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Assays for the Specific Growth Rate and Cell-binding Ability of Rotavirus
Published on: January 28, 2019
Protein-losing enteropathy in an infant with rotavirus infection
Adriana Parisi1, Alessandro Cafarotti1, Roberta Salvatore1
1a Department of Paediatrics , University of Chieti , Chieti , Italy.
Insights
Rotavirus infection can cause protein-losing enteropathy (PLE) in infants, a rare gastrointestinal condition. Prompt diagnosis and supportive care, including albumin infusions if needed, are crucial for recovery.
Area of Science:
- Gastroenterology
- Pediatrics
- Infectious Diseases
Background:
- Protein-losing enteropathy (PLE) is a rare condition characterized by excessive protein loss through the intestines, leading to hypoproteinemia and edema.
- While rotavirus is a common cause of gastroenteritis in children, its association with PLE is infrequently reported.
Observation:
- A 6-month-old infant presented with diarrhea, fever, generalized edema, and laboratory findings consistent with PLE, including low serum proteins and albumin.
- Diagnostic tests confirmed PLE and identified rotavirus antigen in stool using a rapid immunochromatographic test.
- Abdominal ultrasound revealed bowel distension and thickening, with ascites, while echocardiography ruled out pericardial effusion.
Findings:
- The case highlights a rare presentation of rotavirus infection causing symptomatic protein-losing enteropathy in an infant.
- The patient required albumin infusions to maintain normal serum albumin levels.
- Recovery was observed over two weeks with supportive care, including gradual normalization of stools and reduction of edema.
Implications:
- Rotavirus should be considered in the differential diagnosis of acute, symptomatic PLE in children.
- Rapid diagnostic tests for rotavirus facilitate timely diagnosis.
- While supportive care is often sufficient, albumin infusions may be necessary for severe cases of rotavirus-induced PLE.
Abstract:
Protein-losing enteropathy (PLE) is a rare gastro-intestinal complication characterised by intestinal loss of proteins with consequent hypoproteinaemia and generalised oedema. Rotavirus infection associated with PLE in children has rarely been reported. A 6-month-old girl presented with diarrhoea, fever and generalised oedema. Total serum proteins were 34 g/L (61-79) and plasma albumin 16.8 g/L (40-50), serum sodium was 126 mmol/L and there was mild metabolic alkalosis (pH 7.46). Stool for alpha-1 antitrypsin was >1.2 mg/g (<0.6) which supported the diagnosis of PLE. Stool examination demonstrated the presence of rotavirus antigen by the rapid immunochromatographic test. Abdominal ultrasound showed bowel distension and intestinal wall thickening with a small amount of ascites. Echocardiography excluded pericardial effusion. Two albumin infusions (1 g/kg) were required to sustain normal serum albumin levels. Over the next 2 weeks, there was gradual normalisation of stools and progressive reduction of oedema. In children with acute and symptomatic PLE, rotavirus should be considered in the differential diagnosis. The availability of the rapid immunochromatographic test facilitates the diagnosis. In most cases, supportive care alone is sufficient, but albumin infusions may be required in more severely affected children.
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