Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between 1967 and 1985 95 patients with pituitary adenoma received radiation therapy at the University of California, Los Angeles (UCLA), and the West Los Angeles Veterans' Administration (VA) Medical Center. Seventy of these patients received radiation therapy immediately as adjuvant therapy following incomplete resection, and 25 were irradiated as primary treatment or after surgical failure. The majority of cases (87%) presented clinically with macroadenomas. Two-thirds of the patients were treated with parallel opposed lateral portals to a midline total dose of 50 Gy. The mean follow-up was 7 years (range: 30-250 months). In our series, there is a difference in response by disease subtype. The control rates were 83% (30 of 36) for nonfunctioning adenoma, 60% (nine of 15) for growth-hormone secreting adenoma, 44% (16 of 36) for prolactin secreting adenoma, three of five for Nelson's syndrome, and three of three for Cushing's disease. There was a tendency for a better response rate with a total dose of greater than or equal to 50 Gy for prolactinoma. None of the patients were known to develop brain necrosis or radiation-induced sarcoma. An analysis of these results and a review of the literature is presented here.
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PMID:Radiation therapy of pituitary tumors: results in 95 cases. 198 33

TSH-producing adenomas of the pituitary gland are very rare. Synchronous combinations of TSH-producing adenomas with other causes of hyperthyroidism are certainly extremely rare. We present the second known case, reported in the literature, consisting of observations for 12 years in a woman aged 43 years, who presented with active Graves' disease and an apparently inactive pituitary macro-adenoma. However, after normalisation of serum T3 and serum T4 levels by antithyroid medication for one year, the serum TSH rose inappropriately and continued to rise for the following 11 years. Insidious growth of the adenoma also occurred. After one year of medical treatment, a huge goitre was resected (210 g) leaving the patient euthyroid, clinically and biochemically, for four years. Hereafter, hyperthyroidism developed again this time without Graves' disease. We conclude that the patient experienced hyperthyroidism on two occasions, the first caused by Graves' disease and then caused by a TSH-producing pituitary adenoma.
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PMID:[Basedow's disease and thyroid stimulating hormone producing pituitary adenoma in a patient]. 201 75

In order to study the mechanism of GH secretion from somatotroph adenoma cells, we have compared the effect of 12-O-tetradecanoyl phorbol-13-acetate (TPA) with that of growth hormone releasing factor (GRF) on GH secretion from human somatotroph adenoma cells cultured in monolayer. Pituitary adenoma cells were obtained from 13 patients with acromegaly undergoing surgery. On the 7th day of culture, the cells were exposed for 2 h to secretagogues. All 13 adenoma cell cultures (100%) responded to TPA (1.6-16.0 nmol/l) with a two- to six-fold increase in GH release (240 +/- 37% increase of control: mean +/- SE). The response was detectable within 10 min, and was maximal at 2 h. Phospholipase C (7.7 mmol/l) also stimulated a two- to ten-fold increase in GH release in all four adenomas examined (100%). GH release was stimulated by GRF (2.0 nmol/l) in eight out of 12 adenoma cells (67%), but the magnitude of the responses to GRF (60 +/- 18% increase of control: mean +/- SE) were much smaller than that of TPA. Five out of 13 adenomas secreted detectable amount of PRL into the medium and these five adenomas (100%) responded to TPA (16.0 nmol/l) with a two- to six-fold increase. These observations indicate that the activation of protein kinase C is the consistent stimulator in GH and PRL secretion in human somatotroph adenoma cells. However, it is not determined whether the protein kinase C is involved in the in-vivo production of GH in patients with acromegaly.
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PMID:Phorbol ester, not growth hormone releasing factor, consistently stimulates growth hormone release from somatotroph adenomas in culture. 206 Jan 47

23 cases of nonfunctional pituitary adenoma were studied with light and electron microscopy as well as with immunohistochemical stains PAP technique. Under routine light microscopy, 17 cases were chromophobic adenomas; anyhow, electron microscopy showed that there were 6 cases of oncocytoma; 7 cases of undifferentiated cell adenoma; 4 cases of gonadotropic adenoma; 4 cases of mixed adenomas 1 cases of sparsely granulated GH cell adenoma and 1 case of sparsely granulated PRL cell adenoma. Immunohistochemical stain showed: null cell adenomas 7 cases, FSH cell adenoma 3 cases, LH cell adenoma 1 case, GH cell adenoma 2 cases and other mixed adenoma 10 cases. Therefore, the nonfunctional pituitary adenoma is actually a mixture, and the null cell adenoma was only about 1/3 in this series. Among them, most of the hormones gave no function expression themselves.
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PMID:[Pathological study of 23 cases of nonfunctional pituitary adenoma]. 206 77

This case report describes a 38-year-old male who was hospitalized for further clarification of clinically mild hyperthyroidism. His increased total hormone levels, the elevated free thyroid hormones and the elevated basal TSH with blunted response to TRH strongly suggested a pituitary adenoma with inappropriate TSH incretion. Transmission computed tomography showed an intrasellar expansion, 16 mm in diameter. The neoplastic TSH production was confirmed by an elevated alpha-subunit and a raised molar alpha-sub/TSH ratio. However, T4 distribution on prealbumin (PA, TTR), albumin (A) and thyroxine binding globulin (TBG) showed a clearly increased binding to PA (39%), indicating additional prealbumin-associated hyperthyroxinemia. The absolute values of PA, A and TBG were within the normal range. After removal of the TSH-producing adenoma, basal TSH, the free thyroid hormones and T4 binding to prealbumin returned to normal. Therefore, the prealbumin-associated hyperthyroxinemia had to be interpreted as a transitory phenomenon related to secondary hyperthyroidism (T4 shift from thyroxine binding globulin to prealbumin) rather than a genetically conditioned anomaly of protein binding.
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PMID:Transient prealbumin-associated hyperthyroxinemia in TSH-producing pituitary adenoma. 210 34

Serum concentrations of LH and FSH and their response to the separate administration of GnRH (100 micrograms i.v.) and TRH (200 micrograms i.v.) have been studied preoperatively in 12 patients with a clinically functionless pituitary adenoma, of whom nine (3F: 6M) were found to secrete gonadotrophins in vitro. In three patients with a gonadotrophin-secreting adenoma (GSA) the pulsatile release of LH and FSH was also assessed preoperatively. An elevated serum FSH was recorded in six of nine patients with a GSA, and was subnormal in one, whilst an elevated LH was recorded in only two and was subnormal in six. A doubling of LH occurred in only four of the nine patients after GnRH and in three of six after TRH. None of the three patients with a non-GSA was shown to have an aberrant response to GnRH or TRH. In patients with a GSA, pulsatile release of LH and FSH was usually asynchronous and neither hormone demonstrated any regular harmonic pattern. These data show that in patients with a GSA the serum FSH level is usually elevated but this is not invariable, and the LH may well be low. Pathological responses of LH are frequently found following the administration of either GnRH or TRH and these stimulation tests should be performed separately in patients presenting with a clinically 'non-functioning' pituitary tumour to assist in the preoperative diagnosis. The absence of normal LH and FSH pulsing also appears to be a feature of GS adenomas, and suggests that tumorous gonadotrophin secretion is not under physiological control by hypothalamic GnRH.
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PMID:LH and FSH secretion and responses to GnRH and TRH in patients with clinically functionless pituitary adenomas. 211 44

Hypersecretion of TSH by a pituitary adenoma is thought to be a rare form of hyperthyroidism. We describe three such patients, each of whom presented with clinical hyperthyroidism and a diffuse goitre, without eye signs or dermatopathy. Two were receiving long-term phenothiazine, one of these was also acromegalic. Plasma thyroxine, free T4 and tri-iodothyronine were repeatedly raised in each; plasma TSH was grossly elevated in one and inappropriately normal in the other two. Plasma TSH did not rise in response to thyrotrophin-releasing hormone or metoclopramide and was not suppressed by L-dopa in any patient. Anti-thyrotrophin receptor antibodies were undetectable. Skull radiographs showed erosion and expansion of the pituitary fossa and CT scans confirmed a pituitary mass in each patient. A pituitary adenoma was removed by transphenoidal surgery in two patients and a TSH-secreting adenoma was confirmed by immunocytochemical staining and electron microscopy. Both patients were clinically euthyroid post-operatively but still had evidence of TSH excess. Pituitary surgery was technically unsuccessful in the third patient. Although two patients had hyperthyroidism of long duration, all three were diagnosed within one year of the introduction of a sensitive TSH assay to our laboratory. A TSH-secreting pituitary adenoma may be a more common cause of hyperthyroidism than has been believed.
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PMID:Hyperthyroidism, inappropriate plasma TSH and pituitary adenoma in three patients, two receiving long-term phenothiazine therapy. 211 96

Fifty-seven patients with pituitary-dependent Cushing's syndrome and eight with Nelson's syndrome underwent transsphenoidal pituitary exploration, with removal of macroscopically abnormal tissue in 64 patients and detailed histology of this in 63. The cure rate by stringent criteria 1 month later was 48 (83%) of the 58 with assessable data, who were followed for 225 patient-years. Two patients relapsed later, a rate of one per 112 patient-years of follow-up. In 27% of patients, the macroscopically abnormal tissue removed was histologically indistinguishable from normal pituitary gland but the cure rate was 82%, and a quarter of the patients in this group assessable for recovery of normal ACTH function gained it. Another 53% of biopsies showed corticotroph adenomas, and the cure rate in these was 89% though rather more (69%) recovered normal ACTH function. The remaining 20% of biopsies were consistent with corticotroph hyperplasia. The cure rate varied little whether the lesion was diffuse or localized, whether or not it was in the invasion zone/interlobar cleft, whether or not there was pituitary enlargement, or whether the surgery was radical or selective. Six patients, of whom three are cured, showed surgical or radiological evidence of invasion outside the pituitary fossa. The data are consistent with the idea that pituitary adenoma is merely the end stage of some other process in the corticotrophs, and cure often follows removal of a lesion other than adenoma. Of patients who were permanently cured, 47% regained normal ACTH function within 3 years of operation (none later), 53% remaining ACTH-deficient at 3 years or more. Of all patients 48% acquired gonadotrophin deficiency, 28% have TSH deficiency and 25% permanent diabetes insipidus. All these pituitary function deficits were more common after radical surgery and in patients with normal histology, The literature contains so little objective data on these functions that we cannot say whether the endocrine damage in our patients is exceptional or not.
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PMID:Transsphenoidal surgery for Cushing's disease: does what is removed determine the endocrine outcome? 217 17

Thyrotropin-secreting pituitary adenomas have been diagnosed more frequently as radiographic techniques and biochemical assays have improved; however, they remain uncommon and are unfamiliar to most neurosurgeons. This report concerns eight patients with hyperthyroidism, inappropriately elevated levels of serum thyrotropin and alpha-subunit, and radiographic evidence of pituitary tumor. All underwent surgery and had pathological confirmation of a thyrotropin-secreting adenoma, and most had been subjected to prior ablation of the thyroid gland. Only one tumor was a microadenoma; the others ranged in size from 1.4 to 12 cm, and invasion of parasellar structures was common. Thyrotropin, triiodothyronine, thyroxine, and alpha-subunit were measured preoperatively and at intervals postoperatively. Coexistent hormonal abnormalities (which occurred in all patients) included acromegaly and hyperprolactinemia and were also monitored. All four patients who had tumors less than 2 cm in diameter remain alive. Complete extirpation of tumor in these patients produced rapid correction of all hormonal abnormalities and resolution of clinical hyperthyroidism. The other four patients had larger invasive tumors: two died soon after surgery, one died of disseminated tumor 8 years after presentation, and one remains alive with residual tumor. Tumors secreting thyroid-stimulating hormone are less easily cured by surgery than are other types of pituitary adenoma because of the large size and invasive features that many attain during the delay to diagnosis; medical therapy can subdue the tumor but not cure it. The experience with these patients establishes the importance of early diagnosis and surgical excision for successful treatment, and demonstrates the utility of modern diagnostic techniques for finding these lesions. As occurs in Nelson's syndrome after adrenalectomy for Cushing's disease, ablation of the target organ may allow the tumor to convert to a more clinically malignant form which is resistant to cure.
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PMID:Surgical treatment of thyrotropin-secreting pituitary adenomas. 221 57

A 36-year-old woman is reported with a possible variant of the McCune-Albright syndrome. The triad was incomplete because of the absence of skin pigmentation and since the sexual precocity was not evident. The presence of a pituitary mass and the secretory dynamics of growth hormone and prolactin were suggestive of a mammosomatotroph cell adenoma. A toxic multinodular goiter was also associated, but unique was the spontaneous normalization of the thyroid function. Unusual was the silent evolution of the polyostotic fibrous dysplasia, which was only fortuitously discovered during magnetic resonance imaging of the pituitary region. Treatment of the acromegaly with the long-acting somatostatin analogue octreotide resulted in an important inhibition of the GH secretion and in a reduction of the volume of the pituitary adenoma.
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PMID:Acromegaly, multinodular goiter and silent polyostotic fibrous dysplasia. A variant of the McCune-Albright syndrome. 227 9


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