Bioavailability of Bumetanide in Grossly Oedematous Patients

Bailie, George R.; Grennan, A; Waldek, Stephen

doi:10.2165/00003088-198712060-00004

Cited by 10 publications

(6 citation statements)

References 6 publications

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“…These findings of an overall potency ratio P/F of approximately 6:40, on a weight to weight basis, is in agreement with other reports of relative potency ratios for comparative short-term studies (Clissold & Brogden, 1985). In previous reports from this laboratory the bioavailability of piretanide in patients with severe CCF was found to be 68 ± 7% (n = 3) compared with 79 ± 6% (n = 4) in normal subjects (McNabb et al, 1984b (Bailie et al, 1987). (84.0 ± 9.9 mmol mg-1; n = 13; P < 0.01, unpublished observations).…”

Section: Resultssupporting

confidence: 92%

“…While there was no change in tmax (time for maximal plasma concentration), the Cmax (maximum plasma concentration) tended to be lower in the cardiac failure group, the mean values were, however, not significantly different from those obtained in normajs [tma (min) 60 ± 12 (n = 4) vs 58 ± 6 (n = 13) and Cmax (ng ml-) 189 ± 36 (n = 4) vs 273 ± 38 (n = 13) respectively (unpublished observations)]. A recent report has shown that oral bioavailability of bumetanide, a closely related sulphamoylbenzoate diuretic, is not diminished in grossly oedematous patients (Bailie et al, 1987).…”

Section: Discussionmentioning

confidence: 78%

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Acute and long‐term renal and metabolic effects of piretanide in congestive cardiac failure.

McNabb

Noormohamed

Lant

1988

Brit J Clinical Pharma

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1 The renal and metabolic effects of the sulphamoylbenzoic acid diuretic, piretanide, have been studied, under controlled dietary conditions, in 39 patients with congestive cardiac failure.2 In acute studies, peak saluresis occurred within 4 h of oral piretanide administration; saluresis was complete within 6 h, after which a significant antidiuretic effect was observed. Addition of triamterene, 50 mg, blunted the 0-6 h kaliuretic effect of piretanide. Over 24 h, piretanide, alone, caused insignificant urinary losses of potassium when compared with control. 3 In comparative studies, the piretanide dose-response curve was found to be parallel to that of frusemide over the dose range studied. The 0-6 h saluretic responses of piretanide, 6, 12 and 18 mg, were found to be equivalent to frusemide, 40,80 and 120 mg respectively. The collective mean ratios of all the saluretic responses to each dose of piretanide with the corresponding dose of frusemide was observed to be 0.99 ± 0.12, over 0-6 h period, and 0.86 ± 0.09 over the 24 h period. The relative potency of piretanide, when compared with frusemide was found to be 6.18 (95% confidence limits 4.87 -8.33), over the 0-6 h period, and 4.73 (95% confidence limits 3.65 -6.14), over 24 h period. 4 In 15 patients in severe cardiac failure, urinary recovery of piretanide, over first 6 h, at the start of treatment was 21.2 ± 2.1% while efficiency of the diuretic (mmol Na/mg drug) was 47.3 ± 4.1. Long-term piretanide therapy was continued in the same group for up to and in some cases over 3 years. No other diuretics or potassium supplements were given.Piretanide dosage ranged from 6 to 24 mg day-' according to clinical need. Plasma potassium fell significantly at 12 and 24 months, though remaining within the normal range. At these same times, significant elevations in both plasma urate and total fasting cholesterol were observed. Two patients developed overt gout on high dose piretanide therapy (24 mg day-1). Piretanide was well tolerated, and effective in the management of congestive cardiac failure without any other recognized metabolic or electrolyte changes.

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Section: Resultssupporting

confidence: 92%

Section: Discussionmentioning

confidence: 78%

Acute and long‐term renal and metabolic effects of piretanide in congestive cardiac failure.

McNabb

Noormohamed

Lant

1988

Brit J Clinical Pharma

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“…A recent study from our laboratory reports fewer hospitalizations and better quality of life in patients with heart failure treated with a completely absorbed loop diuretic as represented by torsemide compared with furosemide (67). Edematous disorders do not cause malabsorption of loop diuretics (6,13,18,34,86,91,94,95). Absorption is slowed, particularly in patients with decompensated heart failure (95), but the total amount absorbed is the same as in healthy individuals.…”

Section: Pharmacokinetcs Of Loop Diureticsmentioning

confidence: 99%

“…In patients with congestive heart failure and preserved renal function, delivery of loop diuretics to the tubular fluid is normal (5,39,74). Historically, the possibility has been raised that patients with overt heart failure likely have gut wall edema causing diuretic malabsorption; studies have shown that the same quantity of loop diuretic is absorbed in such patients as occurs in healthy control subjects (6,13,92,95). Thus malabsorption does not occur.…”

Section: Pharmacodynamics Of Loop Diuretics In Edematous Disordersmentioning

confidence: 99%

Loop diuretics: from the Na-K-2Cl transporter to clinical use

Shankar

Brater

2003

American Journal of Physiology-Renal Physiology

155

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The diuretic response to loop diuretics in various disease states has consistently been found to be subnormal. One of the key determinants of the degree of diuretic response is the functional integrity of the sodium-potassium-chloride transporter in the loop of Henle. Studies in animal models suggest that expression/activity of the transporter may be affected by factors such as altered natural splicing events of NKCC2 (the gene encoding for the renal transporter), renal prostanoids, vasopressin, and other autacoids. We have reviewed the pharmacokinetics and pharmacodynamics of loop diuretics in health and in edematous disorders for which they are used. On the basis of evidence reviewed in this paper, we propose that altered expression or activity of the sodium-potassium-chloride transporter in the loop of Henle, in conjunction with events occurring in other segments of the nephron, possibly accounts for the altered diuretic response to these agents. Thus the modulators of this altered expression/activity could serve as important therapeutic targets for alternative diuretic regimens in these conditions.

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“…8,9 In contrast, bumetanide and torsemide are less affected by intestinal wall edema, allowing for higher and more predictable bioavailability ranging from 80% to 100%. 8,10 Once in the blood, concentration kinetics also differ; furosemide and bumetanide have half-lives of 1 to 3 hours and a 6-to 8-hour duration of action, and torsemide has a longer half-life at 4 to 6 hours, with a 12-to 18-hour duration of action. 8,11 Compared with other loop diuretics, torsemide intrinsically blocks sympathetic nervous system and aldosterone activity, which may lead to favorable cardiac remodeling and decreased kaliuresis.…”

Section: Diuretic Therapymentioning

confidence: 99%

Volume Overload in Heart Failure

Houston

Kalathiya

Kim

et al. 2015

Mayo Clinic Proceedings

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Acute decompensated heart failure is the leading cause of hospital admission in the United States, with a high risk of readmission within 30 days. Most acute decompensated heart failure admissions are driven by congestive signs and symptoms resulting from fluid and sodium overload. We reviewed the evidence base addressing the management and prevention of fluid overload in heart failure, focusing on recent clinical trials. All the references in this review were obtained through PubMed and had at least 1 of the following key words: heart failure and volume overload, congestion, loop diuretics, thiazide diuretics, aldosterone antagonists, dopamine, cardiorenal syndrome, nesiritide, vasopressin antagonists, ultrafiltration, sodium restriction, fluid restriction, telemonitoring, and invasive hemodynamic monitoring. We also reviewed relevant references cited in the obtained articles, especially articles addressing methods of treating or preventing volume overload in patients with heart failure.

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Bioavailability of Bumetanide in Grossly Oedematous Patients

Cited by 10 publications

References 6 publications

Acute and long‐term renal and metabolic effects of piretanide in congestive cardiac failure.

Acute and long‐term renal and metabolic effects of piretanide in congestive cardiac failure.

Loop diuretics: from the Na-K-2Cl transporter to clinical use

Volume Overload in Heart Failure

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