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Related Experiment Videos

[The vaso-active intestinal polypeptide in Verner-Morrison syndrome].

F J Seif, P Sadowski, F Heni

    Deutsche Medizinische Wochenschrift (1946)
    |February 28, 1975
    PubMed
    Summary

    A non-B-cell pancreatic tumor caused Verner-Morrison syndrome by releasing vasoactive intestinal polypeptide (VIP). Surgical removal normalized VIP levels, resolving severe watery diarrhea, with glucocorticoids offering additional relief.

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    Area of Science:

    • Endocrinology
    • Gastroenterology
    • Oncology

    Background:

    • Verner-Morrison syndrome, characterized by refractory watery diarrhea and hypokalemia, is often associated with pancreatic islet-cell tumors.
    • Non-B-cell islet-cell carcinomas can secrete hormones, leading to distinct clinical manifestations.

    Observation:

    • A 40-year-old male presented with Verner-Morrison syndrome due to a non-B-cell islet-cell carcinoma with liver and mesenteric lymph node metastases.
    • Tumor tissue and plasma exhibited high concentrations of vasoactive intestinal polypeptide (VIP).

    Findings:

    • Radioimmunological tests confirmed elevated VIP levels in both tumor tissue and patient plasma.
    • Immunohistochemistry revealed exclusive high fluorescence for VIP in the tumor cells.
    • Post-surgical tumor removal led to a normalization of plasma VIP concentrations.

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    Implications:

    • Vasoactive intestinal polypeptide (VIP) is strongly implicated as the causative agent for the severe watery diarrhea in this Verner-Morrison syndrome case.
    • Surgical resection of the VIP-secreting tumor effectively managed the syndrome, highlighting the importance of identifying the hormonal source.
    • Glucocorticoid administration provided symptomatic relief for the severe watery diarrhea, suggesting a potential adjunctive treatment strategy.