we may cite Hippocrates’ BC observation that eunuchs did not develop baldness. Later, Joseph Plenck, in his book ” Doctrina de Morbis Cutaneis ” Vienna, Vienna, identified, in teminina cases, the miniaturization of hair follicles, which he called “c alvities “. He also distinguished the disease in two ways, according to its extension: Initially, fsminina term “diffuse alopecia in women” alopecla widely used to characterize the disease.
Although the follicular changes that lead to alopecia are similar between men and women, clinical presentation and response to antiandrogen therapy are different. In addition, the participation of androgens in the development of female pattern baldness has not yet been fully elucidated.
Given these differences in relation to male pattern baldness, the term Female Pattern Hair Loss FPHL has been preferred over female androgenic alopecia. Despite this division, women may eventually present baldness similar to the male pattern and vice versa. FPHL is characterized as a non-scarring diffuse alopecia, evolving from the progressive miniaturization of hair follicles and subsequent reduction of the number of hairs, especially in the central, frontal and parietal scalp regions Figure 1.
Female Pattern Hair Loss. Diffuse thinning of the hairs in the frontal and parietal regions, preserving the anterior hair implantation line. FPHL is the condition that most commonly leads to hair loss in adult females. Its prevalence increases with age and the disease shows an inconsistent response to treatment.
Hair loss and hair thinning complaints are common in dermatological practice. According to a census conducted by the Brazilian Society of Dermatology in with 36, female patients, non-scarring alopecia unspecified was one of the ten most common diagnoses.
The frequency of FPHL varies among population groups and increases with age. However, a comparison between prevalence studies is hampered by the lack of universally accepted criteria for fejinina diagnostic definition of the disease. In general, FPHL has its onset during the reproductive years.
More androgeneticca cases of the disease are already noticeable at puberty. However, there is a greater demand for treatment among patients aged years.
There is androgendtica second peak incidence at menopause, between 50 and 60 years of age. Since the disease has a slow and progressive course, studies considering only clinical criteria usually identify cases with marked reduction of hair volume and show modest prevalence among young people.
Nevertheless, if more sensitive diagnostic procedures, such as dermoscopic identification of hair miniaturization, start to be used, the prevalence of FPHL might become higher in all age groups. The highest prevalence was found among women over 70 years of age: A study conducted with Korean women in found an overall prevalence of 5. Ina population study involving Chinese women found similar amdrogenetica rates to the ones found in the Korean study.
Table 1 summarizes the weighted results of different studies on the prevalence of FPHL in Caucasoid and Asian women, according to age. These studies show a higher frequency in Caucasoid women at all ages. Prevalence of Female Pattern Hair Loss in each age group, according to epidemiological studies indifferent population groups.
Although FPHL more frequently manifests in adulthood, it may also occur in childhood and adolescence. InTosti and colleagues reported 20 cases of children aged between years 12 of whom were girls with diffuse-pattern androgenetic alopecia.
None of them had laboratory abnormalities, however, they all had strong family history. Only one subject experienced hormonal changes.
There is evidence that FPHL has a phenotype independently associated with insulin androgeneyica and atherosclerosis. The causal model for this finding has not yet been established, but it may be related to a hyperandrogenic state induced by insulin resistance, which also favors atherosclerosis. A case-control study conducted androgenetuca Spain in evaluated subjects 60 men and 60 women with hair loss and controls without alopecia. There was no association between low levels of SHBG and hyperglycemia in the controls.
In order to investigate the relationship between baldness and metabolic syndrome, an epidemiological study was conducted in Korea in This relationship, however, was not observed in the male population, which suggests that follicle miniaturization in FPHL and MPA arises from different stimuli. The pathophysiology of FPHL is not yet completely understood.
There is evidence that genetic, hormonal and possibly environmental factors are involved. The biological cycle of the hair follicles is not synchronized among the adjacent units, assuming a mosaic pattern in the scalp. It is didactically divided into three phases: At the end of the telogen phase, the original hair falls out exogenous phase and is replaced by a new hair at femiina growth stage. Normally, the anagen phase lasts between 2 and 8 years; the catagen phase last between 2 and 3 weeks, and the telogen phases lasts about 3 months.
This can ceminina evidenced by trichogram or anatomopathological examination. In FPHL there is a femminina in the duration of the anagen phase and a miniaturization of the dermal papilla thinning of the hair.
Thick pigmented hairs are gradually replaced by miniaturized hairs Figure 2. Moreover, there is a delay between the end of femknina telogen phase and the beginning of the new anagen phase.
Representative schemes of the hair cycle. A – Normal cycle of the follicle.
B – Alterations occurring in baldness: The hair follicle is a complex structure in constant activity. An imbalance between various growth factors and cytokines which mantain the anagen phase and promote apoptosis can determine the beginning of the catagen phase Chart 1.
Main factors associated with the transition from the anagen hair phase to the catagen hair phase. The diffuse apoptosis of the follicular keratinocytes leads to the follicular regression observed in the catagen phase.
The premature termination of the anagen phase is a landmark event in the development of FPHL. Apoptosis can be triggered in two ways: In the hair follicle, the apoptosis starts in the melanogenic area late anagenpropagates to the array premature catagen and then to the internal and external root sheath. Apoptosis in the various sites of the hair follicle present different forms of regulation.
The direct role of cytokines and alopeecia factors in the control of the apoptosis of follicular keratinocytes in this process has not yet been fully established. The diameter of the follicles is directly determined by the size of the dermal papilla. As the hair keeps the same thickness from the tip to the proximal andgogenetica, it is concluded that no thinning occurs during the anagen phase. Thus, it is understood that miniaturization occurs sometime between the catagen phase and the formation of the new hair.
The miniaturized hair is very similar to vellus hair, but is not a true vellus hair.
Although the hair is thin, it has a developed piloerector muscle, unlike the vellus hair, which has no or absent muscle. A possible mechanism of follicle miniaturization is the decrease in the number of papilla cells due to apoptosis. Despite the importance of hormonal factors in the development of baldness, the action mechanisms through which they lead to shortening of the anagen phase and the miniaturization of the follicles have not yet been elucidated.
The dependence on androgens for the development of baldness in men was observed by Hippocrates BC and established by Hamilton in It was observed that eunuchs and men castrated before puberty did not develop baldness. However, the administration of testosterone T induced alopecia in individuals with a family history of baldness.
Female Pattern Hair Loss: a clinical and pathophysiological review
Androgens spread through the cytoplasmic membrane and connect themselves to specific intracellular receptors. This complex hormone-receptor promotes the transcription of genes that are primarily responsible for its tissue actions. The miniaturization of the hair follicle caused by androgens occurs primarily due to the action of DHT, which has five times greater affinity for the androgen receptor AR than testosterone.
Representative scheme of the cellular action of androgens. In addition, DHT may interfere with the follicular cycle by interacting with the Wnt signaling pathway. The Wnt pathway induces dermal papilla cells to maintain the anagen phase.
A recent phase I clinical trial showed improvements in hair density and thickness in men with MPA through the infiltration of a complex containing Wnt activity. Despite the fact that the evidence indicating that androgens participate in baldness has emerged from studies in men, androgens were also assumed to play such role in female baldness, due to the idea that, in spite of the clinical differences, male and female baldness are the same entity.
However, finasteride and dutasteride even at higher doses showed less consistent results in the treatment of FPHL. Aromatase is an enzyme that converts androstenedione to estrone and testosterone to estradiol, exerting an antiandrogenic action. Inin a study by Sawaya involving 12 men and 12 women with baldness, the aromatase levels of the follicles of the frontal region of women with FPHL were half as high as those of the occipital region.
When compared with the follicles of the frontal region of men showed, these levels were six times greater.
In baldness, the miniaturization process may be accompanied by a mild to moderate lymphohistiocytic inflammatory infiltrate in the peri-infundibular region. To term microinflamation has been used in order to differentiate it from the inflammation that occurs in scarring alopecia. The frequency of this process is abdrogenetica. InWhiting evaluated the presence of inflammatory infiltrate in men with MPA and 22 controls 13 men and 9 women.
The fact that the inflammatory process occurs in the upper part of the follicle suggests that the causal factor may affect this region. External factors androgenetiica as ultraviolet radiation, environmental pollutants, inhabitants of the skin microbiota and follicle such as Propionibacterium sp. The real meaning of this inflammatory process for development of FPHL, as well as its possible relation to the miniaturization process and the hormonal elements involved in FPHL have not yet been established.
Family segregation is not yet fully understood, however, the high prevalence of FPHL and the fact that FPHL manifests with varying degrees of intensity and has its onset at different ages, suggest a polygenic pattern with incomplete penetrance.
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