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[Functional condition of the stomach, pancreas, liver and gallbladder in celiac disease]
Insights
Celiac disease (CD) significantly impacts digestive organs, causing stomach issues, pancreatic enzyme decline, and gallbladder dysfunction. These contribute to malabsorption and other CD symptoms.
Area of Science:
- Gastroenterology
- Pediatric Gastroenterology
- Digestive System Physiology
Background:
- Celiac disease (CD) is an autoimmune disorder triggered by gluten ingestion.
- Understanding gastrointestinal manifestations beyond the small intestine is crucial for comprehensive CD management.
Purpose of the Study:
- To investigate the condition of the stomach, gallbladder, pancreas, and liver in celiac disease patients.
- To determine the contribution of dysfunction in these organs to the clinical presentation of CD symptoms.
Main Methods:
- Studied 215 celiac disease patients and 25 healthy controls.
- Assessed gastric acid secretion, gastrin levels, pancreatic enzyme activity (trypsin, amylase, lipase), and bile acid composition.
- Utilized duodenal intubation, biochemical assays, liver biopsy, and histological examination.
Main Results:
- Celiac disease patients exhibited high gastric acid secretion and gastrin levels, with lymphocytic gastritis.
- Pancreatic enzyme secretion was inert, and gallbladder function showed hypokinesia or atony.
- Liver pathology included hypertransaminasemia and steatohepatitis.
Conclusions:
- Gastric changes in new-onset CD may promote ulcer formation.
- Impaired pancreatic exocrine function, gallbladder hypokinesia, and liver dysfunction contribute to significant maldigestion and malabsorption in CD patients.
Aim:
To study condition of the stomach, gall-bladder, pancreas, liver in celiac disease (CD) and contribution of their dysfunction to clinical presentation of CD symptoms.
Material And Methods:
A total of 215 CD patients entered the study (191 females and 24 males) aged under 20 years (n=100), 20 to 50 (n=74) and over 50 years (n=41). The control group consisted of 25 healthy volunteers. Acid-forming function of the stomach, blood serum gastrin level were studied. Bile for biochemical test was obtained at duodenal intubation using 40 ml of 40% glucose solution or 25% magnesium solution as food stimulators, and intravenous injection of cholecystokininpancreosimin. Cholic acid was assayed in bile portions B and C. Two-channel probe was used to obtain duodenal content before meal and after intravenous injection of pancreosimin for tripsin, amylase and lipase assay. Clinical and biochemical blood tests were made as well as puncture biopsy of the liver with histological study of biopsy material.
Results:
CD patients were found to have high basal and stimulated acid-forming function, high gastrin concentration in the blood. The morphological examination detected lymphocytic gastritis. There were an inert type of pancreatic enzyme secretion, gall-bladder hypokinesia or atony. Gall-bladder contracted only after intravenous injection of cholecystokinin. Changes in the liver were characterized by hypertransaminasemia, steatohepatitis.
Conclusion:
Changes in the stomach in patients with new-onset CD promote formation of ulcer. Decline in excretory pancreatic function, slow enzyme secretion, marked hypokinesia of the gall-bladder, hyperenzymemia and steatohepatitis as manifestations of hepatic pathology result in dramatic disorder of digestion and absorption of food substances.
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