eMedicine Specialties > Dermatology > Allergy & Immunology

Urticaria, Solar

Elma D Baron, MD, Assistant Professor of Dermatology, Case Western Reserve University, University Hospitals of Cleveland; Director of Skin Study Center, University Hospitals Research Institute; Acting Chief of Dermatology, Veterans Affairs Medical Center, Cleveland
Charles R Taylor, MD, Assistant Professor of Dermatology, Harvard Medical School; Director of Phototherapy Unit, Department of Dermatology, Massachusetts General Hospital

Updated: Mar 29, 2007

Introduction

Background

Solar urticaria is a rare photodermatosis characterized by pruritus, stinging, erythema, and wheal formation after a brief period of exposure to natural sunlight or an artificial light source emitting the appropriate wavelength.

Initially described by Merklen in 1904, the reaction is localized to exposed areas of the skin, although it can occur through thin clothing. Solar urticaria disappears within several minutes to a few hours, without pigmentary change if further sun exposure is avoided. This disorder can be quite disabling and difficult to manage. It often has a sudden, dramatic onset, and little information is available regarding its duration and eventual outcome.

Pathophysiology

Solar urticaria is possibly caused by an antigen-antibody reaction. Solar irradiation may induce an antigen in the serum or plasma of affected individuals. Intradermal injection of serum from a solar urticaria patient passively, but not consistently, transfers the condition to a healthy individual.

The following types of solar urticaria have been proposed:

• Type I: This type is an immunoglobulin E (IgE)–mediated hypersensitivity to specific photoallergens generated only in solar urticaria patients.
• Type II: This type is an IgE-mediated hypersensitivity to nonspecific photoallergens found in both solar urticaria patients and healthy individuals.

Passive transfer test findings are positive in patients with type II solar urticaria, but they may be positive or negative in those with type I.

The wide action spectrum (290-800 nm) implicated for this condition may be related to the specific photoallergen and its molecular weight. Diversity in the reported action spectra may be due to differences in photoallergens. In addition, spectra believed to be responsible for either inhibition or augmentation of the reaction have been detected. Complex interactions occur between the various wavelengths and the photoallergen.

The result of these interactions is mast cell degranulation with subsequent histamine release. Mediators other than histamines may also be involved. Inhibition of solar urticaria with light suppresses the wheal-flare response following intradermal injection of photoactivated autologous serum but does not suppress the wheal and flare associated with compound 48/80.

Frequency

United States

Solar urticaria comprises only 4% of US patients with photosensitive disorders.

International

Solar urticaria comprises 5.3% of the cases of photosensitive dermatoses worldwide.

Mortality/Morbidity

The mortality rate has not been determined. In some cases, skin eruption is accompanied by symptoms such as headache, nausea, vomiting, bronchospasm, and syncope.

Race

The condition occurs in all races.

Sex

A slight female predilection is noted.

Age

Solar urticaria has a wide range of onset (10-70 y). The mean age of onset is 35 years, but it has been reported to occur in infancy.

Clinical

History

An accurate history is important for the diagnosis of solar urticaria because of the transient nature of the eruption. Patients often have no obvious lesions.

• Patients may report pruritus, erythema, and wheal formation of varying degrees after a short period (<30 min) of sun exposure.
  • As with most other photodermatoses, skin lesions in solar urticaria may occur on any exposed area, even if skin was covered with thin clothing.
  • The face and the dorsal aspect of the hands, which are chronically exposed to the sun, are less severely affected than other parts of the body, perhaps owing to acclimatization and "hardening."
• Mucosal involvement (eg, tongue and/or lip swelling) has been reported.
• Other symptoms, such as headache, nausea, vomiting, bronchospasm, and syncope, have been reported but are considered rare.
• Upon cessation of sun exposure, the rash begins to disappear within several minutes to a few hours and rarely lasts beyond 24 hours. Rapid disappearance of the rash upon cessation of further sun exposure is essential to the diagnosis of solar urticaria.
• Ascertain the following aspects of history to exclude other differential diagnoses:
  • Oral medication intake (eg, chlorpromazine), which may cause a similar photo-induced reaction
  • Currently used topical agents (eg, sunscreen, fragrance), which can cause photocontact dermatitis
  • Family history of photosensitivity (as may occur in some porphyrias)
  • Medical history regarding other body systems in order to detect other underlying causes of photosensitivity (eg, connective-tissue disorders)

Physical

In most cases, physical examination findings will be normal.

• During an acute episode, vital signs are usually unaffected; however, systemic symptoms accompanying the cutaneous eruption have been reported.
  • In rare cases, cardiac and respiratory rates increase and blood pressure decreases.
  • Wheezing may be heard upon auscultation of the chest when bronchospasm is present.
• Examination of the skin during an acute episode may reveal lesions in the form of erythematous macules to distinct wheals, the morphology of which may be no different from that of lesions found in acute urticaria secondary to other causes.
  • Eruption follows a photodistribution modified by the type of clothing worn by the affected individual at the time of exposure.
  • Lesions may be present in areas covered with thin clothing, depending on the causative light wavelength and sheerness of the fabric.
  • Mucosal areas, such as the tongue and lips, may be swollen or edematous.
  • The reaction leaves no residual skin changes. Consequently, examination of the skin after the acute eruption reveals no evidence of the condition.

Causes

Solar urticaria may be caused by an antigen-antibody reaction. Solar irradiation may induce an antigen in the serum or plasma of affected individuals. Intradermal injection of serum from a solar urticaria patient passively, but not consistently, transfers the condition to a healthy individual.

Differential Diagnoses

Other Problems to Be Considered

• Polymorphous light eruption is much more common than solar urticaria and may affect the same sites, but the lesions do not subside as quickly upon cessation of sun exposure.
• Erythropoietic protoporphyria usually manifests earlier in life.
• Lupus erythematosus is more common in women, and signs and symptoms, other than dermatologic ones, accompany the acute systemic form. Localized cutaneous forms have different morphologies (eg, discoid, papulosquamous, annular); however, lupus erythematosus should be excluded through laboratory test findings.
• Photocontact dermatitis manifests in a pattern suggestive of the contactant or allergen and does not totally disappear upon discontinuation of sun exposure.
• Miliaria rubra (heat rash) can be mistaken for solaria urticaria.
• Churg Strauss syndrome may manifest solar urticaria.

Workup

Laboratory Studies

• Perform serologic tests for antinuclear antibody, Ro, and La antibodies to exclude connective-tissue disease (eg, lupus erythematosus).
• Perform testing to exclude metabolic causes (eg, porphyrias).
  • Evaluate the plasma porphyrin level.
  • If abnormal results are found, follow with a quantitative 24-hour urinary and fecal porphyrin measurement, as well as erythrocyte porphyrin determination.

Other Tests

• Phototesting confirms the diagnosis, identifies the action spectrum, and establishes baseline data (eg, minimum urticarial dose [MUD]) for possible therapeutic interventions and monitoring in the future.
  • Solar urticaria has a wide action spectrum. Perform phototesting using broadband UV-B (290-320 nm), UV-A (320-400 nm), and visible light sources (400-800 nm). Most patients with solar urticaria have provocative wavelengths in the UV-A and visible ranges, especially green or blue.
  • Duration of exposure under visible light should be less than an hour. Typically, the light emitted by a slide projector is used. Measures must be taken to avoid excessive heat output from the light source in order to eliminate the possibility of cholinergic- or heat-induced urticaria, instead of actual solar urticaria. A water filter may be placed in front of the light source to absorb excess heat.
  • Phototesting with narrowband UV-B (311-313 nm) is recommended if therapy with this light source is being considered. Occasionally, these tests do not produce the expected reaction.
  • Phototesting with other light sources (eg, solar simulators, lasers) may be necessary in difficult-to-establish cases.
  • Provocation with natural sunlight may be performed if ambient conditions allow.
  • Many patients with solar urticaria have an inhibition spectrum. If their skin is first exposed to wavelengths known to induce solar urticaria and is then immediately afterward, or possibly concurrently, exposed to radiation within the inhibition spectrum, the urticarial reaction is either eliminated or diminished.

Histologic Findings

Histologic changes are typically found in the dermis in the form of vasodilatation, increased permeability of the vascular endothelium, and edema. Eosinophil infiltration and deposition of eosinophil granule proteins in the dermis are prominent during early stages of the lesion. Neutrophils are found in increased numbers around the upper dermal vessels. Dermal mast cells may increase in number. After 24 hours, the dermal infiltrate is predominantly composed of mononuclear leukocytes.

Treatment

Medical Care

In rare systemic cases, supportive medical measures to maintain blood pressure and adequate ventilation may be required if extensive cutaneous surfaces are simultaneously involved.

Medication

Treatment of solar urticaria can be frustrating. A combination of different modalities is often necessary, but the success of these methods is highly variable. Taking measures to avoid or minimize sun exposure is the most important step. Unfortunately, this often requires major adjustments in lifestyle, which might be impractical for some patients.

Antihistamines

Because solar urticaria involves IgE-mediated mast cell degranulation with consequent histamine release, the first line of treatment consists of long-acting, nonsedating H1-receptor blockers. Often, such agents achieve a protective factor of 10 or more. The extent to which this is useful depends on the severity of the disease itself. For example, someone who gets hives after just a few seconds of sun exposure is unlikely to benefit from antihistamine monotherapy. A patient requiring 10 minutes or more of exposure would show more benefit. Antihistamines seem to block wheal response and minimize pruritus, but they do not entirely eliminate an erythematous reaction. This tendency should be explained to the patient.

Cetirizine (Zyrtec)

Forms complex with histamine for H1-receptor sites in blood vessels, GI tract, and respiratory tract.

Dosing

Adult

5-10 mg PO qd

Pediatric

<2 years: Not established
2-5 years: 2.5 mg PO qd
>5 years: Administer as in adults

Interactions

Increases CNS toxicity of depressants

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Because it is related to the highly sedating antihistamine hydroxyzine, some patients also experience drowsiness; caution in hepatic or renal dysfunction; doses >10 mg/d may cause drowsiness

Fexofenadine (Allegra)

Competes with histamine for H1 receptors in GI tract, blood vessels, and respiratory tract, reducing hypersensitivity reactions. Does not sedate.

Dosing

Adult

180 mg/d PO

Pediatric

<6 months to 2 years: Not established; 15 mg (2.5 mL) PO bid recommended for chronic idiopathic urticaria
2-12 years: 30 mg PO bid
>12 years: Administer as in adults

Interactions

Toxicity increases with coadministration of erythromycin and ketoconazole; concurrent administration with aluminum- or magnesium-containing antacids within 15 min decreases absorption

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Cardiac complications (dysrhythmias) may occur in high doses; no data available on use while breastfeeding

Loratadine (Claritin)

Selectively inhibits peripheral H1 receptors.

Dosing

Adult

10 mg PO qd on empty stomach

Pediatric

<2 years: Not established
2-6 years: 5 mg/d PO
>6 years: Administer as in adults

Interactions

Ketoconazole, erythromycin, procarbazine, and alcohol may increase levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Initiate therapy at lower dose in liver or renal impairment

Desloratadine (Clarinex)

Long-acting tricyclic histamine antagonist selective for H1 receptor. Relieves nasal congestion and systemic effects of seasonal allergy. A major metabolite of loratadine, which, after ingestion, is metabolized extensively to active metabolite 3-hydroxydesloratadine.

Dosing

Adult

5 mg PO qd

Pediatric

<6 months: Not established
6-12 months: 2 mL (1 mg) syr PO qd
1-6 years: 2.5 mL (1.25 mg) syr PO qd
6-12 years: 5 mL (2.5 mg) syr or 2.5 mg PO qd
>12 years: Administer as in adults

Interactions

Limited data exist; erythromycin and ketoconazole increase desloratadine and 3-hydroxydesloratadine plasma concentrations, but no increase in clinically relevant adverse effects, including QTc, has been observed

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Decrease dose in hepatic impairment; rarely causes pharyngitis or dry mouth; adjust dose in renal impairment

Antimalarials

Used to treat certain photosensitive eruptions, including solar urticaria. Efficacy is unpredictable.

Hydroxychloroquine (Plaquenil)

Inhibits chemotaxis of eosinophils and locomotion of neutrophils. Impairs complement-dependent antigen-antibody reactions.
Hydroxychloroquine sulfate 200 mg is equivalent to 155 mg hydroxychloroquine base and 250 mg chloroquine phosphate.

Dosing

Adult

200 mg PO bid

Pediatric

10 mg base/kg initially, followed by 5 mg/kg at 6, 24, and 48 h

Interactions

Serum levels increase with cimetidine; magnesium trisilicate may decrease absorption

Contraindications

Documented hypersensitivity; psoriasis; retinal and visual field changes attributable to 4-aminoquinolones

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in hepatic disease, G-6-PD deficiency, psoriasis, and porphyria; not recommended for long-term use in children; perform periodic (q6mo) ophthalmologic examinations (include visual acuity, slit-lamp, funduscopic, and visual field tests); periodically test for muscle weakness; periodic CBC counts should be checked; hemolysis, aplastic anemia, agranulocytosis, and leukopenia can occur

Histamine H2-receptor antagonists

Usually given in addition to H1 blockers.

Ranitidine (Zantac)

H2 antagonist that, when combined with H1 type, may be useful in treating allergic reactions that do not respond to H1 antagonists alone.

Dosing

Adult

150 mg PO bid

Pediatric

<1 month: Not established
>1 month to 12 years: 2-4 mg/kg PO qd; not to exceed 150 mg/d
>12 years: 1.25-2.5 mg/kg/dose PO q12h; not to exceed 300 mg/d; alternatively, 0.75-1.5 mg/kg/dose IV/IM q6-8h; not to exceed 400 mg/d

Interactions

May decrease effects of ketoconazole and itraconazole; may alter serum levels of ferrous sulfate, diazepam, nondepolarizing muscle relaxants, and oxaprozin; may decrease effectiveness of bisacodyl if given within 1 h of H2 blocker; drugs that raise gastric pH, such as H2 blockers, reduce cefpodoxime absorption

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Caution in renal or liver impairment; if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment; elevation of transaminase enzymes has occurred with prolonged IV therapy

Follow-up

Further Outpatient Care

• Phototherapy with UV-A, broadband UV-B, or narrowband UV-B and photochemotherapy with oral methoxsalen (8-MOP) plus UV-A are effective for treating solar urticaria. Desensitization treatments are usually performed in the spring. Unfortunately, the tolerance induced by these modalities is often short-lived, and maintenance therapy is needed.
• A number of treatment protocols are used for the different light sources mentioned, but the optimal protocol is not clearly established.
• The MUD with the specific light box to be used in the treatment must be determined.
  • The MUD is repeated during the course of treatment in order to monitor the patient's progress because development of tolerance is usually paralleled by an increase in the MUD.
  • If the initial MUD is very low, it is difficult to immediately start the patient on oral methoxsalen photochemotherapy. Initial exposures with UV-A alone may be performed until the MUD is increased to a level at which oral methoxsalen photochemotherapy can be initiated.
• Phototherapy and photochemotherapy mechanisms of action in solar urticaria are not entirely known.
  • The resulting increase in skin pigmentation and epidermal thickening may be important factors but are probably not the main mechanisms behind tolerance induction.
  • Some authorities have postulated a UV-induced increase in the mast cell degranulation threshold as a possible mechanism.
• Psoralen–UV-A, or PUVA, can cause disease improvement or remission lasting several months. Based on available evidence, it is probably the treatment of choice for patients not sufficiently helped by antihistamines.
• Plasma exchange therapy has been effective in a few cases, especially in patients with a circulating factor in their serum demonstrated by a positive intradermal test finding (Collins, 1996). However, therapy has been reported ineffective in some centers. Until definitive studies are conducted to evaluate the efficacy of this therapy, it should be reserved as a last resort.

Deterrence/Prevention

• Sun exposure must be avoided or minimized because it is the primary causative agent. Educate patients about practical measures such as wearing protective clothing, judiciously applying sunscreens with adequate protection against the causative wavelengths, using UV protective shields over glass windows, and altering lifestyle to minimize time spent outside during the day (ie, changing job hours, shifting to indoor recreational activities). Some patients with UV-A or visible, induced solar urticaria may find helpful the use of self-tanning lotions containing dihydroxyacetone.
• If medical therapy is unsuccessful, some patients benefit from complete avoidance or, possibly, a combination of avoidance and medical therapy.

Prognosis

• Solar urticaria is usually a chronic condition. Few patients experience spontaneous remission. Continued intake of oral antihistamines may prevent the whealing to a degree, thus allowing some tolerance to sunlight. Significant and more long-lasting improvement is observed in patients who undergo phototherapy or photochemotherapy. Some patients find that following preventive measures makes their condition manageable.

Patient Education

• Educate patients that, despite its persistent and chronic nature, solar urticaria is a benign disorder usually localized to the skin without affecting general health. Emphasize that response to treatment is generally unpredictable and that prevention by avoidance may ultimately be the key to the management of this condition.
• For excellent patient education resources, visit eMedicine's Allergy Center and Skin, Hair, and Nails Center. Also, see eMedicine's patient education article Hives and Angioedema.

Miscellaneous

Medicolegal Pitfalls

• Ensure that an underlying condition that manifests as a photo-induced urticarial reaction (eg, lupus erythematosus, porphyrias) is excluded by conducting the necessary laboratory examinations.
• Patients must be well informed of the risks and benefits of antihistamines, phototherapy, photochemotherapy, or plasma exchange therapy if these modalities are considered.

References

1. Collins P, Ahamat R, Green C, Ferguson J. Plasma exchange therapy for solar urticaria. Br J Dermatol. Jun 1996;134(6):1093-7. [Medline].

2. Dawe RS, Ferguson J. Prolonged benefit following ultraviolet A phototherapy for solar urticaria. Br J Dermatol. Jul 1997;137(1):144-8. [Medline].

3. Fotiades J, Soter NA, Lim HW. Results of evaluation of 203 patients for photosensitivity in a 7.3-year period. J Am Acad Dermatol. Oct 1995;33(4):597-602. [Medline].

4. Fukunaga A, Horikawa T, Yamamoto A, Yamada Y, Nishigori C. The inhibition spectrum of solar urticaria suppresses the wheal-flare response following intradermal injection with photo-activated autologous serum but not with compound 48/80. Photodermatol Photoimmunol Photomed. Jun 2006;22(3):129-32. [Medline].

5. Harris A, Burge SM, George SA. Solar urticaria in an infant. Br J Dermatol. Jan 1997;136(1):105-7. [Medline].

6. Khoo SW, Tay YK, Tham SN. Photodermatoses in a Singapore skin referral centre. Clin Exp Dermatol. Jul 1996;21(4):263-8. [Medline].

7. Miyauchi H, Horio T. Detection of action, inhibition and augmentation spectra in solar urticaria. Dermatology. 1995;191(4):286-91. [Medline].

8. Roelandts R, Ryckaert S. Solar urticaria: the annoying photodermatosis. Int J Dermatol. Jun 1999;38(6):411-8. [Medline].

9. Roelandts R. Diagnosis and treatment of solar urticaria. Dermatol Ther. 2003;16(1):52-6. [Medline].

10. Ryckaert S, Roelandts R. Solar urticaria. A report of 25 cases and difficulties in phototesting. Arch Dermatol. Jan 1998;134(1):71-4. [Medline].

11. Shimauchi T, Kabashima K, Tokura Y. Solar urticaria as a manifestation of Churg-Strauss syndrome. Clin Exp Dermatol. Mar 2007;32(2):209-10. [Medline].

Keywords

solar urticaria, sun hives, allergy, allergic reaction, anaphylaxis, anaphylactoid reaction, angioedema, photodermatosis, pruritus, solar irradiation, minimum urticarial dose, MUD, polymorphous light eruption, PMLE, erythropoietic protoporphyria, lupus erythematosus, photocontact dermatitis, miliaria rubra, psoralen–UV-A, PUVA, phototherapy, UV-A, broadband UV-B, narrowband UV-B, photochemotherapy, methoxsalen

Contributor Information and Disclosures

Author

Elma D Baron, MD, Assistant Professor of Dermatology, Case Western Reserve University, University Hospitals of Cleveland; Director of Skin Study Center, University Hospitals Research Institute; Acting Chief of Dermatology, Veterans Affairs Medical Center, Cleveland
Elma D Baron, MD is a member of the following medical societies: American Academy of Dermatology, American Society for Photobiology, Photomedicine Society, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Coauthor(s)

Charles R Taylor, MD, Assistant Professor of Dermatology, Harvard Medical School; Director of Phototherapy Unit, Department of Dermatology, Massachusetts General Hospital
Charles R Taylor, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society for Laser Medicine and Surgery, Massachusetts Medical Society, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Donald Belsito, MD, Clinical Professor, Department of Internal Medicine, Division of Dermatology, University of Missouri at Kansas City; Private Practice, American Dermatology Associates, LLC
Donald Belsito, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, Dermatology Foundation, Kansas Medical Society, Noah Worcester Dermatological Society, Phi Beta Kappa, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Jeffrey Meffert, MD, Assistant Clinical Professor of Dermatology, University of Texas Health Science Center-San Antonio
Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

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