valganciclovir and Esophagitis

Genetic aberrations in the toll-like receptor (TLR)3 pathway are associated with increased susceptibility to herpes simplex virus (HSV) infections. Leucine-rich repeat and PYD-containing protein (NLRP)12 is a component of the inflammasome apparatus, which is critical to an immediate innate inflammatory response. Aberrations in NLRP12 have been shown to mediate auto-inflammation. In this study, we present a 44-year old patient with severe HSV esophagitis and Crohn's disease. An immune and genetic investigation confirmed two coinciding genetic mutations in TLR3 and NLRP12. Our findings support conducting laboratory workup that targets TLR3 pathway in the immunocompetent host developing recurrent HSV infections.

Topics: Acyclovir; Adult; Antibodies, Monoclonal, Humanized; Antiviral Agents; Crohn Disease; Esophagitis; Female; Gastrointestinal Agents; Herpes Simplex; Humans; Intracellular Signaling Peptides and Proteins; Mutation; Signal Transduction; Toll-Like Receptor 3; Valganciclovir; Whole Genome Sequencing

Topics: Antiviral Agents; Convalescence; Cytomegalovirus; Cytomegalovirus Infections; Endoscopy, Digestive System; Esophagitis; Female; Gastroesophageal Reflux; Humans; Immunocompromised Host; Kidney; Kidney Transplantation; Middle Aged; Renal Insufficiency, Chronic; Valganciclovir

A 64-year-old man with a 2-week history of fatigue and fever presented to the medical admissions unit. He had a background of lymphoplasmacytic lymphoma and had recently completed a course of fludarabine-based chemotherapy. CT of the abdomen demonstrated an increase in spleen size and it was thought that his fevers were most likely due to disease recurrence or high-grade transformation. A bone marrow trephine was organised, which showed no evidence of lymphoma and positron emission tomography-CT demonstrated an area of increased avidity at the gastro-oesophageal junction. An oesophagogastroduodenoscopy was recommended, which revealed ulceration within the oesophagus and stomach. Biopsy of the lesions and immunohistochemistry confirmed a diagnosis of cytomegalovirus oesophagitis. He was treated with intravenous ganciclovir followed by oral valganciclovir for a total of 3 weeks. His fever resolved and he was discharged home approximately 8 weeks after he first presented.

Topics: Antineoplastic Agents; Antiviral Agents; Biopsy; Cytomegalovirus Infections; Diagnosis, Differential; Endoscopy, Digestive System; Esophagitis; Ganciclovir; Humans; Immunocompromised Host; Male; Middle Aged; Positron-Emission Tomography; Tomography, X-Ray Computed; Valganciclovir; Vidarabine; Waldenstrom Macroglobulinemia