Related Experiment Videos
TRH-immunoreactivity in chronic pancreatitis.
L Duntas1, B Glasbrenner, C Wolf
1Department of Internal Medicine I and II, University of Ulm, Germany.
Hepato-Gastroenterology
|October 1, 1992
Summary
Chronic pancreatitis (CP) significantly lowers circulating thyrotropin-releasing hormone (TRH) immunoreactivity (IR). Severe exocrine pancreatic insufficiency (SEI) results in very low TRH-IR, suggesting the pancreas influences TRH release.
Area of Science:
- Endocrinology
- Gastroenterology
- Pancreatic Physiology
Background:
- Thyrotropin-releasing hormone (TRH) is found in the pancreas.
- Chronic pancreatitis (CP) can lead to exocrine pancreatic insufficiency (EPI).
Purpose of the Study:
- To investigate circulating TRH-immunoreactivity (IR) levels in patients with CP and varying degrees of EPI.
- To examine the impact of glucose on peripheral TRH-IR in healthy individuals and patients with severe EPI.
Main Methods:
- Measured basal TRH-IR plasma levels in 27 CP patients and 23 healthy controls.
- Assessed TRH-IR response to oral glucose (100g) in 5 healthy controls and 5 patients with SEI.
Main Results:
- Basal TRH-IR was significantly lower in CP patients (20.8 ± 7 fmol/ml) compared to controls (38 ± 14 fmol/ml).
- Patients with SEI had significantly lower TRH-IR (15.8 ± 3 fmol/ml) than those with normal pancreatic function (28.1 ± 8 fmol/ml).
- Healthy controls showed a significant TRH-IR increase post-glucose, while patients with SEI did not.
Conclusions:
- Circulating TRH-IR appears to be primarily of pancreatic origin.
- Severe exocrine pancreatic insufficiency is associated with markedly reduced peripheral TRH-IR.
- CP demonstrably affects TRH release, particularly in cases of severe EPI.