Currently there is no cure for actinic prurigo, and treatment focuses on relieving the dermatologic symptoms, by way of topical steroid creams or systemic immunosuppressants.

Prescribed treatments include:

- topical creams such as Tacrolimus and Betamethasone.

- systemic immunosuppressants such as Prednisone.

- In some cases, Thalidomide has proven to be effective in controlling the symptoms of actinic prurigo.

All patients with AP are encouraged to minimize sun exposure, and to use strong sunscreen throughout the year, and even on cloudy or overcast days, as UVA light, unlike UVB light, is able to penetrate cloud cover and remains constant throughout the day.

Alternative treatment methods might include UV Hardening, Meditation and/or cognitive behavioral therapy. UV-A desensitization phototherapy has also been shown to be effective in cases.

To prevent AC from developing, protective measures could be undertaken such as avoiding mid-day sun, or use of a broad-brimmed hat, lip balm with anti UVA and UVB ingredients (e.g. para-aminobenzoic acid), or sun blocking agents (e.g. zinc oxide, titanium oxide) prior to sun exposure.

Ultraviolet radiation is believed to contribute to the development of actinic keratoses by inducing mutations in epidermal keratinocytes, leading to proliferation of atypical cells. Therefore, preventive measures for AKs are targeted at limiting exposure to solar radiation, including:

- Limiting extent of sun exposure

- Avoid sun exposure during noontime hours when UV light is most powerful

- Using sun protection

- Frequently applying powerful sunscreens with SPF ratings greater than 30 and that also block both UVA and UVB light

- Wearing sun protective clothing such as hats, long-sleeved shirts, long skirts, or trousers

Recent research implicating human papillomavirus (HPV) in the development of AKs suggests that HPV prevention might in turn help prevent development of AKs, as UV-induced mutations and oncogenic transformation are likely facilitated in cases of active HPV infection.

Prurigo nodularis is very hard to treat, but current therapies include steroids, vitamins, cryosurgery, thalidomide and UVB light. In the event that staphylococcus or other infection is present, antibiotics have proven effective, but tend to cause more harm than good for this particular disease.

A physician may administer a strong dose of prednisone, which will almost immediately stop the itch/scratch cycle. However, cessation of steroids allows relapse to occur, usually within a few weeks. Horiuchi "et al" recently reported significant improvement in PN with antibiotic therapy.

Another drug a physician may administer is Apo-Azathioprine. Azathioprine, also known by its brand name Imuran, is an immunosuppressive drug used in organ transplantation and autoimmune diseases and belongs to the chemical class of purine analogues.

The cause for actinic prurigo is unknown, however researchers believe that protein in our bodies may be a cause to the condition also:

•UV-A and UV-B light seem to be the main provoking agents. This observation is supported by the fact that most patients live at high altitudes (>1000 m above sea level), and the condition improves in many patients when they move to lower altitudes. However, some patients who are affected already live at sea level.18,19,27 •Some authors are considering a food photosensitizer or a nutritional selective deficiency as a cause; however, no evidence proves this theory.27

Diagnostically, researchers are investigating the role of novel biomarkers to assist in determining which AKs are more likely to develop into cutaneous or metastatic SCC. Upregulation of matrix metalloproteinases (MMP) is seen in many different types of cancers, and the expression and production of MMP-7 in particular has been found to be elevated in SCC specifically. The role of serin peptidase inhibitors (Serpins) is also being investigated. SerpinA1 was found to be elevated in the keratinocytes of SCC cell lines, and SerpinA1 upregulation was correlated with SCC tumor progression "in vivo". Further investigation into specific biomarkers could help providers better assess prognosis and determine best treatment approaches for particular lesions.

In terms of treatment, a number of medications are being studied. Resiquimod is a TLR 7/8 agonist that works similarly to imiquimod, but is 10 to 100 times more potent; when used to treat AK lesions, complete response rates have range from 40 to 74%. Afamelanotide is a drug that induces the production of melanin by melanocytes to act as a protective factor against UVB radiation. It is being studied to determine its efficacy in preventing AKs in organ transplant patients who are on immunosuppressive therapy. Epidermal growth factor receptor (EGFR) inhibitors such as gefitinib, and anti-EGFR antibodies such as cetuximab are used in the treatment of various types of cancers, and are currently being investigated for potential use in the treatment and prevention of AKs.

This condition is considered premalignant because it may lead to squamous cell carcinoma in about 10% of all cases. It is not possible to predict which cases will progress into SCC, so the current consensus is that all lesions should be treated.

Treatment options include 5-fluorouracil, imiquimod, scalpel vermillionectomy, chemical peel, electrosurgery, and carbon dioxide laser vaporization. These curative treatments attempt to destroy or remove the damaged epithelium. All methods are associated with some degree of pain, edema, and a relatively low rate of recurrence.

Numerous treatment options are available for photoaged skin, including dermabrasion, topical application of retinoic acid, carbon dioxide laser resurfacing, hyaluronic acid injection into the dermis, imiquimod, tacrolimus ointment, and topical oestrogen therapy. These treatments have variable efficacy.

The most effective prevention strategy for photoaging remains minimization of sun exposure, through use of sunscreen and other sun exposure avoidance measures.

Prurigo is an itchy eruption of the skin.

Specific types include:

- Prurigo nodularis

- Actinic prurigo

- Besnier's prurigo (a specific type of atopic dermatitis).

Actinic granuloma (also known as "O'Brien granuloma") is a cutaneous condition characterized histologically by a dermal infiltrate of macrophages.

Actinic granuloma is an asymptomatic granulomatous reaction that affects sun-exposed skin, most commonly on the face, neck, and scalp.

It is characterized by annular or polycyclic lesions that slowly expand centrifugally and have an erythematous elevated edge and a hypopigmented, atrophic center.

Advise to reduce exposure to the sun and to use sunscreen.

Treatment with topical halometasone cream, pimecrolimus cream.

There is no good evidence that a mother's diet during pregnancy, the formula used, or breastfeeding changes the risk. There is tentative evidence that probiotics in infancy may reduce rates but it is insufficient to recommend its use.

People with eczema should not get the smallpox vaccination due to risk of developing eczema vaccinatum, a potentially severe and sometimes fatal complication.

Evidence suggests that IL-4 is central in the pathogenesis of AD. Therefore, there is a rationale for targeting IL-4 with anti-IL-4 inhibitors. People with atopic dermatitis are more likely to have Staphylococcus aureus living on them. The role this plays in pathogenesis is yet to be determined.

Bathing once or more a day is recommended, usually for five to ten minutes in warm water. Soaps should be avoided as they tend to strip the skin of natural oils and lead to excessive dryness.

There has not been adequate evaluation of changing the diet to reduce eczema. There is some evidence that infants with an established egg allergy may have a reduction in symptoms if eggs are eliminated from their diets. Benefits have not been shown for other elimination diets, though the studies are small and poorly executed. Establishing that there is a food allergy before dietary change could avoid unnecessary lifestyle changes.

People can wear clothing designed to manage the itching, scratching and peeling.

Prurigo simplex is a chronic, itchy, idiopathic skin condition characterized by extremely itchy skin nodules and lesions. Typically, there is no known direct cause of prurigo simplex, but some factors are known to trigger or aggravate it. This condition falls between chronic and acute, sometimes transitioning into a chronic condition. Many people experience a recurrence of the condition after periods of remission. Middle-aged patients are the most prone age group to this condition.

The most common prurigo simplex symptoms are skin nodules resembling insect bites that are intensely itchy. These nodules are frequently scratched open, becoming lesions that continue to itch. Sometimes the skin thickens and becomes discolored around the nodules. The scalp, arms, legs and trunk of the body are the most frequent sites of the bumps and lesions. Itching can become severe and habitual, worsening the condition and possibly causing infections in the open sores.

Sometimes the nodules become less itchy and eventually disappear leaving a discolored area or scar tissue. The same nodules can persist for months or even years, though, without healing. Patients may experience a remission but then relapse with new nodules forming. The condition might also become chronic, with no periods of improvement and relief.

Treatment is challenging, with narrow band UVB or pimozide sometimes helpful.

The cause of prurigo nodularis is unknown, although other conditions may induce PN. PN has been linked to Becker's nevus, linear IgA disease, an autoimmune condition, liver disease and T cells. Systemic pruritus has been linked to cholestasis, thyroid disease, polycythaemia rubra vera, uraemia, Hodgkins disease, HIV and other immunodeficiency diseases. Internal malignancies, liver failure, renal failure, and psychiatric illnesses have been considered to induce PN, although more recent research has refuted a psychiatric cause for PN. Patients report an ongoing battle to distinguish themselves from those with psychiatric disorders such as delusions of parasitosis and other psychiatric conditions.

The role of vitamin D on atopic dermatitis is not clear, but there is some evidence that vitamin D supplementation may improve its symptoms.

Studies have investigated the role of long chain polyunsaturated fatty acids (LCPUFA) supplementation and LCPUFA status in the prevention and treatment of atopic diseases, but the results are controversial. It remains unclear if the nutritional intake of n-3 fatty acids has a clear preventive or therapeutic role, or if n-6 fatty acids consumption promotes atopic diseases.

Several probiotics seem to have a positive effect with a roughly 20% reduction in the rate of atopic dermatitis. The best evidence is for multiple strains of bacteria.

In people with celiac disease or non-celiac gluten sensitivity, a gluten free diet improves their symptoms and prevents the occurrence of new outbreaks.

Actinic elastosis, also known as solar elastosis, is an accumulation of abnormal elastin (elastic tissue) in the dermis of the skin, or in the conjunctiva of the eye, which occurs as a result of the cumulative effects of prolonged and excessive sun exposure, a process known as photoaging.

Photosensitivity with HIV infection is a skin condition resembling polymorphous light eruption, actinic prurigo, or chronic actinic dermatitis, seen in about 5% of HIV-infected people.

Phototherapy in the form of sunlight has long been used for psoriasis. Wavelengths of 311–313 nanometers are most effective, and special lamps have been developed for this application. The exposure time should be controlled to avoid over exposure and burning of the skin. The UVB lamps should have a timer that will turn off the lamp when the time ends. The amount of light used is determined by a person's skin type. Increased rates of cancer from treatment appear to be small. Narrow band UVB light (NBUVB) phototherapy has been demonstrated to have similar efficacy to PUVA.

One of the problems with clinical phototherapy is the difficulty many patients have gaining access to a facility. Indoor tanning resources are almost ubiquitous today and could be considered as a means for patients to get UV exposure when dermatologist provided phototherapy is not available. Indoor tanning is already used by many people as a treatment for psoriasis; one indoor facility reported that 50% of its clients were using the center for psoriasis treatment; another reported 36% were doing the same thing. However, a concern with the use of commercial tanning is that tanning beds that primarily emit UVA might not effectively treat psoriasis. One study found that plaque psoriasis is responsive to erythemogenic doses of either UVA or UVB, as exposure to either can cause dissipation of psoriatic plaques. It does require more energy to reach erythemogenic dosing with UVA.

UV light therapies all have risks; tanning beds are no exception, particularly in the link between UV light and the increased chance of skin cancer. There are increased risks of melanoma, squamous cell and basal cell carcinomas; younger psoriasis patients, particularly those under age 35, are at increased risk from melanoma from UV light treatment. The World Health Organization (WHO) listed tanning beds as carcinogens. A review of studies recommends that people who are susceptible to skin cancers exercise caution when using UV light therapy as a treatment.

A major mechanism of NBUVB is the induction of DNA damage in the form of pyrimidine dimers. This type of phototherapy is useful in the treatment of psoriasis because the formation of these dimers interferes with the cell cycle and stops it. The interruption of the cell cycle induced by NBUVB opposes the characteristic rapid division of skin cells seen in psoriasis. The activity of many types of immune cells found in the skin is also effectively suppressed by NBUVB phototherapy treatments. The most common short-term side effect of this form of phototherapy is redness of the skin; less common side effects of NBUVB phototherapy are itching and blistering of the treated skin, irritation of the eyes in the form of conjunctival inflammation or inflammation of the cornea, or cold sores due to reactivation of the herpes simplex virus in the skin surrounding the lips. Eye protection is usually given during phototherapy treatments.

Psoralen and ultraviolet A phototherapy (PUVA) combines the oral or topical administration of psoralen with exposure to ultraviolet A (UVA) light. The mechanism of action of PUVA is unknown, but probably involves activation of psoralen by UVA light, which inhibits the abnormally rapid production of the cells in psoriatic skin. There are multiple mechanisms of action associated with PUVA, including effects on the skin's immune system. PUVA is associated with nausea, headache, fatigue, burning, and itching. Long-term treatment is associated with squamous cell carcinoma (but not with melanoma). A combination therapy for moderate to severe psoriasis using PUVA plus acitretin resulted in benefit, but acitretin use has been associated with birth defects and liver damage.

A systematic review found that no treatments commonly used for leukoplakia have been shown to be effective in preventing malignant transformation. Some treatments may lead to healing of leukoplakia, but do not prevent relapse of the lesion or malignant change. Regardless of the treatment used, a diagnosis of leukoplakia almost always leads to a recommendation that possible causative factors such as smoking and alcohol consumption be stopped, and also involves long term review of the lesion, to detect any malignant change early and thereby improve the prognosis significantly.

Solar purpura (also known as "Actinic purpura," and "Senile purpura") is a skin condition characterized by large, sharply outlined, 1- to 5-cm, dark purplish-red ecchymoses appearing on the dorsa of the forearms and less often the hands.

The condition is most common in elderly people of European descent. It is caused by sun-induced damage to the connective tissue of the skin.

No treatment is necessary. The lesions typically fade over a period of up to 3 weeks.

Many different topical and systemic medications have been studied, including anti-inflammatories, antimycotics (target Candida species), carotenoids (precursors to vitamin A, e.g. beta carotene), retinoids (drugs similar to vitamin A), and cytotoxics, but none have evidence that they prevent malignant transformation in an area of leukoplakia.Vitamins C and E have also been studied with regards a therapy for leukoplakia. Some of this research is carried out based upon the hypothesis that antioxidant nutrients, vitamins and cell growth suppressor proteins (e.g. p53) are antagonistic to oncogenesis. High doses of retinoids may cause toxic effects. Other treatments that have been studied include photodynamic therapy.

Chronic actinic dermatitis (also known as "Actinic reticuloid," "Chronic photosensitivity dermatitis," "Persistent light reactivity," and "Photosensitive eczema") is a condition where a subject's skin becomes inflamed due to a reaction to sunlight or artificial light. Patients often suffer from other related conditions of the skin that cause dermatitis in response to a variety of stimuli (e.g., flowers, sunscreens, cosmetics, etc.).

Diagnosis can occur at any age, ranging from soon after birth to adulthood. A GP may refer a patient to a dermatologist if the condition is not showing clear symptoms, and a variety of tests - usually completed at a hospital - can then determine the exact nature and cause of the patient's condition.

Reactions, which vary depending on the severity of the case, include rashes, flared 'bumpy' patches, affected areas being extremely hot to touch, and outbreaks shortly (or within 24 hours) after direct or indirect exposure to UVA and/or UVB light. The skin most likely reacts on the upper chest, hands and face, however it is not unlikely for reactions to happen all over the body. The patient may feel burning, stinging or throbbing sensations in these areas, which causes mild, yet uncomfortable pain.

Isotretinoin, high doses of vitamin A and tretinoin cream can be utilized. Also, emollients, oral antihistamines, and antipruritic creams that contain menthol and camphor may be helpful because the lesions can become very itchy.

Prurigo pigmentosa is a rare skin condition of unknown cause, characterized by the sudden onset of erythematous papules that leave a reticulated hyperpigmentation when they heal.