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Description
A 37-year-old male patient with acute myeloid leukaemia presented to us with eruptive lesions over the anterior chest and neck for the past 5 days and severe burning pain over the involved areas. He had earlier received consolidation chemotherapy. On examination, he was afebrile. Multiple papular, vesicular and crusting lesions over C2 to C7 and T1 to T3 dermatomes were noted which were consistent with herpes zoster (HZ; figures 1 and 2). No ocular or neurological symptoms were present except the neuropathic pain. Oral valacyclovir therapy along with opioids and tricyclic antidepressants was started. His lesions resolved over a period of 2 weeks, however neuralgia persisted. Severity of pain was 6 (moderate) on numeric rating scale. He was advised capsaicin cream for topical application and oral pregabalin. He got good symptomatic relief with pain intensity measuring 2 (mild) 3 weeks later.
HZ or shingles is the clinical manifestation of the varicella-zoster virus (VZV). VZV can manifest in two ways namely, chickenpox and HZ. Chickenpox is a self-limiting illness usually seen in children and occurs due to primary infection. HZ occurs due to the reactivation of the latent VZV in dorsal root ganglia. The risk of HZ increases with old age and in patients with reduced cell-mediated immunity such as haematological malignancies, immunosuppressive therapies, HIV infection and transplant recipients. The incidence of HZ has been variably reported as 2% in chronic myeloid leukaemia, 13% in chronic lymphocytic leukaemia and 30% in marrow transplant recipients.1–3 HZ occurring in these settings is usually very severe and may involve multiple contiguous, non-contiguous or bilateral dermatomes. It may be associated with encephalitis, pneumonitis, ocular complications and persistent postherpetic neuralgia.3 These patients require prompt diagnosis and early institution of antiviral therapy.
Learning points
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Extensive dermatomal involvement may be seen in herpes zoster (HZ) occurring in the setting of immunodeficient conditions. Vice versa, an extensive involvement of HZ should prompt a clinician to search for associated immunodeficiency state.
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Patients may develop non-cutaneous complications and must be treated aggressively.
Footnotes
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Contributors DS and NK contributed in the management of the patient, conceptualisation of the manuscript, data acquisition, manuscript drafting and revision, and gave final approval. RK and MW contributed in the management of the patient, conceptualisation of the manuscript, revision and gave final approval.
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Competing interests None.
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Patient consent Obtained.
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Provenance and peer review Not commissioned; externally peer reviewed.