Use of bumetanide in the treatment of ascites due to liver disease

Moult, P. J. A.; Lunzer, Michael; Trash, D. B.; Sherlock, Sheila

doi:10.1136/gut.15.12.988

Cited by 18 publications

(5 citation statements)

References 7 publications

(5 reference statements)

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“…The elimination of BTN is considerably slower in neonatal patients compared with adults (FDA Bumetanide Label, 2009), with ranges from 8 to 27 h in neonates and 33–100 min in adults (Pacifici, 2012; Puskarjov et al, 2014). BTN is also utilized in the treatment of nephrotic syndrome and massive edema (2–6 mg/day) (Lemieux et al, 1981), heart failure (1–3 mg/day) (Kourouklis et al, 1976), and liver disease (0.5–4 mg/day) (Moult et al, 1974). BTN can be administered orally, intravenously, or intramuscularly and increases urinary output by inhibiting Na + and Cl − in the loop of Henle (Figure 1B3) with secondary actions on the proximal tubules (Bourke et al, 1973; Murdoch and Auld, 1975; Ward and Heel, 1984; FDA Bumetanide Label, 2009).…”

Section: Systemic Effectsmentioning

confidence: 99%

Off-Label Use of Bumetanide for Brain Disorders: An Overview

2019

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Bumetanide (BTN or BUM) is a FDA-approved potent loop diuretic (LD) that acts by antagonizing sodium-potassium-chloride (Na-K-Cl) cotransporters, NKCC1 (SLc12a2) and NKCC2. While NKCC1 is expressed both in the CNS and in systemic organs, NKCC2 is kidney-specific. The off-label use of BTN to modulate neuronal transmembrane Cl − gradients by blocking NKCC1 in the CNS has now been tested as an anti-seizure agent and as an intervention for neurological disorders in pre-clinical studies with varying results. BTN safety and efficacy for its off-label use has also been tested in several clinical trials for neonates, children, adolescents, and adults. It failed to meet efficacy criteria for hypoxic-ischemic encephalopathy (HIE) neonatal seizures. In contrast, positive outcomes in temporal lobe epilepsy (TLE), autism, and schizophrenia trials have been attributed to BTN in studies evaluating its off-label use. NKCC1 is an electroneutral neuronal Cl − importer and the dominance of NKCC1 function has been proposed as the common pathology for HIE seizures, TLE, autism, and schizophrenia. Therefore, the use of BTN to antagonize neuronal NKCC1 with the goal to lower internal Cl − levels and promote GABAergic mediated hyperpolarization has been proposed. In this review, we summarize the data and results for pre-clinical and clinical studies that have tested off-label BTN interventions and report variable outcomes. We also compare the data underlying the developmental expression profile of NKCC1 and KCC2, highlight the limitations of BTN’s brain-availability and consider its actions on non-neuronal cells.

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Section: Systemic Effectsmentioning

confidence: 99%

Off-Label Use of Bumetanide for Brain Disorders: An Overview

2019

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“…Distal di uretics like spironolactone on the other hand, inhibit sodium reabsorption in the convoluted distal and collecting tubules, by antagonizing the effects of aldosterone [7], The recommended dose of bumetanide for diuretic action is 0.5-2 mg/day [3] and that of spironolactone is 100-300 mg/day [8], In the present study we planned to use moder ate doses of both diuretics.…”

Section: Discussionmentioning

confidence: 99%

“…These are more marked with the potent loop diuretics furosemide [4] or bumetanide [1,3] than with spironolactone [8,10]. Total exchangeable potassium is low in cirrhotic patients.…”

Section: Discussionmentioning

confidence: 99%

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Bumetanide, Spironolactone and a Combination of the Two, in the Treatment of Ascites due to Liver Disease

Sarin

Sachdev²,

Mishra³

et al. 1988

Digestion

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There are few studies available comparing the efficacy of loop and distal diuretics and a combination of the two groups, in the treatment of ascites due to liver disease. Thirty-seven nonazotemic cirrhotic patients with ascites were randomly allocated to receive for 2 weeks bumetanide (group A, n = 13), spironolactone (group B, n = 12) or a combination of the two drugs (group C, n = 12) after a 5-day stabilization period. The response to the treatment was 69, 42 and 83% in groups A, B and C, respectively; the difference was not significant. Hypokalemia was seen in 4 patients of group A and mild hyperkalemia in 2 patients of group B. Electrolyte disturbances were minimal in patients of group C. The response to diuretic treatment was prompt in groups A and C. It can be concluded that a combination of loop and distal diuretics is superior to a one-drug regimen in achieving a rapid and better diuretic response with fewer side effects.

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“…Occasional drug rashes 75 ,81 usually of a minor nature, have been observed, along with one case of Stevens-Johnson syndrome. 67 Some of the patients treated with parenteral or high doses of bumetanide have experienced gastrointestinal discomfort, usually of a colicky nature, 49,66,69 In some patients, especially those with renal failure receiving high doses of bumetanide, myal-gias and muscular tenderness have been described. 67 ,74, 82,112,113 The etiology of these changes has not been established.…”

Section: Adverse Effectsmentioning

confidence: 99%

Pharmacology, Therapeutic Efficacy, and Adverse Effects of Bumetanide, A New “Loop” Diuretic

Flamenbaum

Friedman

1982

Pharmacotherapy

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Bumetanide is a recently developed natriuretic and diuretic agent, belonging to the "loop" class of diuretics. Since it is rapidly and almost completely absorbed after oral administration, oral and parenteral formulations have a similar pharmacokinetic profile. Peak plasma levels are achieved approximately 30 min after oral administration. The apparent half-life is 1.2-1.5 hr, and the volume of distribution is about 25 liters. Plasma clearance is 228-255 ml/min. Bumetanide is promptly and almost completely eliminated by metabolism of the butyl side chain and urinary excretion of the parent drug and its metabolites. The principle renal site of action is the ascending limb of the loop of Henle, with a minor effect on the proximal tubule. The drug causes decreases in both free water clearance (during water diuresis) and solute free water reabsorption (during hydropenia), increased fractional delivery of sodium chloride to the distal tubule and a natriuresis approaching 20% of the filtered load of sodium, calciuria, phosphaturia, and minimal bicarbonaturia. Extensive clinical studies have been conducted with both oral and parenteral bumetanide in patients with a variety of edematous conditions. The agent has been clearly demonstrated to be an effective diuretic in the treatment of edema due to cardiac disease (congestive heart failure) and edema, with or without ascites, due to hepatic disease. Bumetanide has also been shown effective in treating edema due to renal disease, even when modest to severe renal insufficiency is present, and it may be useful in the treatment of edema refractory to other loop diuretics. As would be predicted for any potent diuretic, bumetanide administration has been associated with hypokalemia, hypochloremia, metabolic aklalosis, hyperuricemia, and prerenal azotemia. Alterations in glucose metabolism are an inconsistent finding. Transient thrombocytopenia and granulocytopenia have been noted, but no consistent or important alterations in biochemical parameters have been observed. In some patients, especially those with renal failure receiving high doses, myalgias and muscle tenderness have been described. To date only a very limited potential for ototoxicity has been observed. Bumetanide has been administered without difficulty to patients having side effects from other loop diuretics.

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Use of bumetanide in the treatment of ascites due to liver disease

Cited by 18 publications

References 7 publications

Off-Label Use of Bumetanide for Brain Disorders: An Overview

Off-Label Use of Bumetanide for Brain Disorders: An Overview

Bumetanide, Spironolactone and a Combination of the Two, in the Treatment of Ascites due to Liver Disease

Pharmacology, Therapeutic Efficacy, and Adverse Effects of Bumetanide, A New “Loop” Diuretic

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