There is no known cure at the moment but there are several things that can be done to relieve the symptoms. Moisturising products are very helpful to minimize the scaling/cracking, and anti-infective treatments are useful when appropriate because the skin is very susceptible to infection. Extra protein in the diet during childhood is also beneficial, to replace that which is lost through the previously mentioned "leaky" skin.

Steroid and retinoid products have been proven ineffective against Netherton syndrome, and may in fact make things worse for the affected individual.

Intravenous immunoglobulin has become established as the treatment of choice in Netherton's syndrome. This therapy reduces infection; enables improvement and even resolution of the skin and hair abnormalities, and dramatically improves quality of life of the patients; although exactly how it achieves this is not known. Given this; it is possible that the reason Netherton's usually is not very severe at or shortly after birth is due to a protective effect of maternal antibodies; which cross the placenta but wane by four to six months.

Because XLI is caused by a gene mutation or deletion, there is no "cure." One of the aims of treatment is to reduce scaling by removing the excess, flaky scales, and keep the skin hydrated. This can be achieved using a variety of topical creams.

- Keratolytic agents such as Ammonium lactate (Lac-Hydrin) are used to facilitate the release of retained corneocytes.

- Topical isotretinoin

- The topical receptor-selective retinoid tazarotene

Research is ongoing with regard to the use of gene therapy to treat XLI.

The infant is intubated post delivery to stabilize the respiratory problems experienced. Often the skin condition becomes less severe resolving itself to flaky dry skin as the individual grows. No intervention is usually required and the condition becomes less severe as the patient grows. The dry skin symptoms can be managed with topical ointments or creams and the individual remains otherwise healthy.

In congenital FXII deficiency treatment is not necessary. In acquired FXII deficiency the underlying problem needs to be addressed.

Management of AOS is largely symptomatic and aimed at treating the various congenital anomalies present in the individual. When the scalp and/or cranial bone defects are severe, early surgical intervention with grafting is indicated.

For patients with vWD type 1 and vWD type 2A, desmopressin is available as different preparations, recommended for use in cases of minor trauma, or in preparation for dental or minor surgical procedures. Desmopressin stimulates the release of vWF from the Weibel-Palade bodies of endothelial cells, thereby increasing the levels of vWF (as well as coagulant factor VIII) three- to five-fold. Desmopressin is also available as a preparation for intranasal administration (Stimate) and as a preparation for intravenous administration. Recently, the FDA has approved the use of Baxalta’s Vonvendi. This is the first recombinant form of vWF. The effectiveness of this treatment is different than desmopressin because it only contains vWF, not vWF with the addition of FVIII. This treatment is only recommended for use by individuals who are 18 years of age or older.

Desmopressin is contraindicated in vWD type 2b because of the risk of aggravated thrombocytopenia and thrombotic complications. Desmopressin is probably not effective in vWD type 2M and is rarely effective in vWD type 2N. It is totally ineffective in vWD type 3.

For women with heavy menstrual bleeding, estrogen-containing oral contraceptive medications are effective in reducing the frequency and duration of the menstrual periods. Estrogen and progesterone compounds available for use in the correction of menorrhagia are ethinylestradiol and levonorgestrel (Levona, Nordette, Lutera, Trivora). Administration of ethinylestradiol diminishes the secretion of luteinizing hormone and follicle-stimulating hormone from the pituitary, leading to stabilization of the endometrial surface of the uterus.

Desmopressin is a synthetic analog of the natural antidiuretic hormone vasopressin. Its overuse can lead to water retention and dilutional hyponatremia with consequent convulsion.

For patients with vWD scheduled for surgery and cases of vWD disease complicated by clinically significant hemorrhage, human-derived medium purity factor VIII concentrates, which also contain von Willebrand factors, are available for prophylaxis and treatment. Humate P, Alphanate, Wilate and Koate HP are commercially available for prophylaxis and treatment of vWD. Monoclonally purified factor VIII concentrates and recombinant factor VIII concentrates contain insignificant quantity of vWF, so are not clinically useful.

Development of alloantibodies occurs in 10-15% of patients receiving human-derived medium-purity factor VIII concentrates and the risk of allergic reactions including anaphylaxis must be considered when administering these preparations. Administration of the latter is also associated with increased risk of venous thromboembolic complications.

Blood transfusions are given as needed to correct anemia and hypotension secondary to hypovolemia. Infusion of platelet concentrates is recommended for correction of hemorrhage associated with platelet-type vWD.

The antifibrinolytic agents epsilon amino caproic acid and tranexamic acid are useful adjuncts in the management of vWD complicated by clinical hemorrhage. The use topical thrombin JMI and topical Tisseel VH are effective adjuncts for correction of hemorrhage from wounds.

As with all types of ichthyosis, there is no cure but the symptoms can be relieved.

- Moisturizers

- Prevention of overheating

- Eye drops (to prevent the eyes from becoming dried out)

- Systemic Retinoids (isotretinoin and acitretin are very effective, but careful monitoring for toxicity is required. Only severe cases may require intermittent therapy.)

Psychological therapy or support may be required as well.

There are no life-threatening complications after the perinatal period (around the time of birth) and the skin conditions persist but to a lesser degree of severity. Individuals have a favourable prognosis as symptoms can be managed and past the infancy stage are not life-threatening. The red skin edema improves after a three-week period but the ichthyosis scaling persists. Asthma has been recorded in some cases later on in the individual's life and sign of atopic dermatitis persist, follicular hyperkeratosis and small amounts of scaling at the scalp that goes on into adulthood but otherwise the individual continues a healthy life.

Treatments for ichthyosis often take the form of topical application of creams and emollient oils, in an attempt to hydrate the skin. Creams containing lactic acid have been shown to work exceptionally well in some cases. Application of propylene glycol is another treatment method. Retinoids are used for some conditions.

Exposure to sunlight may improve or worsen the condition. In some cases, excess dead skin sloughs off much better from wet tanned skin after bathing or a swim, although the dry skin might be preferable to the damaging effects of sun exposure.

There can be ocular manifestations of ichthyosis, such as corneal and ocular surface diseases. Vascularizing keratitis, which is more commonly found in congenital keratitis-ichythosis-deafness (KID), may worsen with isotretinoin therapy.

Treatment is depended on the type of glycogen storage disease. E.g. GSD I is typically treated with frequent small meals of carbohydrates and cornstarch to prevent low blood sugar, while other treatments may include allopurinol and human granulocyte colony stimulating factor.

While there is no cure for haemophilia, treatment improves outcomes.

Desmopressin (DDAVP) may be used in those with mild haemophilia A. Tranexamic acid or epsilon aminocaproic acid may be given along with clotting factors to prevent breakdown of clots.

Pain medicines, steroids, and physical therapy may be used to reduce pain and swelling in an affected joint.

Primary prophylaxis with low-molecular weight heparin, heparin, or warfarin is often considered in known familial cases. Anticoagulant prophylaxis is given to all who develop a venous clot regardless of underlying cause.

Studies have demonstrated an increased risk of recurrent venous thromboembolic events in patients with protein C deficiency. Therefore, long-term anticoagulation therapy with warfarin may be considered in these patients.

Homozygous protein C defect constitutes a potentially life-threatening disease, and warrants the use of supplemental protein C concentrates.

Liver transplant may be considered curative for homozygous protein C deficiency.

In terms of hemophilia C medication cyklokapron is often used for both treatment after an incident of bleeding and as a preventative measure to avoid excessive bleeding during oral surgery.

Treatment is usually not necessary, except in relation to operations, leading to many of those having the condition not being aware of it. In these cases, fresh frozen plasma or recombinant factor XI may be used, but only if necessary.

The afflicted may often suffer nosebleeds, while females can experience unusual menstrual bleeding which can be avoided by taking birth control such as: IUDs and oral or injected contraceptives to increase coagulation ability by adjusting hormones to levels similar to pregnancy.

In December 2017, it was reported that doctors had used a new form of gene therapy to treat haemophilia A.

In regards to the treatment of this genetic disorder, most individuals with severe haemophilia require regular supplementation with intravenous recombinant or plasma concentrate Factor VIII. The preventative treatment regime is highly variable and individually determined. In children, an easily accessible intravenous port ( portacath) may have to be inserted to minimise frequent traumatic intravenous cannulation. These devices have made prophylaxis in haemophilia much easier for families because the problems of "finding a vein" for infusion several times a week are eliminated. However, there are risks involved with their use, the most worrisome being that of infection, studies differ but some show an infection rate that is high These infections can usually be treated with intravenous antibiotics but sometimes the device must be removed, also, there are other studies that show a risk of clots forming at the tip of the catheter.Some individuals with severe haemophilia and most with moderate and mild haemophilia treat only as needed without a regular prophylactic schedule. Mild haemophiliacs often manage their condition with desmopressin, which releases stored factor VIII from blood vessel walls.

Treatment is by intravenous infusion of factor IX, which has a longer half life than factor VIII and as such factor IX can be transfused less frequently. Blood transfusions may be needed, NSAIDS should be discontinued once the individual has been diagnosed with the condition. Any surgical procedure should be done "in concert" with tranexamic acid.

Constant care is required to moisturise and protect the skin. The hard outer layer eventually peels off, leaving the vulnerable inner layers of the dermis exposed. Early complications result from infection due to fissuring of the hyperkeratotic plates and respiratory distress due to physical restriction of chest wall expansion.

Management includes supportive care and treatment of hyperkeratosis and skin barrier dysfunction. A humidified incubator is generally used. Intubation is often required until nares are patent. Nutritional support with tube feeds is essential until eclabium resolves and infants can begin nursing. Ophthalmology consultation is useful for the early management of ectropion, which is initially pronounced and resolves as scale is shed. Liberal application of petrolatum is needed multiple times a day. In addition, careful debridement of constrictive bands of hyperkeratosis should be performed to avoid digital ischemia. Cases of digital autoamputation or necrosis have been reported due to cutaneous constriction bands. Relaxation incisions have been used to prevent this morbid complication.

In the past, the disorder was nearly always fatal, whether due to dehydration, infection (sepsis), restricted breathing due to the plating, or other related causes. The most common cause of death was systemic infection and sufferers rarely survived for more than a few days. However, improved neonatal intensive care and early treatment with oral retinoids, such as the drug Isotretinoin (Isotrex), may improve survival. Early oral retinoid therapy has been shown to soften scales and encourage desquamation. After as little as two weeks of daily oral isotretinoin, fissures in the skin can heal, and plate-like scales can nearly resolve. Improvement in the eclabium and ectropion can also be seen in a matter of weeks. Children who survive the neonatal period usually evolve to a less severe phenotype, resembling a severe congenital ichthyosiform erythroderma. Patients continue to suffer from temperature dysregulation and may have heat and cold intolerance. Patients can also have generalized poor hair growth, scarring alopecia, contractures of digits, arthralgias, failure to thrive, hypothyroidism, and short stature. Some patients develop a rheumatoid factor-positive polyarthritis. Survivors can also develop fish-like scales and retention of a waxy, yellowish material in seborrheic areas, with ear adhered to the scalp.

The oldest known survivor is Nusrit "Nelly" Shaheen, who was born in 1984 and is in relatively good health as of April 2016. Lifespan limitations have not yet been determined with the new treatments.

A study published in 2011 in the Archives of Dermatology concluded, "Harlequin ichthyosis should be regarded as a severe chronic disease that is not invariably fatal. With improved neonatal care and probably the early introduction of oral retinoids, the number of survivors is increasing."

Even though there is no way to cure the disease itself, there are ways to dampen the symptoms. These include medical help in form of pills, and using heavy lotions and oils.

To maintain the good health of the skin after the symptoms have dampened the person with the disease are advised to go on normally with their lives but to take precautions while showering. This is to take shorter, colder baths than usual to not stress the skin. It is also known to help to use bar-soap, instead of a liquid body wash.

The overall prognosis is excellent in most cases. Most children with Adams–Oliver syndrome can likely expect to have a normal life span. However, individuals with more severe scalp and cranial defects may experience complications such as hemorrhage and meningitis, leading to long-term disability.

Netherton syndrome is a severe, autosomal recessive form of ichthyosis associated with mutations in the "SPINK5" gene. It is named after Earl W. Netherton (1910–1985), an American dermatologist who discovered it in 1958.

Often, this disease is treated by giving aspirin to inhibit platelet activation, and/or warfarin as an anticoagulant. The goal of the prophylactic treatment with warfarin is to maintain the patient's INR between 2.0 and 3.0. It is not usually done in patients who have had no thrombotic symptoms.

Anticoagulation appears to prevent miscarriage in pregnant women. In pregnancy, low molecular weight heparin and low-dose aspirin are used instead of warfarin because of warfarin's teratogenicity. Women with recurrent miscarriage are often advised to take aspirin and to start low molecular weight heparin treatment after missing a menstrual cycle. In refractory cases plasmapheresis may be used.

Hystrix-like ichthyosis–deafness syndrome (also known as "HID syndrome") is a cutaneous condition characterized by a keratoderma.

The prognosis is poor; affected individuals are either stillborn or die shortly after birth. The longest survival reported in literature is of 134 days.

This syndrome is transmitted as an autosomal recessive disorder and there is a risk for recurrence of 25% in future pregnancies.

Neonatal ichthyosis–sclerosing cholangitis syndrome (also known as "NISCH syndrome" and "ichthyosis–sclerosing cholangitis syndrome") is a cutaneous condition caused by mutations in the Claudin 1 gene.