Since there is no cure for albinism, it is managed through lifestyle adjustments. People with albinism need to take care not to sunburn and should have regular healthy skin checks by a dermatologist.

For the most part, treatment of the eye conditions consists of visual rehabilitation. Surgery is possible on the extra-ocular muscles to decrease strabismus. Nystagmus-damping surgery can also be performed, to reduce the "shaking" of the eyes back and forth. The effectiveness of all these procedures varies greatly and depends on individual circumstances.

Glasses, low vision aids, large-print materials, and bright angled reading lights can help individuals with albinism. Some people with albinism do well using bifocals (with a strong reading lens), prescription reading glasses, hand-held devices such as magnifiers or monoculars or wearable devices like eSight

and Brainport.

Albinism is often associated with the absence of an iris in the eye. Contact lenses may be colored to block light transmission through the aniridic eye. Some use bioptics, glasses which have small telescopes mounted on, in, or behind their regular lenses, so that they can look through either the regular lens or the telescope. Newer designs of bioptics use smaller light-weight lenses. Some US states allow the use of bioptic telescopes for driving motor vehicles. (See also NOAH bulletin "Low Vision Aids".)

To support those with albinism, and their families, the National Organization for Albinism and Hypopigmentation was set up to provide a network of resources and information.

There is no specific treatment for Chédiak–Higashi syndrome. Bone marrow transplants appear to have been successful in several patients. Infections are treated with antibiotics and abscesses are surgically drained when appropriate. Antiviral drugs such as acyclovir have been tried during the

terminal phase of the disease. Cyclophosphamide and prednisone have been tried. Vitamin C therapy has improved immune function and clotting in some patients.

Different therapeutic modalities have been attempted to repigment the lesions of nevus depigmentosus such as PUVA, excimer laser, and different grafting techniques. PUVA therapy has not been shown to be beneficial. Successful repigmentation was reported in a single case with 14 sessions of excimer laser treatment. Though the repigmentation of nevus depigmentosus is possible by grafting techniques, the results are inconsistent and recurrence is possible. In consideration of the experience of other authors and us, the quality and retention of pigment are unpredictable. These factors need to be considered while consulting and offering any treatment to the patient of nevus depigmentosus.

Genetic testing can confirm albinism and what variety it is, but offers no medical benefits except in the cases of non-OCA disorders that cause albinism "along with" other medical problems which may be treatable. There is no 'cure' for Albinism. The "symptoms" of albinism can be assisted by various methods.

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.

People with hemeralopia may benefit from sunglasses. Wherever possible, environmental illumination should be adjusted to comfortable level. Light-filtering lenses appear to help in people reporting photophobia.

Otherwise, treatment relies on identifying and treating any underlying disorder.

While there is no cure for HPS, treatment for chronic hemorrhages associated with the disorder includes therapy with vitamin E and the antidiuretic dDAVP.

Regular administration of exogenous granulocyte colony-stimulating factor (filgrastim) clinically improves neutrophil counts and immune function and is the mainstay of therapy, although this may increase risk for myelofibrosis and acute myeloid leukemia in the long term.

Over 90% of SCN responds to treatment with granulocyte colony-stimulating factor (filgrastim), which has significantly improved survival.

Bone marrow transplant may be possible for Severe Combined Immune Deficiency and other severe immunodeficiences.

Virus-specific T-Lymphocytes (VST) therapy is used for patients who have received hematopoietic stem cell transplantation that has proven to be unsuccessful. It is a treatment that has been effective in preventing and treating viral infections after HSCT. VST therapy uses active donor T-cells that are isolated from alloreactive T-cells which have proven immunity against one or more viruses. Such donor T-cells often cause acute graft-versus-host disease (GVHD), a subject of ongoing investigation. VSTs have been produced primarily by ex-vivo cultures and by the expansion of T-lymphocytes after stimulation with viral antigens. This is carried out by using donor-derived antigen-presenting cells. These new methods have reduced culture time to 10–12 days by using specific cytokines from adult donors or virus-naive cord blood. This treatment is far quicker and with a substantially higher success rate than the 3–6 months it takes to carry out HSCT on a patient diagnosed with a primary immunodeficiency. T-lymphocyte therapies are still in the experimental stage; few are even in clinical trials, none have been FDA approved, and availability in clinical practice may be years or even a decade or more away.

There is no known curative treatment presently. Hearing aids and cataract surgery may be of use. Control of seizures, heart failure and treatment of infection is important. Tube feeding may be needed.

The treatment of primary immunodeficiencies depends foremost on the nature of the abnormality. Somatic treatment of primarily genetic defects is in its infancy. Most treatment is therefore passive and palliative, and falls into two modalities: managing infections and boosting the immune system.

Reduction of exposure to pathogens may be recommended, and in many situations prophylactic antibiotics or antivirals may be advised.

In the case of humoral immune deficiency, immunoglobulin replacement therapy in the form of intravenous immunoglobulin (IVIG) or subcutaneous immunoglobulin (SCIG) may be available.

In cases of autoimmune disorders, immunosuppression therapies like corticosteroids may be prescribed.

The treatment of genetic disorders is an ongoing battle with over 1800 gene therapy clinical trials having been completed, are ongoing, or have been approved worldwide. Despite this, most treatment options revolve around treating the symptoms of the disorders in an attempt to improve patient quality of life.

Gene therapy refers to a form of treatment where a healthy gene is introduced to a patient. This should alleviate the defect caused by a faulty gene or slow the progression of disease. A major obstacle has been the delivery of genes to the appropriate cell, tissue, and organ affected by the disorder. How does one introduce a gene into the potentially trillions of cells which carry the defective copy? This question has been the roadblock between understanding the genetic disorder and correcting the genetic disorder.

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.

Oculocutaneous albinism (OCA) is a form of albinism involving the eyes (""), the skin ("-"), and according to some definitions, the hair.

Overall, an estimated 1 in 20,000 people worldwide are born with oculocutaneous albinism. OCA is caused by mutations in several genes that control the synthesis of melanin within the melanocytes.

Four types of oculocutaneous albinism have been described, all caused by a disruption of melanin synthesis and all autosomal recessive disorders.

Ocular albinism is a form of albinism which, in contrast to oculocutaneous albinism, presents primarily in the eyes. There are multiple forms of ocular albinism, which are clinically similar.

Both known genes are on the X chromosome. When the term ""autosomal recessive ocular albinism"" ("AROA") is used, it usually refers to mild variants of oculocutaneous albinism rather than ocular albinism, which is "X-linked".

A preoperative pulmonology consultation is needed. The anesthesia team should

be aware that patients may have postoperative pulmonary complications as part

of the syndrome.

Preoperative hematology consultation is advisable prior to elective ocular

surgeries. Since patients with the syndrome have bleeding tendencies,

intraoperative, perioperative, and postoperative hemorrhages should be

prevented and treated. If platelet aggregation improves with desmopressin, it

may be administered in the preoperative period. However, sometimes

plasmapheresis is needed in the perioperative period.

Ophthalmologists should try to avoid retrobulbar blocks in patients with the

syndrome. Whenever possible, patients with HPS may benefit from general

endotracheal anesthesia. Phacoemulsification may help prevent intraoperative

and postoperative bleeding in patients with the syndrome. Prolonged bleeding

has been reported following strabismus surgery in patients with the syndrome.

The best treatment is prevention in patients with a known predisposition. This includes preventing unnecessary trauma or surgery (including ear piercing, elective mole removal), whenever possible. Any skin problems in predisposed individuals (e.g., acne, infections) should be treated as early as possible to minimize areas of inflammation.

Treatment of a keloid scar is age dependent. Radiotherapy, anti-metabolites and corticoids would not be recommended to be used in children, in order to avoid harmful side effects, like growth abnormalities.

In adults, corticosteriods combined with 5-FU and PDL in a triple therapy, enhance results and diminish side effects.

Further prophylactic and therapeutic strategies include pressure therapy, silicone gel sheeting, intra-lesional triamcinolone acetonide (TAC), cryosurgery, radiation, laser therapy, IFN, 5-FU and surgical excision as well as a multitude of extracts and topical agents.

Surgical excision is currently still the most common treatment for a significant amount of keloid lesions. However, when used as the solitary form of treatment there is a large recurrence rate of between 70 and 100%. It has also been known to cause a larger lesion formation on recurrence. While not always successful alone, surgical excision when combined with other therapies dramatically decreases the recurrence rate. Examples of these therapies include but are not limited to radiation therapy, pressure therapy and laser ablation. Pressure therapy following surgical excision has shown promising results, especially in keloids of the ear and earlobe. The mechanism of how exactly pressure therapy works is unknown at present but many patients with keloid scars and lesions have benefited from it.

Should keloids occur, the most effective treatment is superficial external beam radiotherapy (SRT), which can achieve cure rates of up to 90%.

Additionally, intralesional injection with a corticosteroid such as Kenalog does appear to aid in the reduction of inflammation and pruritus.

Cryotherapy or cryosurgery is an application of extreme cold to treat keloids. This treatment method is easy to perform and has shown results with least chance of recurrence.

Phototherapy is considered a second-line treatment for vitiligo. Exposing the skin to light from UVB lamps is the most common treatment for vitiligo. The treatments can be done at home with an UVB lamp or in a clinic. The exposure time is managed so that the skin does not suffer overexposure. Treatment can take a few weeks if the spots are on the neck and face and if they existed not more than 3 years. If the spots are on the hands and legs and have been there more than 3 years, it can take a few months. Phototherapy sessions are done 2–3 times a week. Spots on a large area of the body may require full body treatment in a clinic or hospital. UVB broadband and narrowband lamps can be used, but narrowband ultraviolet picked around 311 nm is the choice. It has been constitutively reported that a combination of UVB phototherapy with other topical treatments improves re-pigmentation. However, some vitiligo patients may not see any changes to skin or re-pigmentation occurring. A serious potential side effect involves the risk of developing skin cancer, the same risk as an over-exposure to natural sunlight.

Ultraviolet light (UVA) treatments are normally carried out in a hospital clinic. Psoralen and ultraviolet A light (PUVA) treatment involves taking a drug that increases the skin's sensitivity to ultraviolet light, then exposing the skin to high doses of UVA light. Treatment is required twice a week for 6–12 months or longer. Because of the high doses of UVA and psoralen, PUVA may cause side effects such as sunburn-type reactions or skin freckling.

Narrowband ultraviolet B (NBUVB) phototherapy lacks the side-effects caused by psoralens and is as effective as PUVA. As with PUVA, treatment is carried out twice weekly in a clinic or every day at home, and there is no need to use psoralen.

Not all genetic disorders directly result in death, however there are no known cures for genetic disorders. Many genetic disorders affect stages of development such as Down syndrome. While others result in purely physical symptoms such as muscular dystrophy. Other disorders, such as Huntington's disease show no signs until adulthood. During the active time of a genetic disorder, patients mostly rely on maintaining or slowing the degradation of quality of life and maintain patient autonomy. This includes physical therapy, pain management, and may include a selection of alternative medicine programs.

In secondary cases, treatment of the cause, where possible, is indicated. Additionally, treatment for HLH itself is usually required.

While optimal treatment of HLH is still being debated, current treatment regimes usually involve high dose corticosteroids, etoposide and cyclosporin. Intravenous immunoglobulin is also used. Methotrexate and vincristine have also been used. Other medications include cytokine targeted therapy.

An experimental treatment, an anti IFN-gamma monoclonal antibody tentatively named NI-0501, is in clinical trials for treating primary HLH. The FDA awarded breakthrough drug status to NI-0501 in 2016.

Piebaldism is a rare autosomal dominant disorder of melanocyte development. Common characteristics include a congenital white forelock, scattered normal pigmented and hypopigmented macules and a triangular shaped depigmented patch on the forehead. There is nevertheless great variation in the degree and pattern of presentation, even within affected families. In some cases, piebaldism occurs together with severe developmental problems, as in Waardenburg syndrome and Hirschsprung's disease. It has been documented to occur in all races; early photographers captured many images of African piebalds used as a form of amusement, and George Catlin is believed to have painted several portraits of Native Americans of the Mandan tribe who were affected by piebaldism. Piebaldism is found in nearly every species of mammal. It is very common in mice, rabbits, dogs, sheep, deer, cattle and horses—where selective breeding has increased the incidence of the mutation-, but occurs among chimpanzees and other primates only as rarely as among humans. Piebaldism is completely unrelated to acquired or infectious conditions such as vitiligo or poliosis.

"Pie" is a word for multi-colored and "bald" is related to a root word for "skin." Although piebaldism may visually appear to be partial albinism, it is a fundamentally different condition. The vision problems associated with albinism are not usually present as eye pigmentation is normal. Piebaldism differs from albinism in that the affected cells maintain the ability to produce pigment but have that specific function turned off. In albinism the cells lack the ability to produce pigment altogether. Human piebaldism has been observed to be associated with a very wide range and varying degrees of endocrine disorders, and is occasionally found together with heterochromia of the irises, congenital deafness, or incomplete gastrointestinal tract development, possibly all with the common cause of premature cutting off of human fetal growth hormone during gestation. Piebaldism is a kind of neurocristopathy, involving defects of various neural crest cell lineages that include melanocytes, but also involving many other tissues derived from the neural crest. Oncogenic factors, including mistranscription, are hypothesized to be related to the degree of phenotypic variation among affected individuals.

In mild cases, vitiligo patches can be hidden with makeup or other cosmetic camouflage solutions. If the affected person is pale-skinned, the patches can be made less visible by avoiding tanning of unaffected skin.

Leucism (; or ) is a condition in which there is partial loss of pigmentation in an animal resulting in white, pale, or patchy coloration of the skin, hair, feathers, scales or cuticle, but not the eyes. Unlike albinism, it is caused by a reduction in multiple types of pigment, not just melanin.

Ocular albinism type 1 (OA1), also called Nettleship–Falls syndrome, is the most common type of ocular albinism, with a prevalence rate of 1:50,000. It is an inheritable classical Mendelian type X-linked recessive disorder wherein the retinal pigment epithelium lacks pigment while hair and skin appear normal. Since it is usually an X-linked disorder, it occurs mostly in males, while females are carriers unless they are homozygous. About 60 missense and nonsense mutations, insertions, and deletions have been identified in "Oa1". Mutations in OA1 have been linked to defective glycosylation and thus improper intracellular transportation.

The eponyms of the name "Nettleship–Falls syndrome" are the ophthalmologists Edward Nettleship and Harold Francis Falls.

These are localized white spots on skin which may affect any area of the body, but these white spots are quite stable lesions. In the majority of patients, the lesions are not completely achromic, but are hypopigmented and resemble splashed paint. The individual lesions are permanent and there are no effective therapies for re-pigmenting this nevus. If there is hair in an affected area, it is usually colourless or white.