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Lasix (Furosemide)

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Lasix is a highly effective FDA approved medication for the treatment of excessive edema (fluid retention) due to kidney disorder (nephrotic syndrome), heart failure, cirrhosis and liver disease. It is also used to treat high blood pressure (hypertension). Lasix works by regulating the way in which the body absorbs salts.

Other names for this medication:
Aldalix, Anfuramide, Ansemid, Apix, Apo-furosemida, Asax, Betasemid, Diaqua-2, Foliront, Salix®, Frusenex, Frusemide, Furantral, Furesis, Furetic, Furide, Furocot, Furovet, Furoxem, Furozenol, Fursemid, Furtenk, Fusix, Hoe 058, Inclens, Intermed, Jufurix, Las 6873, Lasilacton, Lasilactone, Lasiletten, Lasilix, Lo-Aqua, Vesix

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Also known as: Furosemide.


Lasix prevents excessive edema (fluid retention) in people with kidney disorder (nephrotic syndrome), heart failure, cirrhosis and liver disease. It is also used for the treatment of high blood pressure (hypertension), high levels of potassium (hyperkalemia), calcium (hypercalcemia), and magnesium (hypermagnesemia).

The active component, Furosemide, is a potent loop diuretic (water pill) that eliminates water and salt from the body. Furosemide works by blocking the absorption of sodium, chloride, and water from the filtered fluid in the kidney tubules, causing a profound increase in the output of urine (diuresis).

Lasix starts to act within one hour after oral administration, and the effect lasts for about 6-8 hours.


Lasix is available in tablets which should be taken orally with a full glass of water.

The dosage of Lasix depends on the body weight and on the health status of the recipient.

Take Lasix at the same time once a day.

Do not take more than your recommended dose, as high doses of furosemide may cause irreversible hearing loss.

Do not crush or chew the tablet.

To achieve the most effective results, do not stop taking Lasix suddenly.


In case of a Lasix overdose visit your doctor or health care provider immediately. Symptoms of a Lasix overdose include fainting, tinnitus, confusion, weakness, lightheadedness, lack of appetite.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Lasix are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Lasix if you are allergic to any of its components or if you are unable to urinate.

Do not take Lasix if you are pregnant, plan to have a baby, or you are breastfeeding.

Do not take Lasix if you suffer from or have a history of kidney disease, cirrhosis or other liver disease, gout, lupus or diabetes.

Do not take Lasix if you suffer from enlarged prostate, bladder obstruction or other urination problems, or an electrolyte imbalance (such as low levels of potassium or magnesium in your blood).

Do not take Lasix if you suffer from high cholesterol or triglycerides (a type of fat in the blood).

Use Lasix with care if you are taking indomethacin (such as Indocin); steroids (such as prednisone); diabetes medicines; diet pills; sucralfate (such as Carafate); netilmicin (such as Netromycin); amikacin (such as Amikin); streptomycin; tobramycin (such as Nebcin, Tobi); gentamicin (such as Garamycin); digoxin (such as Lanoxin); blood pressure medicines; salicylates (such as aspirin, Tricosal, Disalcid, Dolobid, Salflex, Doan's Pills); cold medicines; lithium (such as Lithobid, Eskalith), ethacrynic acid (such as Edecrin); probenecid (such as Benemid).

This medicine can make your skin more sensitive to the sunlight. Try to protect your skin where possible.

Avoid becoming dehydrated.

If you are going to have surgery, inform your doctor that you are taking Lasix.

Do not stop taking Lasix suddenly.

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The efficacy and tolerability of two combinations, namely 50 mg spironolactone + 20 mg furosemide (SF) or 50 mg spironolactone + 5 mg butizide (SB), were compared in a randomised intraindividual trial in 22 patients with congestive heart failure. The parameters used were: weight, ankle- and calf-circumference, blood pressure, resting pulse, resting ECG, spirometry and blood chemistry. The physicians' judgement of the success of treatment was also recorded. Clinical symptoms improved clearly in both groups and in most cases there was significant improvement of the various parameters. The trend towards improvement was more apparent with SF. The physicians considered SF to be more effective in 12 cases compared to one case with SB. In all other cases both treatments were considered equally effective. The blood chemistry data showed relevant differences: serum-potassium levels were less scattered with SF and showed a - desirable - shift into the upper normal range. The number of patients with elevated serum-creatinin-levels increased during SB-treatment whereas the opposite was noted with SF. This could be due to furosemide's positive effects on renal functions.

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PAC/PRA above 50 was used to denote hyperaldosteronism. Serum K was 4 +/- 0.07 mM/L, PAC 22.8 +/- 1.8 ng/dl, PRA 0.13 +/- 0.02 ng/ml/hour, PAC/PRA 190 +/- 22 (above 100 in 17). After suppression PAC decreased from 25 +/- 1.8 to 11 +/- 1 ng/dl (normal < 5 ng/dl). Stimulation did not affect PRA and PAC/PRA. Abdominal computed tomography scan revealed normal adrenal glands in 15 patients. Spironolactone (116 +/- 60 mg/day) normalized blood pressure in all patients; it was used as a single therapy in 8, and in association with only one anti-hypertensive drug in the remaining 12 patients. In one patient the treatment was discontinued due to the presence of hyperkalemia.

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Furosemide is an effective diuretic that initiates a rapid diuresis and peripheral vasodilatation through renal adenylate cyclase inhibition and prostaglandin synthesis. Recently, it has been shown to be associated with activation of the neurohumoral vasoconstrictor mechanism and a further compromise of left ventricular function in patients with heart failure. The present study was performed to investigate the direct effects of furosemide on myocardial performance in the isolated perfused rabbit heart. Furosemide (10(-3) M) caused a significant decrease in developed pressure as well as a similar fall in coronary perfusion pressure. Furosemide also decreased myocardial contractility when the coronary perfusion pressure was kept constant. The change in developed pressure but not the decrease in coronary perfusion pressure could be blocked by treatment with indomethacin. Furosemide did not antagonize rabbit cardiac membrane adenylate cyclase. Therefore, furosemide has a direct inhibitory effect on cardiac contractility that is related to prostaglandin synthesis.

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To describe a case of a serous choroidal detachment which resulted after discontinuation of furosemide and illustrate the utility of ultrawide-angle fundus imaging in documenting this lesion in the retinal periphery.

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Furosemide treatment produces glomerular hypertrophy and augments glomerular capillary hydraulic pressure in the normal rat. Similar processes have been implicated in the progression of glomerulosclerosis (GS). Whereas prior experiments with furosemide treatment of 6 to 8 weeks duration have produced no detrimental effects on renal function or structure, the effects of more prolonged treatment are unknown. Male Munich-Wistar rats were pair fed with or without furosemide, 40 mg/d, from the time of weaning through 10 months of age. At selected time points, 24-hour urine collections were obtained for total protein and volume determination. At the end of the study, light and electron microscopic morphometric studies were performed. Renal cortical hypertrophy and glomerular hypertrophy were sustained throughout the 9 months of treatment in the group receiving furosemide. The cortical interstitial area was increased in the furosemide group, but this did not appear to be the result of fibrosis. Proximal and distal tubule diameter were unaffected by treatment. No differences in GS or glomerular ultrastructure were shown. This study provides no evidence of detrimental glomerular effects of furosemide in normal animals. Further studies of furosemide treatment under conditions of preexisting renal pathological conditions are warranted to confirm the safety of this treatment in situations analogous to those seen in the clinical setting. Interstitial expansion also warrants further study in this setting.

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(68)Ga-PSMA-11-PET/CT at 3h p.i. showed most lesions characteristic for PCa with higher uptake and contrast. In addition, the radioactivity signal within the urinary bladder was lower at 3h p.i., especially when furosemide was applied. Consequently, scans at 3h p.i. detected more tumor lesions than 1h p.i.

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With the ever-increasing population of cigarette smokers, the potential for cigarette smoke to affect drug therapy both pharmacokinetically and pharmacodynamically is significant. The overriding pharmacokinetic effect is increased drug metabolism through the induction of liver enzymes. The constituents of tobacco smoke, primarily nicotine, have their own pharmacological effects which may potentiate or antagonise the desired pharmacological effect of a particular drug, thereby affecting its efficacy. Furthermore, end-organ responsiveness may also be altered by tobacco. These latter 2 aspects constitute altered clinical pharmacodynamics. Approximately 30 drugs have been evaluated in terms of cigarette smoking. Induction of liver enzymes has been shown to increase the metabolism of imipramine, meprobamate, oestrogens, pentazocine, phenylbutazone, theophylline and warfarin. Nicotine has been shown to inhibit diuresis, alter ulcer healing, impair subcutaneous absorption, affect protein binding and stimulate catecholamine release; these effects have been evaluated in terms of therapy with frusemide (furosemide), histamine H2-antagonists, insulin, lignocaine (lidocaine) and beta-blockers, respectively. The interactions have not been correlated with clinical significance in all cases. Diminished end-organ responsiveness may account for reduced drowsiness in smokers receiving chlorpromazine and benzodiazepines, compared with non-smokers. Smoking has been associated with diminished pain tolerance, requiring increased dosages of morphine, pethidine (meperidine) and propoxyphene. Enzyme-inducers such as carbamazepine, phenytoin and phenobarbitone appear to be minimally affected by cigarette smoke, perhaps because hepatic enzymes are already maximally stimulated. Codeine, corticosteroids and nortriptyline do not appear to be affected by cigarette smoke. The bioavailability of glutethimide is higher in smokers, but this has not been associated with greater efficacy. The effect of smoking on paracetamol (acetaminophen) has been variable, depending on the extent of smoking, and does not appear to be of clinical significance.

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Six infants (6%) had renal calcification at term or before discharge compared with 96 who did not. Factors significantly associated with renal calcification included gestational age (26 weeks vs. 29 weeks, p=0.006), birth weight (851 g vs. 1141 g, p=0.004), duration of mechanical ventilation (69 days vs. 29 days, p=0.002), length of intensive care (72 days vs. 41 days, p=0.013), furosemide therapy (33% vs. 3%, p=0.027), and dexamethasone therapy (50% vs. 2% p=0.001). Birth weight and dexamethasone therapy had significant independent association after stepwise logistic regression analysis. Sex, oliguria, acidosis, duration of oxygen therapy, length of hospital stay, nutrition status, and nephrotoxic drugs did not differ between the two groups. Three of the six infants had spontaneous remission of renal calcification, whereas two patients without the finding in neonatal stage had renal calcification at a corrected age of 1 year.

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Nephrologists should promote the detection of CKD in heart disease patients. The evaluation should include estimation of GFR and detection of microalbuminuria in a recently voided urine sample by the albumin:creatinine ratio. Any patient with stage 3 or 4 CKD and rapid deterioration of GFR should be evaluated by the nephrologist. - Patients with CKD have a high risk of cardiovascular (CV) complications and heart disease patients have a high incidence of CKD and progression is also more rapid (Strength of Recommendation B). The most likely pathophysiological hypothesis is endothelial damage. - The CV risk profile should be established in each patient followed by adequate compliance with control goals for common CV risk factors: smoking, obesity, sedentarism, hypertension, dyslipidemia. Early treatment of anemia and bone mineral disease as CV risk factors requires special mention (Strength of Recommendation B). - Management of these patients will be based on individualization of treatment, close systematic follow-up, and integration between care levels: Specialized care (nephrologists and cardiologists) and primary care. - The cardiorenal syndrome (CRS) is a condition in which both organs are simultaneously affected and their deleterious effects are reinforced in a feedback cycle, with accelerated progression of renal and myocardial damage. Because of its prognostic value, treatment of HF takes precedence over CKD. Most studies on cardiovascular risk and on HF exclude patients with stage 4-5 CKD. We thus do not have sufficient strong evidence and recommendations are based on the extrapolation of data from studies with normal GFR or milder grades of CKD, and on the empirical use of certain treatments. - ARBs and ACEIs are the mainstays of treatment of HF with systolic and diastolic dysfunction, and have been shown to reduce mortality in studies in the general population (Strength of Recommendation A). The may also slow progression of CKD, especially in diabetics. Dual renin-angiotensin blockade with the combined use of lower doses of both drugs has shown promising results for control of CKD progression, but there are no data to recommend its use for control of HF in advanced stages of CKD (stage 4-5) (Strength of Recommendation C). - In these stages of CKD, only loop diuretics have sufficient potency. The therapeutic dose range should be achieved. Lowdose thiazides achieve diuretic synergy. The use of spironolactone and eplerenone has shown benefits in patients with AMI and HF with an ejection fraction < 40% without advanced CKD. They should always be used with strict control of GFR and K+. No benefit has been shown for the use of (may even be harmful) or continuous infusion of furosemide (Strength of Recommendation B). The use of beta-blockers should be increased in these patients. - Treatment-refractory heart failure in the context of stage 3 CKD could be amenable to ultrafiltration techniques. Continuous ambulatory PD could be an alternative treatment to maintain hemodynamic equilibrium while also allowing pharmacological treatments to be prescribed that would not be feasible without dialysis and could even improve myocardial and kidney function (Strength of Recommendation C).

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To address this problem, an International Consensus Committee was appointed by the Ninth International Symposium on Radionuclides in Nephrourology in 1994.

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To assess the efficacy and safety of intravenous (IV) chlorothiazide versus oral metolazone when added to loop diuretics in patients with acute decompensated heart failure (ADHF) and loop diuretic resistance.

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The technique of stationary microperfusion of the early distal tubule used in experiments on male newts (Triturus vulgaris) revealed the intratubular effect of CoCl2 and furosemide on the ion transport. CoCl2 in concentration 5 X 10(-4) M increased Na and Cl reabsorption, reduced Ca, Mg and K reabsorption, and increased (TFexp/TFo)in from 1.14 +/- 0.04 to 1.68 +/- 0.27 (p less than 0.001). CoCl2 in concentration 5 X 10(-5) M enhanced Na and Cl reabsorption, without affecting transport of other ions. 6 X 10(-4) M furosemide decreased reabsorption of water, Na, Cl, Ca and Mg. The combined effect of Co2+ and furosemide inhibited reabsorption of Mg and Ca to a greater extent, but stimulated Na reabsorption. Experiments on frog skin showed that being added to the apical membrane of cells, Co2+ stimulates short circuit current and potential differences, whereas furosemide reducing Cl absorption induces only hyperpolarization. Experimental findings allow to assume that Co2+ on the outer surface of the apical membrane of the distal tubule cells blocks the selective Ca and Mg channels and activates Na channels.

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In order to characterize the driving forces for the concentrative uptake of unconjugated bile acids by the hepatocyte, the effects of pH gradients on the uptake of [3H]cholate by rat basolateral liver plasma membrane vesicles were studied. In the presence of an outwardly directed hydroxyl gradient (pH 6.0 outside and pH 7.5 inside the vesicle), cholate uptake was markedly stimulated and the bile acid was transiently accumulated at a concentration 1.5- to 2-fold higher than at equilibrium ("overshoot"). In the absence of a pH gradient (pH 6.0 or 7.5 both inside and outside the vesicle), uptake was relatively slower and no overshoot was seen. Reductions in the magnitude of the transmembrane pH gradient were associated with slower initial uptake rates and smaller overshoots. Cholate uptake under pH gradient conditions was inhibited by furosemide and bumetanide but not by 4, 4'-diisothiocyano-2,2'-disulfonic stilbene (SITS), 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (DIDS), or probenecid. In the absence of a pH gradient, an inside-positive valinomycin-induced K+ diffusion potential caused a slight increase in cholate uptake which was insensitive to furosemide. Moreover, in the presence of an outwardly directed hydroxyl gradient, uphill cholate transport was observed even under voltage clamped conditions. These findings suggest that pH gradient-driven cholate uptake was not due to associated electrical potentials. Despite an identical pKa to that of cholate, an outwardly directed hydroxyl gradient did not drive uphill transport of three other unconjugated bile acids (deoxycholate, chenodeoxycholate, ursodeoxycholate), suggesting that a non-ionic diffusion mechanism cannot account for uphill cholate transport. In canalicular vesicles, although cholate uptake was relatively faster in the presence of a pH gradient than in the absence of a gradient, peak uptake was only slightly above that found at equilibrium under voltage clamped conditions. These findings suggest a specific carrier on the basolateral membrane of the hepatocyte which mediates hydroxyl/cholate exchange (or H+-cholate co-transport). A model for uphill cholate transport is discussed in which the Na+ pump would ultimately drive Na+/H+ exchange which in turn would drive hydroxyl/cholate exchange.

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Experiments on rats showed that single doses of diuretics furosemide, ethacrynic acid, mannitol, hypertonic solution of sodium chloride administered subcutaneously 30 and 60 min and intravenously 10 and 20 min before complete arrest of the blood flow in the single kidney for 2.5 hours decrease creatinine content in the blood and increase survival rate of the animals. The anti-ischemic protection occurs provided that the natriuretic effect of the drugs coincides with Lopressor Generic Side Effects the ischemic factor action. Morphometry revealed the ability of furosemide to prevent the development of hyperhydration of the epithelial cells, to increase lumina of the proximal and distal tubules. The role of hydrodynamic factors in the mechanism of anti-ischemic protection of the kidneys with diuretics is discussed.

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This is a randomized controlled study of anemic patients with severe congestive heart failure (CHF) to assess the effect of correction of the Cordarone Generic Name anemia on cardiac and renal function and hospitalization.

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One of the potential limitations in the usefulness of both renal output efficiency (ROE) and normalized residual activity (NORA) is their residual dependence on total renal function. The Bystolic Cost Usa purpose of this study was to present and examine a new quantitative method whereby the effects of this dependence may be removed.

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This randomised trial was registered in the European Clinical Trial Database (EudraCT) with the reference number 2008-004488-20. Cozaar Medication Generic Names

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Nephrotic edema are the clinical feature of isolated interstitial expansion. Expanded interstitial compartment compensates sodium accumulation in the extracellular volume due to inappropriate renal sodium retention. Renal sodium retention is brought about by an activation of the molecular structures responsible for the reabsorption of sodium along the cortical collecting duct: amiloride-sensitive epithelial sodium channel at the apical face and sodium pump at the basolateral face of the principal cell. This activation is independent of aldosterone and vasopressin. The asymmetry of expansion between interstitium and plasma compartments is due to impaired Starling forces and increased fluid transfer through the capillary wall. The lack of significant changes in transcapillary oncotic and hydrostatic gradients suggests that increased hydraulic conductivity due to transconformation of endothelial intercellular junctions drives the leakage of fluid into the interstitium and allows to understand the mobility of nephrotic edema. Consistently with the site of renal sodium retention and the activation of the epithelial sodium channel, the association of amiloride and furosemide is efficient to increase urinary sodium excretion, to reverse sodium balance and Augmentin How Much Cost to remove edema from patients with nephrotic syndrome.

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Furosemide causes both diuretic and non-diuretic changes Zocor Cost in renal function. We compared responses to intravenous furosemide 0.5 in 38 subjects (30 males, 8 females) aged 18 to 30 with those in 14 subjects (9 males, 5 females) aged 50 and over. There were no consistent differences attributable to gender. Older persons showed greater natriuresis (47 percent in males and 26 percent in females) but their increment in plasma renin activity was markedly reduced. The urinary excretion of thromboxane B2 was elevated in older subjects (58 +/- 10 vs. 30 +/- 4 ng/4 h, p less than 0.05 for males; 48 +/- 7 vs. 29 +/- 4 ng/4 hr, p less than 0.05 for females) while that of 6-keto prostaglandin F1 alpha was not different. While differences in the diuretic response to furosemide may be due to pharmacokinetic differences, the non-diuretic response differences may reflect age related changes in renal prostaglandin synthesis.

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A case of postoperative rhabdomyolysis following radical prostatectomy for prostate cancer is reported. A 60-year-old man was referred to our hospital because of an elevation of prostate specific antigen detected by the health checkup system. Sextant biopsy for the prostate revealed moderately differentiated adenocarcinoma. Radical prostatectomy was performed after hormonal therapy for 10 months. Two to three days after surgery, the patient complained of a feeling of listlessness. Serum levels of creatine phosphokinase were elevated to 6,584 IU/ml and creatinine slightly elevated to 1.6 mg/dl. Symptoms and Suprax Cost laboratory findings improved after sufficient fluid infusion and injection of furosemide. To our knowledge, this is only the third case report in the world literature of postoperative rhabdomyolysis after urological surgery.

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Polarized arrest, induced by tetrodotoxin (TTX) at an optimal concentration of 22 micromol/L, has been shown to reduce ionic imbalance and improve myocardial preservation compared with hyperkalemic (depolarized) arrest. Additional pharmacologic manipulation of ionic changes (involving inhibition of Na+ influx by the Na+/H+ exchanger [HOE694] and Na+/K+/2Cl- cotransporter [furosemide], and calcium desensitization [BDM]) may further improve long-term preservation. In this study, we (i) established optimal concentrations of each Vytorin Generic drug, (ii) determined additive effects of optimal concentrations of each drug and (iii) compared our optimal preservation solution to an established depolarizing cardioplegia (St Thomas' Hospital solution No 2: STH2) used during long-term hypothermic storage for clinical transplantation.

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A 43-year-old man was admitted to our hospital in January, 1991 for further examination of polydipsia, polyuria and hypertension. He had had a personal history of hypertension since 1976 and of diabetes mellitus since 1982. Physical examination and routine laboratory studies showed that the patient was characterized by asymptomatic hypertension in the presence of hypokalemia and increased urinary potassium excretion. Plasma aldosterone concentrations (PAC) were elevated and plasma renin activity (PRA) was suppressed, resulting in a considerable increase in the ratio of PAC to PRA. PAC was not normally suppressed by saline infusion (2 1/2h, iv). PRA remained suppressed and PAC did not rise after stimulation with iv injection of furosemide (40 mg) in combination with walking for 60 min. PAC was increased in response to ACTH injection (0.25 mg, iv) but not suppressed by dexamethasone administration (2 and 8 mg/day, po). PAC did not rise after iv infusion of angiotensin II (20 ng/kg/min for 30 min). Venous sampling showed that PAC was considerably elevated in the bilateral adrenal vein. CT and MRI demonstrated tumor mass Micardis Generic Release Date in the bilateral adrenal gland and the remaining normal portion in the left adrenal gland. Scintigraphic imaging with 133I-aldosterol during dexamethasone suppression provided bilateral uptake in the adrenals. Oral administration of spironolactone (375 mg/day) suppressed blood pressure and elevated PRA and serum potassium. Elevated PCA and PRA levels as well as hypertension were corrected by right-total and left-subtotal adrenalectomy performed in March, 1991. However, impaired glucose tolerance was not changed after surgery, and plasma glucose levels were well controlled with a small dose of insulin (9U/day). Pathological studies revealed adrenocortical adenoma cells of clear cell type with spironolactone bodies in the bilateral adrenal tumors. These findings indicate that this is a very rare case of primary aldosteronism due to bilateral functioning adrenocortical adenomas, which is accompanied by diabetes mellitus.

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To describe the diagnosis and management of bacterial Cleocin Lotion Generic pericarditis after heart transplantation.

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Two thousand prescriptions received by 600 subjects (M:F= 1.47:1) were analyzed. One thousand and forty-five (50.62%) prescriptions were off-label. The off-label drug use rate was 1.74+/-1.56 per patient. The maximum rate of off-label drugs was in infants (2.33/patient). 'alteration in dosage' was by far the commonest reason for off-label use; followed by 'age' and 'indication'. Furosemide (i. v.), diazepam (i.v), cefotaxime (i.v), ethambutol (tab) and prednisolone (tab) were the five commonest off-label drugs used in the study population.

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To compare en bloc and artery-only clamping techniques on renal function and perioperative outcomes after laparoscopic partial nephrectomy (LPN).