The diagnosis of androgenic alopecia can be usually established based on clinical presentation in men. In women, the diagnosis usually requires more complex diagnostic evaluation. Further evaluation of the differential requires exclusion of other causes of hair loss, and assessing for the typical progressive hair loss pattern of androgenic alopecia. Trichoscopy can be used for further evaluation. Biopsy may be needed to exclude other causes of hair loss, and histology would demonstrate perifollicular fibrosis.

Because they are not usually associated with an increased loss rate, male-pattern and female-pattern hair loss do not generally require testing. If hair loss occurs in a young man with no family history, drug use could be the cause.

- The pull test helps to evaluate diffuse scalp hair loss. Gentle traction is exerted on a group of hairs (about 40–60) on three different areas of the scalp. The number of extracted hairs is counted and examined under a microscope. Normally, fewer than three hairs per area should come out with each pull. If more than ten hairs are obtained, the pull test is considered positive.

- The pluck test is conducted by pulling hair out "by the roots". The root of the plucked hair is examined under a microscope to determine the phase of growth, and is used to diagnose a defect of telogen, anagen, or systemic disease. Telogen hairs have tiny bulbs without sheaths at their roots. Telogen effluvium shows an increased percentage of hairs upon examination. Anagen hairs have sheaths attached to their roots. Anagen effluvium shows a decrease in telogen-phase hairs and an increased number of broken hairs.

- Scalp biopsy is used when the diagnosis is unsure; a biopsy allows for differing between scarring and nonscarring forms. Hair samples are taken from areas of inflammation, usually around the border of the bald patch.

- Daily hair counts are normally done when the pull test is negative. It is done by counting the number of hairs lost. The hair from the first morning combing or during washing should be counted. The hair is collected in a clear plastic bag for 14 days. The strands are recorded. If the hair count is >100/day, it is considered abnormal except after shampooing, where hair counts will be up to 250 and be normal.

- Trichoscopy is a noninvasive method of examining hair and scalp. The test may be performed with the use of a handheld dermoscope or a video dermoscope. It allows differential diagnosis of hair loss in most cases.

There are two types of identification tests for female pattern baldness: the Ludwig Scale and the Savin Scale. Both track the progress of diffused thinning, which typically begins on the crown of the head behind the hairline, and becomes gradually more pronounced. For male pattern baldness, the Hamilton–Norwood scale tracks the progress of a receding hairline and/or a thinning crown, through to a horseshoe-shaped ring of hair around the head and on to total baldness.

In almost all cases of thinning, and especially in cases of severe hair loss, it is recommended to seek advice from a doctor or dermatologist. Many types of thinning have an underlying genetic or health-related cause, which a qualified professional will be able to diagnose.

Hair loss can be slowed or reversed in its early stages with medication. Medications approved by the United States' Food and Drug Administration (FDA) to treat male-pattern hair loss include minoxidil and finasteride.

Alopecia areata is usually diagnosed based on clinical features.

Trichoscopy may aid in establishing the diagnosis. In alopecia areata, trichoscopy shows regularly distributed "yellow dots" (hyperkeratotic plugs), small exclamation-mark hairs, and "black dots" (destroyed hairs in the hair follicle opening).

A biopsy is rarely needed to make the diagnosis or aid in the management of alopecia areata. Histologic findings include peribulbar lymphocytic infiltrate ("swarm of bees"). Occasionally, in inactive alopecia areata, no inflammatory infiltrates are found. Other helpful findings include pigment incontinence in the hair bulb and follicular stelae, and a shift in the anagen-to-telogen ratio towards telogen.

Though not as common as the loss of hair on the head, chemotherapy, hormone imbalance, forms of hair loss, and other factors can also cause loss of hair in the eyebrows. Loss of growth in the outer one third of the eyebrow is often associated with hypothyroidism. Artificial eyebrows are available to replace missing eyebrows or to cover patchy eyebrows. Eyebrow embroidery is another option which involves the use of a blade to add pigment to the eyebrows. This gives a natural 3D look for those who are worried about an artificial look and it lasts for two years. Micropigmentation (permanent makeup tattooing) is also available for those who want the look to be permanent.

Androgen deficiency is not usually checked for diagnosis in healthy women.

Commonly, alopecia areata involves hair loss in one or more round spots on the scalp.

- Hair may also be lost more diffusely over the whole scalp, in which case the condition is called diffuse alopecia areata.

- Alopecia areata monolocularis describes baldness in only one spot. It may occur anywhere on the head.

- Alopecia areata multilocularis refers to multiple areas of hair loss.

- Ophiasis refers to hair loss in the shape of a wave at the circumference of the head.

- The disease may be limited only to the beard, in which case it is called alopecia areata barbae.

- If the person loses all the hair on the scalp, the disease is then called alopecia areata totalis.

- If all body hair, including pubic hair, is lost, the diagnosis then becomes alopecia areata universalis.

Alopecia areata totalis and universalis are rare.

Female patients may show symptoms of hyperandrogenism in their early life, but physicians become more concerned when the patient is in her late teens or older.

Hyperandrogenism is most often diagnosed by checking for signs of hirsutism according to a standardized method that scores the range of excess hair growth.

Checking medical history and a physical examination of symptoms are used for an initial diagnosis. Patient history assessed includes age at thelarche, adrenarche, and menarche; patterns of menstruation; obesity; reproductive history; and the start and advancement of hyperandrogenism symptoms. Patterns of menstruation are examined since irregular patterns may appear with hirsutism. Family history is also assessed for occurrences of hyperandrogenism symptoms or obesity in other family members.

A laboratory test can also be done on the patient to evaluate levels of FSH, LH, DHEAS, prolactin, 17OHP, and total and free testosterone in the patient's blood. Abnormally high levels of any of these hormones help in diagnosing hyperandrogenism.

Since risk factors are not known and vary among individuals with hyperandrogegism, there is no sure method to prevent this medical condition. Therefore, more longterm studies are needed first to find a cause for the condition before being able to find a sufficient method of prevention.

However, there are a few things that can help avoid long-term medical issues related to hyperandrogenism like PCOS. Getting checked by a medical professional for hyperandrogenism; especially if one has a family history of the condition, irregular periods, or diabetes; can be beneficial. Watching your weight and diet is also important in decreasing your chances, especially in obese females, since continued exercise and maintaining a healthy diet leads to an improved menstrual cycle as well as to decreased insulin levels and androgen concentrations.

Latanoprost and bimatoprost are specific PGF2a analogues applied topically, and have been found to lengthen eyelashes, darken hair pigmentation and elongate hair. Bimatoprost is available as treatment for eyelash growth. Latanoprost has shown ability to promote scalp hair density and pigmentation, and is theorized to function at the dermal papilla. A study found latanoprost ineffective on eyelashes in a patient with alopecia areata. It has also been found ineffective in treatment of eyebrow hair loss.

Dietary supplements are not typically recommended. There is only one small trial of saw palmetto which shows tentative benefit in those with mild to moderate androgenetic alopecia. There is no evidence for biotin. Evidence for most other produces is also insufficient. There was no good evidence for gingko, aloe vera, ginseng, bergamot, or hibiscus as of 2011. While lacking both evidence and expert recommendation, there is a large market for hair growth supplements, especially for products that contain biotin.

A scalp biopsy is essential for the diagnosis of cicatricial alopecia and is the necessary first step, as it can be hard to know the diagnosis for sure without a biopsy. Findings of the scalp biopsy, including the type of inflammation present, location and amount of inflammation, and other changes in the scalp, are necessary to diagnose the type of cicatricial alopecia, to determine the degree of activity, and to select appropriate therapy.

Clinical evaluation of the scalp is also important. Symptoms of itching, burning, pain, or tenderness usually signal ongoing activity. Signs of scalp inflammation include redness, scaling, and pustules. However, in some cases there are few symptoms or signs and only the scalp biopsy demonstrates the active inflammation. The overall extent and pattern of hair loss is noted and sometimes photographed for future comparison. A hair "pull test" is performed to see if growing, or "anagen", where hairs are pulled out easily. The pulled hairs are mounted on a slide and the hair bulbs are viewed with a light microscope to determine how many are growing hairs and how many are resting hairs. In addition, if pustules are present, cultures are taken to identify which microbes, if any, may be contributing to the inflammation. A thorough evaluation that includes all of these parameters is important in diagnosing a cicatricial alopecia and in identifying features in individual patients that will help the selection of therapy.

New diagnostic techniques, such as trichoscopy may be used for non-invasive differential diagnosis of cicatricial alopecia.

Diagnosis and treatment of cicatricial alopecias is often challenging. For this reason, it is helpful to be evaluated by a dermatologist with a special interest or expertise in scalp and hair disorders, and who is familiar with current diagnostic methods and therapies.

Treatment may consist of hormone replacement therapy with androgens in either sex. Alternatively, gonadotropin-releasing hormone (GnRH)/GnRH agonists or gonadotropins may be given (in the case of "hypogonadotropic" hypoandrogenism). The Food and Drug Administration (FDA) stated in 2015 that neither the benefits nor the safety of testosterone have been established for low testosterone levels due to aging. The FDA has required that testosterone pharmaceutical labels include warning information about the possibility of an increased risk of heart attacks and stroke.

Early histological features expected to be seen on examination of gynecomastic tissue attained by fine-needle aspiration biopsy include the following: proliferation and lengthening of the ducts, an increase in connective tissue, an increase in inflammation and swelling surrounding the ducts, and an increase in fibroblasts in the connective tissue. Chronic gynecomastia may show different histological features such as increased connective tissue fibrosis, an increase in the number of ducts, less inflammation than in the acute stage of gynecomastia, increased subareolar fat, and hyalinization of the stroma. When surgery is performed, the gland is routinely sent to the lab to confirm the presence of gynecomastia and to check for tumors under a microscope. The utility of pathologic examination of breast tissue removed from male adolescent gynecomastia patients has recently been questioned due to the rarity of breast cancer in this population.

The spectrum of gynecomastia severity has been categorized into a grading system:

- Grade I: Minor enlargement, no skin excess

- Grade II: Moderate enlargement, no skin excess

- Grade III: Moderate enlargement, skin excess

- Grade IV: Marked enlargement, skin excess

There is no cure for any congenital forms of hypertrichosis. The treatment for acquired hypertrichosis is based on attempting to address the underlying cause. Acquired forms of hypertrichosis have a variety of sources, and are usually treated by removing the factor causing hypertrichosis, e.g. a medication with undesired side-effects. All hypertrichosis, congenital or acquired, can be reduced through hair removal. Hair removal treatments are categorized into two principal subdivisions: temporary removal and permanent removal. Treatment may have adverse effects by causing scarring, dermatitis, or hypersensitivity.

Temporary hair removal may last from several hours to several weeks, depending on the method used. These procedures are purely cosmetic. Depilation methods, such as trimming, shaving, and depilatories, remove hair to the level of the skin and produce results that last several hours to several days. Epilation methods, such as plucking, electrology, waxing, sugaring, threading remove the entire hair from the root, the results lasting several days to several weeks.

Permanent hair removal uses chemicals, energy of various types, or a combination to target the cells that cause hair growth. Laser hair removal is an effective method of hair removal on hairs that have color. Laser cannot treat white hair. The laser targets the melanin color in the lower 1/3 of the hair follicle, which is the target zone. Electrolysis (electrology) uses electrical current, and/or localized heating. The U.S. Food and Drug Administration (FDA) allows only electrology to use the term "permanent hair removal" because it has been shown to be able treat all colors of hair.

Medication to reduce production of hair is currently under testing. One medicinal option suppresses testosterone by increasing the sex hormone-binding globulin. Another controls the overproduction of hair through the regulation of a luteinizing hormone.

Hair care products and shampoos can generally be used with any frequency desired, as long as the products are gentle and non-irritating to the scalp. Hair pieces, wigs, hats, and scarves may be used freely.

The preferable way to diagnose the presence of this syndrome would be to use the help of clinical tests and medical reports after the tests and examinations. Now being aware of the subject that HAIR-AN syndrome is caused by genetic, environmental factors and also the hyperandogenism, insulin resistance and acanthosis nigricans, some of the way we could diagnosis this syndrome is by looking for signs in the body for symptoms leading to relate to those key contributors discussed above.

According to studies HAIR-AN is to be found in 1% to 3% women possessing hyperandrogenism. It is an established concept in physiopathology that the androgen in the female body is produced by the stromal ovarian cells, when stimulated by the LH and HCG. The observed activity of these cells was elevated by insulin, and later was found to be used as a determining element to find how severe the hirsutism was. Physicians must look for obesity, as it is also a diagnostic factor in many possible cases.

Hypertrichosis is diagnosed clinically by the occurrence of hair in excess of what is expected for age, sex, and ethnicity in areas that are not androgen-sensitive. The excess can be in the form of excessive length or density and may consist of any hair type (lanugo, vellus, or terminal).

There is no standard treatment for alopecia universalis. Many treatments have been explored, including immunomodulatory agents such as imiquimod. Tofacitinib citrate may also have benefits. In June 2014, it was reported that a 25 year old man with almost no hair on his body grew a full head of hair, and eyebrows, eyelashes, facial, armpit and other hair, following 8 months of treatment.

Some other blood tests are suggestive but not diagnostic. The ratio of LH (Luteinizing hormone) to FSH (Follicle-stimulating hormone), when measured in international units, is elevated in women with PCOS. Common cut-offs to designate abnormally high LH/FSH ratios are 2:1 or 3:1 as tested on Day 3 of the menstrual cycle. The pattern is not very sensitive; a ratio of 2:1 or higher was present in less than 50% of women with PCOS in one study. There are often low levels of sex hormone-binding globulin, in particular among obese or overweight women.

Anti-Müllerian hormone (AMH) is increased in PCOS, and may become part of its diagnostic criteria.

Other causes of irregular or absent menstruation and hirsutism, such as hypothyroidism, congenital adrenal hyperplasia (21-hydroxylase deficiency), Cushing's syndrome, hyperprolactinemia, androgen secreting neoplasms, and other pituitary or adrenal disorders, should be investigated.

There is currently researching being done to find more treatments dependent on the different pre-existing conditions.

Studies are being conducted in which madarosis can be related to malignancy. A study by Groehler and Rose found that there was a statistical significance between these two. They concluded that patients malignancy lesions on the eyelid have a higher chance of having madarosis than a patient with a benign lesion. They stated that despite the fact that it is significant, the absence of madarosis does not mean the lesion cannot be malignant.

In many leprosy cases, madarosis is a symptom or a quality after diagnosis. However, in India, leprosy is common and researchers report a case of madarosis before diagnosis of leprosy with no skin lesions, only madarosis. This allowed for quicker treatment.

A main reason many people have madarosis is due to the chemotherapy drugs. There was a clinical trial in 2011 that tested an eyelash gel called bimatoprost. This gel enhanced the eyelashes in quantity and thickness. They tested this on 20 breast cancer patients who were undergoing chemotherapy. Results seemed positive, in that the group of people who used the gel had growth of eyelashes after the chemotherapy drugs.

Gonadectomy at time of diagnosis is the current recommendation for PAIS if presenting with cryptorchidism, due to the high (50%) risk of germ cell malignancy. The risk of malignancy when testes are located intrascrotally is unknown; the current recommendation is to biopsy the testes at puberty, allowing investigation of at least 30 seminiferous tubules, with diagnosis preferably based on OCT3/4 immunohistochemistry, followed by regular examinations. Hormone replacement therapy is required after gonadectomy, and should be modulated over time to replicate the hormone levels naturally present in the body during the various stages of puberty. Artificially induced puberty results in the same, normal development of secondary sexual characteristics, growth spurt, and bone mineral accumulation. Women with PAIS may have a tendency towards bone mineralization deficiency, although this increase is thought to be less than is typically seen in CAIS, and is similarly managed.

Unfortunately, the number of differentials to consider for PAIS is particularly large. Prompt diagnosis is particularly urgent when a child is born with ambiguous genitalia, as some causes are associated with potentially life-threatening adrenal crises. Determination of testosterone, testosterone precursors and dihydrotestosterone (DHT) at baseline and / or after human chorionic gonadotropin (hCG) stimulation can be used to exclude such defects in androgen biosynthesis.

Approximately one half of all 46,XY individuals born with ambiguous genitalia will not receive a definitive diagnosis. Androgen receptor (AR) gene mutations cannot be found in 27% to 72% of individuals with PAIS. As a result, genetic analysis can be used to confirm a diagnosis of PAIS, but it cannot be used to rule out PAIS. Evidence of abnormal androgen binding in a genital skin fibroblast study has long been the gold standard for the diagnosis of PAIS, even when an AR mutation is not present. However, some cases of PAIS, including AR-mutant-positive cases, will show normal androgen binding. A family history consistent with X-linked inheritance is more commonly found in AR-mutant-positive cases than AR-mutant-negative cases.

The use of dynamic endocrine tests is particularly helpful in isolating a diagnosis of PAIS. One such test is the human chorionic gonadotropin (hCG) stimulation test. If the gonads are testes, there will be an increase in the level of serum testosterone in response to the hCG, regardless of testicular descent. The magnitude of the testosterone increase can help differentiate between androgen resistance and gonadal dysgenesis, as does evidence of a uterus on ultrasound examination. Testicular function can also be assessed by measuring serum anti-Müllerian hormone levels, which in turn can further differentiate PAIS from gonadal dysgenesis and bilateral anorchia.

Another useful dynamic test involves measuring the response to exogenous steroids; individuals with AIS show a decreased response in serum sex hormone binding globulin (SHBG) after a short term administration of anabolic steroids. Two studies indicate that measuring the response in SHBG after the administration of stanozolol could help to differentiate individuals with PAIS from those with other causes of ambiguous genitalia, although the response in individuals with predominantly male phenotypes overlaps somewhat with the response in normal males.