Indian Journal of Dermatology
: 2022  |  Volume : 67  |  Issue : 5  |  Page : 614--615

Post-zoster eosinophilic dermatosis and acquired tufted angioma: Isotopic response

Young Shin Kim, Yeon Seok Lee, Tae Young Han, June Lee, Jae Eun Choi 
 Department of Dermatology, Eulji University Eulji Hospital, Seoul, South Korea

Correspondence Address:
Yeon Seok Lee
Department of Dermatology, Eulji University Eulji Hospital, Seoul
South Korea

How to cite this article:
Kim YS, Lee YS, Han TY, Lee J, Choi JE. Post-zoster eosinophilic dermatosis and acquired tufted angioma: Isotopic response.Indian J Dermatol 2022;67:614-615

How to cite this URL:
Kim YS, Lee YS, Han TY, Lee J, Choi JE. Post-zoster eosinophilic dermatosis and acquired tufted angioma: Isotopic response. Indian J Dermatol [serial online] 2022 [cited 2023 Mar 23 ];67:614-615
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Various benign and malignant cutaneous reactions have been reported to develop at the sites of resolved herpes zoster (HZ) lesions from weeks to years after acute infection. Wolf et al. defined the occurrence of a new skin disorder at sites of other, unrelated, and already healed skin diseases as an isotopic response. HZ is the most common primary disease to induce Wolf's isotopic responses (WIRs). Frequently reported skin diseases that appear as WIRs include granulomatous dermatitis (e.g. granuloma annulare and sarcoidal granulomas), lichen planus and psoriasis.[1],[2] The mechanism underlying the pathogenesis of this phenomenon remains unknown. Here, we describe two patients with post-zoster eosinophilic dermatosis and acquired tufted angioma [Figure 1] and [Figure 2].{Figure 1}{Figure 2}

Case 1: An 88-year-old woman presented with a 2-week history of multiple erythematous to purpuric papules on her left upper arm, limited to the vicinity of the axilla. She had underlying Alzheimer's disease, diabetes, asthma and hypothyroidism. Histopathological examination showed closely set capillaries scattered throughout the dermis. These circumscribed ovoid angiomatous aggregates have been reported to exhibit a 'cannonball' appearance. The lobules were composed of bloodless aggregates of capillaries surrounded by dilated crescent-shaped vascular structures. The patient's children later reported that the patient had previously experienced HZ infection on the same dermatome, several weeks prior to presentation in our clinic. Based on the clinicopathological findings, the patient was diagnosed with acquired tufted angioma after healed HZ. Although complete excision is the treatment of choice for tufted angioma, no treatment was applied as the patient elected watchful waiting.

Case 2: A 76-year-old woman presented with intensely pruritic erythematous xerotic patches on her left lower back. She had underlying hypertension, diabetes and stroke. She had previously experienced HZ infection on the same dermatome several years prior, which had healed after treatment. Skin biopsy specimens revealed dense perivascular inflammatory cellular infiltrates composed of eosinophils, lymphocytes and histiocytes in the upper to middle dermis. Based on the clinical and histopathological findings, the patient was diagnosed with post-zoster eosinophilic dermatosis. Topical corticosteroid treatment was applied but did not effectively control the patient's extreme pruritus. Triamcinolone was subsequently injected into the skin lesions several times, which led to symptom relief.

Since the first description of WIRs by Wolf et al.[3] in 1995, the development of various skin diseases after HZ infection has been reported, although these diseases are rare. WIRs range from benign lesions (e.g. granulomatous dermatitis, psoriasis and lichen planus) to malignant lesions (e.g. basal cell carcinoma, squamous cell carcinoma and angiosarcoma).[4] The interval between acute HZ infection and cutaneous reactions varies from weeks to years. The pathogenesis of WIRs after HZ remains incompletely understood, although viral DNA has been isolated from several patients with postherpetic isotopic response. Recently, it has been suggested that WIRs are caused by neuroimmune dysfunction. HZ can cause the destruction of nerve fibres in the dermis; the secretion of neuropeptides (e.g. substance P and vasoactive intestinal peptide) from damaged nerve fibres has various effects on mast cells, T lymphocytes, monocytes and endothelial cells. Local immunological changes may cause abnormal immune reactions.[1],[5] However, further studies are needed to determine why a single isotopic response manifests as distinct dermatological disorders with various time intervals.

In conclusion, we described two patients with post-zoster eosinophilic dermatosis and tufted angioma, which is considered an isotopic response. Further studies in larger cohorts may help to elucidate the pathological mechanism of this phenomenon. Clinicians should recognize this entity and evaluate the history of HZ in affected patients.

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