Correspondence Address:
Elif Afacan
Dermatology, Faculty of Medicine, Gazi University, Ankara
Turkey

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Sir,

Herpes zoster (HZ) is a common disease caused by reactivation of varicella-zoster virus (VZV).[1] Besides the classical vesicular rash on the skin, VZV is known to cause extra-cutaneous manifestations, including vasculopathy of different sized vessels.[2],[3] VZV vasculopathy is a well-recognised entity in central nervous system (CNS); however, only few data have been published on cutaneous small-vessel vasculitis (CSVV) in HZ. Herein, we present a case of HZ with CSVV and a review of the literature.

A 53-year-old woman with a history of acute myeloid leukaemia and allogeneic stem cell transplantation was admitted to our department with complaints of painful lesions in left gluteal region and upper leg for 2 days. On examination, purpuric papules/plaques with central necrohaemorrhagic crusts were seen in dermatomal distribution [Figure 1]. Punch biopsy showed intraepidermal bulla with viral nuclear inclusions and giant cell formations, as well as perivascular mononuclear inflammation, leukocytoclasia and fibrinoid necrosis around superficial dermal capillaries [Figure 2]. To exclude the presence of herpes simplex virus (HSV), an immunohistochemical staining for HSV and plasma HSV-1/HSV-2 PCR were performed and resulted in negative. After routine laboratory screenings, systemic involvement of vasculitis was excluded. Based on these findings, the patient was diagnosed with HZ with CSVV. She was started on valacyclovir 3 × 1000 mg/day and analgesics. After 7 days, complete resolution of the cutaneous lesions was observed without sequelae and no additional systemic therapy was required for CSVV. She did not develop postherpetic neuralgia (PHN) or vasculopathy of CNS during 2 months of follow-up.{Figure 1}{Figure 2}

Vascular changes associated with VZV are vessel wall thickening, stenosis and inflammatory infiltrate with abundant neutrophils. VZV is suggested to spread transaxonally from neural ganglia to vessel walls.[4] It can infect endothelial cells directly from adjacent nerves and cause vascular damage including microthrombi formation and haemorrhage.[3],[5] In 1984, Cohen and Trapuckd[6] described the first case of CSVV associated with HZ. After a detailed literature review, we found 10 published cases.[6],[7],[8],[9],[10],[11],[12],[13],[14],[15] Clinicopathological features of present and reported cases are summarised in [Table 1]. The mean age was 57.18 ± 17.74 years, which can be explained by the fact that advanced age is a major risk factor for HZ.[1] Most cases, including ours, were immunocompromised individuals. Cutaneous findings were characterised by vesicles, palpable purpura and ulcerated nodules/plaques. The lesions were mostly on the lower extremities. Histopathological findings included intraepidermal blisters, multinucleated giant cells and leukocytoclastic vasculitis. In most cases, complete recovery was achieved with anti-viral agents and no patient required further systemic therapy for CSVV. It is estimated that PHN occurs in 5%–20% of patients with HZ; the absence of postherpetic neuralgia (PHN) in our patient can be explained by early treatment with valacyclovir.[16]{Table 1}

In conclusion, all previously reported cases and our case had a clinically distinctive appearance that prompted dermatologists to obtain a biopsy. Nevertheless, given the well-known vasculopathic effects of VZV, it is possible that this phenomenon is more common than reported. Although the clinical picture is alarming, this association appears quite benign and has no further complications. However, future studies are needed to elucidate the clinical implications of HZ with CSSV.

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Conflicts of interest

There are no conflicts of interest.

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