Prevention includes avoiding exposure to the sun and wearing sun block on the affected area.

- Cover up: wear long sleeves, slacks, and a wide-brimmed hat whenever harsh exposure is probable

- Avoid chemicals that may trigger a reaction

- Wear sunscreen at least factor 30 with a high UVA protection level

- Wear gloves and/or remain indoors after handling fruits or plants which increase sensitivity to light

Many medications and conditions can cause sun sensitivity, including:

- Sulfa used in some drugs, among them some antibiotics, diuretics, COX-2 inhibitors, and diabetes drugs.

- Psoralens, coal tars, photo-active dyes (eosin, acridine orange)

- Musk ambrette, methylcoumarin, lemon oil (may be present in fragrances)

- PABA (found in sunscreens)

- Oxybenzone (UVA and UVB chemical blocker also in sunscreens)

- Salicylanilide (found in industrial cleaners)

- St John's Wort, used to treat clinical depression

- Hexachlorophene (found in some ℞ antibacterial soaps)

- Contact with sap from Giant Hogweed. Common Rue (Ruta graveolens) is another phototoxic plant commonly found in gardens. Phototoxicity caused by plants is called phytophotodermatitis.

- Tetracycline antibiotics (e.g., tetracycline, doxycycline, minocycline)

- Benzoyl peroxide

- Retinoids (e.g., isotretinoin)

- Some NSAIDs (e.g., ibuprofen, naproxen sodium)

- Fluoroquinolone antibiotic: Sparfloxacin in 2% of cases

- Amiodarone, used to treat atrial fibrillation

- Pellagra

Photo dermatitis can also be caused by plants like the Dictamnus (commonly known as the "Burning Bush") which is a genus of the flowering plant in the Rutaceae family. This is called phytophotodermatitis.

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.

With no particular affinity to any particular ethnic group, seen in all age groups and equally amongst males and females, the precise prevalence is not known.

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.

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.

A full recovery is expected with treatment. Recurrent id reactions are frequently due to inadequate treatment of the primary infection or dermatitis and often the cause of recurrence is unknown.

A phototoxic substance is a chemical compound which becomes toxic when exposed to light.

- Some medicines: tetracycline antibiotics, sulfonamides, amiodarone, quinolones

- Many cold pressed citrus essential oils such as bergamot oil

- Some plant juices: parsley, lime, and Heracleum mantegazzianum

- Others: psoralen

Several health authorities have issued related guidance documents, which need to be considered for drug development:

- ICH (International Conference on Harmonisation of Technical Requirements for Registration of Pharmaceuticals for Human Use)

- M3(R2) "Guidance on Nonclinical Safety Studies for the Conduct of Human Clinical Trials and Marketing Authorization for Pharmaceuticals"

- S9 "Nonclinical Evaluation for Anticancer Pharmaceuticals"

- S10 "Photosafety Evaluation"

- EMA (European Medicines Agency)

- "Note for Guidance on Photosafety Testing" (revision on-hold)

- "Question & Answers on the Note for Guidance on Photosafety Testing"

- FDA (U.S. Food and Drug Administration)

- MHLW/PMDA (Japanese Ministry of Health, Labour and Welfare / Pharmaceuticals and Medical Devices Agency)

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.

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

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.

Since PCT is a chronic condition, a comprehensive management of the disease is the most effective means of treatment. Primarily, it is key that patients diagnosed with PCT avoid alcohol consumption, iron supplements, excess exposure to sunlight (especially in the summer), as well as estrogen and chlorinated cyclic hydrocarbons, all of which can potentially exacerbate the disorder. Additionally, the management of excess iron (due to the commonality of hemochromatosis in PCT patients) can be achieved through phlebotomy, whereby blood is systematically drained from the patient. A borderline iron deficiency has been found to have a protective affect by limiting heme synthesis. In the absence of iron, which is to be incorporated in the porphyrin formed in the last step of the synthesis, the mRNA of erythroid 5-aminolevulinate synthase (ALAS-2) is blocked by attachment of an iron-responsive element (IRE) binding cytosolic protein, and transcription of this key enzyme is inhibited.

Low doses of antimalarials can be used. Orally ingested chloroquine is completely absorbed in the gut and is preferentially concentrated in the liver, spleen, and kidneys. They work by removing excess porphyrins from the liver via increasing the excretion rate by forming a coordination complex with the iron center of the porphyrin as well as an intramolecular hydrogen bond between a propionate side chain of the porphyrin and the protonated quinuclidine nitrogen atom of either alkaloid. Due to the presence of the chlorine atom, the entire complex is more water soluble allowing the kidneys to preferentially remove it from the blood stream and expel it through urination. It should be noted that chloroquine treatment can induce porphyria attacks within the first couple of months of treatment due to the mass mobilization of porphyrins from the liver into the blood stream. Complete remission can be seen within 6–12 months as each dose of antimalarial can only remove a finite amount of porphyrins and there are generally decades of accumulation to be cleared. Originally, higher doses were used to treat the condition but are no longer recommended because of liver toxicity. Finally, due to the strong association between PCT and Hepatitis C, the treatment of Hepatitis C (if present) is vital to the effective treatment of PCT.

Chloroquine, hydroxychloroquine, and venesection are typically employed in the management strategy.

Porphyria cutanea tarda has a prevalence estimated at approximately 1 in 10,000. An estimated 80% of porphyria cutanea tarda cases are sporadic. The exact frequency is not clear because many people with the condition never experience symptoms and those that do are often misdiagnosed with anything ranging from idiopathic photodermatitis and seasonal allergies to hives.

There is currently no specific therapy. Intravenous fluids and treatment of the hepatic encephalopathy may help. Increasing dietary levels of branched chain amino acids and feeding low protein diets can help signs of hepatic encephalopathy, which is often accomplished by feeding small amounts of grain and/or beet pulp, and removing high-protein feedstuffs such as alfalfa hay. Grazing on non-legume grass may be acceptable if it is late summer or fall, although the horse should only be permitted to eat in the evening so as to avoid photosensitization. Due to the risk of gastric impaction, stomach size should be monitored.

Sedation is minimized and used only to control behavior that could lead to injury of the animal and to allow therapeutic procedures, and should preferably involve a sedative other than a benzodiazepine. Stressing the animal should be avoided if at all possible. Plasma transfusions may be needed if spontaneous bleeding occurs, to replace clotting factors. Antibiotics are sometimes prescribed to prevent bacterial translocation from the intestines. Antioxidants such as vitamin E, B-complex vitamins, and acetylcysteine may be given. High blood ammonia is often treated with oral neomycin, often in conjunction with lactulose, metronidazole and probiotics, to decrease production and absorption of ammonia from the gastrointestinal tract.

This condition most commonly occurs after the administration of a horse origin biological agent such as equine-derived antiserum, and usually occurs 4–10 weeks after the event. Diseases that have been vaccinated against using equine-origin antiserum, resulting in subsequent Theiler's disease, include: African horse sickness, Eastern and Western Equine Encephalitis, "Bacillus anthracis", tetanus antitoxin, "Clostridium perfringens", "Clostridium botulinum", "Streptococcus equi" subspecies "equi", Equine influenza, Equine herpesvirus type 1, pregnant mare's serum, and plasma. Although it occurs sporadically, It appears to be spreadable within a premises, and there have been outbreaks occurring on farms involving multiple horses over several months. In the Northern hemisphere it is most common between August to November. It is seen almost exclusively in adult horses, and lactating broodmares given tetanus antitoxin post foaling may be more susceptible.