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Corticosteroids with thiazide diuretics

Concomitant internal use of aloe latex is cautioned with thiazide diuretics, corticosteroids, and licorice, and long-term use of aloe latex as a laxative may increase the potassium loss induced by these drugs and botanicals (Brinker 2001). [Pg.45]

CEC-MS is used as an analytical tool for pharmaceutical analysis. The CEC-ESI-MS analysis and quantification of a potential drug candidate from 13 structurally related compounds in extracted plasma were reported by Paterson et al. [26]. The CEC colunm was packed with an experimental mixed mode stationary phase containing both Ci8 and sulfonic acid ligands. These phases promote stable electroosmotic flow across a wide range of pH values and allow a greater choice of buffer pH values. The mobile phase was acetonitrile/25 mM ammonium acetate (75 25) at pH 3.5 adjusted with acetic acid. Taylor et al. reported a CEC-ESI-MS analysis of mixtures of benzodiazepines, corticosteroids and thiazide diuretic drugs [27]. [Pg.183]

Sulfonylureas In acute poisoning with sulfonylureas, the stomach should be washed and treated with activated charcoal, and hypoglycemia must be treated. Sulfonylureas interact with oral contraceptives, thiazide diuretics, corticosteroids, adrenaline, chlorpromazine, ACE inhibitors, some NSAIDs, antihistamines, anticoagulants, MAOIs, antidepressants, and many other drugs. Care must be exercised when treating with sulfonylureas. [Pg.358]

Adverse effects are most commonly manifest as acute pancreatitis. The strongest association is with alcohol abuse. High plasma calcium, including that caused by hypervitaminosis D, and parenteral nutrition also increase the risk. Corticosteroids, didanosine, azathoipurine, diuretics (including thiazides and frusemide), sodium valproate, mesalazine and paracetamol (in overdose) have also been causally related. [Pg.659]

Four children with the nephrotic syndrome developed transient hypercalciuria and intraluminal calcification in renal histopathological specimens without radiological evidence of renal calcification. These children were resistant to corticosteroids and were receiving furosemide plus albumin for the management of edema (10). This result stresses the pervasive effect of furosemide, and probably all loop diuretics, in increasing urinary calcium excretion, with resultant nephrocalcinosis. Whenever possible, steps should be taken to limit the hypercalciuric effect of loop diuretics. Such maneuvers could include limiting the sodium content of the diet and/or combining the loop diuretic with a thiazide diuretic. [Pg.1456]

With long-term use hypokalemia due to intestinal potassium loss could occur (Blumenthal, 1998). Thiazide diuretics, corticosteroids, and licorice could exacerbate hypokalemia. The effects of digoxin can be potentiated by hypokalemia. [Pg.332]

Indapamide is a thiazide diuretic that enhances excretion of sodium, chloride, and water by interfering with transport of sodium ions across renal tubular epithelium. It is indicated in the treatment of edema associated with CHF, hepatic cirrhosis, renal dysfunction, and corticosteroid or estrogen therapy and management of hypertension. [Pg.347]

No interactions are expected at standard therapeutic doses. At higher doses or with long-term use, licorice may potentiate potassium depletion of high-ceiling loop diuretics and thiazide diuretics, stimulant laxatives (Mills and Bone 2005), and corticosteroids such as prednisolone (Cheng et al. 2004 De Smet 1993), and may potentiate the action of cardiac glycosides such as digoxin (Kelly 1990). [Pg.417]

Concomitant use of senna or sickle-pod senna is cautioned with antiarrhythmic drugs, thiazide diuretics, corticosteroids, licorice, and botanicals containing cardiac glycosides, as long-term use of senna or sickle-pod senna as a laxative can cause or exacerbate potassium loss (Brinker 2001 De Smet 1993 ESCOP 2003). [Pg.805]

Drug interactions The extent to which vitamin D supplementation alters drug effectiveness and toxicity in humans has been systematically reviewed. Bile acid sequestrants and lipase inhibitors were found to inhibit the absorption of vitamin D from the gut. Statins, rifampicin, isoniazid, hydroxychloroquine, antiepileptics, corticosteroids, immimo-suppressive and chemotherapeutic agents, antiretroviral drugs and H2 receptor antagonists interfered with vitamin D metabolism. The interaction between vitamin D and thiazide diuretics could result in hypercalcaetnia. Vitamin D supplementation decreases concentrations of atorvastatin, and could cause hypercalcaetnia in elderly individuals or tixose with compromised renal function or hyperparathyroidism [84 ]. [Pg.513]

The risks and benefits of distal tubular diuretics have been assessed in preterm infants under 3 weeks of age with or developing chronic lung disease (36). Acute and chronic administration of distal diuretics improved pulmonary mechanics adverse effects were not reported. However, additional studies are needed to assess whether thiazide administration improves mortality, duration of oxygen dependency, ventilator dependency, length of hospital stay, and long-term outcome in patients exposed to corticosteroids and bronchodilators, and whether adding spironolactone to thiazides or adding metolazone to furosemide has any beneficial effect. [Pg.3378]

Increased risk of toxicity with drugs that alter serum electrolytes (potassium -depleting diuretics, corticosteroids, thiazide and loop diuretics, amphotericin B, quinidine, amiodarone). Blockers of p adrenergic receptors, calcium channels, or acetylcholinesterase increase risk of complete AV block. Drugs which alter Gl absorption may alter bioavallabillty. [Pg.61]

The potassium-depleting diuretics (i.e. loop diuretics or thiazide and related diuretics) are listed in Table 26.1 , (p.944). Acetazolamide, a weak diuretic, has also been predicted to cause hypokalaemia in the presence of corticosteroids. However, hypokalaemia seen with acetazolamide is rarely clinically significant, and therefore the risks are lower... [Pg.1054]

Established interactions. The CSM in the UK advises that, as potentially serious hypokalaemia may result from beta2 agonist therapy, particular caution is required in severe asthma, as this effect may be potentiated by theophylline and its derivatives, corticosteroids, diuretics, and by hypoxia. Hypokalaemia with concurrent use of thiazide and loop diuretics may be reduced or even abolished by the addition of spironolactone or high-dose triamterene. Plasma potassium levels should therefore be monitored in patients with severe asthma. Hypokalaemia may result in cardiac arrhythmias in patients with ischaemic heart disease and may also affect the response of patients to drugs such as the digitalis glycosides and an-tiarrhythmics. [Pg.1162]


See other pages where Corticosteroids with thiazide diuretics is mentioned: [Pg.433]    [Pg.845]    [Pg.266]    [Pg.504]    [Pg.411]    [Pg.218]    [Pg.344]    [Pg.209]    [Pg.153]    [Pg.145]    [Pg.68]    [Pg.209]    [Pg.102]    [Pg.161]    [Pg.10]    [Pg.122]    [Pg.547]    [Pg.65]   
See also in sourсe #XX -- [ Pg.489 ]




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Thiazides

Thiazides Corticosteroids

With corticosteroids

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