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Loop Diuretic (loop + diuretic)

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PRESCRIBER, Issue 9 2008
Article first published online: 21 MAY 200
Dabigatran launched Dabigatran (Pradaxa), an orally active direct thrombin inhibitor, has been introduced for the prophylaxis of venous thromboembolism in patients undergoing elective total hip or knee replacement. Treatment is initiated within four hours of surgery and continued for 10 days after knee replacement and 28-35 days after hip replacement. Dabigatran has been shown to be as effective and well tolerated as enoxaparin (Clexane). The launch was widely publicised in the lay media; the charity Lifeblood claimed it could help prevent tens of thousands of deaths. NICE is preparing a technology appraisal of the new agent but it has not announced a publication date. Loop diuretics may increase bone loss Continuous use of a loop diuretic appears to double the rate of bone loss in men compared with nonusers, an observational study suggests (Ann Intern Med 2008;168: 735-40). Up to five years' follow-up of 3269 men aged over 65 revealed that the mean rate of bone loss in the hip among those who did not use a loop diuretic was 0.33 per cent compared with 0.78 per cent among users and 0.58 per cent in those who had intermittently used a loop diuretic. Use of these agents should be included as a risk factor for fractures, the authors suggest. Rosuvastatin not for heart failure patients? Prescribers should pause before using rosuvastatin (Crestor). in patients with heart failure and ischaemic heart disease, the National Prescribing Centre (NPC). says. Commenting on the CORONA trial (N Engl J Med 2008; published online 5 Nov 2007; 10.1056/NEJMoa 0706201)., which found no reduction in cardiovascular events or mortality in older patients with systolic heart failure despite a reduction in LDL-C, the NPC says GPs should still consider evidence-based statins such as simvastatin in this patient group. The reason for the outcome of CORONA is unclear but the NPC points out that not all statins affect mortality equally. Rimonabant CV benefits sustained Two-year follow-up of the RIO-Europe trial has shown that the benefits of rimonabant (Acomplia). on weight loss and cardiovascular risk factors are sustained with continuing treatment (Eur Heart J 2008; published online doi: 10.1093/ eurheartj/ehn076). In addition to a dietary deficit of 600kcal per day, rimonabant 20mg per day achieved greater mean weight loss (5.5 vs 1.2kg). and improvements in waist circumference, HDL-cholesterol, triglycerides, fasting glucose and insulin levels, insulin resistance, and metabolic syndrome prevalence compared with placebo. Many patients discontinued treatment (placebo 42 per cent, rimonabant 45 per cent). but, although psychiatric events were more common with rimonabant during the first year, there was little difference in patients remaining in the second year. Early glatiramer cuts MS progression risk Early treatment with glatiramer acetate (Copaxone). appears to reduce the risk of progression to multiple sclerosis (MS), according to a study presented at the 60th Annual Meeting of the American Academy of Neurology in Chicago. Interim analysis of the PreCISE trial showed that, in patients with a single episode and MRI suggestive of MS, glatiramer was associated with a lower incidence of progression to a second episode of MS compared with placebo (25 vs 43 per cent). The placebo arm of the trial has now been stopped. NRT before quitting Beginning nicotine replacement therapy (NRT) before stopping smoking may double the six-month success rate compared with beginning treatment on the scheduled quit day, a meta-analysis suggests (Addiction 2008;103: 557-63). The analysis of four trials involving 755 participants found that starting NRT two to four weeks before the agreed quit date was twice as likely as the conventional strategy to achieve abstinence after six weeks and six months. Copyright © 2008 Wiley Interface Ltd [source]

Hospitalized patients with acute decompensated heart failure: Recognition, risk stratification, and treatment review

JOURNAL OF HOSPITAL MEDICINE, Issue S6 2008
Alpesh Amin MD
Abstract Acute decompensated heart failure (ADHF) has emerged as a major healthcare problem. It causes approximately 3% of all hospitalizations in the United States, with the direct medical cost of these hospitalizations estimated at $18.8 billion per year. Early recognition, risk stratification, and evidence-based treatment are crucial in reducing the morbidity, mortality, and costs associated with this disorder. Classic signs and symptoms of ADHF, such as rales, dyspnea, and peripheral edema, may be absent at hospital presentation and, even when present, are not specific to this disorder. As a result, serum B,type natriuretic peptide level is now used to rapidly and accurately detect ADHF. Multivariate analyses have identified renal dysfunction, hypotension, advanced age, hyponatremia, and comorbidities as significant and independent mortality risk factors. Based on these factors, mortality risk can be stratified from very low to very high using published algorithms that have been validated in independent populations. Evidence-based guidelines for the treatment of ADHF are available from both the European Society of Cardiology and the Heart Failure Society of America. In general, an intravenous loop diuretic, either alone or in combination with a vasodilator, is recommended as initial therapy in patients with volume overload, depending on the patient's clinical status. Use of inotropic agents should be limited to the small subset of patients with low-output syndrome and significant hypotension. In any event, frequent monitoring of clinical response is essential, with subsequent therapy determined by this response. Finally, focused patient education during hospitalization may help reduce readmissions for ADHF. Journal of Hospital Medicine 2008;3(Suppl 6):S16,S24. © 2008 Society of Hospital Medicine. [source]

Latest news and product developments

Benefits and risks of furosemide in acute kidney injury

ANAESTHESIA, Issue 3 2010
K. M. Ho
Summary Furosemide, a potent loop diuretic, is frequently used in different stages of acute kidney injury, but its clinical roles remain uncertain. This review summarises the pharmacology of furosemide, its potential uses and side effects, and the evidence of its efficacy. Furosemide is actively secreted by the proximal tubules into the urine before reaching its site of action at the ascending limb of loop of Henle. It is the urinary concentrations of furosemide that determine its diuretic effect. The severity of acute kidney injury has a significant effect on the diuretic response to furosemide; a good ,urinary response' may be considered as a ,proxy' for having some residual renal function. The current evidence does not suggest that furosemide can reduce mortality in patients with acute kidney injury. In patients with acute lung injury without haemodynamic instability, furosemide may be useful in achieving fluid balance to facilitate mechanical ventilation according to the lung-protective ventilation strategy. [source]

Pharmacokinetics and pharmacodynamics of intravenous trasemide in mutant nagase aalbuminemic rats

BIOPHARMACEUTICS AND DRUG DISPOSITION, Issue 1 2003
Eun J. Kim
Abstract The importance of plasma protein binding of intravenous furosemide in circulating blood for its urinary excretion and hence its diuretic effects in mutant Nagase analbuminemic rats (NARs, an animal model for human familial analbuminemia) was reported. Based on the furosemide report, the diuretic effects of another loop diuretic, torasemide, could be expected in NARs if plasma protein binding of torasemide is considerable in the rats. This was proven by this study. After intravenous administration of torasemide, 10 mg/kg, to NARs, the plasma protein binding of torasemide was 23.3% in the rats due to binding to , - and , -globulins (this value, 23.3%, was greater than only 12% for furosemide), and hence the percentages of intravenous dose of torasemide excreted in 8-h urine as unchanged drug was 14.9% in the rat (this value was considerably greater than only 7% for furosemide). After intravenous administration of torasemide to NARs, the AUC (301 versus 2680 µg/min/ml) was significantly smaller [due to significantly faster both Clr (4.81 versus 0.386 ml/min/kg) and Clnr (28.3 versus 3.33 ml/min/kg)], terminal half-life (18.3 versus 73.5 min) and mean residence time (6.97 versus 61.8 min) were significantly shorter (due to faster Cl, 33.2 versus 3.74 ml/min/kg), and amount of 8-h urinary excretion of unchanged torasemide (446 versus 323 µg, due to increase in intrinsic renal excretion) was significantly greater than those in control rats. The 8-h urine output and 8-h urinary excretions of sodium and chloride were comparable between two groups of rats although the 8-h urinary excretion of torasemide was significantly greater in NARs. This could be explained by the following. The amount of urinary excretion of torasemide was significantly greater in NARs than that in control rats only between 0 and 30 min urine collection. In both groups of rats, the urinary excretion rate of torasemide during 0,30 min reached an upper plateau with respect to urine flow rate as well urinary excretion rates of sodium and chloride. Therefore, the diuretic effects (8-h urine output and 8-h urinary excretions of sodium and chloride) were not significantly different between the two groups of rats. Copyright © 2002 John Wiley & Sons, Ltd. [source]

Pharmacokinetics and pharmacodynamics of intravenous bumetanide in mutant nagase analbuminemic rats: importance of globulin binding for the pharmacodynamic effects

BIOPHARMACEUTICS AND DRUG DISPOSITION, Issue 4 2001
Eun J. Kim
Abstract The importance of plasma protein binding of intravenous furosemide in circulating blood for its urinary excretion and hence its diuretic effects in mutant Nagase analbuminemic rats was reported. Based on the furosemide report, the diuretic effects of another loop diuretic, bumetanide, could be expected in analbuminemic rats if plasma protein binding of bumetanide is considerable in the rats. This was proved by this study. After intravenous administration of bumetanide, 10 mg/kg, to analbuminemic rats, the plasma protein binding of bumetanide was 36.8% in the rats mainly due to considerable binding to , - and , -globulins (this value, 36.8%, was considerably greater than only 12% for furosemide), and hence the percentages of intravenous dose of bumetanide excreted in 6 h urine as unchanged drug was 16.0% in the rat (this value was considerably greater than only 7% for furosemide). After intravenous administration of bumetanide to analbuminemic rats, the area under the plasma concentration,time curve from time zero to time infinity (1012 compared with 2472 ,g min/mL) was significantly smaller [due to significantly faster both renal clearance (1.49 compared with 0.275 ml/min/kg) and nonrenal clearance (8.30 compared with 3.71 ml/min/kg)], terminal half-life (9.94 compared with 22.4 min) and mean residence time (4.25 compared with 5.90 min) were significantly shorter (due to faster total body clearance, 9.88 compared with 4.05 ml/min/kg), and amount of 6 h urinary excretion of unchanged bumetanide (559 compared with 261 ,g, due to increase in intrinsic renal excretion) was significantly greater than that in control rats. The 6 h urine output and 6 h urinary excretions of sodium, chloride and potassium were comparable between two groups of rats although the 6 h urinary excretion of bumetanide was significantly greater in analbuminemic rats. This could be explained by the following. The amount of urinary excretion of bumetanide was significantly greater in analbuminemic rats than that in control rats only between 0 and 30 min urine collection. In both groups of rats, the urinary excretion rates of bumetanide during 0,30 min reached a upper plateau with respect to urine flow rate as well urinary excretion rates of sodium, potassium and chloride, therefore, the diuretic effects (6 h urine output and 6 h urinary excretions of sodium, potassium and chloride) were not significantly different between two groups of rats. Copyright © 2001 John Wiley & Sons, Ltd. [source]

Hyponatremia and Heart Failure,Treatment Considerations

CONGESTIVE HEART FAILURE, Issue 1 2006
Domenic A. Sica MD
Hyponatremia as it occurs in the heart failure patient is a multifactorial process. The presence of hyponatremia in the heart failure patient correlates with both the severity of the disease and its ultimate outcome. The therapeutic approach to the treatment of hyponatremia in heart failure has traditionally relied on attempts to improve cardiac function while at the same time limiting fluid intake. In more select circumstances, hypertonic saline, loop diuretics, and/or lithium or demeclocycline have been used. The latter two compounds act by retarding the antidiuretic effect of vasopressin but carry with their use the risk of serious renal and/or cardiovascular side effects. Alternatively, agents that selectively block the type 2 vasopressin receptor increase free water excretion without any of the adverse consequences of other therapies. Conivaptan, lixivaptan, and tolvaptan are three such aquaretic drugs. Vasopressin receptor antagonists will redefine the treatment of heart failure-related hyponatremia and may possibly evolve as adjunct therapies to loop diuretics in diuretic-resistant patients. [source]

Undertreatment of congestive heart failure in an Australian setting

JOURNAL OF CLINICAL PHARMACY & THERAPEUTICS, Issue 1 2004
P. J. Boyles BPharm (Hons)
Summary Aim:, Guidelines for the management of patients with chronic heart failure have undergone change in recent years, with , -blockers and spironolactone shown to reduce mortality when added to angiotensin converting enzyme (ACE) inhibitors, diuretics and digoxin. The aim of this study was to examine the therapeutic management of heart failure in patients admitted to Tasmania's three major public hospitals, with an assessment of the appropriateness of the therapy according to contemporary published guidelines. Methods:, An extensive range of clinical and demographic data was retrospectively extracted from the medical records of consecutive adult patients admitted to the medical wards of the hospitals with heart failure, either as a primary diagnosis or as a comorbidity, during a 6-month period in late 1999,early 2001. Results:, The 450 patients (57% females) had a mean age of 77·8 ± 10·2 years, and were being treated with a median of seven drugs on hospital admission. The percentages of patients being treated with the major drugs of interest were: ACE inhibitors (50%), , -blockers (22%), spironolactone (15%), digoxin (24%), loop diuretics (65%) and angiotensin-II receptor antagonists (8%). Almost 10% were taking a non-steroidal anti-inflammatory agent. Less than one-half the patients who were receiving an ACE inhibitor were taking a target dose for heart failure. There were no significant differences in the pattern of drug use between the three hospitals. Underuse of heart failure medications was most pronounced in women and elderly patients. Conclusions:, The data suggest that current guidelines for the treatment of heart failure are still not being reflected in clinical practice. The relatively low use of drugs shown to improve survival in heart failure is of concern and warrants educational intervention. [source]

Hyponatremia in Heart Failure: Revisiting Pathophysiology and Therapeutic Strategies

CLINICAL CARDIOLOGY, Issue 6 2010
Amir Kazory MD
Hyponatremia is frequently encountered in patients with heart failure (HF), and its association with adverse outcomes is well-established in this population. While hyponatremia is an independent marker for severity of HF, it is not certain whether it has a causal impact on the progression of the disease. There are no universally accepted consensus guidelines regarding therapeutic strategies for HF-associated hyponatremia and volume overload; current societal guidelines do not address management of this complication. Whereas thiazide diuretics are known to induce or worsen hyponatremia in this setting through a number of mechanisms, loop diuretics can be considered a readily available first-line pharmacologic therapy. Consistent with pathophysiology of the disease and mechanisms of action of loop diuretics, available clinical evidence supports such an approach provided that patients can be closely monitored. Use of vasopressin receptor antagonists is an emerging therapeutic strategy in this setting, and the efficacy of these agents has so far been shown in a number of clinical studies. These agents can be reserved for patients with HF in whom initial appropriate loop diuretic therapy fails to improve serum sodium levels. Copyright © 2010 Wiley Periodicals, Inc. [source]

Rapid clinical assessment of hemodynamic profiles and targeted treatment of patient with acutely decompensated heart failure

CLINICAL CARDIOLOGY, Issue S5 2004
Greegg C. Fonarow M.D.
Abstract Acutely decompensated heart failure (ADHF) is characterized by hemodynamic abnormalities and neurohormonal activation that contribute to heart failure (HF) symptoms, end-organ dysfunction, arrhythmias, and progressive cardiac failure. The management of ADHF in the emergency department (ED) can be simplified and improved by a 2-min bedside assessment that identifies any of four possible hemodynamic profiles on the basis of clinical signs and symptoms. The profiles are based on whether congestion is present or absent (wet or dry) and perfusion is adequate or limited (warm or cold). A wet-warm profile is seen more frequently in the ED than any of the other three profiles (wet-cold, dry-warm, and dry-cold). The four clinically determined profiles have been shown to predict clinical outcomes and may be used to guide initial HF therapy. The goals of treating ADHF are to stabilize the patient, reverse acute hemodynamic abnormalities, rapidly reverse dyspnea and/or hypoxemia caused by pulmonary congestion, and initiate treatments that will decrease disease progression and improve survival. An ideal agent for the wet-warm profile would rapidly reduce pulmonary congestion, produce balanced arterial and venous dilation, promote natriuresis, lack direct positive inotropic effects, and not cause reflex neuroendocrine activation. Intravenous nesiritide in conjunction with loop diuretics has been found safe and effective as initial treatment for patients with the wet-warm profile. For the wet-cold profile, more intensive therapy and invasive hemodynamic monitoring may prove useful. This review will discuss the rapid clinical determination of hemodynamic profiles in patients presenting to the ED with ADHF and the options for their initial medical management. Case studies representing the wet-warm, wet-cold, dry-warm, and dry-cold profiles will be presented and discussed. [source]