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.[4]
Epidemiology
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.[5]
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.[6] 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.
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