Wechselwirkung zwischen Amilorid und Fosinopril und Hydrochlorothiazid
Amilorid und Fosinopril und Hydrochlorothiazid: Beide FDA-Fachinformationen versehen diese Kombination mit den stärksten Formulierungen, etwa einer Gegenanzeige, einem umrahmten Warnhinweis (Boxed Warning) oder der Anweisung, sie zu vermeiden.
Nicht ohne ärztliche Anleitung kombinieren. Die unten zitierten Formulierungen der Fachinformation sind die stärksten, die die FDA verwendet.
Was die FDA-Fachinformationen sagen
Aus der FDA-Fachinformation zu Amilorid (amiloride hydrochloride) · Stand 2023-05-05
Hyperkalemia occurs commonly (about 10%) when amiloride is used without a kaliuretic diuretic.
When amiloride HCl is used concomitantly with a thiazide diuretic in patients without these complications, the risk of hyperkalemia is reduced to about 1-2 percent.
It is thus essential to monitor serum potassium levels carefully in any patient receiving amiloride, particularly when it is first introduced, at the time of diuretic dosage adjustments, and during any illness that could affect renal function.
The risk of hyperkalemia may be increased when potassium-conserving agents, including amiloride HCl, are administered concomitantly with an angiotensin-converting enzyme inhibitor, an angiotensin II receptor antagonist, cyclosporine or tacrolimus.
Diabetes Mellitus In diabetic patients, hyperkalemia has been reported with the use of all potassium-conserving diuretics, including amiloride HCl, even in patients without evidence of diabetic nephropathy.
Aus der FDA-Fachinformation zu Fosinopril und Hydrochlorothiazid (Fosinopril Sodium and Hydrochlorothiazide) · Stand 2024-04-28
Symptomatic hypotension is most likely to occur in patients who have been volume- and/or salt-depleted as a result of prolonged diuretic therapy, dietary salt restriction, dialysis, diarrhea, or vomiting.
The thiazide component of fosinopril sodium and hydrochlorothiazide may potentiate the action of other antihypertensive drugs, especially ganglionic or peripheral adrenergic-blocking drugs.
In such patients, fosinopril sodium and hydrochlorothiazide therapy should be started under close medical supervision; they should be followed closely for the first 2 weeks of treatment and whenever the dose of fosinopril or diuretic is increased.
In some studies of hypertensive patients with unilateral or bilateral renal artery stenosis, treatment with ACE inhibitors has been associated with increases in blood urea nitrogen and serum creatinine; these increases were reversible upon discontinuation of ACE inhibitor therapy, concomitant diuretic therapy, or both.
Some ACE-inhibitor-treated hypertensive patients with no apparent preexisting renal vascular disease have developed increases in blood urea nitrogen and serum creatinine, usually minor and transient, especially when the ACE inhibitor has been given concomitantly with a diuretic.
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