HSV-INDUCED APLASTIC ANEMIA

Document Type

Conference Proceeding

Publication Date

6-17-2022

Publication Title

Journal of General Internal Medicine

Abstract

CASE: We present the case of a 56-year-old female with a past medical history of ESRD on hemodialysis, presenting with a three-day history of severe stomatitis, accompanied by odynophagia, dysphagia, blood-tinged sputum, and hoarse voice. Physical exam demonstrated a fever, tachycardia, and extensive desquamation and erythema of the buccal and soft palate mucosa, petechiae, and multiple, bilateral, diffuse gray plaques, necrotic-appearing in the hard palate. Laboratory tests revealed new-onset pancytopenia, including hemoglobin of 6.6 g/dl, WBC count of 0.4 K/uL with an absolute neutrophil count of 0.02 K/uL, and platelet count of 23 K/uL. The absolute reticulocyte count was 4-6 K/uL with a reticulocyte index of 0.04, indicating a hypoproliferative state. Bilateral nasal endoscopy showed no significant findings. An initial frozen biopsy of the oral lesions showed invasive fungal infection, concerning for mucormycosis. Debridement samples showed no evidence of invasive fungal elements. The patient was diagnosed with neutropenic fever and thus started on broad-spectrum antibiotic therapy. Despite this, the pancytopenia and the stomatitis continued to worsen. Blood and oral mucosa cultures were negative. The viral PCR panel revealed the presence of HSV-1 DNA in the oral mucosa. Bone marrow biopsy was hypoplastic with less than 5% cellularity, and normal molecular and cytogenetic profiles. Given all of the objective data, this case was consistent with aplastic anemia secondary to HSV-1 infection. The patient was placed on IV acyclovir, resulting in rapid symptomatic improvement and ultimate recovery of all cell lines. IMPACT/DISCUSSION: Aplastic anemia (AA) is a disease characterized by the destruction of hematopoietic stem cells (HSC), which is induced by oligoclonal expansion of T-cells, resulting in peripheral pancytopenia. Most cases are idiopathic. Other commonly identified etiologies include medication or drug exposure, immunologic disorders, and pregnancy. Viral infections are also associated with AA, although evidence is limited to case reports and case series of HIV, seronegative hepatitis, Parvovirus B19, and Epstein Bar Virus. No reported cases of HSV-1 associated AA have been demonstrated in current medical literature. Although the bone biopsy was negative for HSV-1, it is likely that the mechanism behind virus-induced AA is the induction of autoimmune response and not the result of direct invasion of HSC. The case is also significant for the unusual presentation of herpes stomatitis. Instead of presenting with the typical vesicles and mucosal ulcers, the patient presented with necrotic-appearing plaques. CONCLUSION: Most cases of AA are idiopathic. However, viral etiology should be excluded, since they can respond to treatment The absence of viral presence in the BM does not rule out a viral etiology, since the underlying mechanism is likely immune-mediated. Common etiologies of stomatitis should always be ruled out, even in the presence of atypical features.

Volume

37

Issue

Suppl 2

First Page

S462

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