eMedicine Specialties > Dermatology > Papulosquamous Diseases

Pityriasis Rosea

Robert A Allen, MD, Staff Physician, Department of Dermatology, Drexel University College of Medicine-Hahnemann Hospital
Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School

Updated: Feb 13, 2009

Introduction

Background

Pityriasis rosea (PR) is a common benign papulosquamous disease that was originally described by Camille Melchior Gibert in 1860. Pityriasis denotes fine scales, and rosea translates as rose colored or pink. Pityriasis rosea can have a number of clinical variations. Its diagnosis is important because it may resemble secondary syphilis.

Pathophysiology

Pityriasis rosea has often been considered to be a viral exanthem. Its clinical presentation supports this concept. Pityriasis rosea has been linked to upper tract respiratory infections, it can cluster within families and close contacts, and it has an increased incidence in individuals who are immunocompromised. As with viral exanthems, the incidence may increase in the fall and the spring. A single outbreak tends to elicit lifelong immunity.

Immunologic data suggest a viral etiology. Increased amounts of CD4 T cells and Langhans cells are present in the dermis; this observation may indicate viral antigen processing and presentation. Also, anti-immunoglobulin M (IgM) to keratinocytes has been found in patients with pityriasis rosea; this finding may be associated with the exanthem phase of the presumed viral infection.

Despite these tendencies, no single virus has been proven to cause the disease. A number of viruses have been studied for a link to pityriasis rosea. Picornaviruslike particles have been seen in the tissue of African green monkeys inoculated from human pityriasis rosea lesions. A follow-up study failed to find picornavirus RNA in patients with pityriasis rosea. Serology and polymerase chain reaction for viral DNA have been negative for Epstein-Barr virus, parvovirus B19, cytomegalovirus, human herpesvirus (HHV) – 8,¹  HHV-1, and HHV-2 in patients diagnosed with pityriasis rosea.

Other work demonstrated HHV–7 viral DNA in both the lesions and the plasma in patients with pityriasis rosea.² In addition, a separate study found HHV-7 DNA in lymphocytes in 75% of patients with pityriasis rosea, compared with 9% of controls. Polymerase chain reaction has shown both HHV-7 and HHV-6 DNA in a variety of tissues and secretions from patients with pityriasis rosea. In the same study, in situ hybridization of lesional lymphocytes showed both HHV-7 and HHV-6 mRNA. However, herpesviruslike particles were not seen via electron microscopy.³ Follow-up studies have not confirmed a herpes etiology, and because HHV-7 is frequently found in healthy individuals, its etiologic role is controversial.

Frequency

International

Worldwide, pityriasis rosea has been estimated to account for 2% of dermatologic outpatient visits. The disease is more common in the spring and the fall in temperate climate zones. However, it may be more frequent in the summer in some other regions, and it favors the hot, dry season in Australia, India, and Malaysia.

Mortality/Morbidity

Pityriasis rosea is a benign self-limited disease associated with mild morbidity with rash and occasional pruritus. It has been associated with neonatal hypotonia, hyporeactivity, and premature delivery. An increased risk of miscarriage may occur, especially mothers who developed pityriasis rosea within the first 15 weeks of their pregnancy.⁴

Race

No racial predominance is reported. More intensely pigmented Africans tend to have more widespread disease. The lesions in African Americans may lack a rose color, and they may appear darker than the surrounding skin.

Sex

Pityriasis rosea is more common in women than in men.⁵ One study found it to be twice as common in women as in men.

Age

Pityriasis rosea commonly develops in children and young adults, although any age group can be affected. Most patients are aged 10-35 years.

Clinical

History

The history should include questions about close contacts with similar eruptions. This finding is uncommon because most cases of pityriasis rosea are sporadic, as pityriasis rosea is thought to reflect a weakly contagious disease. A history of medication intake should be obtained because several medications have been shown to cause a similar exanthem.

• The disease typically begins with a solitary macule that heralds the eruption (called the herald spot/patch), which is usually a salmon-colored macule. This initial lesion enlarges over a few days to become a patch with a collarette of fine scale just inside the well-demarcated border.
• Within the next 1-2 weeks, a generalized exanthem usually appears, although it may occur from hours to months after the herald patch. This secondary phase consists of bilateral and symmetric macules with a collarette scale oriented with their long axes along cleavage lines. This phase tends to resolve over the next 6 weeks, but variability is common.
• Pruritus is common, usually of mild-to-moderate severity, and it occurs in 75% of patients.

Physical

• The herald patch is usually a single pink patch, 2-10 cm in diameter, on the neck or the trunk with a fine collarette scale (see Media File 1). It is observed in more than 50% of patients, and it may occur as multiple lesions or in atypical locations.
• About 1-2 weeks after the herald patch is seen, the generalized eruption appears, although it has been known to occur from hours to 3 months later. It consists of salmon-colored macules or patches, 0.5-1.5 cm in diameter, with a collarette scale, often described as having a cigarette paper–like appearance. The long axes of the lesions are oriented in a parallel fashion along cleavage lines, giving the classic Christmas tree pattern (see Media File 2). These secondary lesions most commonly occur on the trunk, the abdomen, the back, and the proximal upper extremities.
• Pruritus occurs in 75% of patients and is severe in 25%.
• Lymphadenopathy is uncommon, but, when present, it is usually observed in African Americans.
• Atypical pityriasis rosea occurs in 20% of patients.
  • These variations can be separated into changes in the lesions and/or their distribution. Variable distribution can be difficult to evaluate.
  • Photosensitivity may occur. Photoexacerbated and photoprotected forms have been documented, although photosensitivity is not a classic manifestation of the disease.
  • Lesions may be localized to single areas, such as the abdomen, the groin, the axilla, the distal extremities, the palms, and the soles.
• An inverse pityriasis rosea may be seen. This form manifests as lesions on the face and the distal extremities, and it is more common in children than in adults. The herald patch may be the only manifestation of the disease.
• A unilateral variant in which the lesions do not cross the midline has been described.
• Drug-induced cases are frequently observed without the herald patch.
• Variations in lesion morphology are noteworthy.
  • Atypical, large patches tend to be fewer in number. They may coalesce to form a variant known as pityriasis circinata et marginata of Vidal. The primary lesions may be papules, vesicles, pustules, or urticarial or purpuric plaques. Pityriasis rosea may first be evident with widespread, intensely pruritic papulovesicles in an unusual distribution, such as on the neck and the scalp.
  • Papular pityriasis rosea tends to have scaling papules in the normal distribution; this form is more common in children than in adults.
  • Erythema multiforme–like plaques may be evident.
  • Oral involvement may occur as punctate hemorrhages, ulcers, papulovesicles, bullae, or erythematous plaques. Most studies find the incidence to be less than 10%; however, one study reported them in as many as 16% of patients.
  • Purpuric pityriasis rosea is seen in both adults and children, and it follows the usual presentation of the disease.
  • African American children may have more frequent papular lesions and facial and scalp involvement than is usually described. Also of interest is that many patients have resolution of lesions within 2 weeks.⁶

Causes

Pityriasis rosea may represent a viral exanthem (and at times enanthem).

• Pityriasis rosea–like drug eruptions may be difficult to distinguish from non–drug-induced cases. Medication-induced eruptions have been reported with captopril, metronidazole, isotretinoin, penicillamine, levamisole, bismuth, gold, barbiturates, ketotifen, clonidine, aspirin, and omeprazole. A single case has been reported with terbinafine. Imatinib mesylate has also been implicated.
• Certain vaccinations, such as the BCG vaccine or the diphtheria vaccine, have been reported to cause similar eruptions.
• Lesions are also thought to be increased in individuals with high stress levels.

Differential Diagnoses

Other Problems to Be Considered

Primary human immunodeficiency viral infection
Viral exanthems

Workup

Laboratory Studies

• One must be careful to rule out syphilis.
  • A screening rapid plasma reagin (RPR) test or a VDRL test should be ordered for appropriate individuals.
  • One should be aware of the prozone phenomenon seen in secondary syphilis and request titration of the RPR test.
  • An HIV test should also be considered in these patients.
• Other laboratory tests are usually normal and, therefore, unhelpful. Changes in the white blood cell count and differential, as well as increases in erythrocyte sedimentation rate, total serum protein level, globulin level, and albumin level, are rarely reported.

Histologic Findings

A biopsy specimen is helpful to confirm the diagnosis, especially in atypical cases. It shows superficial perivascular dermatitis (see Media File 3). Focal parakeratosis in mounds, hyperplasia, and focal spongiosis are observed in the epidermis. The epidermis may show exocytosis of lymphocytes, variable spongiosis, mild acanthosis, and a thinned granular layer. In the dermis, extravasated red blood cells are a helpful finding along with a perivascular infiltrate of lymphocytes, histiocytes, and eosinophils. A number of monocytes are also commonly present.

The herald patch has similar features but has a deeper infiltrate and more acanthosis owing to its chronicity. Such variations as dyskeratotic cells in the epidermis, multinuclear giant cells, and focal acantholytic dysfunction have been observed. These features may closely resemble erythema annulare centrifugum, guttate psoriasis, superficial gyrate erythema, and small plaque parapsoriasis.

Treatment

Medical Care

The most important part of treating patients with pityriasis rosea is reassurance that the rash will resolve.

• Relief of pruritus is helpful and can be accomplished by using topical steroids, oral antihistamines, topical menthol-phenol lotions, and oatmeal baths. Systemic steroids are not recommended. Although they suppress pruritus, systemic steroids do not shorten the overall disease; in fact, they may prolong or exacerbate the disease.
• Ultraviolet B (UV-B) light therapy, starting at 80% of the minimum erythrogenic dose, may rapidly relieve pruritus in resistant cases. If itching is not controlled, the dose of UV-B light should be increased by 20% until symptoms decrease. However, a recent study failed to find improvement in the pruritus but did note decreased lesion severity with UV-B light therapy. One must take into consideration the possibility of postinflammatory pigmentation with light therapy.^7,8
• For vesicular pityriasis rosea, a single case was considerably improved with 20 mg of dapsone twice a day.
• High-dose acyclovir (800 mg qid) may help shorten disease, especially if instituted early in the disease course.⁹ Further trials are needed to help confirm this finding. A number of antibiotics have been tried without much success. Both azithromycin and erythromycin¹⁰  have been shown to not shorten the disease course.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Corticosteroids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.

Hydrocortisone (Westcort)

Treats inflammatory dermatosis that is responsive to steroids. Decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability.

Dosing

Adult

Apply a thin film to affected area tid/qid until favorable response achieved

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; viral, fungal, and bacterial skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Products may contain either tartrazine or sodium bisulfite, which may cause allergic reactions in susceptible individuals; prolonged use, application over large surface areas, application of potent steroids, and use of occlusive dressings may increase systemic absorption of corticosteroids and may cause Cushing syndrome, reversible HPA-axis suppression, hyperglycemia, and glycosuria

Betamethasone (Diprolene, Betatrex)

For inflammatory dermatoses responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Affects production of lymphokines and has an inhibitory effect on Langerhans cells.

Dosing

Adult

Apply thin film bid/qid until response

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; paronychia; cellulitis; impetigo; angular cheilitis; erythrasma; erysipelas; rosacea; perioral dermatitis; acne

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use on skin with decreased circulation; can cause atrophy of groin, face, and axillae; if infection develops and is not responsive to antibiotic treatment, discontinue until infection is under control; do not use monotherapy to treat widespread plaque psoriasis

Clobetasol (Temovate)

Class I superpotent topical steroid. Suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction.

Dosing

Adult

Apply bid for up to 2 wk; not to exceed 50 g/wk

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; viral or fungal skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May suppress adrenal function in prolonged therapy; may cause atrophy of skin with prolonged therapy; can cause atrophy of groin, face, and axillae; if infection develops and is not responsive to antibiotic treatment, discontinue until infection is under control

Antihistamines

These agents may control itching by blocking effects of endogenously released histamine.

Diphenhydramine (Benadryl, Belix)

For symptomatic relief of pruritus symptoms caused by release of histamine in allergic reactions.

Dosing

Adult

25-50 mg PO q6-8h prn; not to exceed 400 mg/d; 10-50 mg IV/IM q6-8h prn; not to exceed 400 mg/d

Pediatric

12.5-25 mg PO tid/qid, or 5 mg/kg/d PO/IV/IM or 150 mg/m²/d PO/IV/IM divided tid/qid; not to exceed 300 mg/d

Interactions

Potentiates effect of CNS depressants; because of alcohol content, do not give syrup form to patient taking medications that can cause disulfiramlike reactions

Contraindications

Documented hypersensitivity; MAOIs

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, and urinary tract obstruction

Follow-up

Further Outpatient Care

• Generally, the disease resolves within 12 weeks.
• Most cases do not recur, but some patients may develop pityriasis rosea more than once. In cases where the diagnosis is in doubt or if the disease persists past this period, further evaluation is advised. Persistent pityriasis rosea of more than a 3-month duration is often better classified as pityriasis lichenoides chronica.

Complications

• The main morbidity is from pigmentary changes, which are possible with the healing lesions.
• Both postinflammatory hyperpigmentation and hypopigmentation may occur.
• Pregnancy complications, including an increased risk of miscarriage, have been reported.⁴

Prognosis

• The prognosis for pityriasis rosea is excellent. Patients may return to work or school because they are not considered to be contagious.

Multimedia

Media file 1: Herald patch. Courtesy of the Drexel Department of Dermatology slide collection.

Media file 2: Christmas tree distribution of lesions on the trunk. Courtesy of the Drexel Department of Dermatology slide collection.

Media file 3: Histopathologic features of pityriasis rosea. Courtesy of Gary R. Kantor, MD, Department of Dermatology, Drexel University, Philadelphia, Pa.

References

1. Chuh AA, Chan PK, Lee A. The detection of human herpesvirus-8 DNA in plasma and peripheral blood mononuclear cells in adult patients with pityriasis rosea by polymerase chain reaction. J Eur Acad Dermatol Venereol. Jul 2006;20(6):667-71. [Medline].

2. Drago F, Ranieri E, Malaguti F, Battifoglio ML, Losi E, Rebora A. 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. Broccolo F, Drago F, Careddu AM, et al. Additional evidence that pityriasis rosea is associated with reactivation of human herpesvirus-6 and -7. J Invest Dermatol. Jun 2005;124(6):1234-40. [Medline].

4. Drago F, Broccolo F, Zaccaria E, Malnati M, Cocuzza C, Lusso P, et al. Pregnancy outcome in patients with pityriasis rosea. J Am Acad Dermatol. May 2008;58(5 Suppl 1):S78-83. [Medline].

5. Chuang TY, Ilstrup DM, Perry HO, Kurland LT. Pityriasis rosea in Rochester, Minnesota, 1969 to 1978. J Am Acad Dermatol. Jul 1982;7(1):80-9. [Medline].

6. 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].

7. Arndt KA, Paul BS, Stern RS, Parrish JA. Treatment of pityriasis rosea with UV radiation. Arch Dermatol. May 1983;119(5):381-2. [Medline].

8. Leenutaphong V, Jiamton S. UVB phototherapy for pityriasis rosea: a bilateral comparison study. J Am Acad Dermatol. Dec 1995;33(6):996-9. [Medline].

9. 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].

10. Rasi A, Tajziehchi L, Savabi-Nasab S. Oral erythromycin is ineffective in the treatment of pityriasis rosea. J Drugs Dermatol. Jan 2008;7(1):35-8. [Medline].

11. Ackerman AB. Pityriasis rosea. In: Ackerman AB, ed. Histiologic Diagnosis of Inflammatory Skin Disease: A Method by Pattern Analysis. Philadelphia, Pa: Lea & Febiger; 1978.

12. Bjornberg A, Hellgren L. Pityriasis rosea. A statistical, clinical, and laboratory investigation of 826 patients and matched healthy controls. Acta Derm Venereol Suppl (Stockh). 1962;42(Suppl 50):1-68. [Medline].

13. Bjornberg A, Tegner E. Pityriasis rosea. In: Freedberg IM, Eisen AZ, Wolff K, et al, eds. Dermatology in General Medicine. 5^th ed. New York, NY: McGraw-Hill; 1999:541-6.

14. Miljkovic J, Bercic M, Belic M. Pityriasis rosea with unusual papulovesicular presentation. Acta Derm Venerol. 1996;5:61-3.

15. Parsons JM. Pityriasis rosea update: 1986. J Am Acad Dermatol. Aug 1986;15(2 Pt 1):159-67. [Medline].

16. Sezer E, Saracoglu ZN, Urer SM, Bildirici K, Sabuncu I. Purpuric pityriasis rosea. Int J Dermatol. Feb 2003;42(2):138-40. [Medline].

17. Toussant S, Kareino H. Pityriasis rosea. In: Elder D, Elenitsas R, Jaworsky C, et al, eds. Lever's Histopathology of the Skin. 8^th ed. Philadelphia, Pa: Lippincott-Raven; 1997:164-5.

Keywords

pityriasis rosea benign papulosquamous disease, herald spot, herald patch, picornavirus, human herpesvirus-6, HHV-6, human herpesvirus-7, HHV-7

Contributor Information and Disclosures

Author

Robert A Allen, MD, Staff Physician, Department of Dermatology, Drexel University College of Medicine-Hahnemann Hospital
Robert A Allen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

Mark G Lebwohl, MD, Chairman, Department of Dermatology, Mount Sinai School of Medicine
Mark G Lebwohl, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Abbott Laboratories Honoraria Consulting; Actelion Honoraria Consulting; Amgen Honoraria Consulting; Astellas Honoraria Consulting; Basilea Honoraria Consulting; Briston-Myers Squibb Honoraria Consulting; Celtic Pharma  Other; Centocor Honoraria Consulting; Chattem Honoraria Other; DermiPsor Honoraria Consulting

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, 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, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of 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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