Twice-a-day quadruple therapy for eradication of Helicobacter pylori in the elderly.

Background: Midday and evening twice-a-day quadruple therapy appears to be the most effective therapy for Helicobacter pylori infection in Northern Sardinia, a site where antibiotics resistance is common.

Aim: The objective of our study was to estimate the efficacy, side-effects, and compliance of a quadruple therapy containing esomeprazole in a group of dyspeptic elderly patients.

Patients And Methods: Consecutive elderly patients positive for H.

Does kidney transplantation normalise cortisol metabolism in apparent mineralocorticoid excess syndrome?

The syndrome of apparent mineralocorticoid syndrome (AME) results from defective 11beta-hydroxysteroid dehydrogenase 2 (11beta-HSD2). This enzyme is co-expressed with the mineralocorticoid receptor (MR) in the kidney and converts cortisol to its inactive metabolite cortisone. Its deficiency allows the unmetabolized cortisol to bind to the MR inducing sodium retention, suppression of PRA and hypertension.

Molecular basis for hypertension in the "type II variant" of apparent mineralocorticoid excess.

The syndrome of apparent mineralocorticoid excess (AME) is a heritable form of hypertension in which cortisol acts as a potent mineralocorticoid. The type I variant results in a severe clinical and biochemical phenotype and arises because of mutations in the gene encoding the type 2 isozyme of 11beta-hydroxysteroid dehydrogenase (11beta-HSD2), an enzyme responsible for the peripheral inactivation of cortisol to cortisone. Only mild abnormalities of cortisol metabolism have been found in the type II variant of AME, suggesting that it may be a separate gene defect.

Apparent mineralocorticoid excess: type I and type II.

The syndrome of apparent mineralocorticoid excess (AME) is a heritable form of hypertension due to an inborn error of cortisol metabolism and is characterized by hypokalemia and low renin levels despite subnormal or normal levels of aldosterone and other known mineralocorticoids. The syndrome is attributable to congenital deficiency of the enzyme 11 beta-hydroxydehydrogenase (11 beta-HSD), which converts cortisol (F) to biologically inactive cortisone. This results in a prolonged half-life of F, which acts at the kidney level as a potent mineralocorticoid (MC).

Hyperinsulinemia and hypertension. Do intestinal hormones play a role?

Gastric inhibitory polypeptide (GIP) is one of the strongest insulinotropic gut factors. Its secretion is induced by oral (but not intravenous) glucose and it has been implicated in the pathogenesis of hyperinsulinemic states (NIDDM, obesity). To determine its relevance to hypertension, 54 subjects were studied: 26 normotensives (12 with and 14 without family history of essential hypertension), and 28 essential hypertensive subjects.

[Insulinemia and intraerythrocytic sodium in normotensive normal-weight subjects with and without a family history for essential arterial hypertension].

To investigate whether the hyperinsulinemia observed in essential hypertensive subjects anticipates the onset of hypertension, and if it may play a role in predisposing to hypertension, we examined the relationships between fasting insulinemia (F.IRI), C-peptide (C-pep), and some known predictive factors of essential hypertension (EH), such as prehypertensive blood pressure, erythrocyte sodium concentration (ESC) and family history of hypertension. Sixty-two normotensive, lean, euglycemic subjects with no family history of diabetes were subdivided in 2 groups: 32 subjects without (F-) and 30 with (F+) family history of EH (at least one parent).

Apparent mineralocorticoid excess type II.

The syndrome of apparent mineralocorticoid excess (AME) is currently understood to reflect impaired peripheral metabolism of cortisol, which is then able to activate the non-selective mineralocorticoid (MC) receptor. The failure of glucocorticoid inactivation at the MC target tissue level in AME involves abnormal activity of 11 beta-hydroxysteroid dehydrogenase, with impaired conversion of cortisol to cortisone, and also of 5 beta-reductase. We have discovered a new form of AME (Type II) in four patients with the same clinical picture of hypertension, hypokalemia, and suppressed renin-angiotensin-aldosterone system, but in whom this conversion seems either to be normal (since cortisol to cortisone metabolite ratio is normal) or to be impaired in both directions, leaving the ratio unchanged.

Beta-blockers and thimidine-3H captation in the human foetal heart.

In the present research the effects that the beta-blockers may express on the development of foetal myocardium have been studied "in vivo" and "in vitro". On the basis of previous researches (7), the beta-blocker effects have been observed by utilizing low doses in comparison with the therapeutic levels. Wistar rats affected by a surgically elicited renal hypertension and "in vitro" cultivated human heart buds, represent the two models utilized for our research.

Insulin hypersecretion: a distinctive feature between essential and secondary hypertension.

Several studies have demonstrated that patients with hypertension have greater plasma insulin levels than normotensive subjects. The aim of the present study was to clarify if hyperinsulinemia in hypertension is a consequence of either increased pancreatic secretion or decreased hepatic clearance, and to determine whether abnormalities of glucose metabolism are equally present in essential and secondary hypertension. In an observational cross-sectional study, fasting blood glucose, plasma insulin, and plasma C-peptide levels were measured in five patient groups: 34 lean normotensive, 19 overweight normotensive, 25 lean essential hypertensive, 27 overweight essential hypertensive, and 20 secondary hypertensive subjects.

Evidence for cortisol as the mineralocorticoid in the syndrome of apparent mineralocorticoid excess.

The hypothesis that cortisol is the functioning mineralocorticoid in the syndrome of apparent mineralocorticoid excess was tested by suppressing its secretion with dexamethasone. The subjects were two siblings with the type 2 form of this syndrome in which the defect in the peripheral metabolism of cortisol lies predominantly in ring A reduction but not in 11 beta-hydroxy dehydrogenation of cortisol to cortisone. Low dosage dexamethasone improved the hypokalemia within several days and hypertension was corrected after 3 weeks of treatment.

Heterogeneous derangement of cellular sodium metabolism in Bartter's syndrome. Description of two cases and review of the literature.

The basic tubular alteration present in Bartter's syndrome is still a subject of controversy. The possibility that a generalized defect in transmembrane ion transport underlies the disease has been extensively investigated. Previous evaluations of cellular sodium metabolism in Bartter's patients showed extremely variable findings.

Defective ring A reduction of cortisol as the major metabolic error in the syndrome of apparent mineralocorticoid excess.

Impaired peripheral metabolism of cortisol in the syndrome of apparent mineralocorticoid excess is currently understood to be causally related to the severe but otherwise unexplained manifestations of mineralocorticoid excess. A normally ambivalent mineralocorticoid receptor responding equally well to glucocorticoids and mineralocorticoids requires prereceptor inactivation of glucocorticoids to elicit a specific mineralocorticoid effect. The failed inactivation step in the form of the syndrome of apparent mineralocorticoid excess first described (type 1) involves the 11 beta-hydroxydehydrogenation of cortisol to cortisone.

Serum insulin, insulin sensitivity, and erythrocyte sodium metabolism in normotensive and essential hypertensive subjects with and without overweight.

Increased insulin circulating levels and perturbations of intracellular sodium metabolism have been reported in essential hypertensive patients, leading to postulate their involvement in the pathophysiology of the disease. In-vitro studies have shown that insulin modulates the activity of some transmembrane sodium transporters. The aim of this investigation was to assess in subjects with essential hypertension and/or overweight, the levels of fasting serum insulin, the activity of sodium transporters and their possible relationships.

Evaluation of insulin-induced changes in the renal response to furosemide in normal subjects.

Over the last years, a large mass of information has accumulated indicating that changes in the serum insulin concentration can affect renal electrolyte excretion. We analyzed the response of the kidney to furosemide in 5 healthy men, in the presence of both normal physiological serum insulin levels and levels at the upper limit of the physiological range, obtained by the hyperinsulinemic-euglycemic clamp technique. After furosemide administration, glomerular filtration rate, urine flow, urine sodium excretion, free water clearance, urine pH, plasma renin activity and plasma aldosterone exhibited the same behavior in the presence of both serum insulin concentrations.

[Insulin resistance in the uremic patient: effects of hemodialysis].

The carbohydrate metabolism abnormalities present in uremia have been attributed to a combination of peripheral resistance to insulin and inhibition of insulin release secondary to beta cells insensitivity. Previous studies evaluated the chronic effects of hemodialysis on glucose metabolism, while acute effects were not examined. In 12 uremic subjects undergoing hemodialysis (3 times a week) the fasting serum levels of glucose, insulin and C-peptide were measured, and the glucose/insulin ratio was calculated as an index of peripheral sensitivity to insulin before and after dialysis.

[Increase of circulating levels of insulin and C-peptide: common factors in essential hypertension and overweight].

The aim of our study was to investigate the hypothesis that insulin resistance is involved in the pathogenesis of essential hypertension, and to explain whether hyperinsulinemia in this condition is the result of either pancreas overproduction or defective hepatic insulin clearance. In 14 lean normotensive, 17 overweight normotensive, 17 lean essential hypertensive, and 20 overweight essential hypertensive subjects, we measured, after overnight fasting, blood glucose, serum insulin, and serum C-peptide, and calculated the glucose/insulin and the insulin/C-peptide ratios, which can be commonly taken as indexes of peripheral sensitivity to insulin and hepatic insulin clearance, respectively. When compared to lean normotensives, overweight and/or hypertensive patients exhibited higher serum insulin and C-peptide concentrations, and a lower glucose/insulin ratio.

[Trans-membrane cationic flow and hemodialysis].

Abnormalities of intracellular ion concentrations and transmembrane fluxes were reported in uremia. In RBC from 12 chronically hemodialyzed patients (age 41 + 12, 7 men, 5 women; mean dialysis duration 31 + 24 months), we evaluated the acute effects of hemodialysis on intracellular Na and K concentrations, ouabain sensitive Na/K pump, furosemide sensitive Na/K cotransport, Na/Li countertransport, and passive permeability to Na. Six patients were normotensive and 6 were taking antihypertensive drugs which were withdrawn before the study.

Insulin resistance and beta-cell hypersecretion in essential hypertension.

To determine whether a decreased sensitivity to insulin is involved in the pathogenesis of essential hypertension, fasting blood glucose, serum insulin, serum C peptide, the glucose:insulin ratio and the insulin:C-peptide ratio were measured in 14 lean normotensives, 17 overweight normotensives, 17 lean hypertensives and 20 overweight hypertensives. Compared with the lean normotensives, the patients who were overweight, those with hypertension and those who were both overweight and hypertensive showed increased fasting serum insulin and C-peptide levels, and a lower glucose:insulin ratio. No significant difference between the normotensive and the hypertensive subjects was found in the insulin:C-peptide ratio.

Insulinemia and blood pressure. Relationships in patients with primary and secondary hypertension, and with or without glucose metabolism impairment.

In order to investigate the relationships between insulinemia and hypertension, fasting insulinemia has been assessed in 117 subjects: 69 normotensive subjects, 36 with essential hypertension, and 12 with renovascular hypertension, all untreated and newly diagnosed, classified in subgroups (euglycemic nonobese, euglycemic obese, with impaired glucose tolerance and with non-insulin-dependent diabetes mellitus). In the patients with essential hypertension fasting insulinemia was significantly higher than in normotensive subjects (P less than .0005).

Effects of furosemide on blood pressure in anephric rats.

This study has been performed in order to evaluate whether furosemide can induce changes in blood pressure independently of its diuretic effects,and whether its pressor effects are connected with the ability to synthetize renal prostaglandins. The experiments were performed in four groups of volume-expanded rats: the first (n.5) had bilateral ligation of the renal vessels; the second (n.

Renal response to furosemide in normal subjects during hyperinsulinaemic clamp.

The study has been performed in an attempt to provide further data on the supposed direct action of insulin on the kidney, based on the assumption that any effect of insulin on sodium reabsorption via co-transport should shift the dose-response curve to the furosemide administration. In five normal male volunteers plasma insulin concentration was changed by means of a hyperinsulinaemic euglycaemic clamp. The diuresis and natriuresis following intravenous injections of furosemide (in increasing doses) were measured in basal conditions and during clamp.

Effects of ketanserin on transmembrane sodium transport in erythrocytes.

Ketanserin, an antagonist of 5-HT2-serotonergic and alpha 1-adrenergic receptors, has come into use for the therapy of mild to moderate arterial hypertension. Quite recent observations have shown changes in transmembrane sodium (Na) transport after the acute administration of high doses of this drug to normal subjects. It is well known that some of these transport systems have an altered activity in essential hypertension.

Pathogenesis of the type 2 variant of the syndrome of apparent mineralocorticoid excess.

The syndrome of apparent mineralocorticoid excess, which is not a primary disorder of the adrenal cortex, describes the association of an unexplained hypermineralocorticoid state with a decreased rate of peripheral 11 beta-hydroxydehydrogenation of cortisol to cortisone. Studies in this syndrome have led to the hypothesis that peripheral cortisol inactivation is the normal mechanism permitting specific mineralocorticoid recognition. This view reconciled developing evidence that the mineralocorticoid receptor itself could not distinguish between mineralocorticoids and glucocorticoids.

Evidence for a direct and non-receptor-mediated action of 5HT2 antagonists on transmembrane cation transport systems.

Changes in transmembrane sodium fluxes have been reported in normotensive and in hypertensive subjects after ketanserin administration. In this study, the effects of the serotonergic system on transmembrane sodium transport mechanisms have been investigated in vitro. In erythrocytes drawn from ten healthy subjects, we studied the effects of serotonin (5HT) on the Na/K pump, Na/K cotransport, Na/Li countertransport, and passive permeability of Na.

[Disseminated intravascular coagulation and acute hepatic necrosis at the end of pregnancy. A case report].

A 30-year-old woman in the 36th week of her second pregnancy, suddenly developed jaundice with remarkable liver necrosis, accompanied by generalized bleeding due to disseminated intravascular coagulation (DIC). She underwent a caesarean and a dead foetus was extracted from the uterus. Heparin and frozen plasma infusion resulted in a prompt recovery from the haemostatic disorder.