Pityriasis Rosea

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Background

Pityriasis rosea (PR) is a benign rash first described by Gibert in 1860; the name means “fine pink scale.” It is a common skin disorder observed in otherwise healthy people, most frequently children and young adults. Other types of similar skin eruptions include lichen planus, psoriasis, and pityriasis rubra pilaris.

Pityriasis rosea manifests as an acute, self-limiting, papulosquamous eruption with a duration of 6-8 weeks. It evolves rapidly, usually beginning with patch that heralds the eruption, the so-called “herald patch” (see the image below). It may sometimes occur in atypical variants or may mimic other skin disorders, such as tinea corporis and secondary syphilis.[1, 2, 3, 4] Guidelines for diagnosing syphilis (and distinguishing the roseola from pityriasis rosea) have been established.[5] As a rule, pityriasis rosea requires only symptomatic treatment.



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Herald patch. Image courtesy of Drexel Department of Dermatology slide collection.

See 15 Rashes You Need to Know: Common Dermatologic Diagnoses, a Critical Images slideshow, to help identify and treat various rashes.

Pathophysiology

Pityriasis rosea (PR) has often been considered to be a viral exanthem, a view supported by the condition’s seasonal occurrence, its clinical course, the possibility of epidemic occurrence, the presence of occasional prodromal symptoms, and the low rate of recurrence. However, a 4-year recurrence rate of 25.9% was documented in one survey of 212 patients.[6] Oxidative stress may play a role too.[7]  One survey noted a significant temporal clustering and seasonal variation, and the incidence of dengue fever significantly correlated.[8]

Pityriasis rosea has been linked to upper tract respiratory infections. An increased incidence is reported among groups with close physical contact (eg, families, students, and military personnel), though the condition does not appear to be highly contagious. The incidence of pityriasis rosea among dermatologists is 3-4 times that among other physicians.

A higher incidence of pityriasis rosea is also noted among patients with decreased immunity (eg, pregnant women and bone marrow transplant recipients). Additionally, ampicillin increases the distribution of the eruption, an effect bearing a striking resemblance to the drug’s effect on the rash of infectious mononucleosis.

Some immunologic data also suggest a viral etiology.[9] A lack of natural killer (NK) cell and B-cell activity in pityriasis rosea lesions has been noted, suggesting a predominantly T-cell mediated immunity in the development of the condition. Increased amounts of CD4 T cells and Langerhans cells are present in the dermis, possibly reflecting viral antigen processing and presentation. 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.

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 (see Presentation).

Atopy, seborrheic dermatitis, and acne vulgaris are more common in patients with pityriasis rosea than in control subjects. Pityriasis rosea during pregnancy may foreshadow premature delivery and fetal demise, especially when it develops within the first 15 weeks of gestation.[10]

Recurrences of pityriasis rosea are generally regarded as rare and are thought by some to indicate a lasting immunity when they do occur. However, they may be more common than previously delineated.[11]

A classification based on pathogenetic mechanisms associated wth the different presentations of pityriasis rosea has been proposed.[12]

Etiology

Infectious agents

An infectious etiology for pityriasis rosea (PR) has been sought for many years. It has been suggested that the condition is precipitated by a viral agent. Accordingly, a number of viruses have been studied with a view to determining whether they are linked 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 (PCR) assay for viral DNA have been negative for Epstein-Barr virus (EBV), parvovirus B19, cytomegalovirus (CMV), human herpesvirus (HHV)-8,[13] HHV-1, and HHV-2 in patients diagnosed with pityriasis rosea.

Some initial reports using PCR analysis suggested a role for human herpesvirus (HHV)-7 and HHV-6, but subsequent studies have not been confirmatory.[14, 15, 16, 13, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26] That HHV-7 is frequently found in healthy individuals casts further doubt on its proposed etiologic role.[25] The influenza virus H1N1 has also been proposed as a possible causative pathogen.[27]

Some investigators have suggested that a fungal infection is a more likely cause of pityriasis rosea than a viral infection is. However, no fungus has been isolated as a definite causal agent. No bacterial pathogen, such as Mycoplasma, has been found to be causative either. Thus far, the search for an infectious cause of pityriasis rosea has been unsuccessful.

Drugs

Pityriasis rosea–like eruptions can also occur in association with many drugs (eg, acetylsalicylic acid, barbiturates, bismuth, captopril, clonidine, gold, imatinib, isotretinoin, ketotifen, levamisole, metronidazole, omeprazole, D-penicillamine, and terbinafine), as well as certain vaccines (eg, bacille Calmette-Guérin [BCG], human papilloma virus, and diphtheria).[2, 28, 29]

Anti−tumor necrosis factor (TNF)-α agents such as adalimumab and etanercept have also been implicated.[30, 31] Pityriasis rosea–like drug eruptions have been reported to be related to use of rituximab,[32] nortriptyline,[33] and clozapine.[34]

Pityriasis rosea–like drug eruptions may be difficult to distinguish from non–drug-induced cases. Drug-induced pityriasis rosea often lasts longer than non–drug-induced pityriasis rosea. Lesions are also thought to be increased in individuals with high stress levels.

Epidemiology

United States statistics

Pityriasis rosea (PR) is very common in the general population, and most cases occur in the spring and winter in temperate climates. The estimated frequency of pityriasis rosea in the United States is approximately 0.13% in females and 0.14% in males, with a 0.3-3% prevalence at dermatologic centers.

International statistics

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. It favors the hot, dry season in Australia, India, and Malaysia.

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

Age-, sex-, and race-related demographics

Pityriasis rosea is observed in people of all age groups, though it is most common in persons aged 10-35 years and rare in infants and elderly persons. The youngest patient reported in the literature was aged 3 months, and the oldest was aged 85 years.

Pityriasis rosea occurs slightly more often in females than in males.[35] The female-to-male ratio is reported as 2:1 or 3:2 in the United States.

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.

Prognosis

Pityriasis rosea (PR) is a self-limiting, generally benign disorder for which the prognosis is excellent and the recurrence rate is low (approximately 2%). Because it is not considered a transmissible disease, patients do not require isolation and may return to work or school. Pityriasis rosea usually lasts for 6-8 weeks, but can last as long as 3-6 months. Protracted cases of severe eczematous or drug-induced pityriasis rosea are referred to as pityriasis rosea perstans.

The main morbidity is from pigmentary changes, which may develop as lesions heal, especially in black people. Both postinflammatory hyperpigmentation and hypopigmentation may occur. However, lesions do not result in scars. Bacterial superinfections may occur, but are rare. In pregnant women, pityriasis rosea is sometimes associated with miscarriage if occurring within the first 15 weeks of pregnancy, premature delivery, or neonatal hypotonia and hyporeactivity.[10, 36]

Patient Education

Patients should be instructed to avoid contact with irritants. In addition, patients and families should be educated regarding the benign and noninfectious nature of the rash and the relatively lengthy course of the disease. Typically, the secondary rash develops over 2 weeks, persists for another 2 weeks, and then fades over another 2 weeks, without the need for treatment, though some lesions have persisted for as long as 3-4 months.

For patient education resources, see the Skin Conditions & Beauty Center, as well as Eczema (Atopic Dermatitis).

History

The history should include questions about the following:

The disease typically begins with a solitary patch, usually salmon-colored, that heralds the eruption and thus is commonly referred to as the herald patch or spot (see Physical Examination). This initial lesion enlarges over a few days to become a patch with a collarette of fine scale just inside the well-demarcated border. Dermoscopy evaluation using a triple-light source may be useful.[37]

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 and occasionally persistent.[38]

Pruritus is commonly evident in 25-75% of patients and usually of mild-to-moderate severity. Secondary eczematous changes can occur if pruritus is severe.

A small number (approximately 5%) of patients with pityriasis rosea have mild prodromal symptoms (eg, malaise, fatigue, headache, nausea, anorexia, chills, fever, and arthralgias) that precede the appearance of the herald patch. Lymphadenopathy may occur before the onset of the rash.

A classification dividing pityriasis rosea into classic, relapsing, persistent, pediatric, pityriasis rosea in pregnancy, and pityriasis rosea–like eruptions has been proposed.[12]

Physical Examination

Herald patch

The typical initial skin lesion of pityriasis rosea (PR), seen in more than 50% of patients, is a single pink macule or patch, which gradually expands over a few days to become an oval or round plaque that is 2-10 cm in diameter, generally with a central wrinkled salmon-colored area and a dark red peripheral zone. This lesion, referred to as the herald patch or spot (see the image below), may develop anywhere on the body, including plantar skin, though it is most commonly located on the back.[39]



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Herald patch. Image courtesy of Drexel Department of Dermatology slide collection.

The herald patch usually shows a collarette of fine scales just inside its well-demarcated edges and may exhibit central clearing, much as in tinea corporis. This patch is something of a dermatologic enigma, in that it does not occur in any other known skin disease. The earliest stages of the patch may manifest as pink papules that can be mistaken for other lesions (eg, insect bites).

Subsequent lesions

A generalized eruption then occurs, in which numerous lesions develop in crops over a period of 1-2 weeks (typically about 10 days) after the onset of the herald patch (though this eruption has also been known to occur as early as hours or as late as 3 months after the appearance of the patch). The eruption is symmetric and most commonly involves the thorax, back, abdomen, and adjoining areas of the neck and extremities; lesions are not usually observed on the face, hands, and feet.

These secondary lesions occur as macules and papules that are elliptical or ovular in shape and 0.5-1.5 cm across. Fine scaling and central wrinkling, with a cigarette paper aspect, is usually present. A characteristic feature is the collarette appearance of the scale, with edges peripherally attached and lifted up near the center of the lesion. However, unlike the scale in classic tinea corporis, the scale in pityriasis rosea does not extend to the border of the lesion.

The distribution of the lesions is usually bilateral and diffuse, with the long axes running parallel to skin tension lines. This produces the classic “Christmas tree” pattern on the trunk (see the image below). In children younger than 5 years, papular pityriasis rosea may be seen with a similar distribution. The rash can last as long as 6-8 weeks before fading.



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Christmas tree distribution of lesions on trunk. Image courtesy of Drexel Department of Dermatology slide collection.

Pigment changes

With resolution of the eruption, postinflammatory pigment changes can be observed. Both hypopigmentation and hyperpigmentation can follow the rash. Individuals with dark skin are particularly likely to experience postinflammatory hyperpigmentation that may take a few months to heal.

Oral findings

Oral lesions of various types have been reported with pityriasis rosea, including punctate hemorrhages, ulcers (with or without raised borders), petechiae, papulovesicles, bullae, and erythematous plaques.[40] Most studies have found the incidence of these lesions to be lower than 10%; however, one study found it to be as high as 16%. A resemblance to geographic tongue has been described.[41]

Variants and atypical forms

Approximately 20% of patients present with atypical or variant forms of pityriasis rosea. These variations may involve differences in the lesions themselves, differences in how they are distributed, or both.

Photosensitivity may occur. Photoexacerbated and photoprotected forms of pityriasis rosea have been documented, though photosensitivity is not a classic manifestation of the disease.

In 10-50% of cases, the herald patch may be absent, a finding that is more frequently observed in drug-induced pityriasis rosea. Alternatively, the herald patch may occur as multiple lesions or in atypical locations, such as the soles or the scalp.[39, 42] Sometimes, it is the only manifestation of the disease and is not followed by the typical rash.

An inverse pityriasis rosea may be seen, in which the generalized rash spreads to areas it usually does not affect, such as the face, hands, and feet. The face may be more commonly affected in young children, pregnant women, and black people. In such cases, the physician should consider secondary syphilis in the differential diagnosis, especially when involvement of the palms and soles is present.

Lesions may be localized to single areas, such as the abdomen, the groin, the axilla, the distal extremities, the palms, and the soles. A unilateral variant in which the lesions do not cross the midline has been described.[43]

A morphologic variant characterized by atypical large patches that tend to be fewer in number and coalescent has been described. In this variant, commonly referred to as pityriasis circinata et marginata of Vidal or limb-girdle pityriasis rosea, the eruption generally appears in the axillae, the groin, or both, with the trunk and extremities usually spared.[44] Individual patches are 3-6 cm in diameter, exhibiting the characteristic central clearing and collarette of scale with surrounding erythema.

The primary lesions may be papules, vesicles, pustules, or urticarial or purpuric plaques.[45, 46, 47] Papular pityriasis rosea tends to have scaling papules in the normal distribution; this form is believed to be more common in young children, pregnant women, and black people. Purpuric pityriasis rosea is seen in both adults and children and follows the usual presentation of the disease.[48] Erythema multiforme–like plaques may be evident.

Pityriasis rosea may occur along the lines of Blaschko[49, 50] or may be segmental.[51]

Additional considerations in black patients

Black people are more likely to experience widespread forms of disease and concurrent lymphadenopathy, with hyperpigmentation upon resolution (48% of black children have residual hyperpigmentation[52] ). Black children are also more likely to have papular lesions (33%), scalp (8%) or facial (30%) involvement, and a shorter course of disease, with resolution sometimes coming within 2 weeks.[52]

Laboratory Studies

The diagnosis of pityriasis rosea (PR) is made clinically in most cases. In general, laboratory tests are not necessary or helpful, with a few exceptions.

Changes in the white blood cell (WBC) count and differential, as well as increases in the erythrocyte sedimentation rate (ESR), total serum protein level, globulin level, and albumin level, have been reported but are rare and usually minimal. Test results for rheumatoid factor (RF), cold agglutinins, and cryoglobulins have been normal. When only the herald patch is present, a potassium hydrochloride (KOH) test may be especially useful for helping to diagnose tinea corporis.

Because PR can be confused with secondary syphilis, a rapid plasma reagin (RPR) or Venereal Disease Research Laboratory (VDRL) test should be performed to rule out this condition. Titration of the RPR test is recommended to detect the prozone phenomenon. Other features that would suggest syphilis include patchy alopecia, salmon-colored plaques on the palms of the hands and soles of the feet, diffuse adenopathy, white papules of the oral mucosa, and condylomata lata.

An HIV test should also be considered in these patients.

Skin Biopsy and Histologic Findings

Histologic examination is usually unnecessary, but may be useful in selected situations. A skin biopsy can be obtained when the eruption is atypical, the diagnosis is uncertain, or the disease has not resolved after 3-4 months. It shows nonspecific features of a subacute or chronic dermatitis, but may be helpful in ruling out other diseases in the differential diagnosis.

The biopsy specimen shows superficial perivascular dermatitis (see the image below). Focal parakeratosis in mounds, hyperplasia, and focal spongiosis are observed in the epidermis.[9] 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. Histopathologic features of syphilis can be seen in pityriasis rosea[4] ; accordingly, neutrophils in the stratum corneum, plasma cells, interface dermatitis with lymphocytes and vacuoles, and lymphocytes with ample cytoplasm need to be delineated.



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Histopathologic features of pityriasis rosea. Image courtesy of Gary R Kantor, MD, Department of Dermatology, Drexel University, Philadelphia, PA.

The herald patch has similar features but, as a consequence of its chronicity, has a deeper infiltrate and more acanthosis. 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.

Approach Considerations

Pityriasis rosea (PR) is a self-limited disease; 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 pityriasis rosea), topical or oral steroids may be used. Ultraviolet (UV) radiation therapy has been demonstrated to be effective for pityriasis rosea but may leave postinflammatory pigmentation at the site of the pityriasis rosea lesion.[54]

For patients in whom superficial tinea infection is a concern or possibility, topical antifungal therapy can be used. Some data suggest that the antiviral agent acyclovir could hasten resolution.[55, 56]

No restriction of activity or isolation is necessary. No evidence suggests that children with pityriasis rosea should be prevented from attending school.

Pharmacologic Therapy and Phototherapy

In most cases, it is not necessary to treat pityriasis rosea (PR).[57] The rash usually disappears in a few weeks, with no sequelae. Although various treatments have been attempted, the efficacy of most of them has not been definitively proved.[58]

Generally, patient education (eg, to avoid exposure to irritant agents [eg, harsh soaps, fragrances, hot water, wool, and synthetic fabrics], tight clothing, and scratching), coupled with reassurance that the rash will resolve, is all that is needed. However, it can be helpful to institute measures aimed at relieving bothersome symptoms (eg, pruritus).

Pruritus is commonly associated with pityriasis rosea and often responds to bland emollients, oral antihistamines, or topical preparations containing calamine, menthol-phenol, pramoxine, colloidal starch, or oatmeal. If the rash is severe, topical steroids can be applied. It must be kept in mind that although steroids alleviate the pruritus, they do not modify the eruption. The sedative effect of the antihistamines may help the patient to sleep better at night.

Systemic steroids are not recommended because they may exacerbate the disease. However, some dermatologists use prednisone (0.5-1 mg/kg/day for 7 days) in selected patients with severe pruritus, vesicular lesions, or the potential for significant postinflammatory hyperpigmentation, to suppress both pruritus and the exanthem. A double-blind, randomized, placebo-controlled trial evaluated short-course, low-dose oral prednisolone and suggested its use only for those with extensive high symptomatic pityriasis rosea.[59]

UV-B phototherapy, starting at 80% of the minimum erythrogenic dose, may rapidly relieve pruritus in resistant cases.[54] If itching is not controlled, the dose should be increased by 20% until symptoms decrease. However, one study failed to find improvement in pruritus with UV-B light therapy but did note decreased lesion severity. The possibility of postinflammatory pigmentation with light therapy must be kept in mind.[60, 61] An alternative approach is to administer low-dose UV-A1 phototherapy 2-3 times a week until resolution.[62]

In an atypical case of vesicular pityriasis rosea, considerable improvement was noted with the administration of 20 mg of dapsone twice daily.[45]

Some evidence suggests that acyclovir may be useful. Treatment in the first week of symptom onset with 1 g of acyclovir taken orally 5 times a day for 7 days in adults has been shown to shorten the duration of disease and may be of benefit.[63, 64] Lower dosages of 400 mg 5 times a day for 1 week may be equally effective.[55] However, acyclovir has been shown to be ineffective against HHV-6 and HHV-7.[63]

A number of antibiotics have been tried, without much success. In a small clinical trial, 1 g of erythromycin taken orally 4 times daily in adults or 25-40 mg/kg divided 4 times daily in children for 2 weeks led to early resolution of symptoms.[65] However, another study did not find erythromycin to be useful in this condition.[66] Azithromycin also was not found to be effective for children with pityriasis rosea.[67]

In a randomized trial involving 42 patients with a clinical diagnosis of pityriasis rosea who were treated with either high-dose oral acyclovir or standard-dose oral erythromycin, all of the patients in the 2 groups exhibited a complete response after 8 weeks.[68] Although the study findings indicated that both agents were helpful, patients receiving acyclovir showed a better response, which was statistically significant in weeks 1, 2, 4, and 6.

Management of pityriasis rosea in patients with evidence of group A streptococcal infection may be warranted. The possible risk of scarlet fever and poststreptococcal sequelae should be considered.[69]

Consultations

Consultation with a dermatologist is warranted for patients with severe pruritus or disease that necessitates systemic steroid therapy, patients who desire UV-B therapy, or patients with atypical presentations of pityriasis rosea (PR).

Consultation with an infectious disease specialist should be considered for individuals with immunosuppression, such as recipients of solid organ transplants or hematopoietic stem cell transplants.

Pregnant women with pityriasis rosea should be referred to a high-risk maternal-fetal medicine specialist.

Long-Term Monitoring

Generally, pityriasis rosea (PR) resolves within 12 weeks, and no follow-up is necessary in most cases. However, follow-up care may be provided to ensure that the rash is improving. Patients with moderate-to-severe pruritus who are receiving topical steroids should be followed up by phone or in a return visit in 1-2 weeks.

Most cases of pityriasis rosea do not recur,[70] but some patients may develop the condition more than once, in which event alternative diagnoses or immune suppression should be considered. If the diagnosis is in doubt or if the disease persists past the expected duration period, further evaluation is advised. Pityriasis rosea that has persisted for longer than 3 months is often better classified as pityriasis lichenoides chronica.

Medication Summary

Pityriasis rosea (PR) is a self-limited disease; treatment is supportive. Drug therapy for pityriasis rosea primarily consists of symptomatic treatment of pruritus. Topical zinc oxide and calamine lotion may be helpful. Oral antihistamines and topical corticosteroids can be used as needed. For patients in whom superficial tinea infection is a concern or possibility, topical antifungal therapy can be used. There is no evidence-based medicine for pityriasis rosea, a self-limited disorder.[71]

Management of pityriasis rosea in patients with evidence of group A streptococcal infection may be warranted. The possible risk of scarlet fever and poststreptococcal sequelae should be considered. Acyclovir may hasten resolution, especially if given within 1 week of rash, but the data are not conclusive.

Hydrocortisone topical (Westcort, U-Cort, Ala-Cort, Caldecort)

Clinical Context:  Topical hydrocortisone is an adrenocorticosteroid derivative that is suitable for application to skin or external mucous membranes and is used to treat inflammatory dermatosis that is responsive to steroids. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes (PMNs) and reversing capillary permeability.

Betamethasone topical (Diprolene, Luxiq)

Clinical Context:  Topical betamethasone is used to treat inflammatory dermatoses responsive to steroids. It decreases inflammation by suppressing migration of PMNs and reversing capillary permeability. It affects production of lymphokines and has an inhibitory effect on Langerhans cells.

Clobetasol (Temovate, Temovate E, Olux, Olux-E)

Clinical Context:  Clobetasol is a class I superpotent topical steroid. It suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction.

Triamcinolone topical (Kenalog, Triderm)

Clinical Context:  Topical triamcinolone decreases inflammation by suppressing migration of PMNs and reversing capillary permeability.

Prednisone (Rayos)

Clinical Context:  Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body’s immune response to diverse stimuli. Over-the-counter (OTC) steroid preparations of low-to-medium potency steroids may help relieve the itching associated with pityriasis rosea.

Diphenhydramine (Benadryl, Aler-Cap, Altaryl)

Clinical Context:  Diphenhydramine, which is available as an OTC product, is a very safe oral antihistamine that can be used safely in pregnancy. It is highly effective for controlling pruritus symptoms caused by release of histamine in allergic reactions.

Hydroxyzine (Vistaril)

Clinical Context:  Hydroxyzine is a sedating agent that antagonizes H1 receptors in the periphery and may suppress histamine activity in the subcortical region of the central nervous system (CNS). It is effective against pityriasis rosea–related pruritus.

Class Summary

Antihistamines may control pityriasis rosea–related itching by blocking effects of endogenously released histamine.

Erythromycin (E.E.S., Ery-Tab, Erythrocin, EryPed)

Clinical Context:  Erythromycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes and causing RNA-dependent protein synthesis to arrest. It may have anti-inflammatory and immunomodulatory effects. In children, age, weight, and severity of infection determine the proper dosage. When twice-daily dosing is desired, half of the total daily dose may be taken every 12 hours.

Class Summary

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

Acyclovir (Zovirax)

Clinical Context:  Acyclovir is a prodrug activated through phosphorylation by a virus-specific thymidine kinase that inhibits viral replication. Herpesvirus thymidine kinase (TK), but not host-cell TK, converts acyclovir into acyclovir monophosphate, a nucleotide analogue. Guanylate kinase converts the monophosphate into diphosphate and triphosphate analogues that inhibit viral DNA replication. Once phosphorylated, the drug causes DNA chain termination when acted on by DNA polymerase. It interferes with DNA replication within the virions.

Class Summary

Antiviral agents may improve the rate of resolution if given within 1 week of the appearance of the rash.

What is pityriasis rosea (PR)?What is the disease course of pityriasis rosea?Why is pityriasis rosea considered a viral exanthem?Which groups have increased risk of developing pityriasis rosea?Which patients have a higher incidence of pityriasis rosea?What is the viral etiology of pityriasis rosea?What is the onset of pityriasis rosea?What are the risks to the fetus of pityriasis rosea during pregnancy?What do recurrences of pityriasis rosea indicate?How is pityriasis rosea classified?What is the role of drugs in the etiology of pityriasis rosea?What is the role of infections in the etiology of pityriasis rosea?What is the prevalence of pityriasis rosea in the US?How does the incidence of pityriasis rosea vary by age?How does the incidence of pityriasis rosea vary by sex?What is the global prevalence of pityriasis rosea?What are the racial predilections of pityriasis rosea?What is the prognosis of pityriasis rosea?What is the morbidity associated with pityriasis rosea?What information about pityriasis rosea should patients be given?What should be the focus of the history for pityriasis rosea?What is the clinical history of pityriasis rosea?What is the prevalence of pruritus in pityriasis rosea?What are the prodromal symptoms of pityriasis rosea?How is pityriasis rosea classified?How are the initial skin lesions of pityriasis rosea characterized?How are the secondary lesions of pityriasis rosea characterized?How are the pigment changes in pityriasis rosea characterized?What are oral findings characteristic of pityriasis rosea?How frequently is the presentation of pityriasis rosea atypical?What are the signs and symptoms of variant and atypical forms of pityriasis rosea?What are the racial differences in presentation of pityriasis rosea?What should be included in the differential diagnosis of pityriasis rosea in patients with risk factors for sexually transmitted diseases?Which conditions should be included in the differential diagnoses of pityriasis rosea?What are the differential diagnoses for Pityriasis Rosea?What is the role of lab studies in the diagnosis of pityriasis rosea?When is skin biopsy indicated in the diagnosis of rosea and what are the expected histologic findings?What are the treatment options for pityriasis rosea?What is the most effective treatment for pityriasis rosea?What is the role of patient education in the treatment of pityriasis rosea?How is pruritus in pityriasis rosea treated?What is the role of systemic steroids for treatment of pityriasis rosea?What is the role of phototherapy for treatment of pityriasis rosea?What is the role of dapsone for the treatment of pityriasis rosea?What is the role of acyclovir for the treatment of pityriasis rosea?What is the role of antibiotics in the treatment of pityriasis rosea?What are increased health risks of comorbid group A streptococcal infection and pityriasis rosea?Which specialist consultations are should be considered for the treatment of pityriasis rosea?What monitoring is needed following treatment of pityriasis rosea?When should an alternative diagnosis or immune suppression be considered in patients with pityriasis rosea?Which drugs are used in the treatment of pityriasis rosea?How is group A streptococcal infection managed in patients with pityriasis rosea?Which medications in the drug class Antiviral Agents are used in the treatment of Pityriasis Rosea?Which medications in the drug class Antibiotics, Other are used in the treatment of Pityriasis Rosea?Which medications in the drug class Antihistamines are used in the treatment of Pityriasis Rosea?Which medications in the drug class Corticosteroids are used in the treatment of Pityriasis Rosea?

Author

Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Pathology, Professor of Pediatrics, Professor of Medicine, Rutgers New Jersey Medical School

Disclosure: Nothing to disclose.

Coauthor(s)

Camila K Janniger, MD, Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of Pediatric Dermatology, Rutgers New Jersey Medical School

Disclosure: Nothing to disclose.

Richard Lichenstein, MD, Professor, Pediatric Emergency Department, University of Maryland School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Disclosure: Nothing to disclose.

Acknowledgements

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.

Jerry Balentine, DO Professor of Emergency Medicine, New York College of Osteopathic Medicine; Executive Vice President, Chief Medical Officer, Attending Physician in Department of Emergency Medicine, St 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.

Kevin P Connelly, DO Clinical Assistant Professor, Department of Pediatrics, Division of General Pediatrics and Emergency Care, Virginia Commonwealth University School of Medicine; Medical Director, Paws for Health Pet Visitation Program of the Richmond SPCA; Pediatric Emergency Physician, Emergency Consultants Inc, Chippenham Medical Center

Kevin P Connelly, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association

Disclosure: Nothing to disclose.

Burke A Cunha, MD Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Pamela L Dyne, MD Professor of Clinical Medicine/Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center

Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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.

Rajendra Kapila, MD, MBBS Professor of Medicine, Department of Medicine, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Rajendra Kapila, MD, MBBS is a member of the following medical societies: American College of Physicians, American Medical Association, Infectious Diseases Society of America, and Infectious Diseases Society of New Jersey

Disclosure: Nothing to disclose.

Thomas M Kerkering, MD Chief of Infectious Diseases, Virginia Tech Carilion School of Medicine

Thomas M Kerkering, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Public Health Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Medical Society of Virginia, and Wilderness Medical Society

Disclosure: Nothing to disclose.

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: Amgen/Pfizer Honoraria Consulting; GlaxoSmithKline None Investigator; Novartis Honoraria Consulting; Ranbaxy None Consulting; Pfizer None Consulting; BioLineRX, Ltd. Honoraria Consulting; Celgene Corporation Consulting; Clinuvel None Investigator; Eli Lilly & Co. Honoraria Consulting; Genentech None Consulting

Daniel R Lucey, MD, MPH Chief, Fellowship Program Director, Department of Internal Medicine, Division of Infectious Diseases, Washington Hospital Center; Professor, Department of Internal Medicine, Uniformed Services University of the Health Sciences

Daniel R Lucey, MD, MPH is a member of the following medical societies: Alpha Omega Alpha and American College of Physicians

Disclosure: Nothing to disclose.

Amal Mattu, MD, FACEP, FAAEM Professor and Vice Chair, Department of Emergency Medicine, University of Maryland School of Medicine

Amal Mattu, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at 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.

Giuseppe Micali, MD Head, Professor, Department of Dermatology, University of Catania School of Medicine, Italy

Giuseppe Micali, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Maria R Nasca, MD, PhD Assistant Professor, Department of Dermatology, University of Catania School of Medicine, Italy

Disclosure: Nothing to disclose.

Robert L Rogers, MD Staff Physician, Departments of Internal Medicine and Surgery, Division of Emergency Medicine, University of Maryland

Robert L Rogers, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and American College of Physicians-American Society of Internal Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster 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.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Herald patch. Image courtesy of Drexel Department of Dermatology slide collection.

Herald patch. Image courtesy of Drexel Department of Dermatology slide collection.

Christmas tree distribution of lesions on trunk. Image courtesy of Drexel Department of Dermatology slide collection.

Histopathologic features of pityriasis rosea. Image courtesy of Gary R Kantor, MD, Department of Dermatology, Drexel University, Philadelphia, PA.

Herald patch. Image courtesy of Drexel Department of Dermatology slide collection.

Christmas tree distribution of lesions on trunk. Image courtesy of Drexel Department of Dermatology slide collection.

Histopathologic features of pityriasis rosea. Image courtesy of Gary R Kantor, MD, Department of Dermatology, Drexel University, Philadelphia, PA.