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Published on: December 15, 2011
Protein-losing enteropathy in an infant with severe atopic dermatitis
Yuji Fujita1, Kohei Nomura2, Shigemi Yoshihara2
1Department of Pediatrics, Dokkyo Medical University, Shimotsuga, Tochigi, Japan fujitay@dokkyomed.ac.jp.
Insights
Severe atopic dermatitis (AD) can cause protein-losing enteropathy (PLE). This case highlights the importance of considering PLE in infants with severe AD and low protein levels, even after eczema treatment.
Area of Science:
- Pediatric Dermatology
- Gastroenterology
- Clinical Case Study
Background:
- Severe atopic dermatitis (AD) is a chronic inflammatory skin condition.
- Hypoproteinaemia is a potential complication of severe AD.
- Protein-losing enteropathy (PLE) is characterized by excessive protein loss through the gastrointestinal tract.
Observation:
- A 7-month-old infant with severe AD, untreated with topical corticosteroids due to familial steroid phobia.
- Infant presented with decreased feeding, diarrhea, reduced urine output, and vomiting.
- Despite initial improvement of eczema with topical corticosteroids, persistent hypoproteinaemia, oliguria, and worsening edema were noted.
Findings:
- Serum albumin scintigraphy confirmed protein-losing enteropathy (PLE) in the distal duodenum.
- Treatment with systemic prednisolone and albumin resolved PLE symptoms and prevented relapse.
- This case represents one of the few reported instances of PLE associated with AD in infancy.
Implications:
- PLE should be considered in the differential diagnosis of infants presenting with severe atopic dermatitis and persistent hypoproteinaemia.
- Early recognition and management of PLE are crucial in pediatric patients with severe AD.
- This case underscores the complex interplay between severe skin inflammation and gastrointestinal dysfunction in infants.
Abstract:
Severe atopic dermatitis (AD) may lead to various complications such as hypoproteinaemia. We describe the case of a 7-month-old male infant with severe AD complicated with protein-losing enteropathy (PLE). He was diagnosed with AD at 2 months of age; however, because of familial steroid phobia, topical corticosteroids were not administered. At 7 months of age, he was admitted to our hospital for decreased feeding, diarrhoea, reduced urine volume and recurrent vomiting. Class 3 topical corticosteroid treatment was initiated. On day 3, eczema had almost resolved. However, serum protein levels had not improved; oliguria persisted and oedema worsened. Serum albumin scintigraphy revealed radioisotopes in the distal duodenum, leading to PLE diagnosis. Systemic prednisolone and albumin were administered, with no PLE relapse after discontinuation. To our knowledge, only two infant PLE cases associated with AD were reported to date. PLE should be considered in patients with severe AD and persistent hypoproteinaemia.
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