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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a case of Nelson's syndrome in which the clinical, radiographic, and surgical findings are indicative of a discrete microadenoma rather than of diffuse pituitary hyperplasia. Ultrastructural analysis reveals this to be the first example of a sparsely granulated lesion in Nelson's syndrome and only the second such adrenocorticotropic hormone-secreting tumor reported. Unfortunately, there do not seem to be any firm ultrastructural features that differentiate between hyperplasia and discrete adenoma. Separation of the two entities may be important in delineating the pathogenesis and treatment of Nelson's syndrome; these are discussed.
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PMID:Nelson's syndrome: one disease or two? 23 Apr 24

Eleven women with secondary amenorrhea associated with hyperprolactinemia were studied. Base line evaluations, visual field determinations, and routine sella turcica x-rays were normal. Prolactin-secreting pituitary microadenomas were found in all of the patients only after further diagnostic studies were carried out. These studies included polytomography of the sella turcica; dynamic pituitary testing of growth hormone reserve, adrenocorticotropic hormone reserve, and gonadotropin reserve; and prolactin suppression with L-dopa. The early diagnosis of a small prolactin-secreting adenoma may be possible if several diagnostic criteria are utilized. The most sensitive diagnostic indices available are (1) polytomography, (2) the magnitude of the plasma prolactin elevation, and (3) the failure to suppress prolactin secretion with L-dopa. Our findings emphasize the importance of an extensive evaluation of all women with amenorrhea associated with hyperprolactinemia.
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PMID:Prolactin-secreting pituitary microadenoma: detection and evaluation. 64 47

A case of Cushing's syndrome associated with a bronchial adenoma treated eight years before with bilateral adrenalectomy was cured by surgical excision of the bronchial adenoma. A discussion of clinical and hormonal features of this lesion is presented. It is concluded that this tumor manifested a capability of synthesizing and releasing substances which are chemically and biologically similar to adrenocorticotropic hormone andmelanocyte-stimulating hormone (MSH). Stimulation of the adrenal cortex by this material results in hyperplasia and hypersecretion, and stimulation of the melanocytesy MSH resulted in excessive pigmentation. Acknowledgment: We are indebted to Doctors Wendell Nicholson, David N. Orth, and Grant W. Liddle of Vanderbilt University for determinations of ACTH and MSH levels and to Mrs. E.P. Jessup for assistance in preparation of statistical data for this manuscript.
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PMID:Cushing's syndrome associated with bronchial adenoma. 83 99

It has been hypothesized by Lamberts and coworkers in their analysis of 15 cases that adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas may be derived from either the anterior lobe or the intermediate lobe. The intermediate lobe type of Cushing's disease is thought to be controlled through a hypothalamic pathway and is characterized by hyperprolactinemia; suppressibility of cortisol with bromocriptine, and lower sensitivity to dexamethasone. The authors investigated the validity of this hypothesis in 125 cases of ACTH-secreting pituitary microadenomas by analyzing the endocrine findings, the locations of the microadenomas, and alpha-melanocyte stimulating hormone (alpha-MSH) immunoreactivity in the adenoma cells. No significant differences in the basal hormone levels, cortisol suppressibility with bromocriptine, sensitivity to dexamethasone, and recurrence rate were observed between patients with the microadenoma adjacent to the posterior lobe (considered typical of the intermediate lobe-derived tumor) or those with the microadenoma located in the anterior lobe. The locations of the microadenoma were not correlated with alpha-MSH immunoreactivity in the adenoma cells. No significant differences in endocrine findings were noticed between adenomas positive or negative for alpha-MSH. Thus, Cushing's disease cannot be simply divided into either the anterior lobe type or the intermediate lobe type by endocrinological evaluation as described by Lamberts, et al.
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PMID:Endocrinological evaluation of ACTH-secreting pituitary microadenomas: their location and alpha-melanocyte stimulating hormone immunoreactivity. 131 55

A 57-year-old obese woman with hypertension, diabetes mellitus, osteoporosis, and a 40-year history of secondary amenorrhea was diagnosed with corticotropin-dependent Cushing's syndrome. Dynamic endocrine testing and radiological evaluation did not reveal definitively the source of the excess corticotropin. Bilateral adrenalectomy was performed with resolution of the signs and symptoms of hypercortisolism. Four years later, the patient was noted to have rising serum corticotropin levels and an enlarging pituitary mass; hyperprolactinemia also was documented. A diagnosis of Nelson-Salassa syndrome was made, and she underwent a transsphenoidal adenomectomy. A histological examination of the specimen revealed two distinct, albeit contiguous, adenomas: a corticotroph adenoma and a lactotroph adenoma. Postoperatively, the serum prolactin and corticotropin levels decreased significantly. Although the stalk section effect resulting from compression by a pituitary adenoma can raise serum prolactin levels, a concurrent lactotroph adenoma should be considered in patients with nonfunctional or functional pituitary adenomas of other types associated with significantly elevated prolactin levels. The mechanisms underlying simultaneous adrenocorticotropic hormone and prolactin excess are discussed.
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PMID:Coexisting corticotroph and lactotroph adenomas: case report with reference to the relationship of corticotropin and prolactin excess. 131 62

This study describes a case of pituitary-dependent Cushing's syndrome where standard biochemical and radiological techniques were discordant in localizing the origin of the autonomous adrenocorticotropic hormone (ACTH) hypersecretion in the pituitary. Hormonal evaluation suggested a pituitary genesis for the disease, but both sellar computed tomography and cranial magnetic resonance (MR) were unable to give clear-cut evidence for a pituitary neoplasm. Simultaneous and bilateral inferior petrosal sinus sampling (SBIPS) correctly identified the left side of the pituitary gland as the source of autonomous ACTH production. One year later, the shaded signs of a pituitary lesion in the left side of the gland were seen with MR imaging, and a 0.5-cm in height adenoma was surgically removed. At the 2-year follow-up the patient's symptoms had completely disappeared, and her menses were restored. In this case, SBIPS correctly diagnosed the presence of an ACTH-secreting pituitary microadenoma one year before shaded signs of the pituitary lesion appeared with MR imaging. This is a clear-cut demonstration of the accuracy of the SBIPS technique in localizing small pituitary lesions.
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PMID:Bilateral and simultaneous inferior petrosal sinus sampling in the early diagnosis of an ACTH-producing pituitary microadenoma and its detection by magnetic resonance one year later. 132 6

The topographical distribution of adrenocorticotropic hormone, growth hormone and prolactin was studied in nine multihormonal pituitary adenomas and two normal adenohypophyses using quantitative immunohistochemical methods. For each pituitary hormone paraffin sections stained by antihormone antibodies were scanned with a light microscope equipped with a projection and scanning device. The number of immunoreactive cells of each square in the grid was counted and transformed into pseudocolors. In this way, the distribution of each hormone was documented. A chi-square test was applied to these distribution patterns to prove randomness. A nonrandom distribution of immunoreactive cells was observed in all pituitary adenomas and normal pituitary glands. Cluster formations of immunoreactive cells were found for each hormone. The clusters were surrounded by halo-like areas of decreasing number of immunoreactive cells from center to periphery. The cluster-halo type of immunoreactive cells was found not only in the adenomas but also in the normal pituitary gland. This may be explained by the similarity of biological processes during cell proliferation either in normal development or in adenoma formation. It can be concluded from our studies that pituitary adenomas in most cases develop by multicentric but not diffuse proliferation of cell clones of different endocrine activity.
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PMID:Pituitary adenomas: tumor cell growth by cluster formation. Pattern analysis based on immunohistochemistry. 133 27

A cat that was suspected some insulin resistance was diagnosed as pituitary dependent hyperadrenocorticism from an adrenocorticotropic hormone (ACTH) stimulation test, dexamethasone suppression test and measure of endogenous plasma ACTH concentration. Histopathological examination revealed chromophobe adenoma in pituitary gland and hyperplasia in adrenal cortex.
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PMID:Pituitary dependent hyperadrenocorticism in a cat. 147 72

We studied four patients with adrenocorticotropic hormone (ACTH)-independent hypercortisolism due to bilateral massive enlargement of the adrenal glands. The combined weight of the adrenal glands ranged from 69 to 149 g and the adrenal cortex was replaced in three of four patients by multiple nodules ranging from microscopic to 4 cm in diameter. One patient had massive diffuse enlargement. All patients had low or undetectable levels of serum ACTH, absence of petrosal sinus to peripheral gradients of ACTH in bilateral samples from the inferior petrosal sinuses before and after stimulation by corticotropin releasing hormone, and absence of an adenoma on MR imaging of the pituitary gland. The marked degree of adrenocortical enlargement and absence of ACTH dependency separates this massive macronodular disease from the more common ACTH-dependent macronodular hyperplasia encountered in older patients with pituitary-dependent Cushing disease. All patients required bilateral adrenalectomy to control hypercortisolism. We present the spectrum of nodular adrenal disease associated with hypercortisolism and a differential diagnosis based on morphologic criteria.
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PMID:CT and MR imaging of massive macronodular adrenocortical disease: a rare cause of autonomous primary adrenal hypercortisolism. 165 80

Eight surgical and one autopsy specimen of pituitary adenomas (six cases of Cushing's disease, two of Nelson's syndrome, and one of hypopituitarism) were studied by histochemical, immunohistocytological, and ultrastructural methods. Eight tumors showed the characteristic histochemical profile of corticotroph adenoma--amphophilic to basophilic, and periodic acid-Schiff-positive to some extent. In all tumors, immunohistochemical studies revealed adrenocorticotropic hormone (ACTH) and alpha-subunit in the cytoplasm of some adenoma cells. By electron microscopy, seven tumors were found to be monomorphous; six were typical corticotroph adenomas and one was a subtype II silent corticotroph adenoma. One unique lesion was bimorphous--i.e., composed of corticotrophs as well as cells resembling glycoprotein cells. Immunoelectron microscopy by the double-labeling immunogold technique, performed on one corticotroph adenoma, demonstrated the presence of ACTH and alpha-subunit not only within the same adenoma cells but also within the same secretory granules. The cytogenesis of ACTH alpha-subunit tumors, a rare form of plurihormonal adenoma, remains to be elucidated. The duration of disease associated with these tumors exceeded the duration in patients with ordinary corticotroph adenomas. Given the low frequency with which increases in serum alpha-subunit are detectable in patients with such tumors--13% in this series--hormone production is not recognized at preoperative evaluation.
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PMID:Pituitary adenomas that produce adrenocorticotropic hormone and alpha-subunit: clinicopathological, immunohistochemical, ultrastructural, and immunoelectron microscopic studies in nine cases. 169 Aug 66


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