Androgenetic (or pattern) alopecia is a genetically determined disorder characterized by the gradual conversion of terminal hairs into indeterminate, and finally into vellus, hairs. It is an extremely common disease that affects men and women.  Only two drugs currently have US Food and Drug Administration (FDA)–approved indications for treatment of androgenetic alopecia: minoxidil and finasteride.
Signs and symptoms
Signs of androgenetic alopecia include the following:
Increased hair shedding
Transition in the involved areas from large, thick, pigmented terminal hairs to thinner, shorter, indeterminate hairs and finally to short, wispy, nonpigmented vellus hairs
End result can be an area of total denudation; this area varies from patient to patient and is usually most marked at the vertex
Diffuse alopecia areata may mimic the androgenetic form. The presence of exclamation point hairs, pitted nails, or a history of periodic regrowth or tapered fractures noted on hair counts suggests the diagnosis of diffuse alopecia areata.
Men note a gradual recession of the frontal hairline early in the process
Men present with gradual thinning in the temporal areas, producing a reshaping of the anterior part of the hairline
Hair generally is lost diffusely over the crown; this produces a gradual thinning of the hair rather than an area of marked baldness; the part is widest anteriorly
The frontal hairline is often preserved in women
Bitemporal recession does occur in women but usually to a lesser degree than in men
See Clinical Presentation for more detail.
History and the physical examination are the most important aspects of diagnosis in patients with androgenetic alopecia. The following laboratory tests, however, can play a role in patient assessment:
Dehydroepiandrosterone (DHEA)-sulfate and testosterone analysis: In women, if virilization is evident
Iron, total iron-binding capacity, and transferrin saturation: To test for iron deficiency, if telogen effluvium is present
Thyrotropin level: If a thyroid disorder is suspected
Biopsy and histology
A biopsy is rarely necessary to make the diagnosis of androgenetic alopecia. If a single biopsy specimen is obtained, it should generally be sectioned transversely if pattern alopecia is suspected.
In androgenetic alopecia, hairs are miniaturized. Although the condition is considered a noninflammatory form of hair loss, a superficial, perifollicular, inflammatory infiltrate is noted at times. A mildly increased telogen-to-anagen ratio is often observed.
See Workup for more detail.
The following drugs have been approved by the FDA for the treatment of androgenetic alopecia:
Minoxidil: Androgen-independent hair-growth stimulator
Finasteride: 5-Alpha reductase type 2 inhibitor
The cosmetic results of surgical treatment for androgenetic alopecia are often satisfactory. Micrografting produces a more natural appearance than does the old technique of transplanting plugs.
See Treatment and Medication for more detail.
Androgenetic alopecia, or pattern alopecia, is an extremely common disorder affecting both men and women. The incidence of androgenetic alopecia is generally considered to be greater in males than females, although some evidence suggests that the apparent differences in incidence may be a reflection of different expression in males and females.
Androgenetic alopecia is a genetically determined disorder and is progressive through the gradual conversion of terminal hairs into indeterminate hairs and finally to vellus hairs. Patients with androgenetic alopecia have a reduction in the terminal-to-vellus hair ratio, normally about 4:1. Following miniaturization of the follicles, fibrous tracts remain. Patients with this disorder usually have a typical patterned distribution of hair loss.
In androgenetic alopecia, studies have indicated a self-renewal of the hair follicle via keratinocyte stem cells located at the area of the bulge of the hair follicle. In addition, a series of studies using mice has indicated that interfollicular keratinocyte stem cells could generate de novo hair follicles in adult mouse skin. These regenerated hair follicles cycled through stages of telogen to anagen. However, these transitions between bulge and epidermal keratinocytes have not been seen yet in human studies. 
Another report has indicated that mice lacking in functional vitamin D receptors develop a functional first coat of hair but lack the cyclic regeneration of hair follicles, leading to the development of alopecia.  Whether these findings will lead to a new area of exploration into the cause of androgenetic alopecia in humans is unknown at this time.
A lymphocytic microfolliculitis targeting the bulge epithelium, along with deposits of epithelial basement membrane zone immunoreactants, are frequently seen in androgenetic alopecia in both sexes. Those cases with a positive immunoreactant profile respond better to combined-modality therapy than do those with a negative result. 
Numerous studies have identified 2 major genetic risk loci for androgenetic alopecia. These are the X-chromosomal AR/EDA2R locus and the PAX1/FOXA2 locus on chromosome 20. A recent genome-wide association study compared move than 1100 severely affected cases of androgenetic alopecia and controls to note differences in the 2 groups. The study indicated that HDAC9 is the third androgenetic alopecia susceptibility gene. The results of this German study were further analyzed by fine-mapping and then individually replicated in an Australian sample. 
A Japanese study of the sebaceous glands was performed to note whether the distribution of the bulge stem cells play a role in the development of androgenetic alopecia.  Biopsies from 250 cases of men with androgenetic alopecia were reviewed. Twenty-three vertical sections of areas of androgenetic alopecia were studied, and each sebaceous gland area was measured and statistically analyzed. For identification of the bulge area, immunochemical study was carried out in the cases of androgenetic alopecia. The result of the study was that the sebaceous gland area of the androgenetic alopecia group was noticeably increased, while the size of each sebaceous gland remained unchanged. This suggests that overgrowth of the sebaceous gland and relative preservation of the follicular stem cells could be an important factor in the pathology of androgenetic alopecia.
A study by Kaya Erdogan et al suggested that younger patients with early onset androgenetic alopecia have greater oxidative stress than do individuals without the disease. The study, on males aged 18 to 30 years, found higher total oxidant levels and oxidative stress index values in patients, all of whom had early onset androgenetic alopecia, than in healthy controls. The investigators also reported that within the patient group, the total antioxidant level was negatively correlated with patient age and disease duration. 
A literature review by Kim et al indicated that patients with androgenetic alopecia have abnormal lipid profiles, which may be a factor in the disorder’s association with cardiovascular disease. In the study, significantly higher levels of serum total cholesterol, serum triglyceride, and low-density lipoprotein cholesterol, as well as significantly lower levels of high-density lipoprotein cholesterol, were found in patients with androgenetic alopecia than in controls. [8, 9]
Male androgenetic alopecia has been suggested as a risk factor for severe coronavirus disease 2019 (COVID-19) owing to the finding that males hospitalized with COVID-19 have a high incidence of the condition. Moreover, research indicates that infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes COVID-19, may be promoted by androgen signaling, which is itself essential to the etiology of androgenetic alopecia. There is also indication that a link exists between androgen signaling and severe COVID-19 symptoms in men. 
However, a study by Henne et al using regression, genetic correlation, and polygenic risk score (PRS) analyses found no significant epidemiologic or genome-wide genetic association between androgenetic alopecia and severe COVID-19. Nonetheless, evidence indicated that a genetic component is shared between androgenetic alopecia and COVID-19, in signaling pathways for vitamin metabolism, natural killer cell–mediated cytotoxicity, Wnt signaling, and aryl hydrocarbon receptor signaling. 
Androgenetic alopecia is an extremely common disorder that affects roughly 50% of men and perhaps as many women older than 40 years. As many as 13% of premenopausal women reportedly have some evidence of androgenetic alopecia. However, the incidence of androgenetic alopecia increases greatly in women following menopause, and, according to one author, it may affect 75% of women older than 65 years.
A community-based study of androgenetic alopecia in 6 cities in China indicated that the prevalence of androgenetic alopecia in both Chinese males and females was lower than that seen in whites but similar to the incidence among Koreans. 
The incidence and the severity of androgenetic alopecia tend to be highest in white men, second highest in Asians and African Americans, and lowest in Native Americans and Eskimos.
Almost all patients with androgenetic alopecia have an onset prior to age 40 years, although many of the patients (both male and female) show evidence of the disorder by age 30 years.
The prognosis of androgenetic alopecia is unknown. Some patients progress to the point where they lose almost all of the hair on the scalp. Others have a patterned or nonpatterned thinning but retain a considerable number of scalp hairs. Women with androgenetic alopecia usually show thinning of the crown rather than developing truly bald areas.
Along with affecting the patient psychologically,  androgenetic alopecia is significant in that it allows ultraviolet light to reach the scalp and, thus, increases the amount of actinic damage. In addition, males with androgenetic alopecia may have an increased incidence of myocardial infarction. 
An increase in benign prostatic hypertrophy has also been associated with androgenetic alopecia.  Arias-Santiago et al measured prostatic volume by transrectal ultrasound and urinary flow by urinary flowmetry in order to study this hypothesis. Their findings suggest that a relationship exists between early onset androgenetic alopecia and prostate growth associated urinary symptoms, most likely owing to their pathophysiological similarity. They suggest that future studies may clarify whether treatment of patients with androgenetic alopecia might benefit concomitant benign prostatic hypertrophy. 
If these associations are proven conclusively, androgenetic alopecia will be of greater clinical significance.
A study by Sanke et al indicated that early androgenetic alopecia (ie, prior to age 30 years) in males is the phenotypic equivalent of polycystic ovarian syndrome (PCOS) and that these males may be at risk of developing complications found in association with PCOS, such as obesity, metabolic syndrome, insulin resistance, cardiovascular disease, and infertility. The investigators reported that the endocrinologic profile of the males with early androgenetic alopecia was similar to that of females with PCOS. Compared with controls, mean levels of testosterone, dehydroepiandrosterone (DHEA)-sulfate, luteinizing hormone, and prolactin were significantly higher in individuals with early androgenetic alopecia, while the mean free androgen index was also higher and mean levels of follicle-stimulating hormone were lower. 
A study by Polat et al indicated that men with androgenetic alopecia have a higher likelihood of developing urolithiasis than do those with no hair loss, with the risk being 1.3-fold greater in males with vertex-pattern alopecia, and 2.1-fold greater in those with total alopecia. The study included 200 men with urolithiasis and 168 males with no history of renal stones.