eMedicine Specialties > Emergency Medicine > Dermatology

Pityriasis Rosea

Richard Lichenstein, MD, Director, Pediatric Emergency Medicine Research, Associate Professor, University of Maryland Medical Center

Updated: Mar 27, 2008

Introduction

Background

Pityriasis rosea (PR) is an acute and characteristic exanthem that has been described for more than 2 centuries. Initially, a primary plaque, called a herald patch, is seen. The herald patch is followed by a distinctive, generalized rash 1-2 weeks later. The rash lasts approximately 2-6 weeks.

Pathophysiology

The primary plaque is seen on the skin in 50-90% of cases a week or more before the onset of the eruption of smaller lesions. This secondary eruption occurs 2-21 days later in crops following the lines of cleavage of the skin. On the back, this eruption produces a "Christmas tree" pattern.

Frequency

United States

The overall prevalence of PR has been calculated to be 0.13% in men and 0.14% in women. The prevalence reported at dermatologic centers has been between 0.3 and 3%.

International

An increase in the prevalence of PR has been reported in Uganda. No change in the prevalence of PR has been reported in Sweden. It has also been seen in the United Kingdom, Nigeria, Sudan, Brazil, Lagos, Singapore, Turkey, Kuwait, and Hong Kong.

Mortality/Morbidity

PR is a self-limited benign illness.

Sex

PR is reported to occur equally in the two sexes or slightly more often in females. The ratio of men to women varies from 1:1.43.

Age

PR is most common in children and young adults. Prevalence of PR rises during childhood and is most common in persons aged 15-40 years. PR is rare in infants and in elderly persons; however, it has been reported in infants as young as 3 months.

Clinical

History

• Pityriasis rosea (PR) may have prodromal symptoms (eg, malaise, nausea, anorexia, fever, joint pain, lymph node swelling, headache) that may precede the appearance of the herald patch.
• Pruritus, which may be intense, is present in 75% of cases.
• Ask the patient whether this is the first episode or a recurrence.

Physical

• The herald patch measures 1-2 cm in diameter. The patch is characterized as oval or round with a central, wrinkled, salmon-colored area and a dark red peripheral zone. The areas are separated by a collarette of fine scales. The herald patch is usually located on the trunk but can be seen on the neck or extremities.
• The secondary eruption appears at its maximum in about 10 days.
  • The secondary eruption is symmetric and localized, predominantly to the trunk and adjacent areas of the neck and extremities.
  • Involvement is maximal over the abdomen and anterior and dorsal surfaces of the thorax.
  • The secondary lesions appear as the primary patch in miniature, with the two red zones separated by the scaling ring. They are distributed in a Christmas tree pattern with their long axes following the lines of cleavage of the skin. In children under the age of 5 years, papular PR may be seen with a similar distribution.
• In atypical PR (20% of patients), the herald patch may be missing or confluent with other lesions.
  • The distribution of the rash may be peripheral, and facial involvement may be seen in children. Involvement of the axilla and groin (inverse variant) can also be seen.
  • The lesions of PR may be large (PR gigantea), urticarial (PR urticata), vesicular, pustular, purpuric, and erythema multiforme–like.
• Hypopigmentary and hyperpigmentary skin changes may follow the inflammatory stage. In patients with black skin, hyperpigmentation is more common.
• African American children have been shown to have more facial involvement (30%) and scalp involvement (8%) than white children. Approximately one third of African American children will have papular lesions, and 48% will have residual hyperpigmentation.¹
• Oral lesions of various types have been reported with PR, including erythematous plaques, hemorrhagic puncta, and ulcers.

Causes

• PR is similar to infectious exanthems in that it occurs in clusters among contacts, has a seasonal predilection to spring and autumn, and has a low rate of recurrence (3%).
• No bacteria, virus, or fungus has been isolated as a definite causal agent, although human herpesvirus 6 (HHV-6) and human herpesvirus 7 (HHV-7) may play a role.²
• Drugs such as bismuth, barbiturates, captopril, gold, organic mercurials, methoxypromazine, metronidazole, D-penicillamine, isotretinoin, tripelennamine hydrochloride, ketotifen, and salvarsan have been implicated in causing drug-induced PR.
• Atopy, seborrheic dermatitis, acne vulgaris, and dandruff are more common in patients with PR than in control subjects.

Differential Diagnoses

Erythema Multiforme
Pityriasis Alba
Psoriasis
Syphilis
Tinea

Other Problems to Be Considered

Nummular eczema
Seborrheic dermatitis
Drug eruptions
Erythema dyschromicum perstans
Lichen planus
Lichenoid reactions
Pityriasis lichenoides
Kaposi sarcoma

Workup

Laboratory Studies

• No diagnostic blood test is available.
• Laboratory testing is usually unnecessary; however, a rapid plasma reagin (RPR) test should be drawn, as PR can be confused with secondary syphilis.
• Blood profiles are normal; however, leucocytosis, neutrophilia, basophilia, and lymphocytosis have been seen.
• Minimal increases in the erythrocyte sedimentation rate (ESR), total protein, albumin, alpha1-globulin, and alpha2-globulin have been noted.
• Test findings for rheumatoid factor (RF), cold agglutinins, and cryoglobulins have been normal.

Procedures

• A skin biopsy may be needed to diagnose pityriasis rosea (PR). Findings are nonspecific and are supportive of the diagnosis and can help rule out other conditions. A positive KOH preparation of a skin scraping of a herald patch can rule out tinea corpora. PR presents as superficial perivascular dermatitis with epidermal and dermal changes. More than half of specimens have epidermal cells that contain dyskeratotic degeneration.
  • The granular cell layer is reduced or absent.
  • Slight acanthosis and spongiosis may be present.
  • Microscopic vesicles may be present in a clinically dry lesion.
  • Superficial perivascular infiltration by lymphocytes, histiocytes and, rarely, eosinophils is present.
  • Extravasated red blood cells (RBCs) may be seen in the papillae and epidermis

Treatment

Emergency Department Care

• In most cases, treatment is not necessary for this self-limited condition. In one study, the use of erythromycin in patients older than age 2 years with pityriasis rosea has been shown to be useful.³ A more recent study has shown that azithromycin is not effective for children with pityriasis rosea.⁴
• There is no reason to exclude children with pityriasis rosea from school.

Consultations

Consultation with a pediatric dermatologist may be required for atypical presentations of PR.

Medication

PR is a self-limited disease, and treatment is supportive. Water, sweat, and soap may cause irritation and should be avoided early in the disease. Topical zinc oxide and calamine lotion are useful for pruritus. If the disease is severe or widespread (eg, vesicular PR), topical or oral steroids may be used. Ultraviolet radiation therapy has been demonstrated to be effective for PR but may leave postinflammatory pigmentation at the site of the PR lesion.⁵ Acyclovir has been shown in one study to hasten resolution especially if given within 1 week of rash but this was a nonrandomized nonblinded trial.⁶

Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. Modify the body's immune response to diverse stimuli.

Prednisone (Deltasone, Meticorten, Orasone)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Dosing

Adult

5-60 mg/d PO qd or divided bid/qid; taper over 2 wk as symptoms resolve

Pediatric

4-5 mg/m²/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid; taper over 2 wk as symptoms resolve

Interactions

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Contraindications

Documented hypersensitivity; fungal, tubercular skin, connective tissue, or viral infections; peptic ulcer disease; hepatic dysfunction; GI disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

Hydrocortisone (Cortaid, Cortef, Hycort)

Adrenocorticosteroid derivative suitable for application to skin or external mucous membranes. Mineralocorticoid and glucocorticoid effects resulting in anti-inflammatory activity.

Dosing

Adult

Apply sparingly to affected areas bid/qid

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; viral, fungal, and bacterial skin infections

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Prolonged use, applying over large surface areas, applying potent steroids, and using occlusive dressings may increase systemic absorption of corticosteroids and may cause Cushing syndrome, reversible HPA axis suppression, hyperglycemia, and glycosuria

Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Erythromycin (E.E.S., E-Mycin, Eryc, Ery-Tab)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes and causing RNA-dependent protein synthesis to arrest.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half-total daily dose may be taken q12h. May have anti-inflammatory and immunomodulatory effects.

Dosing

Adult

250 mg erythromycin stearate/base (or 400 mg ethylsuccinate) PO 1 h ac q6h, or 500 mg q12h
Alternatively, 333 mg PO q8h; increase to 4 g/d depending on severity of infection

Pediatric

30-50 mg/kg/d (15-25 mg/lb/d) PO divided q6-8h; double dose for severe infection

Interactions

Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin, increases risk of rhabdomyolysis; decreases metabolism of repaglinide, thus increasing serum levels and effects

Contraindications

Documented hypersensitivity; hepatic impairment

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI side effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur

Antiviral agents

These agents may improve rate of resolution if given within 1 week of rash.

Acyclovir (Zovirax)

Prodrug activated by phosphorylation by virus-specific thymidine kinase that inhibits viral replication. Herpes virus thymidine kinase (TK), but not host cells TK, uses acyclovir as a purine nucleoside, converting it into acyclovir monophosphate, a nucleotide analogue. Guanylate kinase converts the monophosphate form into diphosphate and triphosphate analogues that inhibit viral DNA replication.
Has affinity for viral thymidine kinase and, once phosphorylated, causes DNA chain termination when acted on by DNA polymerase. Interferes with DNA replication within the virions.

Dosing

Adult

800 mg PO 5 times daily for 5 d

Pediatric

10-20 mg/kg PO q6h for 5-10 d

Interactions

Concomitant use of probenecid or zidovudine prolongs half-life and increases CNS toxicity of acyclovir

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal failure or when using nephrotoxic drugs

Follow-up

Inpatient & Outpatient Medications

• A mild topical steroid or an emollient with 0.25% menthol may relieve the itching.
• Oral antipruritics may be helpful.
• Ultraviolet B therapy may be used to hasten resolution of the rash.⁵
• Oral erythromycin has been used with success in one study in patients with pityriasis rosea who were older than 2 years.³
• Acyclovir may hasten resolution if given within 1 week of illness.⁶

Prognosis

• The prognosis of PR is excellent.
• Fewer than 3% of affected individuals experience recurrences.

Patient Education

• The long duration of PR must be explained to patients and their families.
• The secondary rash develops over 2 weeks, persists for another 2 weeks, and then fades over another 2 weeks.
• Some lesions have persisted for as long as 3-4 months.

Miscellaneous

Medicolegal Pitfalls

• Other treatable conditions (eg, syphilis) may be missed if not considered.

References

1. Amer A, Fischer H, Li X. The natural history of pityriasis rosea in black American children: how correct is the "classic" description?. Arch Pediatr Adolesc Med. May 2007;161(5):503-6. [Medline].

2. Drago F, Ranieri E, Malaguti F. Human herpesvirus 7 in patients with pityriasis rosea. Electron microscopy investigations and polymerase chain reaction in mononuclear cells, plasma and skin. Dermatology. 1997;195(4):374-8. [Medline].

3. Sharma PK, Yadav TP, Gautam RK. Erythromycin in pityriasis rosea: A double-blind, placebo-controlled clinical trial. J Am Acad Dermatol. Feb 2000;42(2 Pt 1):241-4. [Medline].

4. [Best Evidence] Amer A, Fischer H. Azithromycin does not cure pityriasis rosea. Pediatrics. May 2006;117(5):1702-5. [Medline].

5. Stulberg DL, Wolfrey J. Pityriasis rosea. Am Fam Physician. Jan 1 2004;69(1):87-91. [Medline].

6. Drago F, Vecchio F, Rebora A. Use of high-dose acyclovir in pityriasis rosea. J Am Acad Dermatol. Jan 2006;54(1):82-5. [Medline].

7. Chuh A, Chan H, Zawar V. Pityriasis rosea--evidence for and against an infectious aetiology. Epidemiol Infect. Jun 2004;132(3):381-90. [Medline].

8. Chuh A, Lee A, Zawar V. Pityriasis rosea--an update. Indian J Dermatol Venereol Leprol. Sep-Oct 2005;71(5):311-5. [Medline].

9. Coustou D, Leaute-Labreze C, Bioulac-Sage P, et al. Asymmetric periflexural exanthem of childhood: a clinical, pathologic, and epidemiologic prospective study. Arch Dermatol. Jul 1999;135(7):799-803. [Medline].

10. Hartley AH. Pityriasis rosea. Pediatr Rev. Aug 1999;20(8):266-9, quiz 270. [Medline].

11. Horio T. Skin disorders that improve by exposure to sunlight. Clin Dermatol. Jan-Feb 1998;16(1):59-65. [Medline].

12. Kay MH, Rapini RP, Fritz KA. Oral lesions in pityriasis rosea. Arch Dermatol. Nov 1985;121(11):1449-51. [Medline].

13. Kempf W, Burg G. Pityriasis rosea--a virus-induced skin disease? An update. Arch Virol. 2000;145(8):1509-20. [Medline].

14. Nanda A, Al-Hasawi F, Alsaleh QA. A prospective survey of pediatric dermatology clinic patients in Kuwait: an analysis of 10,000 cases. Pediatr Dermatol. Jan-Feb 1999;16(1):6-11. [Medline].

15. Pomeranz AJ, Fairley JA. The systematic evaluation of the skin in children. Pediatr Clin North Am. Feb 1998;45(1):49-63. [Medline].

16. Scott LA, Stone MS. Viral exanthems. Dermatol Online J. Aug 9 2003;9(3):4. [Full Text].

17. Wyndham M. Pityriasis. Practitioner. Jun 1997;241(1575):358. [Medline].

Keywords

pityriasis rosea, PR, pityriasis rosea gigantica, pityriasis rosea urticata, papular PR, atypical PR, drug-induced PR, keratosis, vesicular PR, herald patch, rash, pruritus, exanthem

Contributor Information and Disclosures

Author

Richard Lichenstein, MD, Director, Pediatric Emergency Medicine Research, Associate Professor, University of Maryland Medical Center
Richard Lichenstein, MD is a member of the following medical societies: Ambulatory Pediatric Association and American Academy of Pediatrics
Disclosure: Nothing to disclose.

Medical Editor

Jerry Balentine, DO, Professor of Emergency Medicine, New York College of Osteopathic Medicine; Senior Vice President, Chief Medical Officer, Medical Director, Attending Physician in Department of Emergency Medicine, Saint Barnabas Hospital
Jerry Balentine, DO is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American College of Physician Executives, American Osteopathic Association, and New York Academy of Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Mark W Fourre, MD, Program Director, Department of Emergency Medicine, Maine Medical Center; Associate Clinical Professor, Department of Surgery, University of Vermont School of Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Pamela L Dyne, MD, Associate Professor, Program Director, Department of Medicine, Division of Emergency Medicine, University of California at Los Angeles School of Medicine
Pamela L Dyne, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)