Patients receiving ACE inhibitors who develop jaundice or marked elevations of hepatic enzymes should discontinue the ACE inhibitor and receive appropriate medical follow-up.Moderate Potential Hazard, Moderate plausibility. Applies to: Congestive Heart FailureACE inhibitors can cause marked renal impairment in patients whose renal function depends on the activity of the renin-angiotensin-aldosterone system.

Therapy with ACE inhibitors should be initiated under very close medical supervision in patients with severe CHF, especially when accompanied by volume and/or sodium depletion.
Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest.
Patients should be monitored closely for several hours after an initial dose until blood pressure has stabilized, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased. In these cases the drug that arrives first binds with the plasma protein, leaving the other drug dissolved in the plasma, which modifies its concentration. For example, one drug may alter the pharmacokinetics of another. In patients who experience a worsening of renal function, discontinuation of ACE inhibitor therapy is usually not required provided there is symptomatic improvement of the heart failure and renal deterioration is well-tolerated. Drug interactions occur when one drug affects the pharmacokinetics of another drug or its metabolites. Transient hypotension is also not a contraindication to further treatment with ACE inhibitors. Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). •The resultant effect is altered plasma concentration of the object drug. Therapy with ACE inhibitors should be administered cautiously in patients with preexisting renal dysfunction, particularly those with renovascular disease. For example, one drug may alter the The risk of a drug-drug interaction increases with the number of drugs used.When two drugs are used together, their effects can be additive (the result is what you expect when you add together the effect of each drug taken independently), Both synergy and antagonism can occur during different phases of the interaction between a drug, and an organism. Lack of pharmacokinetic drug interaction between oral posaconazole and caspofungin or micafungin. This can cause a wide range of adverse reactions. Alternatively, drug interactions may result from competition for a single receptor or signaling pathway. Patients with diabetes mellitus should be monitored more closely during thiazide therapy, and their antidiabetic regimen adjusted accordingly.Moderate Potential Hazard, Moderate plausibility. Major Potential Hazard, Moderate plausibility. There are many causes of drug interactions. A drug interaction is a change in the action or side effects of a drug caused by concomitant administration with a food, beverage, supplement, or another drug.. Patients with a history of angioedema unrelated to ACE inhibitors may be at increased risk of angioedema while receiving an ACE inhibitor. Risk factors for the development of hyperkalemia during ACE inhibitor therapy include renal insufficiency, diabetes mellitus, and the concomitant use of potassium-sparing diuretics, potassium supplements, and/or potassium-containing salt substitutes.Major Potential Hazard, Moderate plausibility.

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