Purpuric pityriasis rosea in a 7-year-old girl: A rare variant with generalized involvement

Case report

A 7-year-old girl presented with a 10-day history of generalized purpura and petechiae. The eruption began with a solitary violaceous macule on the trunk and progressed within 1 week to multiple oval and round dark-red to violaceous purpuric macules, ecchymoses, and petechiae affecting the face, trunk, and extremities. Lesions were distributed parallel to skin cleavage lines with a characteristic “Christmas-tree” pattern on the back (Fig 1). No oropharyngeal lesions were noted on examination, and the patient denied sore throat or oral discomfort. She reported no pruritus, pain, fever, or systemic symptoms.

Fig 1.

Clinical presentation of purpuric pityriasis rosea. A and B, Multiple oval and round violaceous macules on the extremities. C, Confluent purpuric patches on the face. D and E, Generalized oval and round purpuric lesions on the trunk, aligned with cleavage lines; the back shows a “Christmas-tree” distribution. Note that peripheral scaling was clinically subtle and may be inconspicuous on overview photographs due to the hemorrhagic component.

Her medical history was notable for precocious puberty, previously treated with several traditional Chinese medicines (Dabu-yin pill, Qizao granule, Zhibai Dihuang pill). The family provided a detailed drug history. The herbal formulations had been stopped 1 week prior to onset and no other medications or vaccinations were reported around the time of eruption. She denied recent infections, medication allergies, or family history of similar skin disorders.

Laboratory studies, including complete blood count, urinalysis, coagulation profile, and syphilis serology (RPR, TPPA), were all within normal limits.

Skin biopsy showed basket-weave hyperkeratosis, mild acanthosis, superficial-to-mid dermal perivascular lymphocytic infiltrates, erythrocyte extravasation, and focal basal vacuolar change (Fig 2). In our patient, the histology was interpreted in conjunction with the characteristic clinical distribution and self-limited course, supporting a diagnosis within the purpuric pityriasis rosea (PPR) spectrum.

Fig 2.

Histopathologic findings of lesional biopsy. A, Orthokeratotic basket-weave stratum corneum with mild acanthosis, superficial-to-mid dermal perivascular lymphocytic infiltrates, and conspicuous erythrocyte extravasation (H&E, ×200). B, Higher magnification highlighting focal basal vacuolar/interface change, perivascular lymphocytes, and extravasated erythrocytes (H&E, ×400).

The patient was treated with oral levocetirizine 5 mg once daily, compound glycyrrhizin tablets 25 mg 3 times daily, vitamin C 100 mg 3 times daily, and calcium gluconate with zinc 10 mL twice daily. Topical corticosteroids were avoided at parental request. After 1 week, truncal lesions lightened slightly, though new purpura appeared on the lower extremities (Fig 3). By week 8, most lesions resolved, and complete clearance was achieved by week 16 (Fig 4). No recurrence was observed during a 3-year follow-up.

Fig 3.

Lesions after 1 week of treatment. A, persistent and increased purpura on the lower extremities; B, partial fading of truncal lesions on the abdomen; C, residual truncal lesions on the back; D, purpuric lesions on the upper extremities.

Fig 4.

Lesions after 8 weeks of treatment. A, near-complete resolution of lesions on the upper extremities; B, resolution of truncal lesions on the chest/abdomen; C, resolution of lesions on the back; D, resolution of lesions on the lower extremities.

Discussion

Pityriasis rosea is a self-limited dermatosis usually presenting with erythematous scaly plaques and a herald patch. Atypical variants comprise up to 20% of cases, including vesicular, inverse, urticarial, giant, and purpuric subtypes.1, 2 In purpuric variants, hemorrhagic changes may obscure surface scale, making collarette scaling subtle or absent on photographs, especially in children. Consequently, diagnosis relies on clinicopathologic correlation, including a herald-patch–like onset, cleavage-line alignment with a Christmas-tree pattern, benign laboratory evaluation, and a self-limited course. Although scaling is a classic feature of PR, purpuric variants may show clinically inconspicuous scale, possibly because the hemorrhagic component obscures the surface changes. While HHV-6/7 reactivation has been implicated in PR, serology/PCR is not routinely required and is neither specific nor diagnostic in isolation; in this case, the diagnosis was made on clinicopathologic grounds and longitudinal follow-up.

PPR, first described by Hartman in 1944,³ is rare and predominantly occurs in children and adolescents. Histopathologic findings in classic PR are often non-specific, typically showing variable spongiosis. Prior reports of hemorrhagic or purpuric variants have described prominent red-cell extravasation and, in some cases, interface-type changes. Clinical features include purpura, ecchymoses, or petechiae within or in place of classical PR lesions.4, 5 Etiology is unclear, but viral reactivation (HHV-6/7) and drug exposure have been implicated.^6,7 Tamer et al⁴ described an adolescent with PPR and HSV-1 IgM positivity, supporting a viral trigger. In our case, the use of multiple herbal medicines may have contributed.

Differential diagnoses include pigmented purpuric dermatoses, lichen planus, and immune thrombocytopenic purpura. Characteristic lesion distribution, normal laboratory results, and absence of systemic bleeding manifestations helped exclude hematologic disease. PR-like drug eruption (PR-LE) was considered given the history of traditional Chinese medicines (herbal formulations). Several features favored PR/PPR over PR-LE in our case: the medications were stopped 1 week before onset rather than taken continuously; the child had no pruritus and no eosinophilia; the eruption showed a herald-patch–like onset and cleavage-line distribution typical of PR; and lesions resolved spontaneously over 16 weeks with no recurrence during 3-year follow-up. While a drug-related trigger cannot be excluded with certainty, the overall presentation and evolution were most consistent with PPR. These considerations are consistent with published distinctions between PR and PR-LEs.⁸ Nevertheless, a drug-related trigger cannot be excluded with certainty.

Treatment is primarily supportive. Antihistamines, vitamin C, and glycyrrhizin may be helpful; corticosteroids, antivirals, or phototherapy have been used in refractory cases.⁹ While typical PR resolves within 6-8 weeks, our patient required 16 weeks, possibly reflecting the widespread hemorrhagic involvement and relative immune immaturity of children.

Limitations include the absence of high-magnification clinical images and dermoscopy, which limits photographic demonstration of subtle peripheral scale. Future reports of purpuric PR may benefit from dermoscopic documentation of scaling and hemorrhagic dots. In addition, HHV-6/7 serology or PCR was not performed, and future studies may clarify the utility of viral testing in pediatric purpuric variants.

This case underscores that PPR can present with minimal or nonphotogenic scaling, and that clinicopathologic correlation and longitudinal follow-up are crucial to avoid unnecessary hematologic work-ups in children.

Conflicts of interest

None disclosed.