A case report of PLEVA after Herpes Zoster infection: is there a correlation?

Sir, Pityriasis Lichenoids Et Varioliformis Acute (PLEVA) is a rare inflammatory skin condition that often affects children and young adults and is marked by the sudden appearance of erythematous papules that evolve into vesicles and/or pustules that may undergo central necrosis and hemorrhagic crusts. These lesions usually appear on the trunk, buttocks, and proximal extremities, resolving within weeks but sometimes leading to dyschromia and varioliform scars [1,2]. The exact cause is unknown, although studies suggest it may be triggered by medications or infectious agents [2–4]. A 63-year-old woman presented with a sudden onset of 3 days of a generalized and itchy skin rash. Three weeks before, the patient was diagnosed with a herpes zoster infection of the right upper limb and treated with acyclovir and paracetamol. No epidemiological context or other possible triggers were identified. The patient had a history of rheumatoid arthritis, type 2 diabetes mellitus, hypertension and dyslipidemia, clinically stabilized with adalimumab, prednisolone (5 mg daily), glulisine and glargine insulin, sitagliptin, atorvastatin, ezetimibe, valsartan, hydrochlorothiazide, and lansoprazole. On physical examination, the patient presented multiple erythematous papules spread across the upper limbs and trunk, and some remaining herpes zoster lesions in resolution. Given the scabies-like lesions, topical benzyl benzoate and oral hydroxyzine were prescribed. She returned after 3 days due to worsening of the rash with extension to the lower limbs and lips. Observation revealed numerous erythematous to purpuric papules and plaques, some scattered vesicles all through the body and some necrohemorrhagic crust lesions on the lips. Biopsy of lesions revealed “a paucicellular vaguely lichenoid infiltrate, accompanied by a perivascular lymphomonocytic superficial dermal infiltrate, with the possibility of PLEVA or possibly subacute lupus”. The analytical study was normal. Based on the aforementioned findings, the patient was diagnosed with PLEVA. The oral prednisolone dose was increased and topical betamethasone dipropionate and emollient cream were prescribed with complete resolution of symptoms. The pathogenesis of PLEVA is explained by three main hypotheses: an inflammatory reaction triggered by infections, drugs, or vaccines; immune complex-mediated hypersensitivity vasculitis; and T cell dyscrasia, involving the loss of mature CD2, CD3, and CD5 T cell antigens and clonal T cell proliferation in some cases [2,3,5]. In our case, the trigger was probably the Herpes Zoster infection 3 weeks before. The potential etiological role of varicella-zoster virus in PLEVA has already been suggested by Horie et al. [4]. The histopathological findings increase the likelihood of this diagnosis, as described in some studies stating the presence of edema with moderately dense lymphohistiocytic infiltrate, which can extend to the epidermis as a common finding in PLEVA [1,5]. Although this disease is self-limited, the use of topical and systemic corticosteroids, antibiotics and/or phototherapy may be useful in relieving symptoms [1,2,5]. We report this case to enrich the literature on PLEVA by providing detailed insights, enhancing understanding of its causes and epidemiology, and potentially improving diagnosis accuracy. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.