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.

A doctor will take a thorough medical history, and may take blood tests as well as examining liver and kidney function. Improvements have also been reported from treating malnutrition associated with zinc deficiency and other minerals. Intracellular (red blood cell) assays are more sensitive than tests for plasma levels.

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.

The main diagnosis technique is observing the area. Then blood tests can be done to determine if there is a pre-existing condition. Family history can be considered because some of the related causes/conditions can be inherited.

This is historically the first classification system proposed, and is still in use for the classification of patients with skin/dermatologic diseases (i.e., psoriasis, HS, acne). Hurley separated patients into three groups based largely on the presence and extent of cicatrization and sinuses. It has been used as a basis for clinical trials in the past and is a useful basis to approach therapy for patients. These three stages are based on Hurley's staging system, which is simple and relies on the subjective extent of the diseased tissue the patient has. Hurley's three stages of hidradenitis suppurativa are:

The Sartorius staging system is more sophisticated than Hurley's. Sartorius "et al." suggested that the Hurley system is not sophisticated enough to assess treatment effects in clinical trials during research. This classification allows for better dynamic monitoring of the disease severity in individual patients. The elements of this staging system are:

- Anatomic regions involved (axilla, groin gluteal, or other region or inframammary region left or right)

- Number and types of lesions involved (abscesses, nodules, fistulas [actually sinuses], scars, points for lesions of all regions involved)

- The distance between lesions, in particular the longest distance between two relevant lesions (i.e., nodules and fistulas in each region or size if only one lesion present)

- The presence of normal skin in between lesions (i.e., are all lesions clearly separated by normal skin?)

Points are accumulated in each of the above categories, and added to give both a regional and total score. In addition, the authors recommend adding a visual analog scale for pain or using the dermatology life quality index (DLQI, or the Skindex) when assessing HS.

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.

Using non-oily cleansers and mild soap may not cause as much irritation to the skin as regular soap. Blackheads can be removed across an area with commercially available pore-cleansing strips or the more aggressive cyanoacrylate method used by dermatologists.

Squeezing blackheads and whiteheads can remove them, but it can also damage the skin. Doing so increases the risk of causing or transmitting infection and scarring, as well as potentially pushing any infection deeper into the skin. Comedo extractors are used with careful hygiene in beauty salons and by dermatologists, usually after using steam or warm water.

Complementary medicine options for acne in general have not been shown to be effective in trials. These include aloe vera, pyridoxine (vitamin B6), fruit-derived acids, kampo (Japanese herbal medicine), ayurvedic herbal treatments and acupuncture.

Some acne treatments target infection specifically, but there are treatments that are aimed at the formation of comedones as well. Others remove the dead layers of the skin and may help clear blocked pores.

Dermatologists can often extract open comedones with minimal skin trauma, but closed comedones are more difficult. Laser treatment for acne might reduce comedones, but dermabrasion and laser therapy have also been known to cause scarring.

Macrocomedones (1 mm or larger) can be removed by a dermatologist using surgical instruments or cauterized with a device that uses light. The acne drug isotretinoin can cause severe flare-ups of macrocomedones, so dermatologists recommend removal before starting the drug and during treatment.

Some research suggests that the common acne medications, retinoids and azelaic acid, are beneficial and do not cause increased pigmentation of the skin.

Many skin conditions can mimic acne vulgaris and are collectively known as acneiform eruptions. Such conditions include angiofibromas, epidermal cysts, flat warts, folliculitis, keratosis pilaris, milia, perioral dermatitis, and rosacea, among others. Age is one factor which may help distinguish between these disorders. Skin disorders such as perioral dermatitis and keratosis pilaris can appear similar to acne but tend to occur more frequently in childhood, whereas rosacea tends to occur more frequently in older adults. Facial redness triggered by heat or the consumption of alcohol or spicy food is suggestive of rosacea. The presence of comedones helps health professionals differentiate acne from skin disorders that are similar in appearance. Chloracne, due to exposure to certain chemicals, may look very similar to acne vulgaris.

Comedones (blackheads and whiteheads) must be present to diagnose acne. In their absence, an appearance similar to that of acne would suggest a different skin disorder. Microcomedones (the precursor to blackheads and whiteheads) are not visible to the naked eye when inspecting the skin and can only be seen with a microscope. There are many features that may indicate a person's acne vulgaris is sensitive to hormonal influences. Historical and physical clues that may suggest hormone-sensitive acne include onset between ages 20 and 30; worsening the week before a woman's menstrual cycle; acne lesions predominantly over the jawline and chin; and inflammatory/nodular acne lesions.

Several scales exist to grade the severity of acne vulgaris, but no single technique has been universally accepted as the diagnostic standard. Cook's acne grading scale uses photographs to grade severity from 0 to 8 (0 being the least severe and 8 being the most severe). This scale was the first to use a standardized photographic protocol to assess acne severity; since its creation in 1979, the scale has undergone several revisions. The Leeds acne grading technique counts acne lesions on the face, back, and chest and categorizes them as inflammatory or non-inflammatory. Leeds scores range from 0 (least severe) to 10 (most severe) though modified scales have a maximum score of 12. The Pillsbury acne grading scale simply classifies the severity of the acne from 1 (least severe) to 4 (most severe).

There are a wide range of depigmenting treatments used for hyperpigmentation conditions, and responses to most are variable.

Most often treatment of hyperpigmentation caused by melanin overproduction (such as melasma, acne scarring, liver spots) includes the use of topical depigmenting agents, which vary in their efficacy and safety, as well as in prescription rules. Several are prescription only in the US, especially in high doses, such as hydroquinone, azelaic acid, and koijic acid. Some are available without prescription, such as niacinamide, or cysteamine hydrochloride. Hydroquinone was the most commonly prescribed hyperpigmentation treatment before the long-term safety concerns were raised, and the use of it became more regulated in several countries and discouraged in general by WHO. For the US only 2% is at present sold over-the-counter, and 4% needs prescription. In the EU hydroquinone was banned from cosmetic applications. Treatments that do not involve topical agents are also available, including fraction lasers and dermabrasion.

The most effective prevention is to grow a beard. For men who are required to; or simply prefer to shave, studies show the optimal length to be about 0.5 mm to 1 mm to prevent their hair growing back into the skin. Using a beard trimmer at the lowest setting (0.5mm or 1mm) instead of shaving is an effective alternative. The resulting faint stubble can be shaped using a standard electric razor on non-problematic areas (cheeks, lower neck).

For most cases, completely avoiding shaving for three to four weeks allows all lesions to subside, and most extrafollicular hairs will resolve themselves in about ten days.

Permanent removal of the hair follicle is the only definitive treatment for PFB. Electrolysis is effective but limited by its slow pace, pain and expense. Laser-assisted hair removal is effective. There is a risk of skin discoloration and a very small risk of scarring.

Exfoliation with various tools such as brushes and loofahs also helps prevent bumps.

Some men use electric razors to control PFB. Those who use a razor, should use a single blade or special wire-wrapped blade to avoid shaving too closely, with a new blade each shave. Shaving in the direction of hair growth every other day, rather than daily, may improve pseudofolliculitis barbae. If one must use a blade, softening the beard first with a hot, wet washcloth for five minutes or shave while showering in hot water can be helpful. Some use shaving powders (a kind of chemical depilatory) to avoid the irritation of using a blade. Barium sulfide-based depilatories are most effective, but produce an unpleasant smell.

The diagnosis of IP is established by clinical findings and occasionally by corroborative skin biopsy. Molecular genetic testing of the NEMO IKBKG gene (chromosomal locus Xq28) reveals disease-causing mutations in about 80% of probands. Such testing is available clinically.

In addition, females with IP have skewed X-chromosome inactivation; testing for this can be used to support the diagnosis.

Many people in the past were misdiagnosed with a second type of IP, formerly known as IP1. This has now been given its own name - 'Hypomelanosis of Ito' (incontinentia pigmenti achromians). This has a slightly different presentation: swirls or streaks of hypopigmentation and depigmentation. It is "not" inherited and does not involve skin stages 1 or 2. Some 33–50% of patients have multisystem involvement — eye, skeletal, and neurological abnormalities. Its chromosomal locus is at Xp11, rather than Xq28.

Methotrexate and corticosteroids are proposed treatments.

Scalp cooling has specifically been used to prevent alopecia in docetaxel chemotherapy, although it has been found prophylactic in other regimens as well. Treatment effects may take time to resolve, with one study showing breast cancer survivors wearing wigs up to 2 years after chemotherapy.

Telogen effluvium is a scalp disorder characterized by the thinning or shedding of hair resulting from the early entry of hair in the telogen phase (the resting phase of the hair follicle). Emotional or physiological stress may result in an alteration of the normal hair cycle and cause the disorder, with potential causes including eating disorders, fever, childbirth, chronic illness, major surgery, anemia, severe emotional disorders, crash diets, hypothyroidism, and drugs.

Diagnostic tests, which may be performed to verify the diagnosis, include a trichogram, trichoscopy and biopsy. Effluvium can present with similar appearance to alopecia totalis, with further distinction by clinical course, microscopic examination of plucked follicles, or biopsy of the scalp. Histology would show telogen hair follicles in the dermis with minimal inflammation in effluvium, and dense peribulbar lymphocytic infiltrate in alopecia totalis.

Vitamin D levels may also play a role in normal hair cycle.

The most simple treatment for PFB is to let the beard grow. Existing razor bumps can often be treated by removal of the ingrown hair. Extrafollicular hairs can usually be pulled gently from under the skin with tweezers. Using the fingernails to "break" razor bumps can lead to infection and scarring, and should be avoided. Complete removal of the hair from its follicle is not recommended. Severe or transfollicular hairs may require removal by a dermatologist.

Medications are also prescribed to speed healing of the skin. Clinical trials have shown glycolic acid-based peels to be an effective and well-tolerated therapy which resulted in significantly fewer PFB lesions on the face and neck. The mechanism of action of glycolic acid is unknown, but it is hypothesized that straighter hair growth is caused by the reduction of sulfhydrylbonds in the hair shaft by glycolic acid, which results in reduced re-entry of the hair shaft into the follicular wall or epidermis. Salicylic acid peels are also effective. Prescription antibiotic gels (Benzamycin, Cleocin-T) or oral antibiotics are also used. Retin-A is a potent treatment that helps even out any scarring after a few months. It is added as a nightly application of Retin-A Cream 0.05 - 0.1% to the beard skin while beard is growing out. Tea tree oil, Witch Hazel, and Hydrocortisone are also noted as possible treatments and remedies for razor bumps.

Trichorrhexis invaginata (also known as "Bamboo hair" ) is a distinctive hair shaft abnormality that may occur sporadically, either in normal hair or with other hair shaft abnormalities, or regularly as a marker for Netherton's syndrome. The primary defect appears to be abnormal keratinization of the hair shaft in the keratogenous zone, allowing for intussusception of the fully keratinized and hard distal shaft into the incompletely keratinized and soft proximal portion of the shaft.

Genetic forms of localized autosomal recessive hypotrichosis include:

In 1937, Touraine and Solente first noted the association between hair-shaft defects (bamboo node) and ichthyosiform erythroderma. Còme first coined the term ichthyosis linearis circumflexa in 1949, although Rille had previously recorded the distinctive features of ichthyosis linearis circumflexa by 1922. In 1958, Netherton described a young girl with generalized scaly dermatitis and fragile nodular hair-shaft deformities, which he termed trichorrhexis nodosa. Later, this was more appropriately renamed as trichorrhexis invaginata (bamboo hair) for a ball-and-socket–type hair-shaft deformity at the suggestion of Wilkinson et al.

In 1974, Mevorah et al. established the clinical relationship between ichthyosis linearis circumflexa and Netherton syndrome, and an atopic diathesis was found to occur in approximately 75% of patients with Netherton syndrome.

Hypotrichosis ("" + "" + "") is a condition of abnormal hair patterns, predominantly loss or reduction. It occurs, most frequently, by the growth of vellus hair in areas of the body that normally produce terminal hair. Typically, the individual's hair growth is normal after birth, but shortly thereafter the hair is shed and replaced with sparse, abnormal hair growth. The new hair is typically fine, short and brittle, and may lack pigmentation. Baldness may be present by the time the subject is 25 years old.

Hypotrichosis is a common feature of Hallermann–Streiff syndrome as well as others. It can also be used to describe the lack of hair growth due to chemotherapy.

The opposite of hypotrichosis is hypertrichosis, where terminal hair (thick) grows in areas that would otherwise normally have vellus hair (thin), for example abnormally thick facial hair growth in women.

The physical examination of the skin and its appendages, as well as the mucous membranes, forms the cornerstone of an accurate diagnosis of cutaneous conditions. Most of these conditions present with cutaneous surface changes termed "lesions," which have more or less distinct characteristics. Often proper examination will lead the physician to obtain appropriate historical information and/or laboratory tests that are able to confirm the diagnosis. Upon examination, the important clinical observations are the (1) morphology, (2) configuration, and (3) distribution of the lesion(s). With regard to morphology, the initial lesion that characterizes a condition is known as the "primary lesion," and identification of such a lesions is the most important aspect of the cutaneous examination. Over time, these primary lesions may continue to develop or be modified by regression or trauma, producing "secondary lesions." However, with that being stated, the lack of standardization of basic dermatologic terminology has been one of the principal barriers to successful communication among physicians in describing cutaneous findings. Nevertheless, there are some commonly accepted terms used to describe the macroscopic morphology, configuration, and distribution of skin lesions, which are listed below.

Favre–Racouchot syndrome occurs in sun-damaged skin and includes open and closed comedones.

Nevus comedonicus or comedo nevus is a benign hamartoma (birthmark) of the pilosebaceous unit around the oil-producing gland in the skin. It has widened open hair follicles with dark keratin plugs that resemble comedones, but they are not actually comedones.

Dowling-Degos disease is a genetic pigment disorder that includes comedo-like lesions and scars.

Familial dyskeratotic comedones is a rare autosomal dominant genetic condition, with keratotic (tough) papules and comedo-like lesions.

Longitudinal leukonychia is far less common and features smaller 1mm white longitudinal lines visible under the nail plate. It may be associated with Darier's disease.

Acanthosis nigricans should be distinguished from the casal collar appearing in pellagra.

Elevated IgE is the hallmark of HIES. An IgE level greater than 2,000 IU/mL is often considered diagnostic. However, patients younger than 6 months of age may have very low to non-detectable IgE levels. Eosinophilia is also a common finding with greater than 90% of patients having eosinophil elevations greater than two standard deviations above the normal mean. Genetic testing is available for "STAT3" (Job's Syndrome), "DOCK8 (DOCK8 Immunodeficiency or DIDS)", "PGM3" (PGM3 deficiency), "SPINK5" (Netherton Syndrome - NTS), and "TYK2" genetic defects.