Pityriasis rosea (PR) is a common, benign, self-limited whole body rash with a seasonal prevalence that is clinically characterized by a solitary “herald patch” lesion followed by a whole body exanthem.
INSIGHT 
Particularly in patients with darker skin types, pityriasis rosea may be more papular and present in an “inverse pattern” (favoring the body folds such as axillae and inguinal creases).
SYNONYMS Pityriasis rosea Gibert, roseola annulata (historical).
AGE 10 to 35 years. Rare in <2 years.
INCIDENCE Up to 2% of all dermatology visits.
GENDER F > M, 2:1.
PREVALENCE Common, especially in fall and spring.
ETIOLOGY Human herpes viruses HHV6 and HHV7 have been postulated, but not proven.
A solitary “herald” patch (Fig. 14-1) typically precedes the exanthematous phase by 1 to 2 weeks. The exanthem develops over a period of a week and self-resolves in 6 to 14 weeks without intervention. A generalized prodrome similar to viral infection—upper respiratory symptoms, fevers, myalgias—may be present in more than 60% of individuals.
HERALD PLAQUE Ovoid patch or plaque with collarette of scale (80%). May rarely have ≥2 herald patches or individual presents for evaluation after patch has faded.
EXANTHEM Papules and plaques with fine scale.
COLOR Pink or red.
SIZE Herald patch: 1 to 10 cm. Exanthem: 5 mm to 3 cm.
SHAPE Round to oval.
ARRANGEMENT Lesions follow the lines of cleavage in a “Christmas tree” distribution.
DISTRIBUTION Trunk > proximal arms, legs. Head, face (Fig. 14-2), palms and soles typically spared. Herald patch most often on the trunk but rarely can occur on limbs.
SITES OF PREDILECTION Axillae, back, inguinal areas.
Headache, malaise, pharyngitis, or lymphadenitis (5%).
The diagnosis of PR is made on history of herald patch and clinical findings. PR can be confused with tinea corporis, secondary syphilis, guttate psoriasis, tinea versicolor, parapsoriasis, pityriasis lichenoides (PL), nummular eczema, seborrheic dermatitis, or a drug eruption (gold, ACE inhibitors, metronidazole, isotretinoin, arsenic, β-blockers, barbiturates, sulfasalazine, bismuth, clonidine, imatinib and other tyrosine kinase inhibitors, mercurials, D-penicillamine, tripelennamine, ketotifen).
DERMATOPATHOLOGY Small mounds of parakeratosis, spongiosis, lymphohistiocytic infiltrate.
PR is typically asymptomatic and self-resolves in 6 to 14 weeks. Atypical cases may have severe pruritus, have a more vesicular, purpuric, or pustular presentation, or may last as long as 5 months. Once cleared, it is uncommon for PR to recur.
Because PR is benign and self-limited, no treatment is needed. In atypical PR or at-risk individuals, serologic testing for syphilis (RPR) should be performed as secondary syphilis can have a similar presentation. Pruritus can be improved with topical steroids, judicious ambient sunlight exposure, and/or oral antihistamines. Systematic reviews regarding the use of oral erythromycin or oral acyclovir for PR have not yielded any definitive benefit from either agent. In more severe, prolonged cases, UVB light therapy or a short course of oral steroids may be indicated for symptomatic relief and eruption clearance.
PL is a papular, clonal T-cell disorder, characterized by recurrent crops of spontaneously regressing papules. Clinically, the spectrum ranges from an acute form, pityriasis lichenoides et varioliformis acuta (PLEVA), to a more chronic form, pityriasis lichenoides chronica (PLC).
INSIGHT 
Pityriasis lichenoides chronica may manifest as predominantly hypopigmented patches, which are akin to postinflammatory hypopigmentation from primary lesions.
SYNONYMS Acute guttate parapsoriasis, parapsoriasis varioliformis, Mucha–Habermann disease, guttate parapsoriasis of Juliusberg.
AGE
PLEVA: Any age.
PLC: Adolescents and adults.
GENDER M > F.
ETIOLOGY Clonal T-cell disorder.
The etiology of PLEVA and PLC is unclear. Theories include an infectious course, a postinfectious hypersensitivity reaction, an autoimmune mechanism, or an adverse reaction to drugs. PLEVA shows a predominance of CD8+ T cells. PLC shows a predominance of CD4+ T cells.
Self-resolving skin lesions tend to appear in crops over a period of weeks or months. Cutaneous lesions are usually asymptomatic, but may be pruritic or sensitive to touch.
TYPE PLEVA: Papules (Fig. 14-3), vesicles, pustules, scale. PLC: Papules, crusts, scars.
COLOR PLEVA: Pink, red. May have a hemorrhagic appearance. PLC: Red, brown. White scars.
DISTRIBUTION Generalized distribution (Fig. 14-4), including palms, soles, and mucous membranes.
Rare fever, malaise, and headache.
PLEVA can be confused with lymphomatoid papulosis, vasculitis, drug reaction, bites, scabies, varicella, folliculitis, impetigo, or prurigo nodularis. PLC can be confused with parapsoriasis, lichen planus (LP), guttate psoriasis, PR, or secondary syphilis.
DERMATOPATHOLOGY Skin biopsy shows epidermal spongiosis, keratinocyte necrosis, vesiculation, ulceration, and exocytosis. There is also dermal edema, a wedge-shaped inflammatory cell infiltrate extending to deep reticular dermis; hemorrhage; vessels congested with blood, and swollen endothelial cells.
PL skin lesions continue to appear in crops, but both disorders tend to have a relapsing benign course. PLEVA may last a few weeks to months, and PLC may last years. Individuals with PL should have continued follow-up because rare cases have been reported to progress to cutaneous T-cell lymphoma (CTCL).
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