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Medical research on aldactazide
Angiotensin-converting enzyme inhibitors and obstructive sleep apnea.
Mayo Clin Proc. 2006 Jan; 81(1): 53-5
Cicolin A, Mangiardi L, Mutani R, Bucca C
Angiotensin-converting enzyme (ACE) inhibitors may induce cough and rhinopharyngeal inflammation. Obstructive sleep apnea (OSA) is characterized by upper airway inflammation. We describe a patient who, during enalapril treatment, developed cough, upper airway symptoms, and diurnal sleepiness, with an increased number of obstructive apnea-hypopnea episodes (apnea-hypopnea index [AHI], 25) during sleep. Her symptoms and AHI improved 1 month after enalapril was discontinued and diuretic therapy (hydrochlorothiazide-spironolactone) was initiated. Similar findings were observed in 4 other patients with OSA who had ACE inhibitor-induced cough. The mean +/- SD AHI was 33.8+/-21.0 during enalapril treatment and 20.0+/-17.0 after withdrawal of this drug (P = .04). Exhaled nitric oxide, a marker of airway inflammation, was increased during enalapril treatment (15.0 +/- 4.3 parts per billion) and decreased after discontinuation of this drug (9.0 +/- 2.6; P = .03). No significant difference in the AHI and exhaled nitric oxide was observed in 4 patients with OSA who did not experience cough, before or after withdrawal of ACE inhibitor treatment. These findings suggest that ACE inhibitor treatment may contribute to OSA by inducing upper airway inflammation.
Bone loss in rats with aldosteronism.
Am J Med Sci. 2005 Jul; 330(1): 1-7
Runyan AL, Chhokar VS, Sun Y, Bhattacharya SK, Runyan JW, Weber KT
OBJECTIVE: We hypothesized that aldosteronism is accompanied by hypercalciuria and hypermagnesuria that lead to bone loss, which could be rescued by hydrochlorothiazide and spironolactone. METHODS: We monitored 24-hour urinary Ca and Mg excretion; plasma ionized [Ca]o and [Mg]o and plasma K; and bone mineral density of the femur. The following groups (n=5 in each group) were studied: age- and gender-matched, untreated controls; controls + 4 weeks hydrochlorothiazide; 4 weeks aldosterone/salt treatment (ALDOST, 0.75 mug/h and dietary 1% NaCl/0.4% KCl); 4 weeks ALDOST+hydrochlorothiazide (50 mg/kg in prepared food); and 4 weeks ALDOST+hydrochlorothiazide+spironolactone (200 mg/kg day in divided doses by twice-daily gavage). RESULTS: ALDOST increased (P
European experience with spironolactone and thiazide diuretic as antihypertensive therapy.
Am J Cardiol. 1990 Jun 19; 65(23): 18K-19K
Lauler DP
J Pediatr. 1989 Apr; 114(4 Pt 1): 619-24
Engelhardt B, Blalock WA, DonLevy S, Rush M, Hazinski TA
To test the hypothesis that spironolactone-hydrochlorothiazide (Aldactazide) will improve urine output and lung function in infants with bronchopulmonary dysplasia, we studied 21 hospitalized, spontaneously breathing, oxygen-dependent infants with chronic bronchopulmonary dysplasia. Infants were randomly assigned to receive either a 1:1 mixture of spironolactone and hydrochlorothiazide orally (n = 12) (3 mg/kg/day of both compounds) or no treatment (n = 9) for 6 to 8 days each. Dynamic lung compliance, total pulmonary resistance, and hemoglobin oxygen saturation were measured on the first and last days of each study period. Fluid intake and urine output were measured each day. Although the treatment significantly increased urine output, neither lung mechanics nor oxygenation were improved by the drug. The magnitude of the diuresis achieved with spironolactone-hydrochlorothiazide treatment was comparable to the diuresis achieved in a previous study of furosemide treatment (J Pediatr 1986:109;1034-9). Statistical analysis indicated that a type II error was an unlikely explanation for our failure to detect a beneficial effect. In three patients, doubling the oral dose did not improve lung mechanics or oxygenation. We speculate that diuresis per se is not responsible for lung function improvement during treatment with other drugs with diuretic properties.
Efficacy of verapamil--hydrochlorothiazide-spironolactone therapy in hypertensive black patients.
Clin Pharm. 1987 Apr; 6(4): 322-6
Hughes GS, Cowart TD, Conradi EC
Pediatrics. 1986 Feb; 77(2): 212-6
Perlman JM, Moore V, Siegel MJ, Dawson J
A retrospective analysis of infants with bronchopulmonary dysplasia requiring prolonged hospitalization (greater than 100 days) was carried out to determine those factors associated with fatal outcome. Twenty-three infants made up the study population. Eleven infants died and 12 survived (survivors). No differences were noted between the groups regarding ventilator requirement, radiographic changes, and medication use (digoxin, aldactazide), except for furosemide which was used twice as frequently in the group of infants who died v the group of infants who survived (P less than .001). Differences noted between the groups included moderate hypochloremia (chloride less than 80 mEq/L) in all 11 infants who died v six of 12 survivors, severe hypochloremia (chloride less than 70 mEq/L) in the nine of 11 infants who died v two of 12 survivors, metabolic alkalosis (pH greater than 7.45) in nine of 11 infants who died v three of 12 survivors, hypertension (systolic BP greater than 113 mm Hg) in eight of 11 infants who died v one of 12 survivors, decrease in head growth in ten of the 11 infants who died v one of the 12 survivors; these differences were all significant (P less than .001). The metabolic alkalosis and head growth changes appear to be related to the hypochloremia. The data suggest that chloride deficiency may be an important contributing factor in the genesis of poor outcome in infants with bronchopulmonary dysplasia and that close attention to chloride supplementation might influence outcome.
Soins Cardiol. 1986 Jan; I-II
de Roquefeuil F, Goupil C
Step 1 1/2 therapy for the treatment of hypertension.
Ohio State Med J. 1985 Jan; 81(1): 57, 59-61, 63
Miller SA, Cobb SD, Petrulis AS, Vertes V
Hydrochlorothiazide-induced pulmonary edema.
Drug Intell Clin Pharm. 1984 Mar; 18(3): 238-9
Levay ID
A patient with probable hydrochlorothiazide-induced pulmonary edema is described. A 70-year-old woman experienced nausea, diaphoresis, and severe respiratory distress approximately 1/2 hour after taking an Aldactazide tablet. She had experienced a flu-like syndrome after taking a single tablet two weeks previously. The patient was mildly tachycardic with a blood pressure of 74/0 mm Hg. A chest X-ray revealed cardiomegaly and bilateral pulmonary edema suggestive of congestive heart failure. The pulmonary capillary wedge pressure was normal. It was felt that the patient had developed a noncardiac pulmonary edema possibly secondary to hydrochlorothiazide ingestion. Nine other cases reported in the literature also are described. Pharmacists should be aware of this potential life-threatening reaction and avoid patient reexposure to the drug.
The bioavailability of spironolactone hydrochlorothiazide combination preparation.
Int J Clin Pharmacol Ther Toxicol. 1982 Jul; 20(7): 327-33
Rameis H, Hitzenberger G, Horwatitsch H
In a single-blind, randomized cross-over study the bioavailability of Spironothiazid (50 mg spironolactone, 50 mg hydrochlorothiazide) was investigated in six healthy male volunteers by comparing the same dose of the well-established drugs Aldactone dragees, 50 mg, and Esidrex tablets, 25 mg. After 6 days treatment with 2 X 1 Spironothiazid or 2 X 1 Aldactone dragees, 50 mg, plus Esidrex tablets, 25 mg daly, orally, the serum concentrations and the cumulative renal excretion of the active substances were measured after the morning dose on the 7th day of the study. Canrenone (the main metabolite of spironolactone) was measured fluorimetrically, hydrochlorothiazide was determined by gas chromatography. There was no statistically significant difference between the investigated drugs, neither in the areas under the curves nor in the cumulative renal excretion, thus indicating an identical bioavailability.