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Table of Contents > Conditions > Photodermatitis
Also Listed As:  Skin Disorders, Photodermatitis; Sunburn
Signs and Symptoms
What Causes It?
Who's Most At Risk?
What to Expect at Your Provider's Office
Treatment Options
Treatment Plan
Drug Therapies
Complementary and Alternative Therapies
Prognosis/Possible Complications
Following Up
Supporting Research

Photodermatitis is an abnormal skin response to ultraviolet (UV) rays, particularly sunlight. It can be acute or chronic. UV rays are classified by wavelength and the greater the wavelength, the greater the risk of developing photodermatitis. UVB rays range from 290 to 320 nm and may cause sunburn, tanning, aging, or cancer-causing changes to the skin. UVA rays range from 320 to 400 nm and may cause reactions to light even through window glass. Ninety percent of the UV radiation from sunlight comes from UVA rays, 10% from UVB. Photoreactions from UV rays depend upon the amount of light reaching the earth. This is influenced by the season or time of year, latitude, thickness of the ozone layer, and topography.

Signs and Symptoms
  • Itchy bumps, blisters, or raised areas
  • Lesions that resemble eczema
  • Hyperpigmentation (darkened discoloration compared to one's normal skin tone)
  • Outbreaks in areas of skin exposed to light
  • Pain, redness, and swelling
  • Chills, headache, fever, and nausea
  • Less severe symptoms after repeated exposure

What Causes It?

Certain chemical agents and drugs may predispose an individual to sunburn, an eczema-like reaction, or hives in reaction to UV rays. In the United States alone, there are more than 115 chemical agents and drugs that are ingested or applied to the skin that may elicit photodermatitis. The reaction may be related to an allergy or it may be a direct toxic effect from the substance. Below are examples of agents or circumstances that may trigger one or the other type of reaction:

Direct toxic effect:

  • Tetracycline and sulfonamides, medications used for bacterial infections
  • Griseofulvin, used for fungal infections
  • Coal tar derivatives and psoralens, such as methoxsalen and trioxsalen, used for psoriasis
  • Tretinoin and other medications containing retinoic acid used for acne
  • Nonsteroidal anti-inflammatory drugs (NSAIDs), such as piroxicam
  • Chemotherapy agents used to treat cancer, such as 5-fluorouracil and vinblastine
  • Sulfonylureas, such as glyburide and glipizide, oral medications used for diabetes
  • Quinine and other medications used to treat malaria
  • Thiazide diuretics, such as hydrochlorothiazide
  • Desipramine and other medications used for depression (known as tricylics)
  • Phenothiazines, a class of medications used for psychosis
  • Benzodiazepines, such as alprazolam and tetrazepam, medications used for anxiety disorders

Allergic reactions:

  • Fragrances containing, for example, musk ambrette and methylcoumarin
  • Sunscreens with p-aminobenzoic acid (PABA) esters
  • Industrial cleaners that contain salicylanilide

Photodermatitis may also result from some immune-related disorders such as systemic lupus erythematosus (SLE) or certain states of nutrient deficiencies, including pellagra, which is caused by niacin (vitamin B3) deficiency.

Who's Most At Risk?
  • Skin type may influence the likelihood of a photodermatitis reaction. Those with fair to light skin, or those with red or blond hair, and green or blue eyes tend to be most sensitive, regardless of their racial or ethnic background. This is categorized as skin type I.
  • Exposure to UV rays for 30 minutes to several hours increases risk of photodermatitis (outbreaks in spring and summer months are common)
  • Exposure to UV rays from 11 a.m. to 2 p.m. also increases risk of photodermatitis since 50% of UV radiation is emitted during this time.

What to Expect at Your Provider's Office

A physical exam and a detailed history of exposure to sensitizers (see section entitled What Causes It?) and UV rays are important for diagnosis. A review of all body systems, including blood and urine tests, helps detect any related disease. Allergy tests may help identify substances that trigger or worsen the condition.

Treatment Options

These measures may help prevent photodermatitis:

  • Limit skin exposure to sun, especially intense midday sun.
  • Use sunscreens that protect against UVA and have a sun protection factor (SPF) of 30 to 50.
  • Cover up with a long-sleeved shirt, long pants, and a wide-brimmed hat.
  • Beware of using any product that causes sun sensitivity. (If you are already taking a prescription medication, however, do not stop taking it without consulting your healthcare provider.)

Treatment Plan

For blisters or weepy eruptions, apply cool, wet dressings. With certain types of photodermatitis, doctors may actually use phototherapy (controlled exposure to light for treatment purposes) to desensitize the skin or to help control symptoms.

Drug Therapies

For extremely sensitive patients, doctors may prescribe azathioprine to suppress the immune system. Short-term use of glucocorticoids may help control eruptions. For those who cannot be treated with phototherapy, doctors may prescribe hydroxychloroquine, thalidomide, beta-carotene, or nicotinamide (see section entitled Nutrition for details regarding the latter two). Note: Thalidomide causes severe birth defects and therefore should never be used by women who either are or wish to become pregnant.

Complementary and Alternative Therapies

Particular nutritional deficiencies can contribute to photosensitivity. Pellagra, for example, is caused by a niacin deficiency. Recent research results suggest that antioxidant nutrients, including beta-carotene, may help lessen the severity of photodermatitis.

  • Beta-carotene and Other Carotenoids: Despite the fact that beta-carotene is considered part of standard treatment for photodermatitis, the results of studies regarding this supplement have been mixed. One study of the effect of beta-carotene supplements on sunburns in humans showed no significant protection. In another trial, though, 20 healthy subjects received either carotenoids alone, mainly from beta-carotene, or carotenoids plus vitamin E. Both groups improved significantly. Vitamin E did not appear to add to the benefits of the carotenoids alone.
  • Fish Oil/Omega-3 Fatty Acids: In one study, 13 patients with a particular type of photodermatitis received supplements of fish oil, which contains omega-3 fatty acids, for three months. Tests afterward showed that the patients were significantly less sensitive to UV rays. Similarly, case reports of three children with hydroa vacciniforme, a rare scarring photosensitivity disorder, found that omega-3 supplements lessened symptoms for two of the three children. Photosensitive patients could consider eating a diet rich in omega-3 fatty acids, such as from cold water fish.
  • Protein: Actinic prurigo, a form of photosensitivity marked by ongoing outbreaks of itchy bumps during hot weather, is seen mainly in malnourished individuals. Research suggests that the condition is related to a diet deficient in protein or a specific amino acid (the building blocks of protein). Patients treated with a high-protein diet have improved but tend to relapse a few weeks after returning to their standard diet.
  • Vitamin B3: Nicotinamide (a form of niacin, or vitamin B3) may make a photosensitive reaction less likely. In a pilot study, 42 people with photodermatitis were given nicotinamide; despite extensive sun exposure, 25 of these people did not develop lesions.
  • Vitamins C and E: Antioxidants, including vitamins C and E, help remove free radicals, harmful by-products that result from cells' use and generation of energy. Free radicals are linked to skin damage. Oral supplements of vitamins C and E seem to work together to possibly reduce UV-induced skin reactions.
  • Vitamin D: In animal studies, vitamin D helped trigger the effects of an antioxidant protein found in skin cells of rats. This protein helps to protect against damage from UVB rays. It is not clear yet whether vitamin D supplements may help protect humans in the same way.

  • Green Tea: The antioxidant properties in green tea (Camellia sinensis) may provide protection against reddening of the skin caused by UV light. Epigallocatechin-3-gallate (EGCG), an active component of green tea has demonstrated photoprotection in animal studies. In a human study, tests on skin samples showed that EGCG does not block the absorption of UVB light but it does appear to inhibit redness, some cell damage, and other changes normally associated with UVB rays.
  • Calendula: Although not studied scientifically, this herb has been used clinically for skin conditions including sunburn. It may also be used as a homeopathic remedy at doses consistent with that kind of therapy.

Similar to photosensitizing medications, certain herbs can trigger photodermatitis; such herbs include St. John's wort (Hypericum perforatum), angelica seed or root (Angelica archangelica), celery stems (Apium graveolens), rue (Rutae folium), and lime oil/peel ( Citrus aurantifolia).


While scientific studies of homeopathy specifically addressing photodermatitis have not been conducted to date, individual reports suggest that homeopathic remedies may be a useful adjunct for the prevention and treatment of photodermatitis. An experienced homeopath considers each individual case and may recommend treatments tailored to address both the underlying condition and any current symptoms.

Prognosis/Possible Complications

Most photosensitivity reactions go away on their own and cause no permanent harm. However, symptoms can be severe when associated with a systemic disorder or when the exposure has been severe. Some photosensitivity reactions can continue for years after exposure ends.

Complications may include:

  • Ongoing photosensitivity, resulting in chronic photodermatitis
  • Hyperpigmentation or dark discoloration compared to normal skin tone even after inflammation has resolved
  • Premature aging of the skin
  • Squamous cell or basal cell skin cancer or melanoma

Following Up

Patients who need steroids to treat photosensitivity reactions must be monitored closely. In addition, anyone with a history of photodermatitis or photoreactivity should keep track of the frequency and duration of symptoms. This information can help determine the cause and appropriate treatment.

Supporting Research

Abramowitz AI, Resnik KS, Cohen KR. Margarita photodermatitis [letter]. N Engl J Med. 1993;328(12):891.

Adamski H, Benkalfate L, Delaval Y, et al. Photodermatitis from non-steroidal anti-inflammatory drugs. Contact Dermatitis. 1998;38(3):171-174.

American Academy of Pediatrics. Ultraviolet light: a hazard to children. Pediatrics. 1999;104(2):328-333.

Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines.Boston, Mass: Integrative Medicine Communications; 1998:35-36; 214-215; 245-249.

Callen JP. Photodermatitis in a 6-year-old child. Arthritis Rheum. 1993;36(10):1483-1485.

Darr D, Dunston S, Faust H, Pinnell S. Effectiveness of antioxidants (vitamin C and E) with and without sunscreens as topical photoprotectants. Acta Derm Venereol (Stockh). 1996;76(4):264-268.

Durán MM, Ordoñez CP, Prieto JC, Bernal J. Treatment of actinic prurigo in Chimila Indians. Int J Dermatol. 1996;35(6):413-416.

Eberlein-König B, Placzek M, Przybilla B. Protective effect against sunburn of combined systemic ascorbic acid (vitamin C) and d-alpha-tocopherol (vitamin E). J Am Acad Dermatol. 1998;38(1):45-48.

Enta T. Dermacase. Contact photodermatitis. Can Fam Physician. 1995;41:577, 586-587.

Enta T. Dermacase. Photodermatitis reaction to chlorothiazide. Can Fam Physician. 1994;40:1269, 1276.

Fernandez de Corres L, Diez JM, Audicana M. Photodermatitis from plant derivatives in topical and oral medicaments. Contact Dermatitis. 1996;35(3):184-185.

Freedberg IM, Eisen AZ, Wolff K. Fitzpatrick's Dermatology in General Medicine. Vol. 1. 5th ed. New York, NY: McGraw-Hill; 1996:1573-1586.

Fuchs J, Kern H. Modulation of UV-light-induced skin inflammation by D-alpha-tocopherol and L-ascorbic acid: a clinical study using solar simulated radiation. Free Radic Biol Med. 1998;25(9):1006-1012.

Garmyn M, Ribaya-Mercado JD, Russell RM, Bhawan J, Gilchrest BA. Effect of beta-carotene supplementation on the human sunburn reaction. Exp Dermatol. 1995;4(2):104-111.

Goldman L, Bennett JC. Cecil Textbook of Medicine. 21st ed. Philadelphia, Pa: W.B. Saunders; 2000:2295-2296.

Hadshiew I, Stäb F, Untiedt S, Bohnsack K, Rippke F, Hölzle E. Effects of topically applied antioxidants in experimentally provoked polymorphous light eruption. Dermatology. 1997;195(4):362-368.

Hanada K, Sawamura D, Nakano H, Hashimoto I. Possible role of 1,25-dihydroxyvitamin D3-induced metallothionein in photoprotection against UVB injury in mouse skin and cultured rat keratinocytes. J Dermatol Sci. 1995;9(3):203-208.

Kamat JP, Devasagayam TP. Methylene blue plus light-induced lipid peroxidation in rat liver microsomes: inhibition by nicotinamide (vitamin B3) and other antioxidants. Chem Biol Interact. 1996;99(1-3):1-16.

Katiyar SK, Matsui MS, Elmets CA, Mukhtar H. Polyphenolic antioxidant (-)-epigallocatechin-3-gallate from green tea reduces UVB-induced inflammatory responses and infiltration of leukocytes in human skin. Photochem Photobiol. 1999;69(2):148-153.

Leroy D, Dompmartin A, Szczurko C, Michel M, Louvet S. Photodermatitis from ketoprofen with cross-reactivity to fenofibrate and benzophenones. Photodermatol Photoimmunol Photomed. 1997;13(3):93-97.

Leung AY, Foster S. Encyclopedia of Common Natural Ingredients Used in Food, Drugs and Cosmetics. 2nd ed. New York, NY: Wiley and Sons; 1996.

Magaña-Garcia M, Magaña M. Actinic prurigo. The possible etiologic role of an amino acid in the diet. Med Hypotheses. 1993;41(1):52-54.

Moschella SL, Hurley HJ. Dermatology. 3rd ed. Philadelphia, Pa: W.B. Saunders; 1992:507-530.

Murata Y, Kumano K, Ueda T, Araki N, Nakamura T, Tani M. Photosensitive dermatitis caused by pyridoxine hydrochloride. J Am Acad Dermatol. 1998;39(2 pt 2):314-317.

Neumann R, Rappold E, Pohl-Markl H. Treatment of polymorphous light eruption with nicotinamide: a pilot study. Br J Dermatol. 1986;115(1):77-80.

Newall CA, Anderson LA, Philpson JD. Herbal Medicines: A Guide for Health-care Professionals. London: The Pharmaceutical Press; 1996.

Pigatto PD, Legori A, Bigardi AS, et al. Multicenter study of allergic contact photodermatitis: epidemiological aspects. Am J Contact Dermat. 1996;7(3):158-163.

Quinones D, Sanchez I, Alonso S, et al. Photodermatitis from tetrazepam. Contact Dermatitis. 1998;39(2):84.

Rhodes LE, Durham BH, Fraser WD, Friedmann PS. Dietary fish oil reduces basal and ultraviolet B-generated PGE2 levels in skin and increases the threshold to provocation of polymorphic light eruption. J Invest Dermatol. 1995;105(4):532-535.

Rhodes LE, White SI. Dietary fish oil as a photoprotective agent in hydroa vacciniforme. Br J Dermatol. 1998;138(1):173-178.

Ross JB, Moss MA. Relief of the photosensitivity of erythropoietic protoporphyria by pyridoxine. J Am Acad Dermatol. 1990;22(2 pt 2):340-342.

Scholzen TE, Brzoska T, Kalden DH, et al. Effect of ultraviolet light on the release of neuropeptides and neuroendocrine hormones in the skin: mediators of photodermatitis and cutaneous inflammation. J Invest Dermatol Symp Proc. 1999;4(1):55-60.

Stahl W, Heinrich U, Jungmann H, Sies H, Tronnier H. Carotenoids and carotenoids plus vitamin E protect against ultraviolet light-induced erythema in humans. Am J Clin Nutr. 2000;71(3):795-798.

Tanaka M, Niizeki H, Shimizu S, Miyakawa S. Photoallergic drug eruption due to pyridoxine hydrochloride. J Dermatol. 1996;23(10):708-709.

Tierney LM, McPhee SJ, Papadakis MA. Current Medical Diagnosis and Treatment 2000. New York, NY: Lange Medical Books/McGraw-Hill; 2000:177-178.

Review Date: December 2000
Reviewed By: Participants in the review process include: Robert A. Anderson, MD, President, American Board of Holistic Medicine, East Wenatchee, WA; Constance Grauds, RPh, President, Association of Natural Medicine Pharmacists, San Rafael, CA; Jacqueline A. Hart, MD, Department of Internal Medicine, Newton-Wellesley Hospital, Harvard University and Senior Medical Editor Integrative Medicine, Boston, MA; Leonard Wisneski, MD, FACP, George Washington University, Rockville, MD.

Copyright © 2004 A.D.A.M., Inc

The publisher does not accept any responsibility for the accuracy of the information or the consequences arising from the application, use, or misuse of any of the information contained herein, including any injury and/or damage to any person or property as a matter of product liability, negligence, or otherwise. No warranty, expressed or implied, is made in regard to the contents of this material. No claims or endorsements are made for any drugs or compounds currently marketed or in investigative use. This material is not intended as a guide to self-medication. The reader is advised to discuss the information provided here with a doctor, pharmacist, nurse, or other authorized healthcare practitioner and to check product information (including package inserts) regarding dosage, precautions, warnings, interactions, and contraindications before administering any drug, herb, or supplement discussed herein.

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