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Hyperprolactinemia and the Multiple Endocrine Adenomatosis Type 1 (MEA-1) Syndrome

Jon H. Levine, MD; Julius Sagel, MB, ChB; George L. Rosebrock Jr, MD; Jorge Gonzalez, MD
Arch Intern Med. 1978;138(12):1777-1778. doi:10.1001/archinte.1978.03630370007006.
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The multiple endocrine adenomatosis, type 1 (MEA-1) syndrome, first described 75 years ago, includes the simultaneous or sequential occurrence of tumors of the parathyroid, pancreas, and pituitary glands. More recently the familial nature of the syndrome with the typical autosomal dominant pattern of inheritance has been recognized.1 Most of the pituitary tumors in this syndrome have been considered to be of the nonfunctioning chromophobe variety. Occasional reports of functioning pituitary tumors causing acromegaly or hypercortisolism as part of the MEA-1 syndrome have appeared, but in the latter cases proof of involvement of the pituitary gland has been inferential.

Within the last decade, four major advances have increased the clinician's awareness of the frequency of prolactin-secreting pituitary tumors. First, reliable radioimmunoassays for prolactin measurements are now readily available. Second, increased sensitivity in detecting microadenomas has been achieved with introduction of polytomography. In addition, revival and refinement of the transseptal transsphenoidal


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