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.

Treatment of manifestations: special hair care products to help manage dry and sparse hair; wigs; artificial nails; emollients to relieve palmoplantar hyperkeratosis.

There are very few ways to test a patient for HGF. Currently, the most common way to diagnose a patient is by means of a physical evaluation. The physician can make a physical evaluation of the patient and send them to a dentist or better yet a specialist like a periodontist to evaluate signs of gingival overgrowth, quality of gingiva, inflammation, mechanical difficulties of the mouth, tooth conditions, and any sort of discomfort.

Aside from obvious physical symptoms seen in a physical evaluation, molecular tests can be run to check if there is a mutation in the SOS1 gene to confirm the diagnosis. If there is indeed a mutation in this gene coupled with the typical physical symptoms, then it is quite probable that a patient suffers from this disease. Also, looking at family history is also becoming more prominent in aiding to diagnose the patient. Otherwise, researchers are working to find new and better ways to test for the presence of HGF.

Mild forms of IBS should be diagnosable from appearance and patient history alone. Severe cases of IBS are hard to distinguish from mild EHK.

A skin biopsy shows a characteristic damaged layer in the upper spinous level of the skin. Again it may be difficult to distinguish from EHK.

The gene causing IBS is known and so a definite diagnosis can be given by genetic testing.

Diagnosis can be made at birth by identifying the symptoms of the child. Ultrastructural diagnosis where tissues are analyzed is using electron microscopy is also conducted. A specimen of skin is obtained via a skin biopsy and analyzed to see any tell tale characteristics.Genetic testing can also be done to identify the mutation on the FATP4 gene associated with fatty acid synthesis. Genetic consultation through a genetic counsellor is done to determine whether the individual has this syndrome and reduces the chances of misdiagnoses with other cutaneous diseases.

HED2 is suspected after infancy on the basis of physical features in most affected individuals. GJB6 is the only gene known to be associated with HED2. Targeted mutation analysis for the four most common GJB6 mutations is available on a clinical basis and detects mutations in approximately 100% of affected individuals. Sequence analysis is also available on a clinical basis for those in whom none of the four known mutations is identified.

Pachyonychia congenita may be divided into these types:

- Pachyonychia congenita type I (also known as "Jadassohn–Lewandowsky syndrome") is an autosomal dominant keratoderma that principally involves the plantar surfaces, but also with nails changes that may be evident at birth, but more commonly develop within the first few months of life.

- Pachyonychia congenita type II (also known as "Jackson–Lawler pachyonychia congenita" and "Jackson–Sertoli syndrome") is an autosomal dominant keratoderma presenting with a limited focal plantar keratoderma that may be very minor, with nails changes that may be evident at birth, but more commonly develop within the first few months of life.

The diagnosis of harlequin-type ichthyosis relies on both physical examination and certain laboratory tests.

Physical assessment at birth is vital for the initial diagnosis of harlequin ichthyosis. Physical examination reveals characteristic symptoms of the condition especially the abnormalities in the skin surface of newborns. Abnormal findings in physical assessments usually result in employing other diagnostic tests to ascertain the diagnosis.

Genetic testing is the most specific diagnostic test for harlequin ichthyosis. This test reveals a loss of function mutation on the ABCA12 gene. This gene is important in the regulation of protein synthesis for the development of the skin layer. Mutations in the gene may cause impaired transport of lipids in the skin layer and may also lead to shrunken versions of the proteins responsible for skin development. Less severe mutations result in a collodion membrane and congenital ichthyosiform erythroderma-like presentation. ABCA12 is an ATP binding cassette (ABC) transporter, and is a member of a large family of proteins that hydrolyze ATP to transport cargo across membranes. ABCA12 is thought to be a lipid transporter in keratinocytes necessary for lipid transport into lamellar granules during the formation of the lipid barrier.

Biopsy of skin may be done to assess the histologic characteristics of the cells. Histological findings usually reveal hyperkeratotic skin cells, which leads to a thick, white and hard skin layer.

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.

The condition can be diagnosed via exam that reveals; generalized redness; thick, generally dark, scales that tend to form parallel rows of spines or ridges,especially near large joints; the skin is fragile and blisters easily following trauma; extent of blistering and amount of scale is variable

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.

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 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.

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

An extremely rare disease of which only a few isolated cases are known.

People with ED often have certain cranial-facial features which can be distinctive: frontal bossing is common, longer or more pronounced chins are frequent, broader noses are also very common. In some types of ED, abnormal development of parts of the eye can result in dryness of the eye, cataracts, and vision defects. Professional eye care can help minimize the effects of ED on vision. Similarly, abnormalities in the development of the ear may cause hearing problems. Respiratory infections can be more common because the normal protective secretions of the mouth and nose are not present. Precautions must be taken to limit infections.

Since this condition is generally agreed upon to be hereditary, nothing can be done to prevent HGF. However, in some cases where it can develop as a result of rare multi-system syndromes, such as: Zimmerman-Laband, Jones, Ramon Syndrome, Rutherford Syndrome, Juvenile Hyaline Fibromatosis, Systemic Infantile Hyalinosis, and Mannosidosis, it is best for one to simply monitors the possible progression for HGF with regular dental check-ups.

If the patient's disease is treated by means of surgery, it is recommended that the patient undergoes post-surgical therapies for maintenance and periodic monitoring of gums for the sake of the possibility of re-occurrence of HGF.

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.

Reported treatments include topical agents, dermabrasion, cryotherapy, laser therapy, and surgical excision. These therapies have a high failure rate because of incomplete relief of symptoms, scarring, or recurrence .

Though similar in appearance, ILVEN will not respond to therapies known to affect psoriasis. ILVEN can be very difficult to live with but can be treated. The most effective method is full-thickness excision of the lesion. CO2 Laser Surgery can resurface the skin to give a flat, smoother and more normal appearance, but does not remove the lesion.

Acrokeratosis verruciformis (also known as "Acrokeratosis verruciformis of Hopf" is a rare autosomal dominant disorder appearing at birth or in early childhood, characterized by skin lesions that are small, verrucous, flat papules resembling warts along with palmoplantar punctate keratoses and pits. However sporadic forms, whose less than 10 cases have been reported, presents at a later age, usually after the first decade and generally lack palmoplantar keratoses.

Whether acrokeratosis verruciformis and Darier disease are related or distinct entities has been controversial, like Darier's disease, it is associated with defects in the ATP2A2 gene. however the specific mutations found in the ATP2A2 gene in acrokeratosis verruciformis have never been found in Darier's disease.

Meleda disease (MDM) or "mal de Meleda", also called Mljet disease, keratosis palmoplantaris and transgradiens of Siemens, (also known as "Acral keratoderma," "Mutilating palmoplantar keratoderma of the Gamborg-Nielsen type," "Palmoplantar ectodermal dysplasia type VIII", and "Palmoplantar keratoderma of the Norrbotten type") is an extremely rare autosomal recessive congenital skin disorder in which dry, thick patches of skin develop on the soles of the hands and feet, a condition known as palmoplantar hyperkeratosis.

MDM is most common on the Dalmatian island of Mljet (or "Meleda"), thought to be because of a founder effect. It is of autosomal recessive inheritance. It may be caused by a mutation on the "SLURP1" gene, located on chromosome 8.

The symptoms of ichthyosis hystrix Curth-Macklin are similar to epidermolytic hyperkeratosis (NPS-2 type) but there is no blistering and the hyperkeratosis is verrucous or spine-like. The hyperkeratosis is brown-grey in colour and is most obvious on the arms and legs. It is an autosomal dominant condition and can be caused by errors to the KRT1 gene. It is named after Helen Ollendorff Curth (1899-1982), a German-Jewish dermatologist, and Madge Thurlow Macklin (1893–1962), an American medical geneticist, and is one of the first syndromes named after two women.

Hypotrichosis–acro-osteolysis–onychogryphosis–palmoplantar keratoderma–periodontitis syndrome (also known as "HOPP syndrome") is a cutaneous condition characterized by a prominent palmoplantar keratoderma.

-The plaques are characterized histologically by hyperkeratosis which is a thickening of the outer layer of skin. Hyperkeratosis is often associated with an abnormal amount of keratin production. Also characteristic is moderate acanthosis a thickening of the stratum spinosum with elongation of rete ridges.

- Characteristic histologic feature is regular alternation of slightly raised parakeratotic areas without a granular layer (hypogranulosis) and slightly depressed orthokeratotic areas with prominent granular layer (hypergranulosis). Orthokeratotic hyperkeratosis is characterised by hyperkeratosis with non-nucleated cells. Parakeratotic hyperkeratosis is characterised by hyperkeratosis with nucleated cells.

- The orthokeratotic area shows a basket-weave-pattern.

- The dermis shows scattering of chronic inflammatory infiltrate (Munro's microabscess) sometimes giving a spongiform appearance.

This is very similar to linear psoriasis, but it has been noted that the diseases are distinct entities by immunohistochemical analyses.