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

The course of mean arterial pressure was compared in two series concerning 18 primary or tumoral hyperaldosteronism and 8 idiopathic ones. Identification of the nature of the hyperaldosteronism should not yet motivate a decision on principle, surgical in case of tumor, medical in an idiopathic case. In the latter case cooperation and tolerance of medical treatment, severity of hypertension also come into consideration. A positive spirolactone test, a hypertension course of less than six years were in our experience a good indication of successful surgery, as opposed to a normal unilateral renal biopsy. In case of operation, the removal protocol should adapt to the peroperative findings; 80% adrenalectomy is the most common procedure, except in the case of isolated adenoma of more than 10 mm diameter.
Arch Mal Coeur Vaiss 1976 Nov
PMID:[Primary and idiopathic hyperaldosteronism. Course 1 year after operation. Apropos of 28 cases]. 82 53

The purpose of the study was to evaluate the effects of a dihydropyridine calcium antagonist, nicardipine (N), on blood pressure (BP) and aldosterone secretion in hypertensive patients (pt) with primary aldosteronism. The study concerned 8 pts, mean age 55.6 +/- 7.7 years, 1 pt with aldosterone-producing adenoma (APA) and 7 pts with idiopathic aldosteronism: plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were respectively 0.30 +/- 0.2 ng/ml/h) and 314 +/- 109 pg/ml. Acute administration of 12 mg of nicardipine during 90 mn (three periods of N infusion during 30 mn: 0.4 mg/mn-5 mn; then 0.08 mg/mn-25 mn) significantly decreased BP, with an increase in heart rate (HR); the levels of PAC were significantly reduced with a slight but not significant increase in PRA, 60 mn after N: (table; see text) N decreased also PAC in the pt with APA [600 to 410 pg/ml] but did not improve hypokalemia (3.1 vs 3.3 mmol/l, n = 8 N.S.). In contrast, PAC levels were not modified 2 hours after acute oral administration of captopril (1 mg/kg): 302 +/- 164 pg/ml vs 332 +/- 191 pg/ml (NS). This study demonstrated the antihypertensive efficacy of acute infusion of nicardipine in primary aldosteronism; the decrease of PAC under this calcium antagonist suggested its potential interest in the management of idiopathic aldosteronism.
Arch Mal Coeur Vaiss 1989 Jul
PMID:[Effect of a calcium inhibitor, nicardipine, on aldosterone secretion in primary hyperaldosteronism]. 251 Jun 55

The authors report a case of primary hyperparathyroidism in a 47 year old woman presenting with cardiac arrhythmias. She had paraoxystic supraventricular tachycardias and rate-dependent ventricular hyperexcitability suggestive of a catecholamine-induced phenomenon which were resistant to antiarrhythmic therapy over a 3 year period; the plasma calcium concentration was 3.30 mmol/l. An ectopic parathyroid adenoma was removed surgically, normalising the biological changes, and no further arrhythmias were detected by Holter monitoring during the 2 year follow-up period. The association of atrial and ventricular arrhythmias seems to be relatively rate in hyperparathyroidism; patients usually present with atrioventricular block and ventricular hyperexcitability. The other cardiovascular abnormalities observed in hyperparathyroidism are hypertension and myocardial hypertrophy. The electrophysiological mechanisms underlying the clinical manifestations remain obscure.
Arch Mal Coeur Vaiss 1989 Dec
PMID:[Primary hyperparathyroidism disclosed by heart arrhythmia]. 251 34

The term primary hyperparathyroidism currently refers to the clinical and biological manifestations resulting from the hypersecretion of parathyroid hormone by one or several parathyroid adenomas. This entity is a recent one since it goes back to 1925. The clinical picture resulting from this anomaly, were first described as Recklinghausen's fibrous osteitis, which was not justified since Recklinghausen had not established the relationship between the clinical manifestations and the adenoma discovered by Mandl, then under the name of parathyroid osteosis. This term was justified at a time when the disease presented only bony manifestations with biological evidence. Primary hyperthyroidism is the current appellation, demonstrating that the disease is now a biological disease, often discovered systematically, with therapeutic progress, progress in biological identification and possibility of medical forms without mandatory surgical outcome. Bibliographic references accompany the various stages of this historical reminder.
Rev Rhum Mal Osteoartic 1988 May
PMID:[Primary hyperparathyroidism. History]. 305 9

Over a period of 23 years, 3 members of a family of 5 presented with 7 parathyroid adenomas (4 in the first case, 2 in the second case, 1 in the third case). Excision of each adenoma, with systematic pre-operative assessment of the remaining parathyroid tissue, led to complete clinical and laboratory cure of each episode. The delay in the appearance of recurrence was between 3 and 9 years. After reviewing the literature, the authors stress the importance, in any case of hyperparathyroidism, of routinely investigating the serum calcium levels in members of the patient's family, especially if the patient is young and if he has had several episodes or a multiglandular involvement in the one episode. The authors discuss the literature concerning recurrent familial hyperparathyroidism with endocrine polyadenomatosis and the "hypercalcaemia - hypocalciuria" syndrome.
Rev Rhum Mal Osteoartic 1983 Feb
PMID:[Familial and recurrent hyperparathyroidism. Apropos of 7 adenomas in 3 members of the same family. Review of the literature]. 685 34

The level of parathyroid hormone was measured by heterologue C terminal radio-immunological assay in 69 patients with clinical or radiological manifestations of the type seen in primary articular chondrocalcinosis. They were divided into three groups: P1 with undetermined clinical arthropathies; P2 with sub-chondral and arthosic arthropathies; P3 with radiologically definite chondrocalcinosis. They were compared with 57 control subjects broken up into four groups: T1 with chronic rheumatic arthritis, T2 with low back pain, T3 with primary hyperparathyroidism due to adenoma, and T4 with secondary hyperparathyroidism with renal insufficiency. A form of normocalcemic hyperparathormonaemia was demonstrated in more than one out of two patients in group P1 (15/29). It was seen in three-quarters of the cases in group P2 (12/16). And it was seen in more than a quarter of the cases in group P3 (7/24). This hyperparathormonaemia was statistically significant only in groups P1 and P2 compared to the normals in groups T1 and T2. The results we obtained in this study seem to be in complete concordance with those we obtained earlier in idiopathic hemochromatosis. This hyperparathormonaemia seems to regress with age and is often only discovered when the characteristic articular lesions have appeared. The discovery of normocalcemic hyperparathormonaemia several years before the appearance of the radiological signs of the disease would appear to be an important argument in favour of the diagnosis of early articular chondrocalcinosis. The existence of raised parathyroid hormone in primary articular chondrocalcinosis as well as in idiopathic hemachromatosis is special etiopathogenic interest even if there remain numerous questions concerning its origin and mode of action.
Rev Rhum Mal Osteoartic 1981 Dec
PMID:[Normocalcemic hyperparathormonemia and articular chondrocalcinosis. Study of 69 patients compared to 57 controls]. 733 2

Primary aldosteronism comprises two different conditions, the tumoral form usually caused by an adenoma and the idiopathic form due to nodular hyperplasia of the two adenals. More rarely, an adenoma of the adrenal cortex, glucocorticosteroid-sensitive hyperplasia, and angiotensin-sensitive adenoma or an autonomous nodule transformed to primary tumoral hyperplasia, may be observed. Primary alderosteronism may be conceived as a spectrum of genetic abnormalities which express themselves either by hyperplasia or by a tumour. A defect in steroid genesis and prolonged stimulation of the cortex would lead to the formation of nodules which may become autonomous and generate a tumour. Hypertension may be isolated. Detection requires three sampling of serum potassium in all hypertensive patients, a study of the aldosterone-renin axis when the value is less than 3.6 mEq, or whenever the hypertension is severe or resistant to treatment. The diagnosis is made by the association of an increased plasma aldosterone level before getting up in the morning and a plasma renin unaffected by orthostatism. The choice of medical or surgical treatment depends on the uni- or bilateral anatomic substrate. Computerised tomography, very sensitive but not specific, like hormonal studies, often provides incomplete answers. Adrenalectomy is indicated in the presence of a mass of centimetric proportions with concordant results of the dynamic test. In other situations, investigations are continued with the search for an aldosterone gradient by selective venous sampling. This is very valuable to determine the lateralisation but fails in 25% of cases, and its results have to be compared with those of imaging techniques: CT scan, venography and, when necessary, scintigraphy.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1995 Feb
PMID:[Conceptual basis and diagnosis of primary hyperaldosteronism]. 748 76

The purpose of the study was to evaluate the interest of aldosterone precursors assays in arterial hypertension with hypokaliemia and adrenal nodules non due to aldosterone. Seven hypertensive patients, 3 men and 4 women, aged 59.5 +/- 10.1 years were included in the study. After drug withdrawal, kaliemia was 3.1 +/- 0.3 mmol/l (2.7-3.6), active renin 2.9 +/- 1.4 ng/l, plasma aldosterone (aldo) 108 +/- 49.4 pg/ml, cortisol 13 +/- 3.1 micrograms/100 ml, and [S] 0.47 +/- 0.5 micrograms/100 ml. Adrenal CT scan showed an adenoma in 3 patients (30.5 +/- 5 mm) and an unilateral nodular hyperplasia in 4 patients. In all patients, the plasma levels (RIA, chomatographic step) of the following steroids in the mineralocorticoid (MC) pathway were determined: DOC, 18 OH-DOC, B, 18 OH-B and aldosterone. Two from 7 (28%) exerted aldosterone precursors excess, 1 with DOC-producing adenoma (DOC-PA) (table), and 1 with a partial 11 beta hydroxylase deficiency (DOC: 211 pg/ml; S: 1 mu/100 ml). Aldosterone/DOC + 18 OH-DOC ratio proposed as a malignancy index was decreased in the patient with DOC-PA (8.1). No dysfunction in the MC pathway was identified in the 5 other patients. [table: see text] The study suggests the relevance of aldosterone precursors assays in low renin hypertension non due to aldosterone and in incidentally discovered adrenal masses.
Arch Mal Coeur Vaiss 1996 Aug
PMID:[Aldosterone precursors and hypertension with hypokalemia and adrenal module non caused by primary hyperaldosteronism]. 894 78

A 74-year-old woman was hospitalised for pleuro-pneumonia of the right base. The chest x-ray showed the presence of a right paratracheal opacity which persisted during the course of the infectious episode. A computed tomographic scan of the thorax showed a voluminous anterior mediastinal mass which compressed the trachea without invading it. Surgical excision enabled the ablation of a tumour which was haemorrhagic and the histological examination established a diagnosis of cystic parathyroid adenoma. At anytime did the patient present either clinical symptoms or biochemical signs suggesting primary hyperparathyroidism.
Rev Mal Respir 1997 Dec
PMID:[Asymptomatic mediastinal parathyroid adenoma]. 949 10

Hypokalaemic hypertension or resistant hypertension justify investigation for primary hyperaldosteronism. The first step of this investigation is to exclude the ingestion of liquorice, alkalis and diuretics. The second is to make sure that the treatment is compatible with the hormonal tests and that the natriuresis and kaliuresis are normal. The diagnosis then depends on an increased plasma or urinary concentration of aldosterone with a low plasma renin activity. The adenoma of Conn is present in 2/3 of cases and surgically curable, and should be distinguished from adrenal hyperplasia which is treatable with distal diuretics. This is a diagnosis which requires computerised tomography or, when inconclusive, demonstration of unilateral secretion of aldosterone. Adrenalectomy, usually by coelioscopy, is indicated in Conn's adenoma when the patient is young and the hypertension severe or recent. Surgical abstention is strongly advised in cases of adrenal hyperplasia.
Arch Mal Coeur Vaiss 2000 Nov
PMID:[Hypertension and primary hyperaldosteronism]. 1119 Feb 97


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