Pityriasis rosea L42

Author: Prof. Dr. med. Peter Altmeyer

All authors of this article

Last updated on: 19.03.2023

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Erythema anulatum; Floret lichen; herpes tonsurans maculosus; ibertian disease; lichen anulatus; pityriasis maculata circinata; Pityriasis marginé et circiné de Vidal; Pseudoexanthème desquamatif (Besnier); Roseola anulata; Scaly Florets

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Gibert, 1860

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Frequent, exanthematic, self-limiting, inflammatory skin disease of unknown (probably viral etiology) etiology with typical two-phase course.

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Common clinical picture with a prevalence of 0.1%.

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Unknown. Increasingly, the role of the herpesviruses HHV-6(HHV-7), possibly also HHV-8, is discussed, especially since their antigens were detectable in the lesions and the disease responds to antiviral substances such as aciclovir.

Association with H1N1 virus and COVID-19 has been reported in individual cases (Martora F et al. 2022); furthermore, occurrence has been observed after COVID-19 vaccination (Dormann H et al. 2021; Gambichler T et al. 2022).

Associations to other viruses(EBV, CMV) or to streptococcal infections could not be demonstrated.

Furthermore, as triggering moments are discussed: stress, medication, impregnated clothing.

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Occurring in healthy individuals between the ages of 10-35 years (Leung AKC et al. 2021). Occurrence of pityriasis rosea in children <10 years of age is uncommon. Females appear to be preferentially affected (m:w = 1:2). Equal occurrence worldwide. Endemic occurrence possible especially in spring and autumn.

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Trunk (up to the base of the neck) and proximal (approximately upper third) extremities. Head, neck, peripheral extremities remain free. An inverse form(pityriasis rosea inversa) affects the axillae and the groin region.

Clinical features
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Occasionally, mild prodromes such as respiratory symptoms (about 50% of patients), nausea, malaise, lassitude, fever, and headache precede the initial skin lesions. Less commonly, enlarged lymph nodes and arthralgias are detected (in 5% of patients - Leung AKC et al. 2021).

Initially, a 0.4-7.0 cm, oval, light-red to pink, usually scaling (Collerette scaling), marginal plaque ("primary medallion") is seen. The primary medallion (tache mère, herald patch) is a regularly occurring symptom in > 50% of cases and often appears on the trunk.

In the further course, relapsing, exanthematous (symmetrical) spreading (truncal), lasting for 1-2 weeks, of 0.2-1.0 cm, oval or elongated, little raised, scaly patches and scaly papules and plaques (see Fig.), aligned according to the cleavage lines (fir tree pattern; canopy sign). Here, too, evidence of so-called collerette scaling, an inwardly directed delicate scaly ruff, is possible in individual plaques. This type of scaling is a supporting diagnostic phenomenon (see Fig.). The foci that appear later are usually smaller than the primary medallion. This is not always detectable in the exanthema stage.

The face, neck, and distal halves of the extremities usually remain free. Oropharyngeal mucosal lesions are rare but are associated with the clinical picture (Ciccarese G et al. 2017).

Follicular exanthema, hemorrhagic and urticarial exanthema, circine, vesicular, squamous, or psoriasiform variants should be noted as (rare) special forms.

An inverse form is observed preferentially in children as well as African-Americans(pityriasis rosea inversa).

Notice. In colored persons, the exanthema appears more infiltrated than in whites with a clear tendency to hyperpigmentation! Here, depending on the degree of pigmentation, the red tint of the skin manifestations so typical in white skin is missing.

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Nonspecific superficial dermatitis with moderate acanthosis, slightly elongated rice ridges, papilledema, perivascular and interstitial lymphocytic infiltrate; occasionally admixtures of eosinophilic granulocytes. Marked epidermotropia with focal spongiotic loosening of the epithelium and focal, stratified parakeratosis (histologic counterpart of Collerette's pucker). Rarely erythrocyte extravasations.

Differential diagnosis
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  • Clinical Differential Diagnosis:
    • Tinea corporis: never exanthematic, but chronically continuous course (rare exception is microsphere, here there is self-fluorescence under wood light); pathogen detection by native examination and culture is proof.
    • Psoriasis vulgaris: first manifestation of an acute, exanthematic psoriasis as an important DD. The exanthema phenomenon is always negative in pityriasis rosea!
    • Parapsoriasis en plaques (benign small-field form): chronic process, never acute exanthematic. Single florescences significantly larger than in Pityriasis rosea. Typical is a "pseudoatrophy of the surface".
    • Drug exanthema: Acute monomorphic exanthema; rarely eczematous or psoriasiform. Drug anamnesis with prompt re-prescription of a drug.
    • Pityriasis lichenoides: Similar distribution pattern. However, PLEVA and PLC show a groundbreaking polymorphism (colourful picture) of the efflorescences.
    • Early syphilis: Syphillis are usually accompanied by swelling of the LK. Distribution pattern: Frequent infestation of palms and face. Serology is conclusive! Histology is conclusive (plasmacellular dermatitis).
  • Histological differential diagnoses:
    • Acute and subacute eczema: spongiosis, extensive parakeratosis, in atopic eczema possible prominent eosinophilia. Often indistinguishable.
    • Psoriasis guttata: acanthosis, extensive hyper- and parakeratosis with neutrophil inclusions, diffuse, also perivascularly compressed lymphocytic infiltrate with neutrophil granulocytes, no erythrocyte extravasations, strong epidermotropism.
    • Parapsoriasis en plaques: Fibrosis of the papillary stratum; surface epithelium rather atrophic, epidermotropy present, hardly any spongiosis, no parakeratosis!
    • Allergic contact dermatitis: Clinically clearly distinguishable! Prominent, flat spongiosis, surface epithelium acanthotic, long hills of parakeratosis. Histological differentiation can only be reliably made in connection with clinical data.
    • Tinea corporis: Varied histological pattern, which is characterized by the acuteity of the infection. In early stages low superficial perivascular lymphocyte infiltrate, focal spongiosis; later stage with neutrophil component. Compact ortho- and parakeratosis. In the PAS preparation, detection of hyphae (then safe DD); otherwise safe DD is only possible in connection with clinical data.
    • Erythema anulare centrifugum: Clinically clearly distinguishable; histologically safe differentiation only in connection with clinical data! Mostly dense perivascular infiltrate sheaths.
    • Drug exanthema: Cancellous drug exanthema are rare! Mostly combined with interface dermatitis.
    • Early syphilis: Interface dermatitis with psoriasiform epidermal reaction dense, band-shaped infiltrate in the upper and middle dermis (lymphocytes, histiocytes and plasma cells. Extension of the infiltrate to the deep vascular plexus).

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Causal therapy not known. The skin changes heal spontaneously within 3-8 weeks.

General therapy
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Avoidance of heat accumulation, occlusive clothing, sports, sauna and moisturising external agents. No excessively hot and long baths, no sunbathing!

External therapy
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Cave! Irritation from aggressive external agents. No fat creams or ointments. Treatment e.g. with Tannolact Lotio, Tannosynt Lotio (shaking mixture), Optiderm Lotio. Blande skin care with O/W emulsion (e.g. Eucerin O/W). Recommended especially for itching are creams containing 5% polidocanol or shaking mixture R200 or weakly effective glucocorticoids like 0.5% hydrocortisone emulsion R123.

Radiation therapy
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Mild broad-spectrum UVB therapy can be applied to fair-skinned patients with extensive infestation (Villalon-Gomez JM 2018).

Internal therapy
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If necessary, oral antihistamines such as levocetirizine (e.g. Xusal Tbl.) 1 time/day 5 mg p.o. or desloratadine (e.g. Aerius Tbl.) 1 time/day 5 mg p.o.

Alternative: Aciclovir; in a randomized study in a medium-sized collective, a positive clinical effect (shortening of disease duration) was demonstrated by oral administration of aciclovir (OFF label use) for 7 days (400 mg/5xday p.o.). This therapeutic option should be carefully considered with regard to the self-limiting course of the disease.

Alternative: Oral erythromycin (250mg 4x/day for 2 weeks) is significantly successful according to a meta-analysis (Chuh A et al. 2005).

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Healing in 3-8 weeks, generally without permanent skin changes. Hyperpigmentation, leukoderm formation, scarring are possible. Recurrences are rare (<3%) (pityriasis rosea recidivans).

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Remember! A primary medallion is a regularly occurring, diagnostically usable symptom; in > 50% of cases

Notice! Pityriasis rosea (almost) never affects the face and mucous membranes; only rarely the extremities! Patients have no disturbed general condition!

Notice! The course of pityriasis rosea is critical for the fetus up to the 15th week of pregnancy with an increased risk (57%) of miscarriage or premature birth (Monastirli A et al. 2016).

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  1. Chuang TY et al (1983) Recent upper respiratory tract infection and pityriasis rosea: a case-control study of 249 matched pairs. Br J Dermatol 108: 587-591.
  2. Chuh A et al.(2006) Atypical presentations of pityriasis rosea: case presentations. J Eur Acad Dermatol Venereol 19:120-126.
  3. Ciccarese G et al (2017) Oropharyngeal lesions in pityriasis rosea. J Am Acad Dermatol 77:833-837.
  4. Das A et al (2015) Acyclovir in pityriasis rosea: An observer-blind, randomized controlled trial of effectiveness, safety and tolerability. Indian Dermatol Online J 6:181-184.
  5. Demirkan S et al (2019). Does influenza subtype H1N1 have a place in the etiology of pityriasis rosea. Postepy dermatologii i alergologii 36: 164-166 .
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  7. DragoF et al (2008) Pregnancy outcome in patients with pityriasis rosea. J Am Acad DErmatol 58: 78-83.
  8. Gambichler T et al. (2022) Cutaneous findings following COVID-19 vaccination: review of world literature and own experience. J Eur Acad Dermatol Venereol 36:172-180.
  9. Gibert CM (1860) Traite' Pratique des Maladies de la peau et de la Syphilis, 3 rd edn. Plon (Paris) pp:402
  10. Kempf W (2002) Human herpesvirus 7 in dermatology: what role does it play? Am J Clin Dermatol 3: 309-315
  11. Kempf W, Burg G (2000) Pityriasis rosea--a virus-induced skin disease? An update. Arch Virol 145: 1509-1520
  12. Leung AKC et al (2021) Pityriasis rosea: An Updated Review. Curr Pediatr Rev 17:201-211.
  13. Monastirli A et al. (2016) Gestational pityriasis rosea: Suggestions for Approaching Affected Pregnant Women. Acta Dermatovenerol Croat 24:312-313.
  14. Martora F et al (2022) Can COVID-19 cause atypical forms of pityriasis rosea refractory to conventional therapies? J Med Virol 94:1292-1293.
  15. Rassai S et al (2011) Low dose of acyclovir may be an effective treatment against pityriasis rosea: a random investigator-blind clinical trial on 64 patients. JEAV 25: 24-26
  16. Renner R et al (2010) Chronic inflammatory and autoimmune-mediated dermatoses in pregnancy. Dermatologist 61: 1021-1026
  17. Vaccaro M et al (2020) Pityriasis rosea during omalizumab treatment for chronic spontaneous urticaria. Dermatol Ther 33:e14356.
  18. Villalon-Gomez JM (2018). Pityriasis rosea: diagnosis and treatment. Am Fam Physician 97:38-44.
  19. Watanabe T et al. (2002) Pityriasis rosea is associated with systemic active infection with both human herpesvirus-7 and human herpesvirus-6. J Invest Dermatol 119: 793-797.


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