Moduretic is used for treating fluid retention (edema) and high blood pressure. It may be used alone or with other medicines.
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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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The objective of the study is to compare fatal and nonfatal cardiovascular endpoints in hypertensive patients randomised to the calcium-channel blocker, nifedipine GITS or a thiazide diuretic, co-amilozide. A total of 6592 patients from nine countries (UK, France, Israel, Spain, Italy, The Netherlands, Sweden, Denmark and Norway) will be recruited, aged 55-80 and with a blood pressure (BP) > or = 150/95 or > or = 160 mm Hg (systolic). All patients will have at least one other major cardiovascular risk factor. Patients will be minimised by country and risk factors and randomised to double-blind treatment with either nifedipine GITS or diuretic. After a single dose titration, additional treatment will be atenolol or enalapril (where beta-blockade is contra-indicated). After achieving a target BP of 140/90 mm Hg patients will be followed for a total of 3 years. Primary endpoints are myocardial infarction, stroke, subarachnoid haemorrhage, heart failure and sudden cardiac death. The study has a power of 80% at 5% significance to detect a difference between 8% event rate over 3 years in diuretic-treated patients and 6% in those receiving nifedipine.
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A randomized double-blind, crossover trial was carried out in twenty hypertensive patients to evaluate the hypotensive efficacy and safety of indapamide. Indapamide in doses of 2.5 mg per day in combination with other antihypertensive agents was as effective in reducing the blood pressure in hypertensive patients as one tablet of Moduretic (50 mg hydrochlorothiazide and 5 mg amiloride). Indapamide induced no changes in serum potassium or uric acid levels and there were no major side effects.
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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)
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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.
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.
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To evaluate physicians' prescribing of anti-hypertensive drug combinations in a tertiary care setting in southwestern Nigeria, determine the degree of usage of Angiotensin Converting Enzyme (ACE) inhibitor-based combinations and identify specific points of intervention to improve outcomes of anti-hypertensive combination therapy.
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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.
This study investigated the effects of aerobic dance combined with antihypertensive drugs on BP and number of antihypertensive drugs in individuals with hypertension.
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In a double-blind parallel-group study 133 patients with mild to moderate essential hypertension were randomised to felodipine 5mg twice daily or Moduretic mite every morning after a run-in placebo period of 1 to 2 weeks. All previous antihypertensive therapy was withdrawn at the start of the run-in period. After 4 weeks the dose of felodipine was increased to 10mg twice daily, and Moduretic mite was replaced by Moduretic in patients with a diastolic blood pressure of greater than 80mm Hg. On the low dose, the supine blood pressure on felodipine was reduced by 24/14mm Hg from 174/105mm Hg, and on Moduretic mite by 19/11mm Hg from 171/103mm Hg. After the increase in dosage blood pressure was lowered further. There was no statistically significant difference in blood pressure reduction between the 2 groups. Severe adverse drug experiences (ADEs) were few and equally distributed. However, more felodipine patients were withdrawn because of ADEs. Potassium levels decreased and uric acid levels increased significantly in the Moduretic group.
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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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Although aerobic exercise has been shown to lower blood pressure (BP) in human beings, its additive BP-reducing effect on antihypertensive drug therapy seems to have been investigated in only laboratory animals.
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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Patients were referred from general and internal medicine practices following written invitations and included consecutively. Participants were examined and followed-up on an outpatient basis.
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To investigate the impact of treatment on cardiovascular mortality and morbidity, we assessed outcomes in patients with hypertension and diabetes who received co-amilozide or nifedipine in the International Nifedipine GITS Study: Intervention as a Goal in Hypertension. Participants had to be 55 to 80 years of age, with hypertension (> or =150/95 or > or =160 mm Hg) and at least one additional cardiovascular risk factor. Patients received 30 mg nifedipine once daily or co-amilozide (25 mg hydrochlorothiazide and 2.5 mg amiloride) daily. Doses were doubled if target blood pressures (<140/90 mm Hg) were not achieved. Primary (composite of cardiovascular death, myocardial infarction, heart failure, and stroke) and secondary outcomes (composite of primary outcomes, including all-cause mortality and death from vascular and nonvascular causes) were assessed by means of intent-to-treat analyses. There was no significant difference in the incidence of primary outcomes between nifedipine-treated and co-amilozide-treated patients with diabetes at baseline (n=1302) (8.3% versus 8.4%; relative risk, 0.99, 95% CI, 0.69 to 1.42; P=1.00). A significant benefit for nifedipine-treated patients was seen for the composite secondary outcome (14.2% versus 18.7%; relative risk, 0.76, 95% CI, 0.59 to 0.97; P=0.03). Among patients without diabetes at baseline (n=5019), there was a significant difference in the incidence of new diabetes (nifedipine 4.3% versus co-amilozide 5.6%, P=0.023). Nifedipine GITS once daily is as effective as diuretic therapy in reducing cardiovascular complications in hypertensive diabetics. Nifedipine-treated patients were also less likely to have diabetes or have secondary events (a composite of all-cause mortality, death from a vascular cause, and death from a nonvascular cause) than co-amilozide recipients. Our results suggest that nifedipine could be considered as first-line therapy for hypertensive diabetics.
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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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.
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A method has been developed for the separation of hydrochlorothiazide and amiloride by high-performance liquid chromatographic (HPLC) method on a C18 column with detection at 280 nm. The optimal conditions of separation were determined with the aid of 'window diagram' technique of Laub and Purnell. The effect of simultaneously varying the pH, proportion aqueous acetic acid and methanol in the mobile phase were studied to optimize the separation. A response surface diagram was used to optimize the experimental conditions for the separation. The mobile phase composition that provides an acceptable resolution hydrochlorothiazide and amiloride in a short elution time is water:methanol (60:40) and pH 3.2 (pH adjusted to 3.2 with CH3COOH). A method is applied for the quantitative analysis of Moduretic tablets (Merck Sharp & Dokme International). The powdered tablets are extracted with methanol, containing caffeine as the internal standard, and assayed by comparison of peak areas after liquid chromatography.
Three cases are presented which emphasize the importance of hyponatraemia as a cause of grand mal seizures. The combination of hydrochlorothiazide and amiloride appears to increase the risk of hyponatraemia. We discuss the aetiology and treatment of hyponatraemia and review the necessity for such combination therapy. We recommend caution in prescribing diuretics and preparations such as Moduretic should be used only in those few patients shown to need potassium supplementation.
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This preliminary report demonstrates the tendency of aerobic dance to enhance BP control in individuals on two antihypertensive drugs without BP control.
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