INTRODUCTION

Section 2 of 10  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
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• References

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. PR can have a number of clinical variations. Its diagnosis is important because it may resemble secondary syphilis.

Pathophysiology

PR has often been considered to be a viral exanthem. Its clinical presentation supports this concept. PR has been linked to upper 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 PR; 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 PR. Picornaviruslike particles have been seen in the tissue of African green monkeys inoculated from human PR lesions. A follow-up study failed to find picornavirus RNA in patients with PR. A recent study showed no increase in anti-IgM to parvovirus B19, making this etiology less likely. Serology and polymerase chain reaction for viral DNA has been negative for Epstein-Barr virus, parvovirus B19, and cytomegalovirus in patients diagnosed with PR.

Other recent work demonstrated human herpesvirus (HHV)–7 viral DNA in both the lesions and the plasma in patients with PR. In addition, a separate study found HHV-7 DNA in lymphocytes in 75% of patients with PR, 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 PR. 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. 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, PR 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

PR is a benign self-limited disease associated with mild morbidity with rash and occasional pruritus.

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

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

Age

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

CLINICAL

Section 3 of 10  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

History

The history should include questions about close contacts with similar eruptions. This finding is uncommon because most cases of PR are sporadic, as PR 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 Image 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 Image 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 PR 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 PR 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. PR may first be evident with widespread, intensely pruritic papulovesicles in an unusual distribution, such as on the neck and the scalp.
  • Papular PR 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 PR is seen in both adults and children, and it follows the usual presentation of the disease.

Causes

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

• PR-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. Recently, imatinib mesylate has 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.

DIFFERENTIALS

Section 4 of 10  

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• Clinical
• Differentials
• Workup
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• Follow-up
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• References

Other Problems to be Considered

Primary human immunodeficiency viral infection
Viral exanthems

WORKUP

Section 5 of 10  

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• Introduction
• Clinical
• Differentials
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• Medication
• Follow-up
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• References

Lab 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 Image 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

Section 6 of 10  

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Medical Care

The most important part of treating patients with PR 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.
• For vesicular PR, 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. Further trials are needed to help confirm this finding. A number of antibiotics have been tried without much success. Recently, azithromycin has been shown to not shorten the disease course.

MEDICATION

Section 7 of 10  

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

Drug Category: 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.

Drug Name	Betamethasone (Diprolene, Betatrex)
Description	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.
Adult Dose	Apply thin film bid/qid until response
Pediatric Dose	Apply as in adults
Contraindications	Documented hypersensitivity; paronychia; cellulitis; impetigo; angular cheilitis; erythrasma; erysipelas; rosacea; perioral dermatitis; acne
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
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

Drug Name	Clobetasol (Temovate)
Description	Class I superpotent topical steroid. Suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction.
Adult Dose	Apply bid for up to 2 wk; not to exceed 50 g/wk
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; viral or fungal skin infections
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	May suppress adrenal function in prolonged therapy; may cause atrophy of skin with prolonged therapy

Drug Category: Antihistamines

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

FOLLOW-UP

Section 8 of 10  

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Further Outpatient Care

• Generally, the disease resolves within 12 weeks.
• Most cases do not recur, but some patients may develop PR more than once. In cases where the diagnosis is in doubt or if the disease persists past this period, further evaluation is advised. Persistent PR 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.

Prognosis

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

MULTIMEDIA

Section 9 of 10  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
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• Follow-up
• Multimedia
• References

Media file 1:  Herald patch. Courtesy of the MCP-Hahnemann resident slide collection.
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Media file 2:  Christmas tree distribution of lesions on the trunk. Courtesy of the MCP-Hahnemann resident slide collection.
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Media file 3:  Histopathologic features of pityriasis rosea. Courtesy of Gary R. Kantor, MD, Chairman, Department of Dermatology, MCP-Hahnemann University, Philadelphia, Pa.
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Media type:  Image

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
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• References

• Ackerman AB. Pityriasis rosea. In: Histiologic Diagnosis of Inflammatory Skin Disease: A Method by Pattern Analysis. 1978.
• Amer A, Fischer H. Azithromycin does not cure pityriasis rosea. Pediatrics. May 2006;117(5):1702-5. [Medline].
• Aractingi S, Morinet F, Mokni M, et al. Absence of picornavirus genome in pityriasis rosea. Arch Dermatol Res. Dec 1996;289(1):60-1. [Medline].
• Arndt KA, Paul BS, Stern RS, Parrish JA. Treatment of pityriasis rosea with UV radiation. Arch Dermatol. May 1983;119(5):381-2. [Medline].
• 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].
• Bjornberg A, Tegner E. Pityriasis rosea. In: Freedberg IM, Eisen AZ, Wolff K, et al, eds. Dermatology in General Medicine. 5th ed. New York:. McGraw-Hill;1999:541-6.
• Buckley C. Pityriasis rosea-like eruption in a patient receiving omeprazole. Br J Dermatol. Oct 1996;135(4):660-1. [Medline].
• 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].
• Drago F, Ranieri E, Malaguti F, et al. 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].
• 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].
• Gupta AK, Lynde CW, Lauzon GJ, et al. Cutaneous adverse effects associated with terbinafine therapy: 10 case reports and a review of the literature. Br J Dermatol. Mar 1998;138(3):529-32. [Medline].
• Lebbe C, Agbalika F. Pityriasis rosea and human herpesvirus 7, a true association?. Dermatology. 1998;196(2):275. [Medline].
• Leenutaphong V, Jiamton S. UVB phototherapy for pityriasis rosea: a bilateral comparison study. J Am Acad Dermatol. Dec 1995;33(6):996-9. [Medline].
• Marcus-Farber BS, Bergman R, Ben Porath E, et al. Serum antibodies to parvovirus B19 in patients with pityriasis rosea. Dermatology. 1997;194(4):371. [Medline].
• Miljkovic J, Bercic M, Belic M. Pityriasis rosea with unusual papulovesicular presentation. Acta Derm Venerol. 1996;5:61-3.
• Parsons JM. Pityriasis rosea update: 1986. J Am Acad Dermatol. Aug 1986;15(2 Pt 1):159-67. [Medline].
• Sezer E, Saracoglu ZN, Urer SM, et al. Purpuric pityriasis rosea. Int J Dermatol. Feb 2003;42(2):138-40. [Medline].
• Toussant S, Kareino H. Pityriasis rosea. In: Elder D, Elenitsas R, Jaworsky C, et al, eds. Lever's Histopathology of the Skin. 8th ed. Philadelphia:. Lippincott-Raven Publishers;1997:164-5.
• Troiano G, Valente G, Isoppo M. Pitiriasi rosea con lesioni eritema polimorfo-simili. Chron Dermatol. 1997;7:417-21.

Article Last Updated: Jan 26, 2007