Generally, PLE resolves without treatment; also, PLE irritations generally leave no scar. However, in severe cases the use of steroids is necessary to help reduce inflammation and increase quality of life of the patient. There are also other therapies for patients who are severely impacted, such as light therapy to harden the skin's surface.

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.

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.

The cases of this condition are most common between the spring and autumn months in the northern hemisphere.

Typically, 5-20% of fair skinned populations are affected, but it can occur in any skin type. It is more common in females than in males. The condition can affect all ethnic groups and research suggests that 20% of patients have a family history of the complaint. Those suffering from PLE usually do so by age 30.

The condition usually resolves on its own, and treatment is not required. Oral antihistamines or topical steroids may be used to decrease itching. Steroids do provide relief from itching, and improve the appearance of the rash, but they also cause the new skin that forms (after the rash subsides) to take longer to match the surrounding skin color. While no scarring has been found to be associated with the rash, scratching should be avoided. It's possible that scratching can make itching worse and an itch-scratch cycle may develop with regular scratching (that is, you itch more because you scratch, so you scratch more because you itch, and so on). Irritants such as soaps with fragrances, hot water, wool, and synthetic fabrics should be avoided. Lotions that help stop or prevent itching may also be helpful.

Direct sunlight makes the lesions resolve more quickly. According to this principle, medical treatment with ultraviolet light has been used to hasten resolution, though studies disagree whether it decreases itching or not. UV therapy is most beneficial in the first week of the eruption.

Oral erythromycin was effective in treating patients in one early trial, but a later study could not confirm these results. Since Human Herpes Virus 6 or Human Herpes Virus 7 has been hypothesized to be the cause, the antiviral drug Acyclovir may reduce length of duration and severity.

It is self limiting condition

1.reassurence

2.steriod cream for local application

3.moisterizer lotion

Antiviral treatment has been tried with some success in a small number of patients.

In most patients, the condition lasts only a matter of weeks; in some cases it can last longer (up to six months). The disease resolves completely without long-term effects. Two percent of patients have recurrence.

Because the eruption is transient and self-limiting, no treatment is indicated.

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

It is estimated that 2—3 percent of hospitalised patients are affected by a drug eruption, and that serious drug eruptions occur in around 1 in 1000 patients.

Photodermatoses is a skin disease that is caused by exposure to sunlight.

People with photodermatoses may develop skin rashes following exposure to the sun. Polymorphous light eruption is the most common type of photodermatoses. It is most likely due to an abnormal immune system reaction to the sun. Polymorphous light eruption occurs in approximately 10 to 20 percent of otherwise healthy individuals, so it is a relatively common condition.

Phytophotodermatitis, also known as "lime disease" (not to be confused with "Lyme disease"), "Berloque dermatitis", or "Margarita photodermatitis" is a chemical reaction which makes skin hypersensitive to ultraviolet light. It is frequently mistaken for hereditary conditions such as atopic dermatitis or chemical burns, but it is caused by contact with the photosensitizing compounds—such as furanocoumarins—found naturally in some plants and vegetables like parsnips, citrus fruits and more. Symptoms include burning, itching and large blisters that slowly accumulate over time. One of the earliest descriptions of this disease was made by Darrell Wilkinson, a British dermatologist in the 1950s.

In more extreme cases, plasmapheresis can be considered. This technique is used to remove the blood plasma or fluid in the red blood cells and then return the cells to the body. It "removes a circulating factor from the blood that may be involved in causing the urticaria," but is still being tested and is not always effective. When the treatment is a success, the patient's photosensitivity is decreased to the degree that they can undergo PUVA which can result in the relief of the urticarial outbreaks for an extended period of time. The major setback to this treatment is that the side effects can be severe and may include anaphylactoid reactions.

At certain times of the year this can be a problem in some areas of the Bahamas particularly around New Providence.

Histamines are proteins associated with many allergic reactions. When the UV radiation or light comes in contact with a person with solar urticaria, histamine is released from mast cells. When this occurs, the permeability of vessels near the area of histamine release is increased. This allows blood fluid to enter the vessels and cause inflammation. Antihistamines suppress the activity of the histamine.

Diphenhydramine, a first-generation H1 receptor antagonist or medicine that combats the H1 receptor that is associated with many allergic reactions, has been found to be the most potent antihistamine for this particular disease. Patients prescribed 50 milligrams four times per day have been able to sustain normal exposure to the sun without suffering a reaction.

Patients with less potent forms of solar urticaria such as fixed solar urticaria can be treated with the medication fexofenadine, which may also be used prophylactically to prevent recurrence.

Treatment is symptomatic.

Treatment does not require a doctor's attention unless the case is severe, with most affected using a topical anti-itch cream (diphenhydramine) and a cortisone solution (hydrocortisone). Do not scratch the area, and avoid any clothing that may irritate the affected area; scratching will result in localized swelling and intense itching.

Upon exiting the water, prompt removal of swim clothing (while it is still wet) followed by a warm sea-water shower largely negates the risk of Seabather's eruption even in endemic areas. A hot freshwater shower with soap (paying particular attention to the hair and areas covered by the suit) is a somewhat less-effective alternative if uncontaminated seawater is unavailable. The contaminated swimsuit should be machine washed with laundry soap and dried in warm air.

Animals can be affected as well, and a cortisone solution for humans can be used on dogs.

In many children hydroa vacciniforme (HV) regresses spontaneously by early adulthood. In the 29 patients followed by Iwatuski et al., 11 of the 18 with definite or probable HV were available for follow-up and all were alive without progression of their symptoms. Some had recurrent eruptions of HV. In contrast out of 11 severe patients in this study, 6 had evidence of chronic EBV infection, 5 had hypersensitivity to mosquito bites, 4 had virus-associated hemophagocytic syndrome. 6 of the severe group had natural killer-cell lymphocytosis in the peripheral blood.

Infantile acropustulosis (also known as "Acropustulosis of infancy") is an intensely itchy vesicopustular eruption of the hands and feet.

Involvement of scabies has been suggested.

infantile acropustulosis is characterized by itchy papules and vesicles that are similar to those found in scabies "mosquito like bites" but there is absence of the typical burrowing with S like burrows on the skin and can occur in small babies as opposed to scabies mostly found on children and young adults.

Acne aestivalis (also known as Mallorca acne) is a special form of mono-morphic light eruption. It is a monomorphous eruption consisting of multiple, uniform, red, papular lesions, reported to occur after sun exposure.

Lichen striatus (also known as blaschko linear acquired inflammatory skin eruption and linear lichenoid dermatosis) is a rare skin condition that is seen primarily in children, most frequently appearing ages 5–15. It consists of a self-limiting eruption of small, scaly papules.

Pustular bacterid is a skin condition characterized by a symmetric, grouped, vesicular or pustular eruption on the palms and soles marked by exacerbations and remissions over long periods of time.

The culprit can be both a prescription drug or an over-the-counter medication.

Examples of common drugs causing drug eruptions are antibiotics and other antimicrobial drugs, sulfa drugs, nonsteroidal anti-inflammatory drugs (NSAIDs), biopharmaceuticals, chemotherapy agents, anticonvulsants, and psychotropic drugs. Common examples include photodermatitis due to local NSAIDs (such as piroxicam) or due to antibiotics (such as minocycline), fixed drug eruption due to acetaminophen or NSAIDs (Ibuprofen), and the rash following ampicillin in cases of mononucleosis.

Certain drugs are less likely to cause drug eruptions (rates estimated to be ≤3 per 1000 patients exposed). These include: digoxin, aluminum hydroxide, multivitamins, acetaminophen, bisacodyl, aspirin, thiamine, prednisone, atropine, codeine, hydrochlorothiazide, morphine, insulin, warfarin, and spironolactone.

Zirconium granulomas are a skin condition characterized by a papular eruption involving the axillae, and are sometimes considered an allergic reaction to deodorant containing zirconium lactate. They are the result of a delayed granulomatous hypersensitivity reaction, and can also occur from exposure to aluminum zirconium complexes. Commonly, zirconium containing products are used to relieve toxicodendron irritation. The lesions are similar to those from sarcoidosis, and commonly manifest four to six weeks after contact. They appear as erythrematous, firm, raised, shiny papules. Corticosteroids are used to ease the inflammation, but curative treatment is currently unavailable.

Autoimmune progesterone dermatitis may appear as urticarial papules, deep gyrate lesions, papulovesicular lesions, an eczematous eruption, or as targetoid lesions. Autoimmune progesterone dermatitis initially manifests with eye symptoms, e.g. burning, and progresses into rashes. Its relapsing-remitting pattern in women correspond to the progesterone levels during the menstrual cycle, which spike twice a month. It is an extremely rare disease, only perhaps 50 cases have ever been reported.