October 2015 Dermatology Clinic
A 14-year-old male presents with an asymptomatic eruption on his trunk, arms, and legs that appeared 2 weeks ago. The rash began on his thigh and spread from there. On physical examination, scattered small, pink, scaly papules and patches with collarettes are noted on the trunk, proximal arms, and legs. The patient has a single larger pink patch with a collarette of scale on the left inner thigh. There are no lesions on the palms or soles, and the patient reports that he had never been sexually active.
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Pityriasis rosea is an acute, self-healing papulosquamous eruption characterized by erythematous ovoid lesions of the trunk and limbs.1 First described in 1798 by Robert Willan, Camille Gilbert termed the condition pityriasis rosea for its distinctive scaly, pink appearance in 1860.2
The condition tends to occur in healthy adolescents and young adults, and the majority of cases present between age 10 and 35 years. Females are affected more frequently than males. There is no racial predilection. PR exhibits seasonal variation with increased incidence in spring and autumn.2,3 It has been found in association with asthma and eczema, as well as some neoplasms and lymphomas. It has also been found associated with receiving bone marrow transplants. PR is believed to occur more frequently in pregnant women than in the general population, with one study estimating the occurrence at 18% vs 6%.1
In many cases, the first clinical indication of PR is a solitary salmon-colored oval lesion on the trunk, the so-called “herald patch.” Progressively enlarging over several days, the herald patch grows to a size of 3 cm to 10 cm and develops an elevated advancing border with a collarette of fine scale. The herald patch is seen in more than 50% of cases, and in rare cases, may appear on the neck or proximal extremities instead of the trunk.2 Within days to a few weeks of this initial presentation, a secondary eruption of smaller tawny pink papules and patches develops on the trunk and proximal arms and legs.3 These oval lesions are symmetrically oriented with their long axis following Langer’s lines of cleavage in what is known as a “Christmas-tree distribution,” appreciated especially when observed on the posterior trunk.2 The secondary eruption typically spares the face, palms, and soles.1 The condition remits spontaneously in 6 weeks and almost never recurs.3
Approximately 5% of patients experience mild constitutional symptoms preceding the herald patch, including headache, arthralgias, low-grade fever, and malaise.2,4 Pruritus is variable in intensity and characterizes 25% of cases.2 Although uncommon, oral mucosal lesions, when present, follow the course of secondary eruption.1 Atypical presentations of PR include urticarial, vesicular, pustular, and purpuric variants. The inverse pattern affects the groin and axillae and is more common in children and individuals with pigmented skin.2 In a few cases, the herald patch is absent or the only manifestation.3
The pathogenesis of PR is poorly understood, but a viral etiology is most likely, with the probable culprits being human herpesvirus (HHV)-7 and HHV-6.3 With this etiology, the cutaneous eruption of PR would constitute an immunologic defense.2 Epidemiological factors suggestive of a viral etiology include case clustering, seasonal variation, and prodromal features.4 However, the evidence is controversial. Supporting HHV-7 as an etiologic agent of PR, Drago et al found the virus in the peripheral blood mononuclear cells and skin and plasma specimens of patients with PR.5 Their results further suggested that the virus invaded the dermal spaces to damage tissues directly or by interaction with the host immune system.1 In contrast, Kempf et al found no difference in the prevalence of DNA from HHV-7 in the peripheral blood mononuclear cells of patients with PR, as compared with controls, and attempts to isolate the viral DNA in skin lesions were unsuccessful.6 Although a viral etiology has not been proven, it has been shown that PR is not related to influenza virus, cytomegalovirus, Epstein-Barr virus, or parvovirus B19.7
With the exception of atypical presentations, the diagnosis of PR is made on the basis of clinical features alone. When uncertain, histopathology is helpful, showing diffuse parakeratosis, a thinned granular layer, spongiosis, and a mild perivascular and dermal infiltrate of lymphocytes and eosinophils.1,2
The differential diagnosis includes secondary syphilis, in which the lesions can mimic the eruption of PR. A history of a chancre and lymphadenopathy will help distinguish syphilis from PR, and the diagnosis can be confirmed with the Venereal Disease Research Laboratory (VDRL) test and fluorescent treponemal antibody absorption test (FTA-ABS). The FTA-ABS test may remain positive for years after a patient has recovered from syphilis. A VDRL test is the only one for which the result can become negative for syphilis after successful treatment and would be useful for ruling out syphilis. Drug eruptions may also mimic PR, but drug eruptions tend to resolve more slowly and do not have the typical features seen on histopathology. Pityriasis lichenoides chronica should be considered if the secondary eruption lasts for more than 4 months.2 Finally, the herald patch of PR may be confused with tinea corporis, nummular eczema, and erythema multiforme.3 A lack of pruritus can be helpful in distinguishing PR from nummular eczema, as PR is often asymptomatic, whereas nummular eczema is expected to be intensely pruritic. Targetoid lesions along with lesions on the palms are characteristic of erythema multiforme but not PR. Because fungal organisms are difficult to visualize on routine biopsy, the histopathology of tinea corporis and PR may look the same. Grocott-Gomori methenamine silver or periodic acid-Schiff staining would be helpful to ensure the correct diagnosis.
As PR is self-limiting, treatment consists of reassurance only. When the pruritus is intolerable, topical steroids can provide symptomatic relief. For severe cases, ultraviolet (UV) B phototherapy or natural sunlight combined with oral antihistamines may be effective. In rare cases, systemic corticosteroids can be given.2,3 One study reported resolution of lesions of PR in 73% of participants taking oral erythromycin, compared with no response in the placebo group.4 Although a viral etiology is implicated in the pathogenesis, antiviral medications are not approved for treatment of PR.7
The patient in our case opted for no treatment, and the rash resolved in approximately 4 weeks.
Lucette Liddell, BA, is a medical student and Maura Holcomb, MD, is a dermatology resident at Baylor College of Medicine in Houston.
- Drago F, Broccolo F, Rebora A. Pityriasis rosea: An update with a critical appraisal of its possible herpesviral etiology. J Am Acad Dermatol. 2009;61(2):303-318.
- Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. Philadelphia, Pa.: Elsevier Saunders; 2012.
- Wolff K, Johnson RA, Saavedra AP, eds. Fitzpatrick’s Color Atlas and Synopsis of Clinical Dermatology. 7th ed. New York, N.Y.: McGraw Hill Education; 2013.
- Scott LA, Stone MS. Viral exanthems. Dermatol Online J. 2003;9(3):4.
- 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):374-378.
- Kempf W, Adams V, Kleinhans M, et al. Pityriasis rosea is not associated with human herpesvirus 7. Arch Dermatol. 1999;135(9):1070-1072.
- González LM, Allen R, Janniger CK, Schwartz RA. Pityriasis rosea: An important papulosquamous disorder. Int J Dermatol. 2005;44(9):757-764.