This site is intended for healthcare professionals

Go to /sign-in page

You can view 5 more pages without signing in

MEN-I

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

Authoring team

The type I form of multiple endocrine neoplasia typically affects the:

  • parathyroid gland
  • pancreatic islets
  • anterior pituitary gland

The gene for MEN-I has been mapped to chromosome 11q13.

Parathyroid tumours occur in over 90% of cases resulting in hypercalcaemia and sometimes, clinical hyperparathyroidism.

Multiple tumours of the endocrine pancreas are present in up to 75% of cases. Gastrinoma leading to the Zollinger - Ellison syndrome is the largest single cause of morbidity and mortality in MEN - I. Other tumours include insulinoma, and rarely, vipoma and glucagonoma.

Anterior pituitary gland tumours are present in about 50% of cases. Most secrete either prolactin, growth hormone or adrenocorticotrophin with associated symptoms of amenorrhoea or galactorrhoea, acromegaly or Cushing's syndrome respectively. Others are clinically non-functional and produce symptoms of pituitary hypofunction or visual field loss.

Occasionally, carcinoid tumours and tumours of the adrenal cortex may occur.

Often, only one major lesion is evident clinically but other asymptomatic tumours are present and discovered when investigated directly. The high occurrence of parathyroid tumours and hypercalcaemia make serum calcium a useful indicator of MEN-I in suspected individuals.


Create an account to add page annotations

Annotations allow you to add information to this page that would be handy to have on hand during a consultation. E.g. a website or number. This information will always show when you visit this page.

The content herein is provided for informational purposes and does not replace the need to apply professional clinical judgement when diagnosing or treating any medical condition. A licensed medical practitioner should be consulted for diagnosis and treatment of any and all medical conditions.

Connect

Copyright 2024 Oxbridge Solutions Limited, a subsidiary of OmniaMed Communications Limited. All rights reserved. Any distribution or duplication of the information contained herein is strictly prohibited. Oxbridge Solutions receives funding from advertising but maintains editorial independence.