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PubMedDate not supplied

Fixed-dose combination diuretics in congestive heart failure: an evaluation.

Thirty-two patients with congestive heart failure were studied for their clinical and biochemical responses to the administration of two combination diuretic products (hydrochlorothiazide/spironolactone and hydrochlorothiazide/triamterene) and the single entity diuretic furosemide. Data from these studies revealed the following: 1. Comparison of the patients on furosemide with those receiving the combination products showed no difference in serum potassium or 24-hour potassium excretion. 2. Significant changes in blood urea nitrogen, plasma renin activity, and urinary aldosterone excretion were noted with both fixed-combination medications but not with furosemide. 3. The combination diuretics offered no clinical benefits over the single agent furosemide. 4. Therapy is best served by the use of a single effective diuretic agent for the treatment of most patients with congestive heart failure.

Blood Urea Nitrogen↗
PubMed2001

Determination and characterization of diuretics in human urine by liquid chromatography coupled to pneumatically assisted electrospray ionization mass spectrometry.

The aim of this work was to develop a method for the characterization and determination of diuretics in human urine samples by liquid chromatography (LC) coupled to pneumatically assisted electrospray ionization (ES) mass spectrometry (MS). The diuretics studied were substances forbidden by the IOC such as trichlormethiazide, furosemide, canrenoic acid, benzthiazide, bendroflumethiazide, bumetanide, etacrynic acid and spironolactone. For this purpose, the operational parameters of electrospray, such as counter electrode voltage, capillary voltage, sample cone voltage and source temperature, were optimized in order to obtain the best signal stability and the highest sensitivity for the greatest number of diuretic agents. The optimized separation method was successfully coupled with the MS system to analyze the above-mentioned diuretics extracted from spiked urine samples by a liquid extraction and clean-up procedure at basic pH, using ethyl acetate as solvent and the salting-out effect (NaCl). The mass spectra obtained provide adequate information for identification purposes. Positive urine samples obtained from athletes were also analyzed. The presence of these substances in human urine was confirmed by this method, making LC/ES-MS an analytical tool to be considered in the area of antidoping control.

Chromatography, Liquid↗
PubMed2002

Gas-phase behaviour of negative ions produced from thiazidic diuretics under electrospray conditions.

A systematic mass spectrometric study of 10 thiazidic diuretics and related compounds was undertaken by mass spectrometry (MS) with electrospray ionization in the negative ion mode. Collisional dissociation 'in-source' (CID-MS) and in a low-pressure collision cell (CID-MS/MS) were compared in both excitation regions. Spectra obtained by CID-MS and by CID-MS/MS were matched. Using the two methods, loss of HCl and consecutive dissociations from 2HCl losses were exhibited from compounds such as methyclothiazide and trichlormethiazide but not from other thiazidic diuretics that contain chlorine substituents in the aromatic moiety. However, deprotonated dichlorphenamide gave rise to loss of HCl by CID-MS and CID-MS/MS. For other diuretics such as hydroflumethiazide and hydrochlorothiazide, the loss of HCN and [HCN + SO(2)] was relevant. Reaction mechanisms were checked by means of deuterium-hydrogen exchange, which showed that deprotonation took place regioselectively on the heterocyclic moiety. The cleavage pathways require molecular isomerization forming ion-dipole complexes prior to decompositions, allowing long-distance proton transfer for neutral elimination. Identifications of the most specific fragmentations presented in this paper were applied to the screening and unambiguous identification of diuretics for horse doping control.

Benzothiadiazines↗
PubMed2005

Simultaneous determination of beta-blocking agents and diuretics in doping analysis by liquid chromatography/mass spectrometry with scan-to-scan polarity switching.

A previously described method for the screening of 18 diuretics and probenecid was substantially extended with 21 beta-blockers and 8 other diuretics allowing simultaneous determination of diuretics and beta-adrenergic blocking agents in human urine. Analysis was performed using an ion trap instrument with an electrospray ionisation (ESI) interface after liquid/liquid extraction with ethyl acetate. Full-scan MS and full-scan MS2 were applied in combination with scan-to-scan polarity switching. All compounds were separated in less than 22 min. The detection limits for the diuretics were between 5 and 100 ng/mL and for the beta-adrenergic blocking agents were between 5 and 500 ng/mL. The excretion of carvedilol was followed after intake of one tablet of Dimitone. Other doping agents including strychnine, norbuprenorphine and mesocarb hydroxysulfate could also be detected with this method.

Adrenergic beta-Antagonists↗
PubMed1992

Diuretics may increase risk of renal cell carcinoma.

The risk for kidney cancer was examined in a Danish cohort of 192,133 people on a hospital discharge register who had been given a diagnosis of hypertension, heart failure, or edema, and were presumed to be probable users of diuretics. The subjects were identified from 1977 to 1987 and followed-up for cancer through 1987. A total of 10,630 cancers was observed. While the risk for all cancers was increased slightly (standard mortality ratio [SMR] = 122, 95 percent confidence interval [CI] = 120-124), the risk for renal cell carcinoma was more than doubled (SMR(men) = 221, CI = 192-253; SMR(women) = 246, CI = 213-283). Increased risks were found in all age groups, and, although surveillance bias was present initially, the risk increased consistently in the years following discharge. Risk estimates for individuals discharged with hypertension were similar to those for the total cohort. Use of diuretics was validated in a random sample of 100 individuals. More than 70 percent were taking diuretics at the time of discharge. The increased risk for renal cell carcinoma in this cohort may indicate either that diuretics are involved in the etiology of renal cell carcinoma or that the risk can be attributed to confounders, including smoking, which affect risk for both the discharge diagnosis and renal cell carcinoma.

Aged↗
PubMed1986

Torasemide, a new potent diuretic. Double-blind comparison with furosemide.

The pharmacodynamic effects of torasemide, a new potent loop diuretic, were compared with those of furosemide in a double blind controlled study in 18 hypertensive patients with oedema of various origins. Given orally for 5 days, torasemide was clinically very effective and well tolerated. On a weight basis, the diuretic, natriuretic and chloruretic effects of torasemide were about 8-times greater than those of furosemide. However, the kaliuretic effect of torasemide was only 3-times greater than that of furosemide, suggesting that torasemide is more potassium sparing than furosemide. Torasemide displayed a rapid onset of action, similar to that of furosemide but had a longer diuretic effect without any rebound phenomenon. Torasemide and furosemide did not effect creatinine clearance or uric acid excretion. Both furosemide and torasemide lowered systolic blood pressure but the effect of torasemide was more marked than that of furosemide. In this group of aged and hypertensive patients with oedema, the pharmacokinetics of torasemide was comparable to that reported in young healthy volunteers, and were similar on the first and fifth days of treatment. The long duration of action and the potassium sparing effect of torasemide compared to furosemide are promising features of this new loop diuretic in the treatment of oedema and hypertension.

Aged↗
PubMed1994

Which diuretic to use?

The choice of a diuretic depends on knowledge of its efficacy in different disease states as well as the complications associated with its use. However, efficacy of the various diuretic agents as determined in healthy subjects may not always be applicable to the sick patient. The thiazide group appears to be the main offender with regard to hypokalemia and metabolic upsets; these complications seem to stem from long-term use and high dosages. Interest has been expressed on the influence of diuretic induced hypokalemia (and intracellular potassium deficiency) in inducing insulin resistance. The lipid abnormalities may arise as a result of this resistance or may be consequent on hyperinsulinemia from other as yet undetermined mechanisms. In addition, hypertension per se may be associated with insulin resistance. It is interesting to speculate that diuretics, which are commonly used in the treatment of hypertension, may, in some way, perhaps via the induction of hypokalemia, unmask this resistance.

Diuretics↗
PubMed1993

Renal excretory responses to single and repeated administration of diuretics in healthy subjects: clinical connotations.

Administration of an initial oral dose of hydrochlorothiazide 25 mg to healthy subjects is followed by increased 24-hour urinary outputs of sodium, chloride, and potassium. On the fourth day of once-daily dosing with hydrochlorothiazide 25 mg, 24-hour natriuresis and chloriuresis are no longer augmented, but the elevation in 24-hour kaliuresis that follows the first dose remains unchanged. Twenty-four-hour urinary calcium output is consistently reduced during repeated once-daily administration of hydrochlorothiazide 25 mg. The first oral dose of the loop diuretic torasemide augments the average natriuresis and kaliuresis in the 6 hours immediately after dosing in healthy subjects, in a dose-dependent fashion, within the 2.5 to 10-mg range. These increased urinary outputs are followed by rebounds below postplacebo values between 6 and 24 hours after dosing. As a result of this biphasic response, torasemide 2.5 mg qualifies as a nondiuretic formulation (it does not elevate 24-hour natriuresis), whereas torasemide 5 and 10 mg qualify as diuretic formulations. After the seventh dose of torasemide 5 or 10 mg during a regimen of once-daily therapy, 24-hour urinary sodium and chloride outputs no longer differ from their postplacebo counterparts. Twenty-four-hour kaliuresis tends to increase in a dose-dependent fashion after the first dose of torasemide (torasemide 2.5 and 5 mg do not augment it significantly), but this tendency is no longer present after the seventh once-daily dose, when torasemide (2.5, 5, or 10 mg) does not elevate the mean 24-hour kaliuresis. Twenty-four-hour calciuresis tends to increase in a dose-dependent manner (torasemide 2.5 mg does not elevate it significantly) after the first dose of torasemide; this calciuretic effect does not change in intensity after 7 days of once-daily treatment. The time course of natriuresis over the 24 hours following the administration of any given formulation of a loop or of an early distal tubular diuretic to healthy subjects is alike after the first and after the nth once-daily dose; therefore, it constitutes a definite characteristic of any given oral formulation. In the case of torasemide, lower doses have more protracted effects on natriuresis, to the extent that the time course of natriuresis over the 24 hours after administration of torasemide 2.5 mg to healthy subjects resembles the time course after administration of hydrochlorothiazide 25 mg, rather than the time course after administration of the overtly diuretic formulation torasemide 10 mg.

Calcium↗
PubMed1982

Interactions of diuretics with the renal kallikrein-kinin and prostaglandin systems.

The renal kallikrein-kinin system may participate in the diuretic, natriuretic and antihypertensive effect of diuretics. This possibility was investigated by studying the influence of hydrochlorothiazide on blood pressure and urinary kallikrein excretion in patients with essential hypertension. Furthermore, the effect of kallikrein-blockade and prostaglandin-synthesis inhibition on the acute furosemide-induced changes of diuresis, natriuresis, GFR and renal plasma flow were studied in normotensive subjects. Thiazide treatment normalized the reduced kallikrein excretion of the hypertensive patients. The fall in mean arterial blood pressure was significantly correlated with the increase in urinary kallikrein excretion. In the normotensive subjects aprotinin-induced kallikrein inhibition failed to alter the acute response to furosemide, whereas indomethacin attenuated the diuretic and natriuretic effect of furosemide. The combination of indomethacin and aprotinin had a greater suppressive effect on plasma renin activity than indomethacin alone, suggesting a participation of kallikrein in renin release. An increase in the activity of the renal kallikrein-kinin system may contribute to the long-term antihypertensive effect of thiazide diuretics but it does not seem to be involved in the acute renal responses to furosemide.

Adult↗
PubMed1984

Influence of digitalis and diuretics on ouabain binding sites on human erythrocytes.

It has been reported that during chronic treatment with digitalis, the number of digitalis binding sites is increased in human erythrocytes [22]. From this finding a tachyphylaxis for cardiac glycosides has been postulated. We reinvestigated this problem in several groups of patients. The number of 3H-ouabain binding sites per erythrocyte in control persons (group I) was 214 +/- 60, n = 43 (means +/- SD). The dissociation constant (KD) was 1.8 +/- 0.5 nM. Thirteen patients (group II) taking cardiac glycosides only, for at least 6 months, had 281 +/- 99 (p less than 0.05) ouabain binding sites per single red cell, KD = 1.8 +/- 0.7 nM. Group III (34 patients) took digitalis for more than 6 months and diuretics for at least 3 months (352 +/- 126 (p less than 0.001), KD = 1.6 +/- 0.6). Twenty-three of these (group IV) were taking a combination with "K+-saving" diuretics (336 +/- 194 (p less than 0.01), KD = 1.6 +/- 0.5) and (group V, 11 patients) a combination with "K+-losing" diuretics (462 +/- 133 (p less than 0.001), KD = 1.4 +/- 0.4). Nine patients (group VI) had a chronic hypokalemia, mainly due to taking furosemide (437 +/- 98 (p less than 0.001), KD = 1.5 +/- 0.4). Four control persons took 50 mg hydrochlorothiazide daily for more than 4 months without measurable K+-losses and without changes in ouabain binding sites. It is concluded from these findings that diuretic treatment with chronic hypokalemia in addition to digitalis is accompanied by a significant increase in ouabain binding sites in human red cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Hemodynamic interactions between diuretics and calcium antagonists in the treatment of hypertensive patients.

To investigate the hypotensive and hemodynamic effects of plain and extended-release (ER) formulations of felodipine added to a diuretic in the treatment of moderate essential hypertension, we studied 18 patients in a randomized, double-blind, cross-over study. Blood pressure (BP), heart rate (HR), hemodynamics (bioimpedance), foot volume (Archimedes' principle), and symptoms were evaluated after a 1-month placebo washout, after 1-month's treatment with a fixed combination of hydrochlorothiazide 50 mg plus amiloride 5 mg (HA), and then after felodipine 5 mg twice daily (F) or felodipine ER 10 mg daily (FER) (double-blind phase), each given for 2 weeks in a randomized sequence together with the diuretic. All measurements were performed at the end of the dosing interval. At baseline, supine SBP/DBP was 175.6 +/- 12.9/113.4 +/- 8.1 mmHg; HR was 77.3 +/- 7.0 beats/min; CO was 5.3 +/- 1.4 l/min; SVR was 2166 +/- 707 dynes sec. cm5, and foot volume was 433 +/- 195 ml (FV). HA induced a reduction (p less than 0.05) in BP; one patient had a DBP = 90 mmHg and was excluded from the combination study; eight patients had a DBP reduction of greater than or equal to 10 mmHg (responders), and their blood pressure was mainly reduced by a fall in SVR. HR, CO, and FV were unchanged. The addition of felodipine to a diuretic induced a further significant (p less than 0.001) reduction in BP with respect to HA alone, with no differences between F and FER. All patients had a DBP fall greater than 10 mmHg, which had no relationship to their response to the diuretic.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Body electrolytes in bronchopulmonary dysplasia and the effects of diuretic therapy.

Body electrolytes and their regulatory hormones were studied in preterm infants who suffered from bronchopulmonary dysplasia under two groups: those who were not treated with diuretics (Group II), and those who were treated with diuretics (Group III). The values were compared with a group of matched healthy controls (Group I). Lower serum Na levels, a need of higher Na intake, and higher urinary Na concentrations and urinary specific gravity were found in Group II infants. FeNa was normal and the urinary flow rate was lower than the controls. These data suggest an inability of these infants to dilute urine. Group III infants who were treated with diuretics showed higher serum Na levels and lower urinary specific gravity than Group II infants. These values, as well as water and Na intake/output ratios, were all similar to the control values. Serum aldosterone level was highest in Group II but did not reach significance. Intracellular K concentration was not different between the groups indicating an optimum total body K balance. A significant negative correlation between serum Na and aldosterone levels was found in Group II infants, which was not noted in the controls. Significant correlations were also found between FeNa and plasma aldosterone level in the BPD groups, unlike the controls. The control group of infants showed significant positive correlation between Na balance and serum Na levels. Our results suggest that inability to dilute urine appropriately might be the reason for the BPD patients to retain body water. Water restriction and diuretic therapy therefore are reasonable therapeutic approaches in such cases.

Bronchopulmonary Dysplasia↗
PubMed2000

Detecting drug-drug interactions using a database for spontaneous adverse drug reactions: an example with diuretics and non-steroidal anti-inflammatory drugs.

OBJECTIVE: Drug-drug interactions are relatively rarely reported to spontaneous reporting systems (SRSs) for adverse drug reactions. For this reason, the traditional approach for analysing SRS has major limitations for the detection of drug-drug interactions. We developed a method that may enable signalling of these possible interactions, which are often not explicitly reported, utilising reports of adverse drug reactions in data sets of SRS. As an example, the influence of concomitant use of diuretics and non-steroidal anti-inflammatory drugs (NSAIDs) on symptoms indicating a decreased efficacy of diuretics was examined using reports received by the Netherlands Pharmacovigilance Foundation Lareb. METHODS: Reports received between 1 January 1990 and 1 January 1999 of patients older than 50 years were included in the study. Cases were defined as reports with symptoms indicating a decreased efficacy of diuretics, non-cases as all other reports. Exposure categories were the use of NSAIDs or diuretics versus the use of neither of these drugs. The influence of the combined use of both drugs was examined using logistic regression analysis. RESULTS: The odds ratio of the statistical interaction term of the combined use of both drugs was increased [adjusted odds ratio 2.0, 95% confidence interval (CI) 1.1-3.7], which may indicate an enhanced effect of concomitant drug use. CONCLUSION: The findings illustrate that spontaneous reporting systems have a potential for signal detection and the analysis of possible drug-drug interactions. The method described may enable a more active approach in the detection of drug-drug interactions after marketing.

Adverse Drug Reaction Reporting Systems↗
PubMed1999

Loop diuretics enhance the secretion of prostacyclin in vitro, in healthy persons, and in patients with chronic heart failure.

BACKGROUND: Previous studies suggest that the acute haemodynamic effects of loop diuretics are due to a direct dilation of blood vessels and are not related to diuretic properties, but possibly to prostaglandin secretion. OBJECTIVES: We investigated whether in vitro human endothelial and renal epithelial cells responded to torasemide or furosemide with enhanced secretion of the vasodilator prostaglandin prostacyclin (PGI2). We also investigated the effects of loop diuretics on plasma concentrations of PGI2 and its physiological antagonist thromboxane after 25 min of administration of drugs in 44 patients with congestive heart failure (CHF) and 44 healthy volunteers. METHODS: The PGI2 levels were measured after extraction in ethyl acetate by RIA as levels of 6-KetoPGF1alpha, a stable metabolite from a non-enzymatic degradation. TxB2 concentration, the stable hydrolysis product of TxA2, was also measured by RIA. RESULTS: In human endothelial and renal epithelial cells, both loop diuretics induced an increase of 6-KetoPGF1alpha secretion that reached a peak after about 5 min and remained stable for 30 min of exposure to the drugs. The magnitude of the phenomenon was lesser in epithelial than in endothelial cells. Moreover, in both cell lines, there was a significantly higher secretion of 6-KetoPGF1alpha to torasemide than furosemide (P < 0.05). Concentrations of 6-KetoPGF1alpha at baseline were similar between the groups of CHF patients receiving the two different drugs. After 25 min of both drugs, 6-Keto-PGF1alpha significantly increased (P < 0.01), and this was significantly higher in patients treated with 10 mg of torasemide (P < 0.05 vs furosemide). Levels of PGI2 at baseline were lower in healthy controls than those reached by CHF patients and similar between groups. After 25 min of both drugs, PGI2 plasma levels were significantly increased (P < 0.01). Baseline values of TxB2 were significantly higher in CHF patients compared with controls (P < 0.01 vs respective groups). and, more importantly, furosemide but not torasemide increased TxB2 levels in patients and controls (P < 0.05 vs baseline). CONCLUSIONS: Our study is the first demonstration in human tissue of increased secretion of PGI2 both in vitro and in vivo, after torasemide or furosemide administration. This phenomenon, which may explain in part the vasodilatory effects of these drugs, was more evident with torasemide and was reached at lower concentrations of the drug. Accordingly, we also found that furosemide but not torasemide stimulated the release of the PGI2 physiological antagonist thromboxane in CHF patients and healthy controls.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Diuretic therapy for mild hypertension: the "real" cost of treatment.

The benefit of any medical intervention, particularly drug therapy, must be weighed against its cost. These costs are not only dollar expenditures but effects on lifestyle and overall health. Diuretic therapy for hypertension has been in use long enough to allow long-term clinical evaluation. It is clear from the numerous prospective drug intervention trials involving hypertensive patients that diuretic therapy is not free of "costs." Aside from the fact that 15 to 20% of diuretic-treated patients reportedly drop out of trials because of side effects, including exertional dyspnea, fatigability, lethargy and impotence, numerous metabolic derangements have been reported with these drugs, i.e., potassium, uric acid, lipid, sodium, glucose and magnesium alterations. Perhaps most important are the changes in lipid fractions, which may be responsible for the failure of antihypertensive therapy to decrease the risk of coronary heart disease. Thus, although diuretics are somewhat less expensive than other antihypertensive drugs in terms of dollars, their overall costs are high. The major alternatives, such as the alpha-blocker prazosin or the central nervous system agent clonidine, are preferable, do not impair a patient's lifestyle and are recommended to be used along with changes in diet and an exercise program for control of mild to moderate hypertension.

Aged↗
PubMed1986

Selected mechanisms of diuretic-induced electrolyte changes.

Thiazide diuretic therapy has been associated with several biochemical electrolyte imbalances including potassium loss. The onset, duration and magnitude of potassium excretion can influence decisions concerning drug therapy, particularly in hypertensive patients at risk if they develop diuretic-induced hypokalemia. The potassium depletion seen during the course of antihypertensive therapy with thiazides is brought about by 2 primary mechanisms: the increased delivery of sodium to the distal tubules for sodium-potassium exchange, and the development of secondary hyperaldosteronism, which causes resorption of sodium with a loss of potassium into the urine. The diuresis caused by thiazides is maximal between 8 and 12 hours. However, resultant volume contraction stimulates elevated serum aldosterone levels, which can be present for 24 hours or longer. Therefore, potassium loss may exceed the period of diuresis. Diuretics are effective antihypertensive therapy in many patients with mild hypertension. Potassium-sparing agents can offset potassium imbalance that often occurs with diuretics, and thus, these agents have become an important addition to the physician's treatment armamentarium for appropriate patients.

Aldosterone↗
PubMed1986

Diuretic therapeutics in the pediatric patient.

Careful management of fluid and electrolytes has long been an intrinsic part of pediatric practice. However, the augmentation of these manipulations through the rational use of diuretic agents requires considerable skill. In pediatric medicine, the regulation of pharmacokinetic processes and their interface with pharmacodynamic processes show dramatic age-related changes. These ontogenetic processes and their modification by various disease states must be considered carefully before selection and application of diuretic agents. The available data concerning the ontogeny of renal function and the attempts to apply diuretic therapy to pediatric disease are reviewed. It is concluded that results obtained to date suffer from the absence of a rigorous attempt to answer the fundamental therapeutic questions: What drug? What dose? What duration of therapy? A rational "target-effect" strategy is proposed for the application of diuretic agents to pediatric medicine.

Acid-Base Equilibrium↗
PubMed1987

Monotherapy with the calcium channel antagonist nisoldipine for systemic hypertension and comparison with diuretic drugs.

A comparative, double-blind, placebo-controlled, double-dummy, randomized, crossover trial was performed in 32 hypertensive patients (initial blood pressure [BP] 165/105 +/- 3/2 mm Hg), most of them obese women, to evaluate the antihypertensive efficacy and tolerability of the new calcium channel blocking drug nisoldipine, 10 mg once or twice daily, over 6 weeks compared with the diuretic hydrochlorothiazide-amiloride (hydrochlorothiazide, 25 mg, in combination with amiloride, 2.5 mg once or twice daily). Adequate 24-hour control of BP (supine diastolic BP less than 90 mm Hg) was achieved in 15 of 32 patients (47%) with monotherapy by 1 agent and in 23 of 32 patients (72%) when including those who responded to either agent. Both nisoldipine and the diuretic had a flat dose-response curve. The larger dose of diuretic yielded lower systolic and exercise BP values (erect and supine) than high-dose nisoldipine (p less than 0.05), with less headache (p less than 0.05). In the other 9 patients who did not respond, the combination of nisoldipine 10 mg plus hydrochlorothiazide (25 mg)-amiloride (2.5 mg) was administered and yielded a response in 8 patients (overall response including monotherapy 96%). Ten patients were given nisoldipine for an additional period of 6 months, and they required an average dose of 33 mg/day for BP control. In both the 6-week and 6-month studies, nisoldipine monotherapy caused frequent subjective adverse effects. In contrast, in the 6-week study the combination of low-dose nisoldipine and low-dose diuretic gave good BP control with no adverse effects.

Adult↗