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Sulphated lithocholic acid conjugates in serum from children with hepatic and intestinal diseases
Insights
Elevated serum sulphated lithocholic acid conjugates (SGLC) in children can indicate cholestasis or intestinal influx. These conjugates may contribute to cholestatic liver disease.
Area of Science:
- Pediatric Gastroenterology
- Hepatology
- Clinical Chemistry
Background:
- Sulphated lithocholic acid conjugates (SGLC) are bile acids with potential roles in liver disease.
- Understanding SGLC levels in pediatric hepatic and intestinal disorders is crucial for diagnosis and management.
Purpose of the Study:
- To investigate the significance of serum SGLC concentrations in children with various gastrointestinal and liver conditions.
- To differentiate between cholestasis and other causes of elevated SGLC.
Main Methods:
- Serum SGLC and glycocholic acid (GC) levels were measured in 268 children.
- Patients were grouped based on SGLC concentrations and the ratio of SGLC to GC.
- Postprandial changes in SGLC (delta SGLC) were analyzed.
Main Results:
- Two groups were identified: low SGLC (≤1.2 mumol/l) and high SGLC (>1.2 mumol/l).
- High SGLC with a low SGLC/GC ratio was associated with cholestasis.
- A significant postprandial increase in SGLC was observed in 81% of patients with high SGLC and a high SGLC/GC ratio, suggesting intestinal influx.
Conclusions:
- Elevated serum SGLC in children can be caused by cholestasis or intestinal influx.
- The hepatotoxic nature of SGLC suggests a role in the pathogenesis of cholestatic liver disease.
- Cholestyramine may mitigate postprandial SGLC increases, potentially by reducing intestinal absorption.
Abstract:
Sulphated lithocholic acid conjugates (SGLC) were measured in the sera of 268 children with various hepatic and intestinal disorders. Two groups were distinguished: (I) SGLC concentration less than or equal to 1.2 mumol/l, n = 198, and (II) SGLC concentration greater than 1.2 mumol/l, n = 70. In 28 patients of the latter group the SGLC concentration was less than 25% of the concentration of glycocholic acid (GC) in the same serum sample. This group (IIA) consisted predominantly of patients with cholestasis, as characterized by high serum bile acid levels and deviating liver function tests. The rest of the group (IIB), with SGLC levels exceeding 25% of the GC concentration and relatively low serum bile acid concentrations, showed no clear cholestatic symptoms. A postprandial increase in serum SGLC (delta SGLC) greater than 1.0 mumol/l was found in only 1 of 32 patients of group I (3%), in 1 of 6 patients of group IIA (17%), but in 9 of 11 patients of group IIB (81%). delta SGLC did not correlate with delta GC in the same test, which indicated that a general hepatic bile acid clearance defect was not responsible. In two patients with intermittent cholestasis, the distinct postprandial rise in serum SGLC that was always found during anicteric periods could be prevented by adding cholestyramine to the test meal. We conclude that elevated serum concentrations of SGLC develop during the course of cholestasis but may also be caused by influx of this bile acid from the intestine. Because of its hepatotoxic properties, SGLC may be involved in the initiation or perpetuation of specific cholestatic phenomena.