CASE REPOR T
JEADV (2004) 18, 622– 625 DOI: 10.1111/j.1468-3083.2004.01021.x
Vesicular pityriasis rosea: response to erythromycin treatment
Blackwell Publishing, Ltd.
SB Miranda,†* O Lupi,‡ E Lucas† † Dermatology Department, Clinical Hospital of Federal University/UFES, Vitória, Brazil, ‡Dermatology Department, Federal University/UFRJ, Rio de Janeiro, Brazil. *Corresponding author, Rua das Palmeiras, 795/603 Santa Luzia, Vitória, ES Brazil, E-mail:
[email protected]
ABSTRAC T Pityriasis rosea (PR) is a relatively common disease although its aetiology has not yet been identified. It occurs worldwide and there is no racial susceptibility factor. It usually affects teenagers and young adults between 10 and 35 years of age. Typical PR is much easier to diagnose than the rare atypical forms. We report a rare case of vesicular PR in a black woman who had vesicular lesions limited to her palms and soles in addition to regular typical lesions. We devised an efficient oral erythromycin treatment for this patient. Key words: atypical pityriasis rosea, erythromycin stearate, pityriasis rosea, vesicular pityriasis rosea Received: 4 July 2003, accepted 31 October 2003
Case report A 32-year-old black woman presented with a generalized rash that was localized mainly on her chest and extremities. Physical examination revealed erythematous papulosquamous eruptions. There were some annular protuberances with marginal collarette of scaly lesions localized on the trunk, neck and arms (fig. 1). Oval erythematous scaly plaques of average diameter 2 cm were found on the dorsal surface of the fourth finger of her left hand (fig. 2). We observed vesicles on her palms, soles and part of the anterior forearm surface (fig. 3). We did not observe any pruritic lesions, lesions on mucous membranes or lymphadenophathy. Scaly plaques found on her fourth finger were first noticed by the patient 1 month prior to physical examination and were the first sign of the disease. Two weeks later, she observed eruptive lesions and vesicles on her palms and soles. Those lesions were not associated with any prodromal symptoms such as fever, malaise, headache or throat infection. She denied the use of any medication and affirmed that no family member had similar eruptive lesions. The following laboratory investigative analyses were all negative: throat swab, antistreptolysin O (ASO) titre, C-reactive protein, venereal disease reference laboratory (VDRL), fluorescent treponemal antibody absorption (FTA/ABS) test, hepatitis B surface antigen and antibody, and anti-human immunodeficiency virus (antiHIV) 1–2. Complete blood count, platelets and erythrocyte sedimentation rate, and urinalysis were all considered normal. We performed two skin biopsies; one included the papulosquamous lesion localized on the trunk. The histological 622
fig. 1 Typical papulosquamous lesions of pityriasis rosea on the arm.
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fig. 2 Herald path on finger.
analysis of this biopsy showed subacute dermatitis with moderate mononuclear perivascular infiltrate in the upper dermis, slight acanthosis, spongiosis, exocitosis and focal parakeratosis (fig. 4). The other biopsy was obtained from the vesicular lesion in the left palm and revealed intraepidermal vesicle with no evidence of acantolytic process (fig. 5). Fungal stain assays, silver impregnation (Grocott) and the periodic acid Schiff (PAS) test were negative for both skin biopsies. The patient was treated with oral erythromycin stearate for 10 days, 1 g per day, prepared from four equally divided 250 mg-aliquots. The lesions faded dramatically in a very short period of time. We observed remarkable involution of nearly all the lesions after only 7 days of oral erythromycin administration. Most lesions, typical and atypical, vanished after the 10th day of treatment, the affected skin had fully cleared after the completion of the treatment, and no postinflammatory hyper- or hypopigmentation macules were detected. During the 4 months of follow-up, no recurrence was observed.
Discussion Pityriasis rosea is an acute or subacute inflammatory skin disease characterized by erythematous papulosquamous eruptions
fig. 3 Intact vesicular lesions on the palms and few ruptured vesicles in the anterior forearm surface.
fig. 4 Focal spongiosis and slight exocitosis in the epidermis as well as overlying parakeratosis. Also, a mononuclear cell infiltrate in the upper-dermis (haematoxylin–eosin stain; original magnification × 100).
localized on the trunk and arms. The eruptions are self-limiting and usually disappear gradually in 2 –10 weeks without any treatment. The aetiology is uncertain although there is evidence of a cause by infection.1,2 The viral hypothesis has been widely studied
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624 Miranda et al.
fig. 5 Intra-epidermal vesicle with marked oedema and minimal mononuclear infiltrate in superficial dermis (haematoxylin–eosin stain; original magnification × 10).
by the scientific community. Recently, the human herpes virus 7 (HHV 7) was thought to be related to the disease development.3 However, scientists were unable to isolate the virus in recent studies, thus failing to support the HHV 7-PR association hypothesis.4 Atypical variants of PR are rare and occur in only 20% of all cases. Atypical forms can differ morphologically or topographically.2,5 Cephalic pityriasis rósea, inverse PR, unilateralis PR, localized PR and pityriasis circinada et marginata of Vidal are the atypical forms most frequently observed with regard to topographic distributions of lesions.2,5,6 With respect to the morphological aspect, the lesions are described as the following variants: generalized papular PR,7 purpuric (haemorragic) PR,8 pustular and vesicular PR.6,9,10 There are few reports of vesicular PR in the literature. Weiss et al. reported only 0.5% of vesicular PR out of a total of 380 PR cases studied so far.6 Vesicular PR is observed more frequently among children and young adults, as for most atypical forms. The vesicular lesions can be generalized, found on the face mimicking a varicellae, or restricted to the palms and soles resembling dishydrosis. Furthermore, the vesicles are usually
associated with typical papulosquamous lesions, favouring a diagnosis of vesicular PR.6,9,10 In general, the evolving course of atypical PR variants is not distinct from that of typical PR forms.2 Histological features can be either subacute or chronic dermatitis with focal parakeratoses, mild acantosis, spongiosis and mononuclear infiltrate on the superior dermis.11 The vesicular lesions of PR are due to severe spongiosis with exocytosis, and intraepidermal vesicles. Histopathological characterization of PR is not specific but can help to diagnose atypical variants. PR is usually treated efficiently with topical corticotherapy, UVB exposure therapies, and oral antihistamines. Systemic steroids are used to treat generalized forms, dapsone is used on severe vesicular PR unresponsive to systemic steroids,12 and oral erythromycin treatment has recently been effective against PR.13 The clinical diagnosis of our case of vesicular PR was based not only on the presence of vesicular lesions in the palms and soles but also on the association of typical erythematous papulosquamous lesions and the herald patch. We opted to use the oral treatment because of the large number of lesions found. The choice for erythromycin treatment was based on the work of Sharma et al., who efficiently treated 45 cases of typical PR with oral erythromycin.13 In our case the majority of lesions regressed by the seventh day of treatment. On clinical grounds, we can conclude that the oral erythromycin treatment was effective against both atypical and typical PR lesions. Furthermore, there was no recurrence of lesions during the 4-month follow-up period. The good response to erythromycin treatment for this atypical and generalized PR case could imply some involvement of aetiological agents such as Streptococcus, Chlamydia, Legionella and Mycoplama.13,14 Such aetiological agents are sensitive to erythromycin and are usually the cause of the upper respiratory tract infections previously associated with PR in the literature.15 However, a correlation between bacterial infectious agents as well as viral infectious agents and the PR pathogen has not yet been clearly established.2,4,14 We suspect that anti-inflammatory and immunomodulary proprieties attributed to erythromycin were the main contributors to the positive response obtained throughout treatment.16 There are studies that show a clear connection between abnormal immunity and high PR incidence such as: during pregnancy,1 after bone marrow transplantation,17 in highly stressed individuals,1 and aggravation of PR after oral corticosteroid treatment.18 It is important to note that the aetiology of PR remains unknown.
References 1 Bjornberg A, Hellgren I. Pityriasis rosea. A statistical, clinical and laboratory investigation of 826 patients and matched healthy controls. Acta Derm Venereol Suppl 1962; 50: 1– 68. 2 Parsons JM. Pityriasis rósea update. J Am Acad Dermatol 1986; 15: 159 –167.
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3 Drago F, Ranieri E, Malaguti F et al. Human herpesvirus 7 in patients with pityriasis rósea. Dermatology 1997; 195: 374 –378. 4 Kempf W, Adams V, Nestle FO et al. Pityriasis rosea is not associated with human herpesvirus 7. Arch Dermatol 1999; 135: 1070–1072. 5 Imamura S, Ozaki M, Horiguchi Y et al. Atypical pityriasis rosea. Dermatologica 1985; 171: 474 – 477. 6 Weiss RL, Lace CW, Showman WA. Pityriasis rosea. Arch Dermatol Syph 1927; 15: 304 –322. 7 Hendricks A, Lohr JA. Pityriasis rosea in infancia. Arch Dermatol 1979; 115: 896–897. 8 Pierson JC, Dijkstra JWE, Elston DM. Purpuric pityriasis rosea. J Am Acad Dermatol 1993; 28: 1021. 9 Baker RJ, Johnson WC. Vesicular pityriasis rosea. Cutis 1971; 8: 341–342. 10 Garcia RL. Vesicular pityriasis rosea. Arch Dermatol 1976; 112: 410. 11 Ackerman AB. Histologic diagnosis of inflammatory skin diseases: a method by pattern analysis. Lee & Febiger, Philadelphia, 1978: 233–235.
12 Anderson CR. Dapsone treatment in a case of vesicular pityriasis rosea. Lancet 1971; 2: 493. 13 Sharma PK, Yadav TP, Gautam RK et al. Erythromycin in pityriasis rosea: a double-blind, placebo controlled clinical trial. J Am Acad Dermatol 2000; 42: 241–244. 14 Chuh AAT, Chan HHL. Prospective case-control study of Chlamydia, Legionella and Mycoplasma infections in patients with pityriasis rosea. Eur J Dermatol 2002; 12: 170 –173. 15 Chuang T, Perry HO, Ilstrup DM et al. Recent upper respiratory tract infection and pityriasis rosea: a case control study of 249 matched pairs. Br J Dermatol 1983; 108: 587–591. 16 Labro MT. Anti-inflammatory activity of macrolides: a new therapeutic potential? J Antimicrob Chemother 1998; 41 (Suppl B): 37–46. 17 Spelman LJ, Robertson IM, Strutton GM et al. Pityriasis rosea-like eruption after bone marrow transplantation. J Am Acad Dermatol 1994; 31: 348 –351. 18 Leonforte JF. Pityriasis rosea: exacerbation with corticosteroid treatment. Dermatologica 1981; 163: 480 –481.
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