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| __NOTOC__
| | #REDIRECT [[Moexipril#Warnings]] |
| {{Moexipril}}
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| {{CMG}}; {{AE}} {{AM}}
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| ==Warnings==
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| ====Anaphylactoid and Possibly Related Reactions====
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| Presumably because [[angiotensin-converting enzyme inhibitors]] affect the metabolism of [[eicosanoids]] and polypeptides, including endogenous [[bradykinin]], patients receiving ACE inhibitors, including moexipril hydrochloride, may be subject to a variety of adverse reactions, some of them serious.
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| ====Head and Neck Angioedema====
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| [[Angioedema]] involving the face, extremities, lips, tongue, glottis, and/or larynx has been reported in patients treated with ACE inhibitors, including moexipril hydrochloride. Symptoms suggestive of [[angioedema]] or facial edema occurred in <0.5% of moexipril-treated patients in placebo-controlled trials. None of the cases were considered life-threatening and all resolved either without treatment or with medication ([[antihistamines]] or [[glucocorticoids]]). One patient treated with [[hydrochlorothiazide]] alone experienced laryngeal edema. No instances of [[angioedema]] were reported in placebo-treated patients.
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| In cases of [[angioedema]], treatment should be promptly discontinued and the patient carefully observed until the swelling disappears. In instances where swelling has been confined to the face and lips, the condition has generally resolved without treatment, although antihistamines have been useful in relieving symptoms.
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| [[Angioedema]] associated with involvement of the tongue, glottis, or larynx, may be fatal due to airway obstruction. Appropriate therapy, e.g., subcutaneous [[epinephrine]] solution 1:1000 (0.3 to 0.5 mL) and/or measures to ensure a patent airway, should be promptly provided.
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| ====Intestinal Angioedema====
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| [[Intestinal angioedema]] has been reported in patients treated with ACE inhibitors. These patients presented with abdominal pain (with or without nausea or [[vomiting]]); in some cases there was no prior history of facial angioedema and [[C-1 esterase]] levels were normal. The angioedema was diagnosed by procedures including abdominal CT scan or ultrasound, or at surgery, and symptoms resolved after stopping the ACE inhibitor. Intestinal angioedema should be included in the differential diagnosis of patients on ACE inhibitors presenting with [[abdominal pain]]. | |
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| ====Anaphylactoid Reactions During Desensitization====
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| Two patients undergoing desensitizing treatment with [[hymenoptera venom]] while receiving ACE inhibitors sustained life-threatening anaphylactoid reactions. In the same patients, these reactions did not occur when ACE inhibitors were temporarily withheld, but they reappeared when the ACE inhibitors were inadvertently readministered.
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| ====Anaphylactoid Reactions During Membrane Exposure====
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| Anaphylactoid reactions have been reported in patients dialyzed with high-flux membranes and treated concomitantly with an ACE inhibitor. Anaphylactoid reactions have also been reported in patients undergoing [[low-density lipoprotein]] apheresis with dextran sulfate absorption.
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| ====Hypotension====
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| Moexipril hydrochloride can cause symptomatic [[hypotension]], although, as with other ACE inhibitors, this is unusual in uncomplicated hypertensive patients treated with moexipril hydrochloride alone. Symptomatic [[hypotension]] was seen in 0.5% of patients given moexipril and led to discontinuation of therapy in about 0.25%. Symptomatic [[hypotension]] is most likely to occur in patients who have been salt- and volume-depleted as a result of prolonged diuretic therapy, dietary salt restriction, [[dialysis]], [[diarrhea]], or [[vomiting]]. Volume- and salt-depletion should be corrected and, in general, diuretics stopped, before initiating therapy with moexipril hydrochloride. | |
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| In patients with congestive heart failure, with or without associated renal insufficiency, ACE inhibitor therapy may cause excessive [[hypotension]], which may be associated with [[oliguria]] or progressive [[azotemia]], and rarely, with acute renal failure and death. In these patients, moexipril hydrochloride therapy should be started under close medical supervision, and patients should be followed closely for the first two weeks of treatment and whenever the dose of moexipril or an accompanying diuretic is increased. Care in avoiding hypotension should also be taken in patients with [[ischemic heart disease]], [[aortic stenosis]], or [[cerebrovascular disease]], in whom an excessive decrease in blood pressure could result in a myocardial infarction or a cerebrovascular accident.
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| If [[hypotension]] occurs, the patient should be placed in a supine position and, if necessary, treated with an intravenous infusion of normal saline. Moexipril hydrochloride treatment usually can be continued following restoration of blood pressure and volume.
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| ====Neutropenia/Agranulocytosis====
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| Another ACE inhibitor, captopril, has been shown to cause [[agranulocytosis]] and bone marrow depression, rarely in patients with uncomplicated hypertension, but more frequently in hypertensive patients with [[renal impairment]], especially if they also have a collagen-vascular disease such as [[systemic lupus erythematosus]] or [[scleroderma]]. Although there were no instances of severe [[neutropenia]] (absolute neutrophil count <500/mm3) among patients given moexipril hydrochloride, as with other ACE inhibitors, monitoring of white blood cell counts should be considered for patients who have collagen-vascular disease, especially if the disease is associated with impaired renal function. Available data from clinical trials of moexipril hydrochloride are insufficient to show that moexipril hydrochloride does not cause [[agranulocytosis]] at rates similar to captopril.
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| ====Fetal Toxicity====
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| ====Pregnancy category D====
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| Use of drugs that act on the [[renin-angiotensin system]] during the secondand third trimesters of pregnancy reduces fetal renal function and increases fetal and neonatal morbidity and death. Resulting [[oligohydramnios]] can be associated with fetal [[lung hypoplasia]] and skeletal deformations. Potential neonatal adverse effects include [[skull hypoplasia]], [[anuria]], [[hypotension]], [[renal failure]], and death. When pregnancy is detected, discontinue moexipril hydrochloride as soon as possible. These adverse outcomes are usually associated with use of these drugs in the second and third trimester of pregnancy. Most epidemiologic studies examining fetal abnormalities after exposure to antihypertensive use in the first trimester have not distinguished drugs affecting the renin-angiotensin system from other antihypertensive agents. Appropriate management of maternal hypertension during pregnancy is important to optimize outcomes for both mother and fetus.
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| In the unusual case that there is no appropriate alternative to therapy with drugs affecting the renin-angiotensin system for a particular patient, apprise the mother of the potential risk to the fetus. Perform serial ultrasound examinations to assess the intra-amniotic environment.
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| If [[oligohydramnios]] is observed, discontinue moexipril hydrochloride unless it is considered lifesaving for the mother. Fetal testing may be appropriate, based on the week of pregnancy. Patients and physicians should be aware, however, that oligohydramnios may not appear until after the fetus has sustained irreversible injury. Closely observe Infants with histories of in utero exposure to Moexipril hydrochloride for [[hypotension]], [[oliguria]], and [[hyperkalemia]]
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| No embryotoxic, fetotoxic, or teratogenic effects were seen in rats or in rabbits treated with up to 90.9 and 0.7 times, respectively, the Maximum Recommended Human Dose (MRHD) on a mg/m2 basis.
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| ====Hepatic Failure====
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| Rarely, ACE inhibitors have been associated with a syndrome that starts with [[cholestatic jaundice]] and progresses to [[fulminant hepatic necrosis]] and sometimes death. The mechanism of this syndrome is not understood. Patients receiving ACE inhibitors who develop jaundice or marked elevations of hepatic enzymes should discontinue the ACE inhibitor and receive appropriate medical follow-up.
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| ==Precautions==
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| ====General====
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| ====Impaired Renal Function====
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| As a consequence of inhibition of the [[renin-angiotensin-aldosterone system]], changes in renal function may be anticipated in susceptible individuals. There is no clinical experience of moexipril hydrochloride in the treatment of hypertension in patients with [[renal failure]].
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| Some 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 moexipril hydrochloride has been given concomitantly with a [[thiazide]] diuretic. This is more likely to occur in patients with preexisting renal impairment. There may be a need for dose adjustment of moexipril hydrochloride and/or the discontinuation of the [[thiazide]] diuretic.
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| Evaluation of hypertensive patients should always include assessment of renal function.
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| ====Hypertensive Patients With Congestive Heart Failure====
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| In hypertensive patients with severe [[congestive heart failure]], whose renal function may depend on the activity of the [[renin-angiotensin-aldosterone system]], treatment with ACE inhibitors, including moexipril hydrochloride, may be associated with [[oliguria]] and/or progressive [[azotemia]] and, rarely, [[acute renal failure]] and/or death.
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| ====Hypertensive Patients With Renal Artery Stenosis====
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| In hypertensive patients with unilateral or bilateral [[renal artery stenosis]], increases in [[blood urea nitrogen]] and [[serum creatinine]] have been observed in some patients following ACE inhibitor therapy. These increases were almost always reversible upon discontinuation of the ACE inhibitor and/or diuretic therapy. In such patients, renal function should be monitored during the first few weeks of therapy.
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| ====Hyperkalemia====
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| In clinical trials, persistent [[hyperkalemia]] (serum potassium above 5.4 mEq/L) occurred in approximately 1.3% of hypertensive patients receiving moexipril hydrochloride. Risk factors for the development of [[hyperkalemia]] with ACE inhibitors include [[renal insufficiency]], [[diabetes mellitus]], and the concomitant use of potassium-sparing diuretics, potassium supplements, and/or potassium-containing salt substitutes, which should be used cautiously, if at all, with moexipril hydrochloride.
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| ====Surgery/Anesthesia====
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| In patients undergoing major surgery or during anesthesia with agents that produce [[hypotension]], moexipril may block the effects of compensatory [[renin]] release. If [[hypotension]] occurs in this setting and is considered to be due to this mechanism, it can be corrected by volume expansion.
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| ====Cough====
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| Presumably due to the inhibition of the degradation of endogenous [[bradykinin]], persistent nonproductive cough has been reported with all ACE inhibitors, always resolving after discontinuation of therapy. ACE inhibitor-induced cough should be considered in the differential diagnosis of cough. In controlled trials with moexipril, cough was present in 6.1% of moexipril patients and 2.2% of patients given placebo.<ref name="dailymed.nlm.nih.gov">{{Cite web | last = | first = | title = MOEXIPRIL HYDROCHLORIDE TABLET [APOTEX CORP.] | url = http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=d18108f5-98ca-1220-d145-bcf4e71ceaee | publisher = | date = | accessdate = }}</ref>
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| ==References==
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| {{Reflist}}
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| {{FDA}}
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| [[Category:Cardiovascular Drugs]]
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| [[Category:Drugs]]
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