Moduretic is used for treating fluid retention (edema) and high blood pressure. It may be used alone or with other medicines.
Other names for this medication:
Also known as: Amiloride hydrochlorothiazide.
Moduretic is a diuretic (water pill) and a combination of a potassium-sparing diuretic (amiloride) and a thiazide diuretic (hydrochlorothiazide). It works by making the kidneys eliminate sodium (salt) and water from the body, which helps to lower blood pressure. The amiloride component helps minimize potassium loss.
Brand name of Moduretic is Moduretic.
Take Moduretic by mouth with food.
Moduretic may increase the amount of urine or cause you to urinate more often when you first start taking it. To keep this from disturbing your sleep, try to take your dose before 6 pm.
If you want to achieve most effective results do not stop taking Moduretic suddenly.
If you overdose Moduretic and you don't feel good you should visit your doctor or health care provider immediately.
Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Do not freeze. Keep container closed tightly. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Moduretic are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Moduretic if you are allergic to Moduretic components or to any ingredient in Moduretic or any other sulfonamide (eg, sulfamethoxazole).
Be careful with Moduretic if you're pregnant or you plan to have a baby, or you are a nursing mother.
Be careful with Moduretic if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.
Be careful with Moduretic if you have allergies to medicines, foods, or other substances.
Be careful with Moduretic if you have cirrhosis or liver problems, diabetes, gout, kidney problems or kidney stones, asthma, heart problems, or systemic lupus erythematosus.
Be careful with Moduretic if you have elevated blood acid, low folic acid levels, or electrolyte problems, or are dehydrated.
Be careful with Moduretic if you take potassium-sparing diuretics (eg, spironolactone), potassium supplements, or salt substitutes containing potassium because high blood potassium levels may occur and cause listlessness, confusion, abnormal skin sensations of the arms and legs, heaviness of limbs, slowed heart rate, irregular heart rhythm, or stopping of the heart; cholestyramine or colestipol because they may decrease Moduretic 's effectiveness; nonsteroidal anti-inflammatory drugs (NSAIDs) (eg, indomethacin) because they may decrease Moduretic 's effectiveness and risk of kidney problems may be increased; barbiturates (eg, phenobarbital), certain chemotherapy medicines, corticosteroids (eg, prednisone), digoxin, dofetilide, ketanserin, narcotic pain medicines (eg, codeine), or medicines for high blood pressure because the risk of their side effects may be increased by Moduretic; diazoxide, lithium, or nondepolarizing neuromuscular blockers (eg, pancuronium) because their actions and the risk of their side effects may be increased by Moduretic; angiotensin-converting enzyme (ACE) inhibitors (eg, enalapril) because the risk of high blood potassium and kidney problems may be increased by Moduretic; diabetes medicines (eg, glipizide) or insulin because their effectiveness may be decreased by Moduretic.
Do not stop taking Moduretic suddenly.
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Amiloride hydrochloride has now been recognized as a safe and effective potassium-sparing diuretic alternative to triamterene with a similar mechanism of pharmacologic activity. Studies were undertaken to assess the difference between therapy with the triamterene-hydrochlorothiazide combination (Dyazide) and an amiloride hydrochloride-hydrochlorothiazide combination (Moduretic) on renal prostaglandin production, since an increase in renal prostaglandin synthesis has been shown to mediate or enhance the pharmacologic action of certain diuretic drugs. Eight subjects treated for four weeks with triamterene-hydrochlorothiazide were compared with nine patients similarly treated with amiloride-hydrochlorothiazide. A 24-hour urine sample for prostaglandin E2 (PGE2) assay was collected under control conditions and after six weeks of therapy with either diuretic in all patients. The PGE2 excretion increased in the amiloride-hydrochlorothiazide-treated group; in the other group PGE2 excretion actually declined. It is concluded from these studies that therapy with amiloride-hydrochlorothiazide enhanced renal PGE2 production, whereas that with triamterene-hydrochlorothiazide actually decreased renal PGE2 production. This difference is an important renal consequence of the use of either drug and should be considered in the choice between these diuretic combinations.
ClinicalTrials.gov number NCT01011660.
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Antihypertensive therapy is effective in reducing the risk of major adverse cardiovascular events. However, blood pressure (BP) control rate remains poor and the optimal combination therapy against hypertension is not established in China. The objective of this study was to evaluate the long-term efficacy and safety of two antihypertensive regimens, amlodipine plus telmisartan and amlodipine plus amiloride/hydrochlorothiazide, in patients with essential hypertension and at least one cardiovascular risk factor.
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Twenty hypertensive outpatients WHO stage I or II, with supine diastolic blood pressure greater than or equal to 95 mmHg at the end of a 4-week treatment period with atenolol (Tenormin) 100 mg daily, continued atenolol in free association with half a tablet of Moduretic (i.e., hydrochlorothiazide 25 mg + amiloride 2.5 mg) for a further 4 weeks. Atenolol monotherapy induced a drop of systolic blood pressure from 175.0 +/- 11 (mean +/- s.d.) mmHg to 158.7 +/- 6 mmHg (p less than 0.01), and of diastolic blood pressure from 113.5 +/- 8 mmHg to 102.7 +/- 5 mmHg (p less than 0.01). After 4 weeks with atenolol in association with half a tablet of Moduretic, systolic blood pressure further decreased to 145.7 +/- 8 mmHg (p less than 0.01), and diastolic blood pressure to 90.2 +/- 10 mmHg (p less than 0.01). Seven out of 20 patients remained with diastolic blood pressure greater than or equal to 95 mmHg despite the above combination therapy. In these patients, the doubling of diuretic dose (hydrochlorothiazide 50 mg + amiloride 5 mg) in combination with atenolol resulted in a further drop in systolic pressure (to 142.1 +/- 9 mmHg) and diastolic (to 92.1 +/- 6 mmHg) (both p less than 0.01). Plasma potassium concentration showed a slight and non-significant increase during atenolol monotherapy (from 4.4 +/- 0.5 mEq/l to 4.6 +/- 0.7 mEq/l; n.s.).(ABSTRACT TRUNCATED AT 250 WORDS)
Moduretic has been reported to inhibit the suppression of plasma norepinephrine (NE) levels by the alpha 2 adrenoceptor agonist, clonidine. To determine whether plasma volume reduction by hydrochlorothiazide (HCTZ) or antagonism of Na+/H+ exchange by amiloride (the constituents of Moduretic) is responsible, the authors performed a modified clonidine suppression test (CST) in nine normal volunteers (aged 25 +/- 2 years), pretreated for 1 week with HCTZ 50 mg daily, amiloride 10 mg daily, or placebo, in a randomized, double-blind, crossover study. Baseline characteristics were identical on all study days, except serum [K+] and weight, which were lowest on HCTZ (3.6 +/- 0.2 mEq/L and 78.7 +/- 2.5 kg), compared with amiloride (4.2 +/- 0.1 mEq/L and 79.9 +/- 2.4 kg) and placebo (4.0 +/- 0.1 mEq/L and 80.2 +/- 2.7 kg, P less than .05). Oral clonidine (0.3 mg) produced a reduction in mean blood pressure by about 20%. Plasma norepinephrine levels were similar in patients receiving placebo, HCTZ, and amiloride (205 +/- 18, 272 +/- 40 and 277 +/- 44 pg/mL, P greater than .20), and decreased significantly during CST. The maximal reduction for each subject averaged 72.7 +/- 12.4%, 87.9 +/- 3.8%, and 82.9 +/- 5.7% for placebo, HCTZ, and amiloride. Clonidine also produced a four to seven-fold increase in plasma growth hormone levels, reduced salivary flow by about 75%, and increased the level of sedation. There were no differences among the three pretreatment regimens in the effects of clonidine, indicating that diuretic therapy does not need to be systematically discontinued in patients undergoing CST.
We did a prospective, randomised, double-blind trial in Europe and Israel in 6321 patients aged 55-80 years with hypertension (blood pressure > or = 150/95 mm Hg, or > or = 160 mm Hg systolic). Patients had at least one additional cardiovascular risk factor. We randomly assigned patients nifedipine 30 mg in a long-acting gastrointestinal-transport-system (GITS) formulation (n=3157), or co-amilozide (hydrochlorothiazide 25 mg [corrected] plus amiloride 2.5 mg; n=3164). Dose titration was by dose doubling, and addition of atenolol 25-50 mg or enalapril 5-10 mg. The primary outcome was cardiovascular death, myocardial infarction, heart failure, or stroke. Analysis was done by intention to treat.
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Nephrogenic diabetes insipidus (NDI) is characterized by the kidney's inability to concentrate urine, which causes intense polyuria that may lead to urinary tract dilation. We report the morphological findings of the urinary tract in ten boys with NDI specifically addressing the presence and changes of urinary tract dilation during treatment.
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In a randomized double-blind study to compare the effect of atenolol vs. hydrochlorothiazide and amiloride (Moduretic) on left ventricular dimensions and systolic function, 100 hypertensive men were followed up during 1 year of treatment, 50 subjects being randomized to each drug. Echocardiography was performed at baseline, and after 3 and 12 months of treatment. A significant reduction in left ventricular mass with atenolol was paralleled by a decrease in left ventricular wall thickness and an increase in stroke volume. A similar reduction of left ventricular mass with Moduretic without a change in relative wall thickness and a decrease in stroke volume was observed. Cardiac output decreased in both groups.
We report a case of lithium overdose in a patient who presented in non-convulsive status epilepticus. The lithium toxicity was probably due to interaction with Moduretic. The diagnosis was not suspected until electroencephalography was performed. This case underscores the importance of therapeutic drug level monitoring of lithium, especially where toxicity is suspected, and the indispensable role electroencephalography plays by allowing a correct diagnosis to be made promptly.
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In order to determine how both diuretics affect water metabolism, we here compare the effects of a rechallenge with either amiloride-hydrochlorothiazide fixed association (AmHTZ; amiloride chlorhydrate 5 mg+hydrochlorothiazide 50 mg; Moduretic) or furosemide (F; 40 mg; Lasix) on water excretion in a 79 year old woman who was previously admitted for severe symptomatic hyponatremia secondary to a 5 days course of AmHTZ for systolic hypertension. After correction of initial hydromineral disturbances, a standard oral water load (WL; 20 mL per kg body weight) was administered before, during and after AmHTZ or F challenges.
An elderly woman who had been taking a fixed-dose combination of a thiazide and potassium-sparing diuretic for eight days, became severely hyponatraemic following total hip replacement. Her hyponatraemia resolved with fluid restriction, intravenous normal saline, and withdrawal of the drug. Hyponatraemia is a well-described side-effect of diuretic therapy; however, we are not aware of any previous reports of this condition developing acutely in the postoperative state. We attribute this to the natriuretic nature of the drug, compounded by the postoperative, anti-diuretic surge which itself may have been exacerbated by the drug. We thus advise caution in the use of this preparation in the elderly patient about to undergo major surgery.
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27 patients with essential hypertension received placebo for 2 weeks, then 1 Moduretic tablet (50 mg hydrochlorothiazide and 5 mg amiloride) daily for 4 weeks, followed by 2 Moduretic tablets daily for a further 10 weeks. The average systolic and diastolic reductions were 26.3/14.0 mm Hg standing and 27.8/19.7 mm Hg lying. 17 of the 27 patients were treated before the beginning of the study with 100 mg hydrochlorothiazide or an equivalent preparation. After 14 weeks' therapy with Moduretic the average systolic/diastolic fall in pressure in these 17 patients was 18.5/9.9 mm Hg standing and 21.6/14.3 mm Hg lying, which was lower than with a thiazide monotherapy. No cases of hyperkalemia or hypokalemia were observed. Moduretic lowers the blood pressure considerably more than thiazide alone and without any concomitant danger of hypokalemia.
Therapy resistance is an enduring problem in clinical hypertension. Our aims were to estimate: (1) the contribution of a low-renin status in therapy resistance; (2) whether such status could give a clue to more successful treatment; and (3) the contribution by adrenal cortical adenomas and by primary aldosteronism.
In a multicenter open-label clinical trial, eligible patients were randomized to receive treatment with amlodipine 2.5-5 mg plus amiloride/hydrochlorothiazide 1.25-2.5 mg/12.5-25 mg (Group A) or amlodipine 2.5-5 mg plus telmisartan 40-80 mg (Group T). If a target BP was not reached, other antihypertensive agents would be added. The target BP was <130/80 mmHg for patients with diabetes mellitus or chronic kidney disease and <140/90 mmHg for others. Efficacy variables were changes from baseline in systolic BP and diastolic BP at the endpoint of 96 weeks. Safety evaluations included monitoring of any adverse events (AEs).
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We here showed that F may be administered to a patient with previous AmHTZ induced hyponatremia without risk for recurrent hyponatremia.
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To estimate the frequency of diuretic-related electrolyte disorders in the elderly, 561 consecutive admissions to three acute geriatric units were studied. For the 287 admissions to one unit, discharge/death diagnoses were also examined in relation to admission diuretic therapy. Sodium concentrations were significantly lower, and urea and creatinine significantly higher, in patients on diuretics, though the size of the differences was small. Comparing different preparations sodium concentrations were significantly lower on Moduretic than on Dyazide or Navidrex K and on frusemide when combined with a potassium-retaining diuretic rather than a potassium supplement. Potassium concentrations were significantly lower on Bendrofluazide alone compared to Navidrex K or Moduretic. Diuretics were positively associated with cardiac failure, ischaemic heart disease, airflow obstruction and obstructive large bowel disorders but negatively with Parkinson's disease. No significant association was found with falls, immobility or confusion. Major electrolyte disorders on diuretics appear to be unusual but important differences exist between preparations. Similarly major illness resulting from diuretic therapy is rare but minor morbidity may be more common.
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Plasma potassium and sodium concentrations were measured in a group of elderly patients taking maintenance thiazide diuretic therapy alone, with a potassium supplement or in combination with a potassium sparing diuretic. Fixed dose combinations of a thiazide and potassium sparing diuretic did not significantly reduce the prevalence of hypokalaemia and the combination of amiloride-hydrochlorothiazide was associated with a disproportionate number of cases of hyponatraemia. The desirability of the current widespread use of fixed dose combination diuretics over less expensive single agents is questioned.
The anti-hypertensive effects of atenolol (Tenormin) 50 mg, a potassium-sparing diuretic (half-strength Moduretic) comprising hydrochlorothiazide 25 mg plus 2.5 mg amiloride hydrochloride, and the 'free' combination of atenolol and diuretic were compared in elderly hypertensive patients aged 60-79 years. After a four-week run-in period on placebo, patients were randomly assigned, in a double-blind manner, to atenolol or diuretic treatment, each for four weeks. Thereafter patients were given the 'free' combination for a further four weeks and this treatment was continued for six months. Blood pressure and heart rate were measured after the patient had rested for five minutes supine and after two minutes standing. These blood pressure measurements were made at least 24 hours after the preceding dose using a Random Zero sphygmomanometer. Results from 26 of the 27 patients entered into the study showed an advantage for combination therapy combined with either atenolol or diuretic treatment alone. No significant difference was found between treatments in the frequency of supraventricular and ventricular ectopic beats occurring in six patients who underwent 24-hour ambulatory ECG monitoring. However, ectopic activity was reduced in some patients during beta-blocker treatment. Few adverse effects occurred with any treatment. Three patients withdrew during the placebo period and three withdrew while taking active treatment. This study has shown that the combination of atenolol, hydrochlorothiazide and amiloride hydrochloride is an effective, safe, well-tolerated antihypertensive drug regimen when used once daily in elderly hypertensive patients.
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73% (138) of the patients were on anti-hypertensive drug combinations, comprising 71.7% (99), 24.4% (34) and 3.6% (5) on combinations of two, three and four drugs respectively. Overall, Thiazide diuretic consisting mainly of fixed dose combination of Amiloride and Hydorchlorothiazide (Moduretic(r)) was the most frequently prescribed drug class in anti-hypertensive combination therapy (83.3%). ACE inhibitor, Lisinopril (Zestril(r)), was prescribed in combination with Moduretic(r), Calcium channel blocker and beta-blocker in 6.5%, 8.5% and 0.7% respectively. Blood pressure control was adequate in only 29% (40) of patients, though adherence with therapy was documented as adequate in 77.5% (107). Type-2 diabetes mellitus (32.7%) and osteoarthritis (21.8%) were the most frequent co-morbidities. Potentially harmful drug-drug interactions in the study sample were identified in 17.5% (46) of patients. Physician documentation of adverse drug reactions among patients was done in only 10.9% of cases. There appear to be no institutionalised system in place to monitor, detect and document adverse drug reactions among patients on anti-hypertensive drug therapy.
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Common carotid artery intima-media thickness (IMT) progression was compared between 4 years of treatment with nifedipine and diuretic.
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A cross-over study was done to compare the effects of doxazosin, moduretic and amlodipine on biochemical values in 9 hypertensive Nigerians aged 35 to 65 years. Doxazosin therapy was characterized by significant increase in the levels of mean plasma total protein and albumin, while moduretic therapy showed significant reduction in the mean values of plasma creatinine and calcium. All other parameters did not show any significant variation during doxazosin and moduretic treatment phases; and amlodipine therapy did not have any effect on the biochemical values of the hypertensive patients.
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This study aims to describe factors associated with cognitive decline among 2584 subjects, aged 65-74, who were followed up for 54 months in the Medical Research Council Elderly Hypertension Trial (1982-1989). The subjects completed a cognitive test, the Paired Associate Learning Test (PALT), five times over this period. Decline on the PALT was associated with advanced age, male sex, rural residence, depression and low intelligence. These effects were modified by gender and level of pre-morbid intelligence. Advanced age, rural residence and number of cigarettes smoked daily were only associated with PALT decline among women of below median intelligence. The association between depression and PALT decline was only apparent in women of below median intelligence and men of above median intelligence. While these findings are consistent with other research into cognitive decline, they differ in some ways from reported risk factors for dementia, suggesting aetiological separateness. That women were more vulnerable than men to the effects of age and smoking raises the question of the impact on cognition of accelerated atherosclerosis after the menopause.
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The purpose of this study was to identify the frequency of cardiac dysrhythmias in two similar groups of hypertensive middle-aged males (age 45-66). They had previously been randomized either to a diuretic treatment (n = 42), or a beta-blocking agent (n = 41). A 24-hour ambulatory Holter monitoring, and serum potassium, was obtained in all patients, serum magnesium was measured in 35 patients. The mean number of ventricular premature beats (VPBs) and the frequency of complex arrhythmias (19 vs. 5) was significantly higher in the diuretic group (p less than 0.01). The serum potassium was significantly lower (p less than 0.001) in the diuretic group, and there was a significant (p less than 0.005) inverse correlation between the number of VPBs and the serum potassium in all treated patients. The patients with complex arrhythmias were older (p less than 0.01) than the remainder of the patients. No correlation between serum magnesium and VPBs or complex arrhythmias was found. This study demonstrates increased frequency of VPBs in older hypertensive males, treated with diuretics, and that hypokalaemia predisposes to increased cardiac arrhythmias. We conclude that in older mildly hypertensive men hypokalaemia should be avoided.
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We report the history of a diabetic man presenting with hyperkalaemia and rapidly progressing muscular paralysis with severe respiratory embarrassment. His symptoms resolved rapidly with reduction of the serum potassium concentration. Similar cases have been reported previously but this is a problem that few will have encountered and is a diagnosis which should not be overlooked before artificial ventilation is commenced.
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To draw attention to primary hyperparathyroidism as a cause of severe hypertension.
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Among 54 patients attending a hospital hypertension clinic and receiving the fixed-combination diuretic Moduretic (hydrochlorothiazide 50 mg, amiloride 5 mg), there was a 44.4% incidence of hypokalaemia. The mean drop in plasma potassium level was 0.69 mmol/L (P less than 0.0001), the mean low level being 2.81 mmol/L. Seventy-four per cent of falls occurred within 52 weeks of the start of therapy, 19.5 weeks being the average period between a normal and a low plasma potassium level. There was no difference in the fall in potassium level between male and female subjects, and beta-blockers were not obviously protective, although there was a statistically significant smaller fall in potassium level in females treated with them. The clinical significance of the unexpected hypokalaemia is uncertain; but even with fixed-combination diuretics, it remains necessary to monitor the plasma potassium level regularly in order to avoid complicating situations. The results of the present study would cast doubt on the efficacy of 5 mg of amiloride with 50 mg of hydrochlorothiazide in fixed-combination form in preventing hypokalaemia in this clinical situation.
A national multicenter study (34 centers) compared six treatments in 328 patients with cirrhotic ascites. Excluded were patients with g.i. bleeding within the last six months, chronic encephalopathy, cancer, tuberculosis or the following complications persisting after three weeks: acute encephalopythy, fever greater than 38 degrees C, infected ascites or biochemical abnormalities: blood urea greater than 8 mmol/l, natremia less than 130 mmol/l, kaliemia less than 2.5 or greater than 5.5 mmol/l, WBC greater than 12000 mm3, total bilirubin greater than 85.5 mumol/l. In each center patients were randomized into two treatment groups, each center using 2 of 6 proposed treatments: (1) Spironolactone and 500 mg Na p.d (77 patients), (2) Spironolactone + furosemide or Moduretic (amiloride + hydrochlorothiazide) and 500 mg Na p.d (80 patients), (3) Spironolactone + Furosemide or Moduretic and unrestricted sodium diet (86 patients), (4) Concentrated ascites reinfusion and 500 mg Na p.d. (36 patients), (5) Unmodified ascites reinfusion and 500 mg Na p.d. (23 patients), (6) Slow ascites drainage and 500 mg Na p.d. (31 patients). Statistical analysis methods were X2, variance analysis and Spotvoll-Stoline and Dunn-Sidak tests. Before treatment, there was no significant difference between the 6 groups.
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