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Related Experiment Videos

Do indole markers predict carcinoid heart disease?

R R Arora, R R Warner

    Chest
    |July 1, 1986
    PubMed
    Summary

    Carcinoid syndrome patients show decreased tryptophan and elevated serotonin and 5HIAA, but cardiac involvement does not alter these indole markers, unlike in animal models.

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    Area of Science:

    • Biochemistry
    • Oncology
    • Cardiology

    Background:

    • Carcinoid syndrome is linked to cardiac lesions in guinea pig models.
    • Tryptophan deficiency and elevated serotonin are implicated in these experimental cardiac issues.
    • Human carcinoid disease requires investigation into indole marker differences with cardiac involvement.

    Purpose of the Study:

    • To compare indole markers in human carcinoid syndrome patients with and without cardiac involvement.
    • To assess plasma tryptophan, serum serotonin, and urinary 5-hydroxyindoleacetic acid levels.
    • To determine if findings in animal models translate to human carcinoid disease.

    Main Methods:

    • Measured plasma tryptophan (T), serum serotonin (5HT), and urinary 5-hydroxyindoleacetic acid (5HIAA).
    • Studied 18 carcinoid syndrome patients (7 with valvular involvement, 11 without) and 24 normal individuals.
    • Utilized clinical, roentgenographic, and echocardiographic techniques for cardiac assessment.

    Main Results:

    • No significant difference in serum tryptophan, serum serotonin, or urinary 5HIAA levels between carcinoid patients with or without cardiac involvement (p > 0.05).
    • Confirmed decreased serum tryptophan (a substrate) in carcinoid syndrome patients.
    • Confirmed elevated serum serotonin and urinary 5HIAA (metabolites) in carcinoid syndrome patients.

    Conclusions:

    • Unlike animal models, cardiac involvement in human carcinoid syndrome does not correlate with altered indole marker levels.
    • Confirms the characteristic biochemical profile of carcinoid syndrome: reduced tryptophan and increased serotonin/5HIAA.
    • Suggests distinct pathophysiological mechanisms for cardiac lesions in human carcinoid disease compared to experimental models.

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