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The predictive value of digoxin and furosemide treatment for identifying patients receiving treatment for congestive heart failure (CHF), the use of angiotensin-converting-enzyme (ACE) inhibitors in this population, and the ability of a pharmacist outreach program to address underutilization of ACE inhibitors were studied. All physicians and owner-managers of community pharmacies on Newfoundland's Avalon Peninsula were asked to participate in the study. Pharmacists who agreed to participate were asked to list patients of the participating physicians with prescriptions for (1) furosemide and digoxin with and without an ACE inhibitor or angiotensin II-receptor inhibitor and (2) an ACE inhibitor. Physicians were visited by a pharmacist and asked whether each of their patients receiving digoxin and furosemide was being treated for CHF and to identify further cases of CHF among their patients receiving an ACE inhibitor. Intervention-group physicians received academic detailing on the use and dosage of ACE inhibitors and angiotensin II-receptor inhibitors for CHF. Both groups were reinterviewed after three months to establish what if any changes in therapy had occurred for each patient discussed during the first visit. The positive predictive value of digoxin and furosemide treatment for identifying patients receiving treatment for CHF was 94%. Seventy-six percent of patients identified by physicians as CHF patients who were taking digoxin and furosemide were treated with an ACE inhibitor. Thirty-six percent of patients treated with an ACE inhibitor for CHF received the targeted dosage. Four physicians stated that the outreach visit influenced their prescribing, but there was no significant difference in ACE inhibitor prescribing between the intervention and control groups. A pharmacist outreach program involving the use of prescription records and academic detailing did not affect prescribing or dosages of ACE inhibitors but demonstrated value as a quality assurance tool.
Delirium may be induced by a variety of reasons, among them drugs and in particular the combination of drugs. In elderly people a delirium is often misinterpreted as dementia. Anticholinergic activity is the mode of action by which drugs cause delirium. Antipsychotic drugs, antidepressants, antihistamines, and of course anticholinergic drugs themselves are the major anticholinergic classes of drugs. In addition some opioids have anticholinergic effects. Other drugs may induce delirium by dehydration (loop diuretics like furosemide) or sedation (benzodiazapines like lorazepam). Elderly people are at especially high risk to develop delirium, because of the multitude of drugs often prescribed to them, because they tend to drink to little, and because their brain is more sensitive to psychoactive drugs.
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A state-of-the-art clinical computing system was investigated to test the hypothesis of whether a completely and predictably absorbed loop diuretic (torasemide) offers clinical advantages over a diuretic that is poorly and erratically absorbed (furosemide).
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Using local intra-arterial administration of losartan, a selective angiotensin II type 1 (AT1) receptor antagonist, we examined the contribution of endogenous angiotensin II to the maintenance of basal and sympathetically stimulated vascular tone in the forearm of healthy man under conditions of sodium repletion and depletion. The effects of losartan on responses to exogenous angiotensin I, angiotensin II, bradykinin and noradrenaline were also determined.
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1896 prescriptions for diuretics prescribed by GPs during two months.
To evaluate the secretory regulation of 19-hydroxyandrostenedione (19-OH-AD), its plasma concentration was measured before and after stimulation and inhibition tests for the ACTH-adrenal axis and the renin-angiotensin system in 50 normal subjects. Basal levels of plasma 19-OH-AD did not correlate with either those of plasma renin activity (PRA) or the plasma aldosterone concentration (PAC), but positively correlated with those of plasma cortisol. Plasma 19-OH-AD was stimulated by 0.25 mg ACTH-(1-24) and was suppressed by 1 mg dexamethasone (DEX) as were plasma cortisol and PAC. On the other hand, with 2-h standing alone or iv 40 mg furosemide plus 2-h standing, plasma 19-OH-AD and cortisol did not increase but PRA and PAC did. With iv furosemide plus 2-h standing with 3 mg DEX pretreatment, plasma 19-OH-AD and cortisol did not respond either, but PRA and PAC increased. With 25 mg oral captopril following 1-h standing with 3 mg DEX pretreatment, plasma 19-OH-AD and cortisol did not change but PAC decreased. These results indicate that the secretion of 19-OH-AD is mainly under the control of the ACTH-adrenal axis rather than the renin-angiotensin system.
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Subjects with ADHF within 12 hours of hospital admission were randomly assigned to continuous infusion or twice daily bolus therapy with furosemide. There were three co-primary endpoints assessed from admission to discharge: the mean paired changes in serum creatinine, estimated glomerular filtration rate (eGFR), and reduction in B-type natriuretic peptide (BNP). Secondary endpoints included the rate of acute kidney injury (AKI), change in body weight and six months follow-up evaluation after discharge.
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LC-MS/MS analysis showed that chlorothiazide typically eluted at 2.6 minutes and furosemide at 4.8 minutes. Each compound was degraded by exposure to strong ultraviolet light in a time-dependent manner. Both unmixed and mixed solutions retained over 90% of the original concentrations of chlorothiazide and furosemide for up to 96 hours. Furosemide and chlorothiazide are commonly used concomitantly to maximize diuresis in pediatric patients; the study findings suggest that solutions of furosemide and chlorothiazide can be combined in the same syringe without loss of stability for up to 96 hours.
In African-American patients with CHF, hypovitaminosis D, aldosteronism, and loop diuretic treatment each exaggerate Ca and Mg losses to stress a fragile Ca balance leading to ionized hypocalcemia and hypomagnesemia with SHPT.
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A 28-year-old white female with primary infertility on hMG (Pergonal; Serono Laboratories, Randolph, MA) therapy.
The objective of this study was to determine which of the many risk factors for nephrocalcinosis (NC) in preterm infants are most relevant.
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Participants' median baseline IVC diameter was 2.38 cm (interquartile range, 1.91-2.55 cm). At 1-2 hours after furosemide, IVC diameters decreased an average of 0.21 cm (95% CI, 0.13-0.29 cm) and remained significantly below baseline at 2-3 hours after furosemide by an average of 0.15 cm (95% CI, 0.07-0.22 cm).
Although ingestion of granulated chlorine is rare in veterinary patients, the resulting disease processes are common and can be treated successfully.
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Previous studies, which have mostly focused on concentrated NaCl solution intake, have suggested sodium depletion may be accompanied with salt taste sensory changes. To further investigate whether the function of the salt taste system changes in different patterns for highly concentrated and diluted NaCl taste stimuli, the effects of sodium depletion on NaCl taste detection threshold in rats were examined. After a conditioned taste aversion (CTA) to a suprathreshold concentration of NaCl (0.1 M) was established, rats were given a series of two-bottle choice tests between distilled water and different concentrations of NaCl. Conditioned rats will generalize the aversion to diluted solutions when they are detected. The taste detection threshold for NaCl is defined as the lowest concentration at which there is a reliable difference in the preference scores between conditioned and control subjects. The results showed that detection threshold for NaCl lay between 0.003 M and 0.005 M in sodium-replete rats, whereas in sodium-depleted rats that have an amplified action of angiotensin II in the brain, the threshold significantly decreased to be between 0.0001 M and 0.0003 M. However, in rats with a blocked action of angiotensin II in the brain the decreased NaCl detection threshold was between 0.001 M and 0.003 M. These findings suggest that sodium-depleted rats could decrease the NaCl taste detection threshold to increase the ability to find sodium ions. And the regulation of the salt taste sensitivity may be related to the action of angiotensin II in brain.
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Several studies have shown that treatment with various neurotrophins protects spiral ganglion cells (SGCs) from degeneration in hair-cell deprived cochleas. In most of these studies the neurotrophins are delivered by means of intracochlear delivery methods. Recently, other application methods that might be more suited in cochlear implant patients have been developed. We have examined if round window membrane application of gelfoam infiltrated with a neurotrophin resulted in SGC survival in deafened guinea pigs. Two weeks after deafening, gelfoam cubes infiltrated with 6 μg of brain-derived neurotrophic factor (BDNF) were deposited onto the round window membrane of the right cochleas. Electric pulses were delivered through an electrode positioned within the round window niche to electrically evoke auditory brainstem responses (eABRs). Two or four weeks after deposition of the gelfoam all cochleas were histologically examined. We found that local BDNF treatment enhances the survival of SGCs in the basal cochlear turn after two and four weeks. The treatment had no effect on SGC size or shape. In animals treated with BDNF, eABR amplitudes were smaller than in normal-hearing control animals and similar to those in deafened controls. We conclude that BDNF delivered by means of local gelfoam application provides a protective effect, which is limited compared to intracochlear delivery methods.
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dry skin, peripheral/periorbital oedema, slow thought and speaking, thyroid increased. Laboratory examinations: high levels of creatine kinase , creatinine, uric acid and lactate dehydrogenase. Free T4 was very low (<0.3 ng/dL) and thyroid-stimulating hormone was high (21.7 µIU/mL). Urinalysis showed haem pigment without haematuria. We performed the diagnosis of AKI secondary to hypothyroidism-induced rhabdomyolysis. Intravenous fluids were started, urinary alkalisation and increased l-thyroxine dose replacement. On the day after admission, forced diuresis with furosemide was introduced leading to a progressive improvement of symptoms. Although hypothyroidism and AKI is unusual, it should be suspected in patients presenting decrease of renal function and high creatine kinase in the absence of other causes of rhabdomyolysis.
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To systematically review clinical studies of co-administration of albumin and loop diuretics in hypoalbuminemic patients as a strategy to overcome diuretic resistance.
It is important to be aware of the influence that medications can have on serum calcium levels when evaluating patients with disorders of calcium homeostasis.
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We studied 20 patients treated with furosemide and spironolactone. Of them, 10 (Group 1) discontinued diuretic treatment for 7 days. Thereafter, for 5 days each patient received subcutaneous octreotide 300 microg b.i.d., in 10 patients (Group 2) in addition to their usual diuretics. We collected data on the patients while they received diuretics (both groups), after discontinuation of diuretics (Group 1), and after octreotide administration (both groups).
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It was hypothesized that the addition of tolvaptan to a background diuretic improved dyspnea early in patients selected for an enhanced vasopressin antagonism response.
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Renal R2* measurements were shown to be reproducible within approximately 12% from day to day based on a coefficient of variance (CV) analysis. The changes in R2* (DeltaR2*) following administration of furosemide were statistically significant, as shown by ANOVA and a paired Student's t-test, and were deemed reliable based on the reliable change index (RCI). However, DeltaR2* values following waterload were not statistically significant, and were not deemed reliable.
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A high performance liquid chromatographic (HPLC) method was proposed for the simultaneous determination of four drugs for kidney disease, enalapril, triamterene, furosemide and valsartan. After proteins being removed by acetone precipitation method, freeze drying and redissolving in mobile phase, the urine samples were analyzed by HPLC. Chromatographic separation was performed on a WondaSil C18-WR (150 mm x 4.6 mm, 5 μm) in gradient elution mode using 10.0 mmol/L ammonium acetate aqueous solution (pH 3.90) and acetonitrile as mobile phases at a flow rate of 1.0 mL/min. The detection wavelength was set at 254 nm. Under the optimized conditions, good linearities were obtained in the range of 0.15-300 mg/L, 0.05-100 mg/L, 0.75-750 mg/L, 0.05-100 mg/L, and the detection limits were 1.38 x 10(-2), 7. 67x103, 3.69x 10-2, 1. 16x 10-2 mg/L for enalapril, triamterene, furosemide and valsartan, respectively. The recoveries were in the range of 89.49%-99.20% with the relative standard deviations (RSDs) among 4.12%-9.44%. The method is simple, accurate and effective, and the results showed the method is applicable for the analysis of the four drugs for kidney diseases in real urine samples.
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Among the patients, 52 (54.2%) had RCHF and 44 (45.8%) did not. Atrial fibrillation was present in 88% of group A and 76% of group B (p = NS). Group A patients had a significantly larger right ventricular area, right atrial area and IVC diameter than group B patients, but a significantly smaller variation in IVC diameter during respiration (11.2 +/- 8.5% versus 24.3 +/- 14.1%, p = 0.001). Right ventricular systolic function and systolic pulmonary pressure were similar in the two groups. On multivariate analysis, respiratory-related variation in IVC diameter (p <0.001) and systolic pulmonary artery pressure (p = 0.04) were the only independent echocardiographic markers of RCHE CONCLUSION: Diminished respiratory variation in IVC diameter and systolic pulmonary artery pressure are independent markers of volume overload in patients with severe TR. These findings may reflect exhaustion of IVC capacitance due to markedly increased right heart filling pressures, though intrinsic changes in IVC tonus may also be involved.
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The aim of the study was to compare sequential versus combined diuretic therapy in patients with cirrhosis, moderate ascites and without renal failure.
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To determine if intensivists given PAC data from critically ill patients make uniform management choices.
We emphasize the importance of early detection of primary and satellite lesions of these tumors including neurohumoral markers and PET/CT scans as in this case, as well as the participation of a multidisciplinary team.
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In the BNP-driven group, furosemide and acetazolamide were given more often and in higher doses than in the control group, resulting in a more negative median (interquartile range) fluid balance during weaning (-2,320 [-4,735, 738] vs. -180 [-2,556, 2,832] ml; P < 0.0001). Time to successful extubation was significantly shorter with the BNP-driven strategy (58.6 [23.3, 139.8] vs. 42.4 [20.8, 107.5] h; P = 0.034). The BNP-driven strategy increased the number of ventilator-free days but did not change length of stay or mortality. The effect on weaning time was strongest in patients with left ventricular systolic dysfunction. The two strategies did not differ significantly regarding electrolyte imbalance, renal failure, or shock.
To analyze interdependent transport of K and Cl, we investigated Rb (K) efflux from in vitro choroid plexus (CP) in isotonic artificial CSF (aCSF) medium containing anions or agents that alter KCl transport. Lateral ventricle CP was loaded with 86Rb for release to enable calculation of the efflux rate coefficient, k. With Cl as the main anion in control aCSF, the k value for 86Rb (K) in CP of 1 week infant rats (0.177 min-1) was 19% lower than in adults (0.218 min-1) (P < 0.005). Replacing CSF Cl with NO3 or SCN, respectively, reduced k for K in infant CP by 73% and 43%; similar anion selectivity was observed in adult tissues (P < 0.05). N-Ethylmaleimide (NEM), which stimulates KCI cotransport, significantly enhanced K efflux in infants and adults. In adult CP, the KCl cotransport inhibitor, furosemide (1 mM), decreased K efflux by 23% or 65%, respectively, when aCSF had Cl or NO3 as the main anion. In infant rat CP, 0.1 mM bumetanide (another KCl cotransport inhibitor), reduced k for K by 65%, whereas the Cl channel blocker diphenylamine carboxylate (1 mM) did not significantly alter K efflux. The collective findings for rat CP indicate a substantial component of K efflux that is associated with Cl concentration and the Cl transport protein sensitive to loop diuretics and NEM. The Cl-dependent K efflux is present in infants.
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Furosemide treatment significantly increased mass-specific VO2max (5.3%), but absolute VO2max was not significantly altered. In the 2 parts of the study, body weights were 2.9 and 2.5% higher when horses were given placebo than when they were given furosemide. Time and distance run at speeds > or = 11.0 m/s were significantly greater following furosemide administration. Furosemide treatment had no effect on breathing mechanics or gas exchange.