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.

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.

Oral retinoids have proven effective in treating this disorder. Depending on the side effects they may improve the quality of life. Examples are etretinate, acitretin, isotretinoin

Gene therapy is really the only true therapy on the horizon for sufferers of EHK.

Over the past 10 years since the first EHK mouse model was developed, many ideas have been discussed about how best to cure EHK. Back as far as 1994 researchers were discussing new promising ideas such as topical lotions that would deliver ribozymes in a liposom cream. Ribozymes are a small piece of synthetic RNA which can digest RNA molecules. When cells make a protein from a gene on a chromosome sitting in the nucleus, the gene is first transcribed as a piece of RNA. This RNA is then translated into a protein. Ribozymes can be designed to destroy RNA molecules with specific sequences. In theory, this will stop the production of the protein encoded by the mutant alleles of the gene.

Successful gene therapy solutions have been recently achieved on mouse models by Jiang Chen M.D., a post-doctoral fellow in the laboratory of Dennis Roop, Ph.D., in the Center for Cutaneous Molecular Biology at Baylor College of Medicine. In 1998 they developed an inducible mouse model for epidermolysis hyperkeratosis which is viable, because the expression of a mutant K10 allele can be restricted to a focal area of the skin. "Once the mutant K10 allele is activated in epidermal stem cells by topical application of an inducer, these stem cells continuously give rise to defective progeny that form hyperkeratotic lesions which persist for the life of the mouse. It was observed that partial suppression of the mutant K10 gene may be sufficient to eliminate the disorder."

To test this observation, Dr. Chen and his team of researchers developed siRNAs that target the mutant K10 gene products for degradation, without affecting normal K10 gene products. Dr. Chen observed that under these conditions, an efficient knock-down of mutant, but not normal, K10 genes could be achieved. The results allowed the normal K10 genes to function properly building healthy skin tissues. He claims that these results may prove to be a very vital step forward in forging a novel gene therapy and possible permanent corrective therapy for this debilitating skin disorder.

There is no cure for IBS but in the future gene therapy may offer a cure.

Treatments for IBS generally attempt to improve the appearance of the skin and the comfort of the sufferer. This is done by exfoliating and increasing the moisture of the skin. Common treatments include:

- Emollients: moisturisers, petroleum jelly or other emolients are used, often several times a day, to increase the moisture of the skin.

- Baths: long baths (possibly including salt) several times a week are used to soften the skin and allow exfoliation.

- Exfoliating creams: creams containing keratolytics such as urea, salicylic acid and lactic acid may be useful.

- Antiseptic washes: antiseptics may be used to kill bacteria in the skin and prevent odour.

- Retenoids: very severe cases may use oral retinoids to control symptoms but these have many serious side effects including, in the case of IBS, increased blistering.

Overheating: The scaling of the skin prevents normal sweating so hot weather and/or vigorous exercise can cause problems.

Eye problems: The eyelids can be pulled down by the tightness of the skin and this can make eyelids (but usually just the lower one) very red and they are prone to drying and irritation.

Constriction bands: Very rarely children with this condition can have tight bands of skin around their fingers or toes (usually at the tips) that can prevent proper blood circulation to the area.

Hair loss: Severe scaling of the skin on the scalp can lead to patchy loss of hair, but this is rarely permanent.

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.

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.

Recent research has focused on changing the mixture of keratins produced in the skin. There are 54 known keratin genes—of which 28 belong to the type I intermediate filament genes and 26 to type II—which work as heterodimers. Many of these genes share substantial structural and functional similarity, but they are specialized to cell type and/or conditions under which they are normally produced. If the balance of production could be shifted away from the mutated, dysfunctional keratin gene toward an intact keratin gene, symptoms could be reduced. For example, sulforaphane, a compound found in broccoli, was found to reduce blistering in a mouse model to the point where affected pups could not be identified visually, when injected into pregnant mice (5 µmol/day = 0.9 mg) and applied topically to newborns (1 µmol/day = 0.2 mg in jojoba oil).

As of 2008 clinical research at the University of Minnesota has included a bone marrow transplant to a 2-year-old child who is one of 2 brothers with EB. The procedure was successful, strongly suggesting that a cure may have been found. A second transplant has also been performed on the child's older brother, and a third transplant is scheduled for a California baby. The clinical trial will ultimately include transplants to 30 subjects. However, the severe immunosuppression that bone marrow transplantation requires causes a significant risk of serious infections in patients with large scale blisters and skin erosions. Indeed, at least four patients have died in the course of either preparation for or institution of bone marrow transplantation for epidermolysis bullosa, out of only a small group of patients treated so far.

A pilot study performed in 2015 suggests that systemic granulocyte-colony stimulating factor (G-CSF) may promote increased wound healing in patients with dystrophic epidermolysis bullosa. In this study seven patients with dystrophic epidermolysis bullosa were treated daily with subcutaneous G-CSF for six days and then re-evaluated on the seventh day. After six days of treatment with G-CSF, the size of the open lesions were reduced by a median of 75.5% and the number of blisters and erosions on the patients were reduced by a median of 36.6%.

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."

The Epidermolysis Bullosa Activity and Scarring index (EBDASI) is a scoring system that objectively quantifies the severity of epidermolysis bullosa. The EBDASI is a tool for clinicians and patients to monitor the severity of the disease. It has also been designed to evaluate the response to new therapies for the treatment of EB. The EBDASI was developed and validated by Professor Dedee Murrell and her team of students and fellows at the St George Hospital, University of New South Wales, in Sydney, Australia. It was presented at the International Investigative Dermatology congress in Edinburgh in 2013 and a paper-based version was published in the "Journal of the American Academy of Dermatology" in 2014.

In 2015, an Italian team of scientists, led by Michele De Luca at the University of Modena, successfully treated a seven-year-old Syrian boy who had lost 80% of his skin. The boy's family had fled Syria for Germany in 2013. Upon seeking treatment in Germany, he had lost the epidermis from almost his entire body, with only his head and a patch on his left leg remaining. The group of Italian scientists had previously pioneered a technique to regenerate healthy skin in the laboratory. They used this treatment on the boy by taking a sample from his remaining healthy skin and then genetically modifying the skin cells, using a virus to deliver a healthy version of the LAMB3 gene into the nuclei. The patient underwent two operations in autumn 2015, where the new epidermis was attached. The graft had integrated into the lower layers of skin within a month, curing the boy. The introduction of genetic changes could increase the chances of skin cancer in other patients, but if the treatment is deemed safe in the long term, scientists believe the approach could be used to treat other skin disorders.

Ichthyosis en confetti, also known as ichthyosis with confetti, congenital reticular ichthyosiform erythroderma (CRIE) and ichthyosis variegata, is a very rare form of congenital ichthyosis in which healthy patches of normal skin co-exist within the abnormal skin areas. The condition is caused by a frameshift mutation in the keratin 10 gene (KRT10); mutant keratin 10 accumulates in the nucleolus, a sub-nuclear structure, rather than within cellular intermedite filaments like the wild-type protein. Children with the condition exhibit red, flaky skin; however, for reasons not yet totally clear, wild type clonal patches of skin start to appear, in place of the red, flaky skin. Due to the clonal nature of the growth of the normal skin cells, it appears the patient is covered with confetti, hence the name of the condition. It has been hypothesized that this is the result of a combination of mitotic recombination and natural selection within the skin.

Ichthyosis bullosa of Siemens is a type of familial, autosomal dominant ichthyosis, a rare skin disorder. It is also known as bullous congenital ichthyosiform erythroderma of Siemens or ichthyosis exfoliativa. It is a genetic disorder with no known cure which is estimated to affect about 1 in 500,000 people.

Because tags are benign, treatment is unnecessary unless the tags become frequently irritated or present a cosmetic concern. If removal is desired or warranted, then a dermatologist, general practitioner, or similarly trained professional may use cauterisation, cryosurgery, excision, or surgical ligation to remove the acrochorda.

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.

Hospitalization for the diseased person is suggested because of the controlled environment because it may prevent nutritional deficiencies and skin infections. A decrease in severity of symptoms usually happens after a few weeks when treated redness and scaliness usually do not recur. In 10 percent of cases, the result of uncontrolled infections or severe electrolyte loss may be fatal.

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.

Since the histopathology of nevus anemicus is normal, nevus anemicus is a pharmacologic nevus and not an anatomic one. In most people a nevus anemicus is on a covered area and so light in appearance that no treatment is needed.

The cause of this disease is unknown; some infants may have a severe case, others may have immunodeficiency.

The cat must have a supply of niacin, as cats cannot convert tryptophan into niacin like dogs. However, diets high in corn and low in protein can result in skin lesions and scaly, dry, greasy skin, with hair loss. Another B vitamin, biotin, if deficient causes hair loss around the eyes and face. A lack of B vitamins can be corrected by supplementing with a vitamin B complex, and brewers yeast.

Oral antibiotics of the tetracycline class such as minocycline, doxycycline, and tetracycline have been recommended for CGPD. However, their use is limited by side effects such as nausea, vomiting, and sensitivity of the skin to sunlight. Tetracycline antibiotics are not recommended for children under the age of 8 since tetracyclines are known to deposit in teeth (thereby staining them) and impair bone growth in children. The use of calcineurin inhibitor creams such as tacrolimus or pimecrolimus on the skin is controversial and results have been mixed. Certain studies have found the use of topical calcineurin inhibitors led to resolution of CGPD whereas others found incomplete resolution or prolonged symptoms. Topical azelaic acid has also been used successfully to treat CGPD.

Ichthyosis vulgaris (also known as "Autosomal dominant ichthyosis," and "Ichthyosis simplex") is a skin disorder causing dry, scaly skin. It is the most common form of ichthyosis, affecting around 1 in 250 people. For this reason it is known as common ichthyosis. It is usually an autosomal dominant inherited disease (often associated with filaggrin), although a rare non-heritable version called acquired ichthyosis exists.

Peeling skin syndrome (also known as "Acral peeling skin syndrome," "Continual peeling skin syndrome," "Familial continual skin peeling," "Idiopathic deciduous skin," and "Keratolysis exfoliativa congenita") is an autosomal recessive disorder characterized by lifelong peeling of the stratum corneum, and may be associated with pruritus, short stature, and easily removed anagen hair.

The acral form can be associated with "TGM5".

"Narrowband UVB therapy as an effective treatment for Schamberg's disease."

This research article proposed that narrowband UVB therapy can be considered as a treatment for pigmented purpura. A study was done on a 33 year old man who had a 3 month history of widespread pigmented purpura. Oral prescription of prednisolone and topical ointment helped controlled the purpuric eruptions, but when the medication was stopped, the rash recurred. Researchers placed the patient on a UV therapy for 5 months. The patient showed signs of improvement, where new purpuric eruptions stopped and some of the pigmented purpura disappeared. However, when the dose of the UV therapy was decreased, the patient showed signs of recurrence. Researchers want to monitor the patient for two years to see if the purpuric eruptions will stop and they believe that this patient will have promising results.

"Successful treatment of generalized childhood Schamberg's disease with narrowband ultraviolet B therapy."

This research article demonstrated two cases where two children had purpuric rashes. The children were placed on UVB therapy and were monitored weekly for purpuric eruptions. One of the child received 10 treatments of UVB therapy, while the other child received 20 treatments. The child that received the 20 treatments did not show signs of purpuric eruptions and the skin lesions disappeared. However, the child that received the 10 treatments, showed signs of recurrence. Most of the rash disappeared, but some of it reappeared on the body. Researchers believe that the narrowband UVB therapy used on children has proven to remove and control the skin lesions.