Usually, a common form of treatment for the condition is a type of hand cream which moisturises the hard skin. However, currently the condition is incurable.

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.

Most patients with hyper IgE syndrome are treated with long-term antibiotic therapy to prevent staphylococcal infections. Good skin care is also important in patients with hyper IgE syndrome. High-dose intravenous gamma-globulin has also been suggested for the treatment of severe eczema in patients with HIES and atopic dermatitis.

Congenital Ichthyosiform Erythroderma (CIE), also known as Nonbullous congenital ichthyosiform erythroderma is a rare type the ichthyosis family of skin diseases which occurs in 1 in 200,000 to 300,000 births.

Also known as ichthyosis hystrix gravior or porcupine man. This disease is characterised by spiny scales which cover the entire body except the face, genitals, palms and soles. The only known cases were in Edward Lambert (known as the porcupine man) who was exhibited in front of the Royal Society in London in 1731 and three generations of his descendants. No cases of this disease are now known though some experts believe that it may have been a type of epidermolytic hyperkeratosis. From the history of the Lambert family the disease appears to have been an autosomal dominant condition.

HID syndrome is also known as ichthyosis hystrix, Rheydt type after the German city of Rheydt near Düsseldorf where it was first discovered. Symptoms are bilateral hearing loss and spiky hyperkeratotic masses which cover the whole body though the palms and soles are less badly affected. It can be differentiated from KID syndrome which also has symptoms of deafness and ichthyosis by the different distribution of hyperkeratosis. It is an autosomal dominant condition caused by a mutation to the GJB2 gene (the same gene affected by KID syndrome).

There is currently no treatment for CHILD syndrome so any treatment would target the symptoms currently present. Emoillents like Lac-Hydran (ammonium lactate) and Ureaphil (urea) are used to treat scaly patches on the skin. A pediatric orthopedic surgeon can evaluate any underdevelopment in the bones and treat them if necessary.

There is a compound that is a topical liquid that can calm lesions down on older adults and make them go away on younger children. The mixture was made by Dr. Amy Paller at Children's Hospital. It is mixed as follows: to make 250 ml: Grind up lovastatin tablets 5g (10-20-40-80 mg); mix with cholesterol NF powder (NDC# 51927-1203-00, PCCA) 5g; mix with preserved water while mixing (eventually mixing for 1/2 hour with electronic mortar and pestle) to bring to full volume with preserved water. 8 oz

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.

Sjögren–Larsson syndrome (SLS) is an autosomal recessive form of ichthyosis apparent at birth.

Sjögren–Larsson syndrome is a rare autosomal, recessive, neurocutaneous disease. This disease can be identified by a triad of medical disorders. The first is ichthyosis, which is a buildup of skin to form a scale-like covering that causes dry skin and other problems. The second identifier is spastic paraplegia which is characterized by leg spasms. The final identifier is intellectual delay.

The gene of SLS is found on chromosome 17. In order for a child to receive SLS both parents must be carriers of the SLS gene. If they are carriers their child has a ¼ chance of getting the disease. In 1957 Sjogren and Larsson proposed that the Swedes with the disease all descended from a common ancestor 600 years ago. Today only 30–40 persons in Sweden have this disease.

Keratitis–ichthyosis–deafness syndrome (also known as "Erythrokeratodermia progressiva Burns," "Ichthyosiform erythroderma, corneal involvement, and deafness," and "KID syndrome,") presents at birth/infancy and is characterized by pregressive corneal opacification, either mild generalized hyperkeratosis or discrete erythematous plaques, and neurosensory deafness.

It is caused by a mutation in connexin 26.

Worth syndrome, also known as benign form of Worth hyperostosis corticalis generalisata with torus platinus, autosomal dominant osteosclerosis, autosomal dominant endosteal hyperostosis or Worth disease, is a rare autosomal dominant congenital disorder that is caused by a mutation in the LRP5 gene. It is characterized by increased bone density and benign bony structures on the palate.

HIES was first described by Davis et al. in 1966 in two girls with red hair, chronic dermatitis, and recurrent staphylococcal abscesses and pneumonias. They named the disease after the biblical figure Job, whose body was covered with boils by Satan. In 1972, Buckley et al. described two boys with similar symptoms as well as coarse facies, eosinophilia, and elevated serum IgE levels. These two syndromes are thought to be the same and are under the broad category of HIES.

Ichthyosis or ichthyosis-like disorders exist for several types of animals, including cattle, chickens, llamas, mice, and dogs. Ichthyosis of varying severity is well documented in some popular breeds of domestic dogs. The most common breeds to have ichthyosis are Golden retrievers, American bulldogs, Jack Russell terriers, and Cairn terriers.

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.

Treatment for autosomal dominant porencephaly type I is based on the symptoms that an individual is experiencing - for example, treatment of seizures with anticonvulsants. It is particularly important for individuals with this disorder and hypertension to control their blood pressure, as they are at higher risk of stroke. Other stroke prevention treatments include avoiding anticoagulants, smoking, and situations that may lead to head trauma.

Worth syndrome is caused by a mutation in the LRP5 gene, located on human chromosome 11q13.4. The disorder is inherited in an autosomal dominant fashion. This indicates that the defective gene responsible for a disorder is located on an autosome (chromosome 11 is an autosome), and only one copy of the defective gene is sufficient to cause the disorder, when inherited from a parent who has the disorder.

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.

Because CHILD syndrome is a congenital disorder, the symptoms may be present at birth or may develop during the first few weeks of life and continue for the lifetime of the patient.

Congenital hereditary corneal dystrophy (CHED) is a form of corneal dystrophy which presents at birth.

Palmoplantar keratodermas are a heterogeneous group of disorders characterized by abnormal thickening of the palms and soles.

Autosomal recessive and dominant, X-linked, and acquired forms have all been described.

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."

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

Trichothiodystrophy (TTD) is an autosomal recessive inherited disorder characterised by brittle hair and intellectual impairment. The word breaks down into "tricho" – "hair", "thio" – "sulphur", and "dystrophy" – "wasting away" or literally "bad nourishment". TTD is associated with a range of symptoms connected with organs of the ectoderm and neuroectoderm. TTD may be subclassified into four syndromes: Approximately half of all patients with trichothiodystrophy have photosensitivity, which divides the classification into syndromes with or without photosensitivity; BIDS and PBIDS, and IBIDS and PIBIDS. Modern covering usage is TTD-P (photosensitive), and TTD.

It is associated with a deficiency of the enzyme "fatty aldehyde dehydrogenase". At least 11 distinct mutations have been identified.