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Spontaneous bacterial peritonitis in children with chronic liver disease: clinical features and etiologic factors
Insights
Children with chronic liver disease and ascites are at risk for spontaneous bacterial peritonitis (SBP). Complement deficiencies, particularly low C3 and C4, may predispose these children to SBP, indicating a potential link in disease development.
Area of Science:
- Pediatric Gastroenterology
- Immunology
- Infectious Diseases
Background:
- Spontaneous bacterial peritonitis (SBP) is a serious complication in children with chronic liver disease and ascites.
- Understanding the factors contributing to SBP pathogenesis in this vulnerable population is crucial for improving outcomes.
Purpose of the Study:
- To investigate the clinical and bacteriologic features of SBP in children with chronic liver disease.
- To explore the role of complement system deficiencies in the development of SBP in pediatric patients.
Main Methods:
- Analysis of clinical data and ascitic fluid cultures from 12 episodes of SBP in 11 children with cirrhosis and ascites.
- Assessment of complement component levels (C3, C4) and opsonization capacity in patients with and without SBP.
Main Results:
- Streptococcus pneumoniae was the most common pathogen identified in SBP episodes.
- Children with SBP frequently exhibited defective yeast opsonization and reduced C3/C4 levels prior to SBP onset.
- Complement component levels were significantly lower in SBP patients compared to cirrhotic children without SBP.
Conclusions:
- The clinical presentation of SBP in children mirrors that seen in adults.
- Complement deficiency, potentially induced by chronic liver disease, appears to be a significant factor in the pathogenesis of SBP in children.
- Early identification and management of complement abnormalities may be important in preventing SBP in at-risk pediatric patients.
Abstract:
We analyzed the clinical and bacteriologic features of 12 episodes of spontaneous bacterial peritonitis (SBP) in 11 children (four boys, median age 5.5 years) with chronic liver disease. All patients had cirrhosis and ascites; four had hypersplenism, and one was asplenic. Symptoms included increasing abdominal distention, pyrexia, abdominal pain, gastrointestinal disturbance, and encephalopathy. Nine had rebound tenderness on abdominal palpation, and 12 had reduced bowel sounds. The most frequent organisms isolated from culture of ascitic fluid were Streptococcus pneumoniae (nine). Klebsiella (two), and Haemophilus influenzae (one); blood cultures grew identical organisms in nine. Seven patients died despite intensive antibiotic therapy. In the 3 months prior to onset of SBP, defective yeast opsonization and reduced serum concentration of C4 were found in all nine children tested; eight had reduced concentration of C3. Functional deficiency of all complement components was present in four tested within 1 to 5 months of the onset. In contrast, only eight of 59 cirrhotic children without SBP had low C3, and eight had defective yeast opsonization, although 35 had low C4 values. Four of the patients with SBP and low C3 and C4 concentrations had normal concentrations at the time of diagnosis of liver disease 2 to 5 years previously. Opsonization of type III pneumococci was reduced in sera from three patients who subsequently developed pneumococcal peritonitis. The incidence of SBP in children with chronic liver disease is similar to that in adults, as are the clinical features. Our observations suggest that complement deficiency induced by chronic liver disease may be important in the pathogenesis of SBP.