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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.
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.
No treatment is required and the patches in time will settle.
The redness, scale and itch if present may be managed with simple emollients and sometimes hydrocortisone, a weak steroid, is also used.
As the patches of pityriasis alba do not darken normally in sunlight, effective sun protection helps minimise the discrepancy in colouration against the surrounding normal skin. Cosmetic camouflage may be required.
Tacrolimus has been reported as speeding resolution.
In exceptionally severe cases PUVA therapy may be considered.
Topical retinoids have been studied in the treatment of AK with modest results. Treatment with adapalene gel daily for 4 weeks, and then twice daily thereafter for a total of nine months led to a significant but modest reduction in the number AKs compared to placebo; it demonstrated the additional advantage of improving the appearance of photodamaged skin. Topical tretinoin is ineffective as treatment for reducing the number of AKs. For secondary prevention of AK, systemic, low dose acitretin was found to be safe, well-tolerated and moderately effective in chemoprophylaxis for skin cancers in kidney transplant patients.
Topical diclofenac sodium gel is a nonsteroidal anti-inflammatory drug that is thought to work in the treatment of AK through its inhibition of the arachidonic acid pathway, thereby limiting the production of prostaglandins which are thought to be involved in the development of UVB-induced skin cancers. Recommended duration of therapy is 60 to 90 days with twice daily application. Treatment of facial AK with diclofenac gel led to complete lesion resolution in 40% of cases. Common side effects include dryness, itching, redness, and rash at the site of application.
Treatments for tinea versicolor include:
- Topical antifungal medications containing selenium sulfide are often recommended. Ketoconazole (Nizoral ointment and shampoo) is another treatment. It is normally applied to dry skin and washed off after 10 minutes, repeated daily for two weeks. Ciclopirox (Ciclopirox olamine) is an alternative treatment to ketoconazole, as it suppresses growth of the yeast "Malassezia furfur". Initial results show similar efficacy to ketoconazole with a relative increase in subjective symptom relief due to its inherent anti-inflammatory properties. Other topical antifungal agents such as clotrimazole, miconazole, terbinafine, or zinc pyrithione can lessen symptoms in some patients. Additionally, hydrogen peroxide has been known to lessen symptoms and, on certain occasions, remove the problem, although permanent scarring has occurred with this treatment in some sufferers. Clotrimazole is also used combined with selenium sulfide.
- Oral antifungals including ketoconazole or fluconazole in a single dose, or ketoconazole for seven days, or itraconazole can be used. The single-dose regimens, or pulse therapy regimens, can be made more effective by having the patient exercise 1–2 hours after the dose, to induce sweating. The sweat is allowed to evaporate, and showering is delayed for a day, leaving a film of the medication on the skin.
There does not yet exist a specific treatment for IP. Treatment can only address the individual symptoms.
Mongolian spots usually resolve by early childhood and hence no treatment is generally needed if they are located in the sacral area. However, sometimes it may be required for extra sacral lesions to have surgical correction. Q-switched alexandrite lasers have been used for treatment. Good results are obtained if treatment is initiated before the age of 20 years. In a study done by the University of Tokyo, the effectiveness of the Q-switched alexandrite laser in treating Mongolian spots was evaluated. A retrospective study was done from April 2003 to September 2011. 16 patients, aged 14-55, were treated with Q-switched alexandrite laser. A good therapeutic outcome was achieved on the whole group, however two patients with sacral Mongolian spots suffered from inflammatory hyperpigmentation, and two patients got post inflammatory hypopigmentation after seven sessions of laser treatment.
Phytophotodermatitis can be prevented by staying indoors after handling the above substances. However, the primary triggering mechanism is UV-A radiation (320–380 nm) which windows are not guaranteed to filter out.
Many different topical and oral medications can be used to treat the inflammatory reaction of phytophotodermatitis. A dermatologist may also prescribe a bleaching cream to help treat the hyperpigmentation and return the skin pigmentation back to normal. If they do not receive treatment, the affected sites may develop permanent hyperpigmentation or hypopigmentation.
Hypopigmentation is the loss of skin color. It is caused by melanocyte or melanin depletion, or a decrease in the amino acid tyrosine, which is used by melanocytes to make melanin.
The exact cause of poikiloderma is unknown; however, extended sun exposure, namely the ultraviolet light emitted by the sun, is the primary factor.
Often, hypopigmentation can be brought on by laser treatments; however, the hypopigmentation can be treated with other lasers or light sources.
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.
Albeit difficult, treatment of poikiloderma involves the delivery of multiple wavelengths of intense pulsed light (IPL) to the affected area.
Types include:
- Poikiloderma vasculare atrophicans
- Poikiloderma of Civatte
- Hereditary sclerosing poikiloderma
Many canine skin disorders can have a basis in poor nutrition. The supplementation of both omega fatty acids, 3 and 6, have been shown to mediate the inflammatory skin response seen in chronic diseases. Omega 3 fatty acids are increasingly being used to treat pruritic, irritated skin. A group of dogs supplemented with omega 3 fatty acids (660 mg/kg [300 mg/lb] of body weight/d) not only improved the condition of their pruritus, but showed an overall improvement in skin condition. Furthermore, diets lacking in essential fatty acids usually present as matted and unkept as the first sign of a deficiency. Eicosapentaenoic acid (EPA), a well known omega 3, works by preventing the synthesis of another omega metabolite known as arachidonic acid. Arachidonic acid is an omega 6, making it pro-inflammatory. Though not always the case, omega 6 fatty acids promote inflammation of the skin which in turn reduces overall appearance and health. There are skin benefits of both these lipids, as a deficiency in omega 6s leads to a reduced ability to heal and a higher risk of infection, which also diminishes skin health. Lipids in general benefit skin health of dogs, as they nourish the epidermis and retain moisture to prevent dry, flaky skin.
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.
This disease has not been shown to be life-threatening or the cause of death in patients. However, treatment is necessary to maintain a healthy lifestyle.
Vitamins are one of many of the nutritional factors that change the outward appearance of a dog. The fat soluble vitamins A and E play a critical role in maintaining skin health. Vitamin A, which can also be supplemented as beta-carotene, prevents the deterioration of epithelial tissues associated with chronic skin diseases and aging. A deficiency in vitamin A can lead to scaly of skin and other dermatisis related issues like alopecia Vitamin E is an antioxidant. Vitamin E neutralizes free radicals that accumulate in highly proliferative cells like skin and prevent the deterioration of fibrous tissue caused by these ionized molecules. There are also a couple of water-soluble vitamins that contribute to skin health. Riboflavin (B2) is a cofactor to the metabolism of carbohydrates and when deficient in the diet leads to cracked, brittle skin. Biotin (B7) is another B vitamin that, when deficient, leads to alopecia.
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.
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.
Dyschromia refers to an alteration of the color of the skin or nails.
"Hyperchromia" can refer to hyperpigmentation, and "hypochromia" can refer to hypopigmentation.
"Dyschromatoses" involve both hyperpigmented and hypopigmented macules.
The patches of pityriasis alba may last from 1 month to about one year, but commonly on the face last a year. However it is possible that the white patches may last for more than 1 year on the face.
Recent research has used induced pluripotent stem cells to study disease mechanisms in humans, and discovered that the reprogramming of somatic cells restores telomere elongation in dyskeratosis congenita (DKC) cells despite the genetic lesions that affect telomerase. The reprogrammed DKC cells were able to overcome a critical limitation in TERC levels and restored function (telomere maintenance and self-renewal). Therapeutically, methods aimed at increasing TERC expression could prove beneficial in DKC.
Several drugs are used off label by patients with EPP:
- Ursodeoxycholic acid is a bile acid that is administered to promote biliary secretion of protoporphyrin. Results of its use in EPP are controversial. However, it is known to alter the composition of bile, to protect hepatocytes from the cytotoxic effect of hydrophobic bile acids, and to stimulate biliary secretion by several distinct mechanisms.
- Hematin appears to reduce excess protoporphyrin production in the bone marrow. It has been administered to patients with EPP (3–4 mg/kg iv) who develop a crisis after liver transplantation.
- Plasmapheresis can also decrease the levels of protoporphyrin in plasma, however its use in treating acute episodes is controversial.
- Cholestyramine is an orally administered resin which reduces circulating levels of protoporphyrin by binding to protoporphyrin in the intestine and, hence, interrupting the enterohepatic circulation. It is usually used in combination with other treatment approaches.
- Activated charcoal, like cholestyramine, binds to protoporphyrin in the intestine and prevents its absorption. It is cheap and readily available. It seems to be effective in reducing circulating protoporphyrin levels.
Bone marrow transplantation, liver transplantation, acetylcysteine, extracorporeal albumin dialysis, parenteral iron and transfusion of erythrocytes are alternative plans for treatment of EEP.
PVA usually has an underlying cause, attributed to existing skin diseases and disorders associated with a cutaneous lymphoma or inflammation. Mycosis fungoides is the common lymphoma believed to cause PVA, although it may be considered a precursor when the lymphoma is (hidden) and undiagnosed. Large plaque parapsoriasis is another common causes of PVA. Less common causes include autoimmune-related connective tissue diseases such as lupus, dermatomyositis and scleroderma. Dermatoses and those that are genetically inspired, called genodermatoses, may also be an underlying cause of PVA. Among them, xeroderma pigmentosum and Rothmund-Thomson syndrome (poikiloderma congenita) are thought to be the most prominent. Ingestion of substances containing arsenic, such as arsphenamine, has also been suggested as a least common cause. PVA can also be idiopathic (of unknown cause), as seen in a small number of cases.