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Acquired angioedema and Helicobacter pylori infection in a child
Jana Varvarovska1, Josef Sykora, Frantisek Stozicky
1Department of Paediatrics, Charles University Hospital, Alej Svobody 80, 304 60 Pilsen, Czech Republic. varvarovska@fnplzen.cz
Insights
Helicobacter pylori infection can cause angioedema in children, a rare condition. Eradicating H. pylori led to remission of angioedema and restored complement function in a pediatric case.
Area of Science:
- Pediatric Gastroenterology
- Immunology
- Infectious Diseases
Background:
- Angioedema is a rare but serious condition characterized by swelling.
- Helicobacter pylori (H. pylori) infection is common in children but rarely associated with angioedema.
Observation:
- A 10-year-old boy presented with generalized angioedema and circulatory shock.
- The patient exhibited severe fluid and protein loss, hemoconcentration, and complement system failure.
- All common causes of angioedema were excluded, implicating H. pylori infection.
Findings:
- Serological and histological evidence confirmed H. pylori infection.
- Eradication therapy successfully cleared the H. pylori infection.
- Following treatment, the patient achieved complete remission of angioedema and restoration of complement function.
Implications:
- This case highlights H. pylori infection as a potential cause of angioedema in children.
- Early consideration of H. pylori in pediatric angioedema cases may improve diagnosis and treatment.
- Further research is warranted to understand the mechanism linking H. pylori and angioedema.
Unlabelled:
We describe a 10-year-old boy with acquired Helicobacter pylori infection and simultaneous angioedema which is a rare but life-threatening condition. Our patient was hospitalised with generalised angioedema and severe circulatory shock due to extreme loss of fluids and proteins into interstitial tissues (weight gain 10 kg within 2 days, extreme haemoconcentration--haemoglobin 206 g/l, haematocrit 0.570, leucocytosis 18,300 /microl, high lactate 13.8 mmol/l) and simultaneous failure of the complement system (C3 <0.16 g/l, C4 <0.13 g/l, CH50 45 U/ml, i.e. 50% of normal value, C1 inhibitor 0.21 g/l at the lower limit). All possible known causes of angioedema were excluded (infection, allergy, auto-immune disease, NSAIDs, lymphoproliferative disease) except for the simultaneous H. pylori infection which was proven serologically and histologically. Eradication therapy led to a complete remission of the H. pylori infection. An absence of angioedema and the restoration of the complement system was later observed. To the best of our knowledge, no similar case report of a child has yet been published.
Conclusion:
Helicobacter pylori infection should be considered in the development of angioedema in childhood.