Prolactin-Producing Pituitary Adenoma Associated with Prolactin Cell Hyperplasia

2002 ◽  
Vol 13 (2) ◽  
pp. 157-166 ◽  
Author(s):  
Sergio Vidal ◽  
Eva Horvath ◽  
Luis V Syro ◽  
Humberto Uribe ◽  
Sandy Cohen ◽  
...  
Author(s):  
Eva Horvath ◽  
Kalman Kovacs ◽  
B. W. Scheithauer ◽  
R. V. Lloyd ◽  
H. S. Smyth

The association of a pituitary adenoma with nervous tissue consisting of neuron-like cells and neuropil is a rare abnormality. In the majority of cases, the pituitary tumor is a chromophobic adenoma, accompanied by acromegaly. Histology reveals widely variable proportions of endocrine and nervous tissue in alternating or intermingled patterns. The lesion is perceived as a composite one consisting of two histogenetically distinct parts. It has been suggested that the neuronal component, morphologically similar to secretory neurons of the hypothalamus, may initiate adenoma formation by releasing stimulatory substances. Immunoreactivity for growth hormone releasing hormone (GRH) in the neuronal component of some cases supported this view, whereas other findings such as consistent lack of growth hormone (GH) cell hyperplasia in the lesions called for alternative explanation.Fifteen tumors consisting of a pituitary adenoma and a neuronal component have been collected over a 20 yr. period. Acromegaly was present in 11 patients, was equivocal in one, and absent in 3.


1980 ◽  
Vol 94 (3) ◽  
pp. 297-303 ◽  
Author(s):  
Adrian M. Schnall ◽  
Kalman Kovacs ◽  
Jerald S. Brodkey ◽  
Olof H. Pearson

Abstract. Recent reports of patients with Cushing's disease who have been explored via the transsphenoidal route indicate that the great majority has pituitary adenomas. We report a patient with biochemically documented pituitary-based hypercortisolism who had a clinical and biochemical remission following hypophysectomy. Serial sections of the pituitary tissue removed showed hyperplasia of corticotroph cells but no adenoma. Hypophysectomy was complete as documented by serum levels of FSH, LH, TSH, prolactin, hGH and ACTH at the lower limits of the respective assays, with no response to appropriate stimuli. This case demonstrates that a minority of patients with Cushing's disease has corticotroph cell hyperplasia without a pituitary adenoma.


1991 ◽  
Vol 2 (4) ◽  
pp. 230-234 ◽  
Author(s):  
Shigeru Furuhata ◽  
Toru Kameya ◽  
Mitsuhiro Otani ◽  
Yoshinori Shimamoto ◽  
Hideo Asada ◽  
...  

1988 ◽  
Vol 29 (3) ◽  
pp. 218-226 ◽  
Author(s):  
Erik P. Pioro ◽  
Bernd W. Scheithauer ◽  
Edward R. Laws ◽  
Raymond V. Randall ◽  
Kalman T. Kovacs ◽  
...  

1982 ◽  
Vol 101 (1) ◽  
pp. 15-24 ◽  
Author(s):  
Mark E. Peterson ◽  
Dorothy T. Krieger ◽  
William D. Drucker ◽  
Nicholas S. Halmi

Abstract. Pituitary adenomas were found in 21 (84%) of 25 dogs with spontaneous pituitary-dependent hyperadrenocorticism. Six dogs had pars intermedia adenomas, whereas 15 had tumours of the pars distalis. Diffuse corticotroph cell hyperplasia was found in 1 of the 4 pituitaries without adenoma; in 2 dogs with pituitary adenoma, coexisting hyperplasia of the surrounding corticotrophs was also present. Immunocytochemical staining of the pituitaries revealed positive staining for ACTH, β-lipotrophin, and β-endorphin in the majority of both pars distalis and pars intermedia adenomas. The most frequent and intense staining was found with anti-β-endorphin. In most part intermedia tumours, many cells stained strongly for α-MSH; double immunostaining of one pars intermedia adenoma for ACTH and α-MSH showed that some tumour cells stained only for ACTH or α-MSH whereas others contained both peptides. Only occasional cells stained for α-MSH in pars distalis adenomas.


1992 ◽  
Vol 3 (4) ◽  
pp. 201-204 ◽  
Author(s):  
Shigeru Furuhata ◽  
Toru Kameya ◽  
Tomoko Tsuruta ◽  
Heiji Naritaka ◽  
Mitsuhiro Otani ◽  
...  

Author(s):  
Michael W. McDermott ◽  
Donald E. Griesdale ◽  
Kenneth Berry ◽  
G. Edward Wilkins

ABSTRACT:Lymphocytic adenohypophysitis (LAH) is an uncommon disorder in the spectrum of pituitary disease. Twenty-three cases proven by biopsy or at autopsy have been reported since 1962. We report 2 further cases and review the etiology, immunology and pathology of the disease. The diagnosis should be considered in afemale patient who presents during the post-partum period with the clinical picture of a non-functional or prolactin cell pituitary adenoma and evidence of hypopituitarism.


1980 ◽  
Vol 12 (2) ◽  
pp. 87-95 ◽  
Author(s):  
K. Kovacs ◽  
G. Ilse ◽  
N. Ryan ◽  
D.J. McComb ◽  
E. Horvath ◽  
...  

Author(s):  
I.C. Murray

In women, hyperprolactinemia is often due to a prolactin (PRL)-secreting adenoma or PRL cell hyperplasia. RRL excess stimulates the mammary glands and causes proliferation of the alveolar epithelium. Bromocriptine, a dopamine agonist, inhibits PRL secretion and is given to women to treat nonpuerperal galactorrhea. Old female rats have been reported to have PRL cell hyperplasia or adenoma leading to PRL hypersecretion and breast stimulation. Herein, we describe the effect of bromocriptine and consequently the reduction in serum PRL levels on the ultrastructure of rat mammary glands.Female Long-Evans rats, 23 months of age, were divided into control and bromocriptine-treated groups. The control animals were injected subcutaneously once daily with a 10% ethanol vehicle and were later divided into a normoprolactinemic control group with serum PRL levels under 30 ng/ml and a hyperprolactinemic control group with serum PRL levels above 30 ng/ml.


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