Related Experiment Videos
[The vaso-active intestinal polypeptide in Verner-Morrison syndrome]
Deutsche Medizinische Wochenschrift (1946)
|February 28, 1975
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.
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.
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.