Several medications can cause generalized or localized acquired hypertrichosis including:

Anticonvulsants: phenytoin

Immunosuppressants: cyclosporine

Vasodilators: diazoxide and minoxidil

Antibiotics: streptomycin

Diuretics: acetazolamide

Photosensitizes: Psoralen.

The acquired hypertrichosis is usually reversible once these medications are discontinued.

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.

Sabinas brittle hair syndrome is inherited as an autosomal recessive genetic trait.

In a study by Howell et al. patients were located and studied by means of complete histories and physical examinations, analyses of serum trace metals, ceruloplasmin concentration, urine and serum amino acids, and routine metabolic urine screens. In addition, serum and urine luteinizing hormone (LH) and follicle-stimulating hormone (FSH) values were determined, and were interpreted in conjunction with total plasma estrogen, estradiol, and testosterone levels. Close examination demonstrated the scalp hairs were very brittle, coarse, wiry in texture, and broke off quite easily with mechanical trauma such as combing and brushing. Some hairs could be visualized in their follicles, which were broken off at the skin line. Most patients had accompanying hyperkeratosis (thickening of the skin) of moderate degree on exposed surfaces. Maxillary hypoplasia (midfacial retrusion) was significant in many patients. The brittle, short hair, reduced eyelashes, crowded teeth, and dull appearance created a characteristic facial appearance. Post-pubertal patients had development of secondary sexual characteristics consistent with their age, except for sparse pubic escutcheons. All cases studied demonstrated some degree of mental deficiency; I.Q.'s ranged between 50–60. A deficiency in eye–hand coordination was also noted.

Avoid aggressive brushing and grooming, strong chemicals, permanents, straightening, and similar hair-damaging habits.

This condition is self-limiting. Improvements in grooming techniques and in environmental conditions will correct the abnormality.

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.

Sabinas brittle hair syndrome, also called Sabinas syndrome or brittle hair-mental deficit syndrome, is an autosomal recessive congenital disorder affecting the integumentary system.

Ear hair generally refers to the terminal hair arising from follicles inside the external auditory meatus in humans. In its broader sense, "ear hair" may also include the fine vellus hair covering much of the ear, particularly at the prominent parts of the anterior ear, or even the abnormal hair growth as seen in hypertrichosis and hirsutism. Medical research on the function of ear hair is currently very scarce.

Hair growth within the ear canal is often observed to increase in older men, together with increased growth of nose hair. Visible hair that protrudes from the ear canal is sometimes trimmed for cosmetic reasons. Excessive hair growth within or on the ear is known medically as "auricular hypertrichosis". Some men, particularly in the male population of India, have coarse hair growth along the lower portion of the helix, a condition referred to as "having "hairy pinnae"" ("hypertrichosis lanuginosa acquisita").

Other syndromes with hair abnormalities may also show features of uncombable hair syndrome such as Rapp–Hodgkin ectodermal dysplasia syndrome, loose anagen syndrome, EEC syndrome (ectodermal dysplasia, ectrodactyly and cleft lip/palate) and familial tricho-odonto-onychial ectodermal dysplasia with syndactyly. However, unlike these conditions, uncombable hair syndrome alone is not associated with physical, neurologic, or mental abnormalities.

There is controversy over whether auricular hypertrichosis is a Y-linked or autosomal trait, or perhaps both (in different families). It was proposed also that this phenotype results from the interaction of two loci, one on the homologous part of the X and Y and one on the nonhomologous sequence of the Y.

Lee et al. (2004), by Y-chromosomal DNA binary-marker haplotyping, suggested that a cohort of southern Indian hairy-eared males carried Y chromosomes from many haplogroups of the Y-phylogeny. According to a hypothesis of Y linkage, it would require multiple independent mutations within a single population. No significant difference between the Y-haplogroup frequencies of hairy-eared males and those of a geographically matched control sample of unaffected males was established. They concluded that the auricular hypertrichosis is not Y-linked in southern India, but it is unlikely to be same in any population.

Genetic forms of localized autosomal recessive hypotrichosis include:

Individuals affected by certain ED syndromes cannot perspire. Their sweat glands may function abnormally or may not have developed at all because of inactive proteins in the sweat glands. Without normal sweat production, the body cannot regulate temperature properly. Therefore, overheating is a common problem, especially during hot weather. Access to cool environments is important.

Pure hair-nail type ectodermal dysplasia is a genetic mutation in the "hair matrix and cuticle keratin KRTHB5 gene" that causes ectodermal dysplasia of hair and nail type. Manifestations of this disorder include onychodystrophy and severe hypotrichosis. It represents as an autosomal dominant trait.

Many medications are being studied, including abatacept, MEXIS/M6S, triamcinolone, secukinumab, tralonkinumab, apremilast, botulinum toxin, INCB018424, bimatoprost, clobetasol, AS101, autologous platelet-rich plasma, topical minoxidil, and nitric oxide gel. Some of these medications are approved for other diseases, others are not available outside of studies.

In 2014, preliminary findings showing that oral ruxolitinib, a drug approved by the US Food and Drug Administration (FDA) for bone marrow disorder myelofibrosis, restored hair growth in three individuals with long-standing and severe disease. The medicine costs almost USD $10,000 a month.

The hair is normal in quantity and is usually silvery-blond or straw-colored. It is disorderly, it stands out from the scalp, and cannot be combed flat. The underlying structural anomaly is longitudinal grooving of the hair shaft, which appears triangular in cross section. This is caused by mutations in one of three possible genes; "PADI3", "TGM" or "TCHH3." The characteristic hair shaft anomaly can be demonstrated in asymptomatic family members by scanning electron microscopy. To be noticeable, 50% of hairs must be affected by the structural abnormality. Improvement often occurs in later childhood. An autosomal dominant mode of inheritance has been suggested though an autosomal recessive pattern with varying degrees of penetrance has also been noted. The stiffness of the uncombable hair has been reasoned to be due to the triangular form of the hair shaft in cross section. It has been suggested that the condition may result from premature keratinization of the inner root sheath.

Focal dermal hypoplasia (also known as "Goltz syndrome") is a form of ectodermal dysplasia. It is a multisystem disorder characterized primarily by skin manifestations to the atrophic and hypoplastic areas of skin which are present at birth. These defects manifest as yellow-pink bumps on the skin and pigmentation changes. The disorder is also associated with shortness of stature and some evidence suggests that it can cause epilepsy.

Focal dermal hypoplasia has been associated with PORCN gene mutations on the X chromosome. 90% of the individuals who are affected with the syndrome are female: the commonly accepted, though unconfirmed, explanation for this is that the non-mosaic hemizygous males are not viable.

The differential diagnosis of focal dermal hypoplasia (Goltz) syndrome includes autosomal recessive Setleis syndrome due to TWIST2 gene mutations. It associated with morning glory anomaly, polymicrogyria, incontinentia pigmenti, oculocerebrocutaneous syndrome, Rothmund-Thomson syndrome and microphthalmia with linear skin defects (also known as MLS) syndrome because they are all caused by deletions or point mutations in the HCCS gene.

Several studies have examined salivary flow rate in individuals and found parotid and submandibular salivary flow ranging from 5 to 15 times lower than average. This is consistent with the salivary glands being of ectodermal origin, although some findings have suggested that there is also mesodermal input.

Prosthetic replacement of missing teeth is possible using dental implant technology or dentures. This treatment can be successful in giving patients with anodontia a more aesthetically pleasing appearance. The use of an implant prosthesis in the lower jaw could be recommended for younger patients as it is shown to significantly improve the craniofacial growth, social development and self-image. The study associated with this evidence worked with individuals who had ectodermal dysplasia of varying age groups of up to 11, 11 to 18 and more than 18 years. It was noted that the risk of implant failure was significantly higher in patients younger than 18 years, but there is significant reason to use this methodology of treatment in those older. Overall the use of an implant-prosthesis has a considerable functional, aesthetic and psychological advantage when compared to a conventional denture, in the patients.

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.

No specific treatment or cure exists. Affected children usually need total parenteral nutrition through a central venous catheter. Further worsening of liver damage should however be avoided if possible. Diarrhea will likely continue even though food stops passing through the gastrointestinal system. They can subsequently be managed with tube feeding, and some may be weaned from nutritional support during adolescence.

Treatment for the disease itself is nonexistent, but there are options for most of the symptoms. For example, one suffering from hearing loss would be given hearing aids, and those with Hirschsprung’s disorder can be treated with a colostomy.

If the Hirschsprung's disease is treated in time, ABCD sufferers live otherwise healthy lives. If it is not found soon enough, death often occurs in infancy. For those suffering hearing loss, it is generally regressive and the damage to hearing increases over time. Digestive problems from the colostomy and reattachment may exist, but most cases can be treated with laxatives. The only other debilitating symptom is hearing loss, which is usually degenerative and can only be treated with surgery or hearing aids.

The genetic determination of presence or absence of hair on the dorsal aspect of the middle phalanx was first suggested by Danforth (1921). From a study of 80 families with a total of 178 children, he suggested that 'a phylogenetically progressive loss of hair is brought about through the action of one or more recessive genes, or of one primary recessive gene with several modifying factors that regulate the distribution of hair when it is present.' Stated conversely, 'despite the fact that in evolutionary progress hair is disappearing from the mid-digital region, its presence...may be regarded as the manifestation of a dominant trait.'

Bernstein and Burks (1942)

suggested that 5 allelic genes, A-0 to A-4, 'control the inheritance and distribution of middigital hair involving but a single gene substitution (the subscript denoting the number of fingers affected with middigital hair),' and that the genes for the presence of hair are dominant over the genes for its absence.

From a literature review and their own study in Brazil, Saldanha and Guinsburg (1961) suggested that lack of middle phalangeal hair may be determined by a pair of recessive genes, but noted that the occurrence of sex, age, and possibly environmental differences make genetic analysis of the trait difficult.

Egesi and Rashid (2010) reviewed the subject of middigital hair and its clinical significance.

Poliosis, also called poliosis circumscripta, is the decrease or absence of melanin (or colour) in head hair, eyebrows, eyelashes or any other hairy area. It is popularly known as white forelock when it affects hair right above the forehead.

This condition can cause single or, less commonly, multiple white patches on the hair. Some mistake these white patches for simple birth marks. In poliosis there is decreased or absent melanin in the hair bulbs of affected hair follicles; the melanocytes of the skin are usually not affected. Poliosis occurs in several genetic syndromes such as piebaldism, Waardenburg syndrome, neurofibromatosis type I, and tuberous sclerosis. It can also occur in conditions such as vitiligo, Vogt–Koyanagi–Harada disease, alopecia areata, sarcoidosis, and in association with neoplasms and some medications.

It can give rise to a "Mallen streak" that can be hereditary. Catherine Cookson wrote a novel and later a TV series called "The Mallen Streak", where a family had the condition. Sports presenter Dickie Davies, runner Sam Brown, and fashion expert Stacy London were famous for their respective Mallen streak.