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Biomedical subjects

C Marone

Publications and source records attributed to C Marone.

At least 37 records · Page 2Linked to original sources
PubMed1991

Cardiovascular pressor reactivity after chronic converting enzyme inhibition.

In addition to inhibiting the formation of angiotensin II, chronic converting enzyme inhibition may affect other blood pressure modulating factors. The influence of an 8 week treatment phase with cilazapril on the activity of the renin-angiotensin-aldosterone and sympathetic nervous systems, the pressor reactivity to infused angiotensin II or norepinephrine, the chronotropic response to isoproterenol, and body sodium and plasma atrial natriuretic peptide concentrations was assessed in 11 normal subjects and 12 patients with essential hypertension. As compared to a 4 week placebo phase, cilazapril decreased arterial pressure in both study groups (from 124/83 +/- 9/6 to 114/77 +/- 9/5 mm Hg and from 143/102 +/- 13/7 to 137/96 +/- 10/10 mm Hg; P less than .025); exchangeable sodium (-158 mmol and, respectively, -104 mmol) and upright plasma aldosterone (-24% and -15%) also tended to fall. Heart rate, the chronotropic response to posture or isoproterenol, plasma norepinephrine levels, the concentration/pressor response curve to norepinephrine, plasma atrial natriuretic peptide concentration, plasma angiotensin II and the responses of blood pressure or plasma aldosterone to angiotensin II were unchanged after 8 weeks of cilazapril. Plasma renin activity increased (+175% to +650%). These findings indicate that the blood pressure lowering effect of cilazapril in the stable phase of pharmacological intervention is not associated with modifications of sympathetic-dependent pressor reactivity or beta-adrenergic sensitivity. Plasma angiotensin II concentration and angiotensin II-dependent pathways including the pressor and aldosterone responsiveness to angiotensin II are also unchanged.

Adolescent↗
PubMed1990

[Acute kidney failure in infectious mononucleosis].

Overt renal disease is a rare complication of infectious mononucleosis (MI). In contrast, up to 16% of patients with MI have been shown to exhibit abnormalities in urinary sediment. Histological abnormalities--usually interstitial nephritis, and occasionally glomerular lesions--are rather common. Clinical symptoms include in rare cases isolated macrohematuria, occasionally a nephrotic or nephritic syndrome, and more commonly acute renal failure due to rhabdomyolysis, hepatorenal syndrome or acute interstitial nephritis. We report two observations of acute renal failure with a typically benign course and discuss these observations in the light of an updated literature survey of 34 patients.

Acute Kidney Injury↗
PubMed1990

[Sicca syndrome in amyloidosis].

We report on two patients with rheumatoid arthritis and sicca syndrome due to secondary amyloidosis (A-amyloid) with involvement of the kidneys and gut. At autopsy, generalized amyloidosis was found with deposits in the salivary and lacrimal glands. Two other patients developed sicca syndrome due to primary systemic L-amyloidosis with Bence-Jones paraproteinuria, renal insufficiency and amyloid cardiomyopathy; both died of cardiac failure. Although sicca syndrome with amyloidosis has been described only occasionally, it is possible that this association is more frequent. These observations suggest that not only Sjögren's syndrome but also amyloidosis should be considered as a possible cause of sicca syndrome.

Amyloidosis↗
PubMed1989

[Severe acute pneumopathy following low-dose methotrexate therapy in chronic polyarthritis].

A 70-year-old patient with a history of rheumatoid arthritis was hospitalized for severe acute pneumonitis after 36 weeks of treatment with low-dose methotrexate (7.5 mg/week). High dose corticotherapy and assisted ventilation were necessary to obtain a clinical response. Medical history, clinical signs, laboratory findings. X-ray films of the chest and special investigations suggest the diagnosis of acute low-dose methotrexate pneumonitis.

Aged↗
PubMed1989

Efficacy and pharmacokinetics of piretanide in patients with congestive heart failure.

The efficacy and pharmacokinetics of the diuretic piretanide were studied in two groups of six patients hospitalized for congestive heart failure. A dosage of 2 x 6 mg day-1 to 2 x 12 mg day-1 of intravenous piretanide for 7 days was sufficient to abrogate most symptoms of cardiac insufficiency. When compared with another group of healthy volunteers, patients with congestive heart failure had reduced total body clearance of piretanide of about 50% which was attributable to a diminished renal but not non-renal clearance. The analysis of the interrelationship between urinary piretanide excretion and diuresis by means of a linearized Emax-model revealed a maximal diuresis of 231 ml h-1 and a urinary piretanide excretion to induce half-maximal diuresis of 245 micrograms h-1. Thus patients with congestive heart failure exhibit a decreased renal clearance of piretanide and a good response to this high ceiling diuretic after intravenous dosing.

Aged↗
PubMed1988

[Plasmapheresis therapy in Guillain-Barré polyneuroradiculitis].

The outcome of Guillain-Barré polyneuritis is not always benign. Since no therapy of proven effectiveness is available and an immunologic etiology is presumed, plasma exchange treatment has been repeatedly used. We report on three patients with severe polyneuritis who were unable to walk. Two were also in acute respiratory failure. All the cases exhibited surprisingly good improvement correlating in time with plasma exchange. A review of the literature suggests that plasma exchange can at least be recommended in severe cases of Guillain-Barré acute polyneuritis with inability to walk. Treatment should be started within 1-2 weeks of onset of the disease.

Adult↗
PubMed1987

[Resistance to diuretics].

Resistance to diuretics may be due to disorders of renal sodium excretion as well as altered pharmacodynamics or -kinetics of the diuretic used. After consideration of some of the factors responsible for diminished natriuresis, some typical clinical examples are discussed.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1987

Massive renal adenomatosis: a case exhibiting low-grade malignancy.

A young man with gradually enlarging kidneys and radiographic findings strongly suggestive of polycystic disease was found on autopsy to have massive bilateral renal enlargement due to innumerable multifocal tumors, arising in atypical renal tubular epithelium, whose microscopic appearance ranged from that of so-called renal adenoma to that of low-grade renal cell carcinoma. Electron microscopy confirmed the epithelial nature of the neoplasms. Local lymph node metastases and pulmonary micrometastases were present. Death was due to renal insufficiency and to refractory hyperkalemia probably secondary to tumor necrosis. Only one similar case is reported in the recent literature.

Adenoma↗
PubMed1987

Cardiovascular effects of verapamil in essential hypertension.

Calcium antagonists may affect the regulation of body sodium and adrenergic-dependent mechanisms. Exchangeable sodium, blood volume, plasma norepinephrine, renin, aldosterone, pressor responsiveness to norepinephrine, heart rate responses to isoproterenol, and lipid metabolism were studied in 15 patients with essential hypertension after 8 weeks of treatment with verapamil (348 +/- 68 (SD) mg/day). Supine blood pressure decreased from 153/103 +/- 19/12 mm Hg to 140/95 +/- 14/12 mm Hg (P less than 0.01). Exchangeable sodium, blood volume, plasma norepinephrine, renin and aldosterone, serum total cholesterol, the lipoprotein fractions, and apoprotein levels were unchanged. The norepinephrine pressor and the isoproterenol chronotropic doses tended to increase, whereas the dose-response curve of blood pressure related to plasma norepinephrine was significantly displaced to the right (F = 5.34; P less than 0.05). The antihypertensive effect of verapamil is associated with a decreased cardiovascular pressor responsiveness to norepinephrine without changes in endogenous noradrenergic activity. Moreover, verapamil does not modify the sodium/fluid volume state, the activity of the renin-angiotensin aldosterone axis, or lipid metabolism.

Adult↗
PubMed1985

Body sodium-blood volume state, aldosterone, and cardiovascular responsiveness after calcium entry blockade with nifedipine.

Exchangeable sodium, blood volume, plasma norepinephrine (NE), epinephrine, renin and aldosterone levels, and pressor responses to infused NE or angiotensin II (AII) were assessed in ten patients with essential hypertension on placebo, following 6 to 8 weeks of calcium-antagonist nifedipine (NIF), 3 X 10 to 20 mg/day, and after 6 to 8 weeks on NIF combined with the diuretic chlorthalidone (CHLOR), 25 to 50 mg/day. Pressor effects of infused calcium also were evaluated on placebo and NIF. Supine blood pressure was decreased from 151/97 +/- 5/2 (SEM) to 132/88 +/- 6/2 mm Hg after NIF alone (P less than 0.05) and to 124/83 +/- 7/3 mm Hg after NIF + CHLOR (P less than 0.01). Body wt was increased from 72.7 to 73.9 kg on NIF alone (P less than 0.05), but decreased to 72.1 (P less than 0.05 compared with placebo) after adding CHLOR. Exchangeable sodium also rose from 2642 +/- 237 to 3360 +/- 266 mmoles on NIF (+ 27%; P less than 0.01) and returned to control values (2638 +/- 248 mmoles) after addition of CHLOR. Plasma volume was only slightly modified on NIF (from 2621 +/- 193 to 2751 +/- 160 ml; + 5%), but was reduced to 2232 +/- 231 ml on NIF + CHLOR (P less than 0.05). Responses of circulating aldosterone to AII were similarly diminished (P less than 0.01) during both conditions. Heart rate, supine and upright plasma renin, aldosterone and catecholamine levels, and pressor responses to NE, AII, or calcium were not consistently changed.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Pharmacokinetic and pharmacodynamic interaction between furosemide and metolazone in man.

In various clinical situations a poor diuretic response to furosemide may be improved by the addition of metolazone. The mechanism of this additive effect is unclear. The purpose of the present investigation was to establish whether metolazone changes the pharmacokinetics of furosemide and by this mechanism enhances the diuretic effect. Eight volunteers were given an intravenous infusion of 4 mg h-1 of furosemide for 12 h. After 6 h 2.5 mg metolazone were administered orally. The addition of metolazone increased diuresis, urinary excretion of sodium and chloride (P less than 0.01), but decreased urinary excretion of calcium (P less than 0.01), while furosemide excretion remained unchanged. Total body clearance and renal clearance values of furosemide were similar before and after administration of metolazone. Our data confirm the additive diuretic effect of the combination treatment metolazone-furosemide and show for the first time a distinct hypocalciuric action of metolazone, similar to thiazides. Moreover metolazone does not affect the pharmacokinetics of furosemide.

Calcium↗
PubMed1985

Antihypertensive efficacy and tolerance of penbutolol: results of a co-operative study in 227 patients.

An open, co-operative study was carried out in 227 patients with mild to severe essential hypertension to assess the efficacy and tolerance of penbutolol, given as monotherapy, in controlling blood pressure. Patients received a single daily dose (40 mg in the majority) for 8 weeks and were assessed every 2 weeks. The results showed that there was a significant reduction (p less than 0.01) in systolic, diastolic and mean arterial blood pressure and in pulse rate after 2 weeks compared with pre-treatment values, and there was a further significant reduction (p less than 0.01) comparing 8-week values with those measured after 2 weeks. Response to treatment did not differ significantly between those patients who were newly diagnosed and those who had received previous antihypertensive medication. The largest percentage reduction in blood pressure from initial values was recorded in those patients with the more severe hypertension (diastolic 116 to 130 mmHg) and a considerable number of all the patients became normotensive during the trial period. Records of side-effects indicated a global incidence of 17.6%, the most frequently reported being dizziness and mild gastro-intestinal disorders; only 1 patient complained of bradycardia and another of cold extremities. Eighteen (7.9%) patients dropped out of the study due to side-effects.

Adult↗
PubMed1984

Comparison of the short-term effects of the loop diuretic piretanide and furosemide in patients with renal insufficiency.

The natriuretic effect of the new loop diuretic piretanide was investigated in patients with severe renal insufficiency and was compared with that of furosemide. In the first study 4 hospitalized patients (serum creatinine 407 to 1220 mumol/l) were examined after administration of piretanide (12, 24, 48 and 96 mg to two patients, and 24, 48, 96 and 192 mg to 2 other subjects, given every third day). In the second study 6 hospitalized patients (serum creatinine 194 to 698 mumol/l) were studied after receiving orally 2 different doses of piretanide and 2 different doses of furosemide orally, given every fourth day. The mean natriuretic effect of 48 mg and 96 mg piretanide was 250 and 340% of the control value for the entire group, and 311 to 480% in the subgroup of patients with serum creatinine below 530 mumol/l. For a given dose the natriuresis was inversely correlated with renal function, and at a given serum creatinine level the natriuretic response was dose-dependent. The drug had less effect on water and potassium diuresis than on natriuresis. No significant difference in natriuretic effect was found on comparison with furosemide given in the ratio furosemide:piretanide 3.33:1. The pharmacokinetic data showed a direct correlation between the dose and the mean plasma concentration and also between urinary recovery of the drug and the measured natriuretic response.

Creatinine↗
PubMed1984

Pharmacokinetics of high doses of piretanide in moderate to severe renal failure.

The pharmacokinetics of piretanide was studied in 10 patients with chronic renal failure. After administration of a high oral dose (12 to 192 mg) of piretanide the kinetics behaved according to an open 2-compartment model. The elimination constant in the first phase (alpha) ranged from 0.385 to 0.756 h-1 and in the second phase (beta) from 0.079 to 0.274 h-1. The corresponding elimination half-lives ranged from 55 to 108 min (t 1/2 alpha) and from 152 to 524 min (t 1/2 beta). Only an average of 2.8% of the orally administered drug was recovered in 24 h urines. Nevertheless, a good correlation was found between urinary recovery or renal clearance of the drug and residual renal function. The elimination of piretanide by non-renal mechanisms appeared to be increased when renal function was greatly diminished.

Adult↗
PubMed1984

Pressor factors and cardiovascular pressor responsiveness after short-term antihypertensive therapy with the calcium antagonist nifedipine alone or combined with a diuretic.

Exchangeable sodium, blood volume, plasma norepinephrine, epinephrine, renin levels, and pressor responses to infused norepinephrine or angiotensin II were assessed in 10 patients with essential hypertension on placebo, following six to eight weeks of monotherapy with nifedipine, 3 X 10-20 mg/day, and after six to eight weeks on nifedipine combined with the diuretic chlorthalidone, 25 to 50 mg/day. Supine blood pressure was decreased after nifedipine alone (P less than 0.05) and even further after nifedipine + chlorthalidone (P less than 0.01). Body weight and exchangeable sodium increased after nifedipine (P less than 0.05), but were decreased after adding chlorthalidone. Blood volume was unchanged after nifedipine, but was reduced on nifedipine + chlorthalidone (P less than 0.05). Heart rate, supine plasma renin, catecholamine levels, and pressor responses to norepinephrine or angiotensin II were not consistently changed on nifedipine alone or combined with chlorthalidone. These findings indicate that in the established phase of treatment, nifedipine may exert its antihypertensive effect without necessarily altering cardiovascular responsiveness to norepinephrine and angiotensin II. Moreover, mild sodium retention may develop on nifedipine at least in some hypertensive patients.

Adult↗
PubMed1982

Effect of standard oral glucose loading on aldosterone secretion in primary hyperaldosteronism.

The effects of mild acute decreases in plasma potassium induced by standard oral glucose loading (100 g) on plasma aldosterone and renin levels were assessed in 10 patients with primary hyperaldosteronism as compared with 10 normal subjects. Following overnight fast, mean plasma glucose was identical in both groups; plasma insulin, potassium and renin levels were lower and plasma aldosterone higher in patients than in controls. Glucose loading significantly increased plasma glucose and insulin concentrations and decreased plasma potassium and aldosterone levels in both groups. The increases in plasma insulin and the decreases in plasma potassium or aldosterone tended to be blunted in primary hyperaldosteronism. glucose-induced changes in plasma aldosterone correlated significantly (P less than 0.025) with those in plasma potassium in the patients and with variations in plasma renin activity in the normal subjects. These findings suggest that the metabolic changes induced by glucose ingestion are capable of modifying aldosterone secretion in primary hyperaldosteronism. However, the glucose-induced decreases in plasma aldosterone are blunted in this disorder; this could be related to the impaired insulin response to glucose loading.

Adult↗