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

Clones of epithelial-like cells were established from urethan-induced mouse lung adenoma. Electron microscopy of one clone showed that the cells contained lamellar inclusion bodies similar in appearance to those seen in the adenoma precursor, the type II alveolar pneumocyte. The clones exhibited characteristics associated with both "transformed" and "normal" cells in culture; i.e., although aneuploid, the cells grew at a slower rate than most transformed cells, did not form colonies in soft agar and, after prolonged subculture, were not tumorigenic when transplanted s.c. into appropriate hosts. Hydrocortisone treatment of the cloned cells led to growth stimulation and the eventual acquisition of neoplastic potential. Epithelial tumors were produced more readily in athymic, nude mice than in antilymphocyte serum-treated A/He mice. The cells are producing a C-type RNA virus into the culture medium.
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PMID:Clonal isolation of epithelial cells from mouse lung adenoma. 16 47

Acute and prolonged alpha 1-24 corticotropin stimulation was performed on a treated chromophobe adenoma patient with partial ACTH deficiency and extreme hyperprolactinemia. Cortisol and aldosterone stimulated normally. However, the basal concentrations of androstenedione (A) and dehydroepiandrosterone (DHA) were low, and that of DHA-sulfate (DHAS) was undetectable. Furthermore, A and DHA did not stimulate normally, and DHAS did not stimulate at all. It has been claimed that adrenal androgen production is increased in hyperprolactinemia. However, the inability of prolactin (Prl) to maintain adrenal androgen (AA) secretion, with and without added ACTH, is demonstrated in this patient.
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PMID:Lack of adrenal androgen stimulation by ACTH in extreme hyperprolactinemia. 22 82

Basal and ACTH-stimulated release of aldosterone and cortisol was studied in slices of adrenocortical adenomas and adrenal cortex from 16 consecutive patients with Conn's syndrome (n = 7), Cushing's syndrome (n = 5) or no signs of steroid hypersecretion (n = 4). Clinical data were reviewed and histologic examination was repeated. The adrenal cortex and all tumours but one (non-hyperfunctioning) secreted cortisol. Cortisol release increased after addition of ACTH in 13/15 tumours and all cortex slices. Aldosterone was secreted from the adrenal cortex in all patients and was increased by ACTH in 75% of the tissue specimens. Adenomas from patients with hyperaldosteronism showed the highest basal aldosterone secretion. This secretion was further increased by ACTH. Tumours from patients without signs of corticosteroid excess also released steroids and responded to ACTH. It is concluded that in vitro studies of steroids released from adrenocortical tumours contribute to their diagnostic and functional evaluation.
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PMID:Basal and ACTH-stimulated cortisol and aldosterone release from adrenocortical adenomas in vitro. 167 26

Fifteen patients with primary aldosteronism were classified as angiotensin II-unresponsive aldosterone-producing adenoma (AII-U APA, n = 9), or angiotensin II-responsive aldosterone-producing adenoma (AII-R APA, n = 6), based on the responsiveness of aldosterone to upright posture and to angiotensin II infusion. Lack of aldosterone response to angiotensin II infusion immediately postoperatively in the AII-R APA subtype was consistent with previous responsiveness residing solely within the adenoma. Cortisol levels in five of the six patients with AII-R APA failed to suppress normally with dexamethasone consistent with some autonomous production of cortisol by the adenoma. In contrast, cortisol levels suppressed normally during dexamethasone administration in all patients with AII-U APA. This biochemical distinction can be added to the previously described overproduction of 18-oxo cortisol in AII-U APA but not in AII-R APA. Histological examination of adenoma sections revealed predominantly (greater than or equal to 50%) zona fasciculata type cells in AII-U APA. In contrast, AII-R APA contained less than 20% zona fasciculata type. Thus, biochemical differences between AII-U APA and AII-R APA subtypes of primary aldosteronism may be due to underlying differences in cellular composition of the aldosterone-producing adenomas.
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PMID:Histological and biochemical distinctiveness of atypical aldosterone-producing adenomas responsive to upright posture and angiotensin. 206 Jan 45

Since calcium entry blocker drugs can interfere with aldosterone secretion in vitro, a similar effect in vivo, in man, has been suggested and partially confirmed. The data available in primary aldosteronism are more controversial. Therefore, we have studied the acute and chronic effect of nifedipine in 7 patients with idiopathic hyperaldosteronism (IHA) and 8 with aldosterone producing adenoma (APA). On 2 different days, 10 mg of nifedipine or placebo were given sublingually to the patients and blood pressure and heart rate were recorded every 5 min. for 60 min. Plasma aldosterone, cortisol, PRA and serum K+ were measured at 0, 30 and 60 min. 5 patients with IHA and 6 with APA received nifedipine 20 mg per os bid for 3 months; the same parameters were evaluated on days 0, 30, 60 and 90; urinary aldosterone was measured on days 0, 30, 60 and 90. BP decreased in both groups both after acute and chronic administration of nifedipine. Plasma aldosterone showed a similar trend either after acute nifedipine or placebo; however, during chronic treatment it was slightly decreased in IHA patients. Cortisol, PRA, urinary aldosterone and K+ remained unchanged. In conclusion, nifedipine is an effective antihypertensive agent also in primary aldosteronism; its aldosterone inhibiting properties are minimal and seem to be present only during long-term therapy in IHA.
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PMID:Acute and chronic effect of nifedipine in primary aldosteronism. 280 62

Tissues from 12 human corticotropin-secreting adenomas, obtained during surgery for Cushing's disease (CD, ten cases) or Nelson's Syndrome (NS, two cases), were exclusively mechanically dispersed. Single cells and cell aggregates were plated on extracellular matrix derived from bovine corneal endothelia. Functional responses to physiological stimuli were analyzed by measuring human beta-endorphin (beta h-EP) immunoreactivity (IR) by radioimmunoassay in the culture medium. All adenomas responded with stimulated secretory activity to arginine vasopressin (AVP), corticotropin-releasing factor (CRF), or both. Cortisol higher than 10(-8) M suppressed basal secretion and CRF- or AVP-stimulated beta h-EP-IR secretion. There was no consistent difference in response of the cells when cultured in medium containing 10% fetal calf serum (FCS) or in serum-free conditions. A change of cells from serum to serum-free conditions usually resulted in 10%-50% reduction in the basal secretion level that remained stable for at least 2 weeks and, in one case (NS), 10 weeks. In cells maintained in medium supplemented with 5% serum obtained from the respective patients 40 min after adenoma removal, basal secretion was suppressed to 60% of the baseline level in a 10% FCS control. Long-term incubation with CRF (10(-9) M) showed sustained stimulation of hormone secretion. No remarkable cell proliferation was observed under basal conditions or during long-term, low-dose incubation with cholera toxin (10(-12) M) in two cases (CD), or CRF (10(-9) M) in two cases (NS, CD). Parallel beta-EP-IR and adrenocorticotropin secretion was verified in selected cases.
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PMID:Long-term culture of human corticotropin-secreting adenomas on extracellular matrix and evaluation of serum-free conditions. Secretory aspects. 302 31

After diagnosis of primary aldosteronism on the basis of biochemical evidence, the detection of the tumour is of crucial importance in the management of the disease. We reviewed the efficacy of CT-Scan, Iodo-Cholesterol Scintigraphy, digitalized phlebography, adrenal vein sampling for steroid measurements (AVS), and Nuclear Magnetic Resonance (NMR) in 160 hypertensive patients with primary aldosteronism. Diagnosis of Conn's adenoma (n = 96) or Adrenal Hyperplasia (n = 40) was confirmed by surgery or at least two concordant tumour localization tests. Scintigraphy gave a correct diagnosis in 53% of the 51 exams, CT-Scan in 82% of the 85 exams, and phlebography in 79% of 61 exams. Plasma Aldosterone/Cortisol ratio was 5 times higher on the side of adenoma in 55% of the 47 cases but this ratio was also present in 23% of 22 patients with adrenal hyperplasia. Each procedure exhibited few false positive and false negative cases. NMR performed in 15 patients with Conn's adenoma identified all the cases. But tumours displayed a signal close to the liver signal and identical to the normal adrenal. These results and the risk of invasive procedure (failure of catheterization of the right adrenal vein (n = 6) and adrenal haematoma (n = 2) lead us to propose a schema of exploration of patients with primary aldosteronism. The CT-Scan could be performed at the first step once the biological diagnosis confirmed. Phlebography and AVS will be performed only if tumour was less than 1 cm at the CT-Scan despite important biological abnormalities. This schema requires to be validated by a prospective evaluation.
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PMID:[Localization of primary hyperaldosteronism]. 320 1

Pituitaries of 137 cases with Cushing's disease were microscopically and immunohistologically studied. Many alterations and parameters (sex, age, anamnesis, cortisol plasma levels, tumor size, invasiveness, localization, differentiation of adenomas, immunohistological hormone content, capillarity, recurrences, peritumorous ACTH cell hyperplasia, and Crooke's cells) were analyzed and compared. Whereas most parameters were not correlated, we found some important statistically significant correlations: Undifferentiated adenomas are more frequently invasive than differentiated ones. Invasive adenomas recur more frequently than non-invasive adenomas. Extremely laterally localized adenomas are more often invasive. Larger adenomas are more frequently invasive than micro-adenomas. ACTH cell hyperplasia are more often demonstrable in specimens from total hypophysectomies (confined to our earlier series) than from partial hypophysectomies and adenomectomies. Recurrences of adenomas are more frequent in pituitaries with periadenomous ACTH cell hyperplasia. Very rarely ACTH cell hyperplasia are the only source of ACTH hyperfunction. The more Crooke's cells are demonstrable, the longer the post-operative replacement dose of Cortisol is required. Adenomas in Cushing's disease and adenomas in Nelson's syndrome differ significantly in the following points: Adenomas in Nelson's syndrome are larger and contain more plurinuclear cells. In the ultrastructure, adenomas in Cushing's disease show more cytofilaments. Paraadenomous Crooke's cells are lacking in Nelson's syndrome.
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PMID:Pituitary pathology in Cushing's disease. 323 49

Isolated adrenocortical cells from 6 patients with a 'normal' zona fasciculata, 4 patients with a 'normal' zona glomerulosa, and tumour cells from 1 adrenocortical adenoma and 1 carcinoma were incubated with and without increasing concentrations of ACTH 1-24 (10(-13) M to 10(-9) M) or Asp1-Ile5-angiotensin II (10(-11) M to 10(-7) M). In 4/5 'normal' cases, cortisol was clearly stimulated by 10(-13) M ACTH. The maximum of the dose-response curve (5-fold stimulation) was reached at 10(-10) M ACTH. Angiotensin II (AII) started to stimulate 'normal' cells at 10(-11) M with a maximum (2-fold stimulation) at 10(-9) M. Aldosterone production by 'normal' cells was less markedly stimulated by ACTH and AII, although the threshold doses for both peptides were similar to those of the cortisol response curves. The cells of the adrenocortical adenoma from a patient with Cushing's syndrome produced large amounts of cortisol and small amounts of aldosterone, both steroids being clearly stimulated by ACTH and AII. The adrenocortical carcinoma cells produced small amounts of cortisol and no aldosterone. Cortisol production responded to ACTH, but not to AII. The results suggest that an activated renin-angiotensin system may stimulate the zona fasciculata, since 10(-11) M AII (= 10 pg AII/ml) is a normal plasma AII concentration on an unrestricted diet. Clinical evidence supporting this thesis is reviewed. However, cortisol production itself will rarely be increased by AII in vivo, since a down-regulation of ACTH would occur.
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PMID:Effects of angiotensin II and ACTH on normal and tumourous human adrenocortical cells. 631 17

In an attempt to test the hypothesis that pituitary adenomas of acromegaly may possess altered cellular membrane receptors, the response of growth hormone (GH) secretion to ovine corticotrophin-releasing factor (CRF) in cultured adenoma cells of acromegaly was studied. In three out of seven experiments using different pituitary adenoma cells in culture, nanomolar concentrations of CRF caused a significant increase in GH release. The CRF-induced GH release was reproducible and a dose-response relationship was observed between the CRF concentrations and the amounts of GH released into the incubation media. Hydrocortisone, at a concentration of 1 microM, on the other hand, resulted in a significant decrease in GH secretion in four out of five experiments. When adenoma cells were co-incubated with CRF and 1 microM hydrocortisone, CRF-induced GH release was partially overcome. In one experiment, the inhibitory effect of hydrocortisone was reversed by co-incubation with CRF, although CRF alone was ineffective in the stimulation of GH. These results suggest that CRF may stimulate GH release in some, though not all, patients with acromegaly, and that glucocorticoids may block this effect of CRF acting directly on the pituitary adenoma cells of acromegaly.
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PMID:Effects of ovine corticotrophin-releasing factor and hydrocortisone on growth hormone secretion by pituitary adenoma cells of acromegaly in culture. 633 44


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