Abstract

<h3>Introduction</h3> While severe manifestations of congenital Cytomegalovirus (CMV) transmission are widely investigated, little is known about postnatal CMV (pCMV) infection. Although pCMV infection in term healthy infant is mostly asymptomatic, serious gastrointestinal symptoms (vomiting, diarrhea, abdominal distension, hepatosplenomegaly, blood stools) are described in literature. We describe two cases of infant hematemesis, focusing on the challenging differential diagnosis between pCMV gastritis and non IgE-mediated Cow’s Milk Protein Allergy (CMPA) enteropathy. Case 1: a 3-month-old female infant presented with growth impairment, hematemesis and melena. Blood and stool analysis (bacterial, viral and parasites panels) resulted normal. Cow’s milk specific-IgE were negative. Viral serologies revealed recent CMV infection with positive CMV-DNA Polimerase Chain Reaction (PCR) on urine and blood samples. Congenital CMV infection was ruled out through negative CMV-DNA PCR on the first day of life saliva sample. Esophagogastroduodenoscopy (EGD) revealed petechial elements in antral and duodenal-bulb mucosa; at biopsies normal eosinophils count and negative morphological research of Helicobacter pylori (HP) were found. Intranuclear CMV inclusion bodies were not detected and CMV immunostaining was negative. Case 2: a 2-month-old male infant presented with dehydration, bloody diarrhoea, vomiting and feeding refusal. Blood analysis revealed severe hypoalbuminemia, anaemia and hypertransaminasemia. Stool examinations (bacterial, viral and parasites panels) and Mycobacterium Tuberculosis screening were negative. Allergological and immunological investigations resulted normal. CMV-DNA PCR on urine, blood and maternal milk samples were positive. CMV-DNA PCR on Guthrie card was negative. EGD and rettosigmoidoscopy revealed exudative active inflammation in duodenal mucosa. HP research was negative while CMV immunostaining visualized duodenal cells viral inclusions. <h3>Discussion</h3> Paediatric hematemesis is mainly caused by foreign bodies ingestion, CMPA, infectious gastritis (Helicobacter pylori, CMV, parasites), drug-induced gastritis (steroids and FANS) and eosinophilic gastropathy. In our cases the differential diagnosis focused on pCMV infection and non IgE-mediated CMPA. Both infants had a partial clinical improvement after starting a cow’s milk protein free diet. However, due to the concomitant pCMV infection and the absence of cow’s milk specific-IgE, a definitive diagnosis could not be established. In conclusion, paediatric hematemesis differential diagnosis turns out particularly challenging when considering non IgE-mediated CMPA and pCMV gastropathy. In fact, neither the absence of cow’s milk specific-IgE

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