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

Angiotensin-converting enzyme (ACE) inhibitors act by lowering the level of angiotensin II. The therapeutic benefits of these drugs and their potential side-effects therefore result from suppression of the physiological effects of angiotensin II. It is rational to prescribe an ACE inhibitor when the renin-angiotensin system is activated, as in renin-dependent essential hypertension, malignant hypertension and hypertension associated with heart failure. The beneficial effects of ACE inhibitor must be weighed against the special risks of renovascular hypertension: risk of renal artery thrombosis in case of unilateral stenosis and risk of renal failure if the stenosis is bilateral or affects a solitary kidney. In some situations the renin-angiotensin system is not directly involved in hypertension but may play a local haemodynamic role, as in some cases of primary or diabetic nephropathy. In such case the ACE inhibitors are thought to exert a protective effect. ACE inhibitors were reputed to be less effective in the elderly than in younger patients, but we now know that they can be prescribed with equal success in both instances to reduce peripheral resistance and improve regional blood flow as well as arterial compliance. Finally, ACE inhibitors can be prescribed, albeit with limited effectiveness, when the renin-angiotensin system is not activated, as in low renin hypertension and idiopathic hyperaldosteronism due to adrenal hyperplasia. They are ineffective in case of Conn's adenoma and contra-indicated in pregnant women.
 ...
PMID:[For which hypertensive patient should angiotensin-converting enzyme inhibitor be prescribed or forbidden?]. 129 38

Twenty-eight patients with primary aldosteronism were treated from 1974 to 1990. The serum potassium concentration was higher than normal level in all patients with the exception of one whose serum potassium concentration was normal. All of 14 tested patients had low renin values. The plasma aldosterone concentration was higher than standard value in all of 5 patients, and the A/PRA ratio was more than 400. Spironolactone administered preoperatively could not only normalize serum potassium concentration level and blood pressure, but also predict postoperative prognosis of hypertension. Only 37.5% of adenomas were detected by retroperitoneal pneumography with tomography in the early period. 80.0% of adenomas were found by B-ultrasonography, and 92.8% by CT after 1982. The operation was done through abdominal incision because of indefinite localization of adenoma before 1982, and the operation was performed through lumbar incision because of definite localization of adenoma after 1982.
 ...
PMID:[Diagnosis and treatment of primary aldosteronism]. 130 99

Altogether 16 persons with STH-producing hypophyseal adenoma were investigated by tacho-oscillography, total rheography, blood taken from the ulnar vein, a radioimmunoassay to determine the levels of STH, ACTH, cortisol, deoxycorticosterone, aldosterone, T3, T4, vasopressin, prostaglandin E2, 6-keto-prostaglandin F1 alpha, and plasma renin activity. Acromegalic patients demonstrated an elevated level of STH, and prostaglandin E2 secretion was inhibited. Two groups of patients were singled out according to the hemodynamic state: the 1st group was characterized by a hyperkinetic type of circulation and normotension of borderline hypertension; the 2nd group was characterized by hypokinetic circulation, increased vascular resistance, labile or stable arterial hypertension. The interrelationship of hemodynamic and hormonal indices was unnoticed. It has been assumed that of pathogenetic importance in the development of arterial hypertension is depletion of E2 production, and at early stages--body liquid retention resulting from hypersomatotropinemia.
 ...
PMID:[State of the endocrine and cardiovascular systems in patients with somatotropin-producing hypophyseal adenoma]. 130 90

A case of primary aldosteronism treated with spironolactone therapy has been followed up for 24 years. This is probably the longest case of spironolactone therapy for primary aldosteronism that has ever been reported. Long-term treatment with spironolactone controlled the hypertension and prevented hypokalemic alkalosis in this patient, without any deleterious effects on steroid biosynthesis. Based on data obtained during dose reduction and subsequent withdrawal of spironolactone, it is suggested that the suppressed plasma renin activity associated with adenoma-induced aldosteronism develops prior to hypokalemia and hypertension.
 ...
PMID:Twenty-four year spironolactone therapy in an aged patient with aldosterone-producing adenoma. 131 94

Exciting developments in knowledge of primary aldosteronism include description of new subtypes and elucidation of the genetic basis of one variety. Furthermore, relatively simple biochemical screening (aldosterone/renin ratio) has disclosed that primary aldosteronism is more common than previously thought, by diagnosing patients at an earlier, normokalaemic stage. The mutant gene discovered in the glucocorticoid-suppressible variety (FHI) codes for an aldosterone biosynythetic enzyme normally controlled by angiotensin II, and now controlled by corticotropin. The zona fasciculata is hyperplastic and makes aldosterone and "hybrid steroids" 18-oxocortisol and 18-hydroxycortisol in excess, in response to ACTH but not to angiotensin II. Adrenal tumours have not yet been described in this condition. Aldosterone-producing adenomas (Conn's syndrome) are also commonly composed of zona fasciculata-like cells, make "hybrid steroids" in excess and are very sensitive to ACTH but not to angiotensin II. We have described a new variety of aldosterone-producing adenoma which is responsive to angiotensin II (AII-responsive APA), consists of at least 20% zona glomerulosa-like cells, and does not make "hybrid steroids" in excess. We have also described a new familial variety of primary aldosteronism that includes tumours and is not glucocorticoid-suppressible (FHII). We propose that primary aldosteronism is a spectrum of genetic diseases expressed as either hyperplasia or neoplasia, and that morphological and genetic diversity explains biochemical and clinical behaviour.
 ...
PMID:Primary aldosteronism: hypertension with a genetic basis. 135 75

The presence of the two components of the renin-angiotensin system (RAS) has been systematically investigated in human normal and pathological adrenal tissues with two aims: 1) the detection of renin and especially angiotensinogen, which has not been reported before; and 2) to study possible differences in the coexpression of renin and angiotensinogen in tissue of cortical and medullary origin. The relative levels of renin and angiotensinogen mRNAs were determined by Northern blot analysis in normal (n = 5) and pathological adrenal tissues of cortical (n = 23) and medullary (n = 10) origin. Renin, prorenin, and angiotensinogen levels were also measured. Renin concentrations in normal and pathological adrenals were around 30-fold higher than those in the plasma of normal subjects, except for a Cushing's adenoma, which contains an extremely high renin content. Renin accounted for 56% of the total renin in normal adrenals and up to 87% in neoplastic tissues. This high proportion of renin indicates a likely conversion of prorenin to renin within these tissues. Renin mRNA was detected in each group of adrenal tissues. There was a significant correlation between the concentration of renin and its mRNA (r = 0.75; P less than 0.05). Angiotensinogen and its mRNA were detected in all normal and pathological adrenals. Compared to normal adrenal tissues, the relative amount of angiotensinogen mRNA was significantly higher in pheochromocytomas. However, the increased mRNA level in these tissues was not accompanied by a parallel increase in tissue angiotensinogen levels. Since the translational efficiency of angiotensinogen was verified by in vitro cell-free translation, the low level of angiotensinogen compared to the relatively high amount of its mRNA suggests a lack of storage of this protein in adrenal cells, as in liver cells. This study demonstrates that renin and angiotensinogen are coexpressed in normal and pathological tissues. Tissues of different cellular origin (zona glomerulosa, fasciculata, and medullary tissue), were able to express, store, and process renin and synthesize angiotensinogen. There was no obvious relationship between the expression of these proteins and the pathophysiology of the adrenal gland.
 ...
PMID:Coexpression of renin, angiotensinogen, and their messenger ribonucleic acids in adrenal tissues. 138 71

The study of structural changes and changes of the aldosterone content (AC) in the surgically removed adrenals of patients with different clinical variants of combination of the arterial hypertension (AH), low--renin hyperaldosteronism and space--occupying lesions in the adrenals found by CT was carried out. In 15 of 20 patients after adrenalectomy the diagnosis of the primary aldosteronism (PA) was established, in 4 cases diagnosis of the hypertension, 2B degree, and in one case the diagnosis of Cushing disease. The functional state was evaluated according to AC in the adenomas and macronodes and in the adjacent cortex as well as by nuclei size of cells producing aldosterone. The aldosterone hyperproduction was shown to be associated with local adenoma in some cases and with hyperactive cortex in the others this being reflected in the course of AH and in the adrenalectomy hypotensive effect.
 ...
PMID:[Functional state of the adrenals in various forms of arterial hypertension]. 147 37

1. Thirteen patients from five families had Familial Hyperaldosteronism Type II (FH-II), a new variety of familial primary aldosteronism not suppressible with dexamethasone that often involves adrenocortical adenoma formation. 2. Five patients had solitary aldosterone-producing adenomas, three had bilateral autonomous overproduction of aldosterone, and in five the subtype is yet to be determined. 3. Comparing FH-II patients with 88 patients with primary aldosteronism of other causes revealed no differences in mean age at presentation or at onset of hypertension, sex incidence, lowest recorded serum potassium, plasma aldosterone, plasma renin activity or adenoma size. 4. Analysis of DNA in peripheral blood of patients with FH-II, their affected and unaffected relatives, and in removed tumours is in progress in order to determine the underlying genetic defect(s) in FH-II, perhaps an abnormality in the P-450aldo gene (CYP11B2). 5. It is recommended that hypertensive relatives of patients with primary aldosteronism should have measurements of the aldosterone/renin ratio.
 ...
PMID:Familial hyperaldosteronism type II: five families with a new variety of primary aldosteronism. 152 63

Urinary excretion of 18-hydroxycortisol (18-OHF), 18-hydroxycorticosterone (18-OHB) and aldosterone 18-glucuronide (Aldo-18-glu) was measured in 10 patients with primary aldosteronism; 5 with aldosterone-producing adenoma (APA) and 5 with idiopathic hyperaldosteronism (IHA), 10 patients with essential hypertension (EHT) and 11 normotensive subjects. In EHT patients, urinary 18-OHF (172 +/- 15 micrograms/24h) and 18-OHB (3.1 +/- 0.6 micrograms/24h) values were not significantly different from 18-OHF (142 +/- 35 micrograms/24h) and 18-OHB (3.6 +/- 0.5 micrograms/24h) in the controls. Urinary 18-OHF values were significantly higher in APA (640 +/- 213 micrograms/24h) when compared with controls and EHT, whereas 18-OHB (11.3 +/- 1.5 micrograms/24h) values were only slightly elevated. Both 18-OHF and 18-OHB were significantly increased in APA compared with 18-OHF (232 +/- 56 micrograms/24h) and 18-OHB (4.6 +/- 0.3 micrograms/24h) in IHA. The two urinary steroids, especially 18-OHF proved to be a useful marker for the diagnosis of APA, confirming the previous findings. Aldo-18-glu was not significantly different between APA and IHA. In normal subjects when sodium intake was restricted to 48meq/day for four days the urinary 18-OHF was increased two fold to 383 +/- 59 micrograms/24h (p less than 0.01 vs control period) associated with comparable rise in plasma renin activity. This suggests that the biosynthesis of 18-OHF is partly under control of renin-angiotensin axis in normal subjects.
 ...
PMID:Determination of urinary 18-hydroxycortisol in the diagnosis of primary aldosteronism. 156 Jan 87

Seven cases of primary aldosteronism were experienced during the 12 years in the Toyama Medical and Pharmaceutical University Hospital. The majority of cases were between 32 and 64 years old with a mean of 51 years. Two cases were male and 5 were female. Hypertension was observed in 6 cases, but one case had normal blood pressure. Hypokalemia was recognized in 6 cases. The plasma level of aldosterone was high in all cases and all the cases showed low levels of plasma renin activity. Concerning the localization of the lesions, CT scan, magnetic resonance imaging and adrenal scintigraphy revealed an accuracy rate of 100%, each. Therefore, these imaging techniques are very useful tools for identifying the locality of the adenoma. On the other hand, the accuracy rates of adrenal venous aldosterone assay and ultrasonography were 83 and 60%, respectively. The cases with rather short duration of hypertension before surgery returned to normal in blood pressure earlier after the operation than the other cases.
 ...
PMID:[Clinical study on primary aldosteronism--localization of adrenal tumors]. 160 57


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>