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Hyperacidity and hypergastrinemia following extensive intestinal resection.

W C Meyers, R S Jones

    World Journal of Surgery
    |September 20, 1979
    PubMed
    Summary

    Extensive intestinal resection leads to increased stomach acid and gastrin levels in humans and animals. This hormonal imbalance, including changes in insulin and glucagon, is a key factor in short gut syndrome.

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    Area of Science:

    • Gastroenterology
    • Endocrinology
    • Physiology

    Background:

    • Extensive intestinal resection is known to cause increased gastric acid secretion.
    • Hypergastrinemia and hyperacidity are observed in short gut syndrome patients and animal models.
    • Hormonal dysregulation is a significant consequence of major intestinal resection.

    Purpose of the Study:

    • To investigate the hormonal changes following extensive intestinal resection.
    • To understand the mechanisms behind postresectional hypergastrinemia.
    • To identify associated alterations in other gastrointestinal hormones.

    Main Methods:

    • Review of existing literature on intestinal resection and hormonal responses.
    • Analysis of data from human and animal studies (dog, rat, monkey).
    • Observation of gastric acid secretion and gastrin levels post-resection.

    Main Results:

    • Gastric acid secretion significantly increases after extensive intestinal resection.
    • Hypergastrinemia is consistently observed post-resection, linked to increased gastrin release and/or decreased degradation.
    • Other hormonal changes include elevated insulin, GIP, and pancreatic glucagon, with decreased enteroglucagon.

    Conclusions:

    • Postresectional hypergastrinemia is a key hormonal consequence of extensive intestinal resection.
    • The hormonal milieu is significantly altered after major intestinal resection, impacting gastrointestinal function.
    • Understanding these hormonal shifts is crucial for managing short gut syndrome.

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