Lisinopril (Page 2 of 7)

3 DOSAGE FORMS AND STRENGTHS

2.5 mg tablet is a white to off-white, round, biconvex, uncoated tablet with “LUPIN” debossed on one side and “2.5” on other side.

5 mg tablet is a pink coloured, round, biconvex, uncoated tablet with “5” debossed on one side and breakline on other side.

10 mg tablet is a pink coloured, round, biconvex, uncoated tablet with “LUPIN” debossed on one side and “10” on other side.

20 mg tablet is a pink coloured, round, biconvex, uncoated tablet with “LUPIN” debossed on one side and “20” on other side.

30 mg tablet is a red coloured, round, biconvex, uncoated tablet with “LUPIN” debossed on one side and “30” on other side.

40 mg tablet is a yellow coloured, round, biconvex, uncoated tablet with “LUPIN” debossed on one side and “40” on other side.

4 CONTRAINDICATIONS

Lisinopril is contraindicated in combination with a neprilysin inhibitor (e.g., sacubitril). Do not administer Lisinopril tablet USP within 36 hours of switching to or from sacubitril/valsartan, a neprilysin inhibitor [see WARNINGS and PRECAUTIONS ( 5.2)].

Lisinopril is contraindicated in patients with:

  • a history of angioedema or hypersensitivity related to previous treatment with an angiotensin converting enzyme inhibitor
  • hereditary or idiopathic angioedema

Do not co-administer aliskiren with lisinopril in patients with diabetes [see DRUG INTERACTIONS ( 7.4)].

5 WARNINGS AND PRECAUTIONS

5.1 Fetal Toxicity

Lisinopril can cause fetal harm when administered to a pregnant woman. Use of drugs that act on the renin-angiotensin system during the second and 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 lisinopril as soon as possible [see USE IN SPECIFIC POPULATIONS ( 8.1)] .

5.2 Angioedema and Anaphylactoid Reactions

Patients taking concomitant mTOR inhibitor (e.g. temsirolimus, sirolimus, everolimus) therapy or a neprilysin inhibitor may be at increased risk for angioedema. [see DRUG INTERACTIONS ( 7.7, 7.8)].

Angioedema

Head and Neck Angioedema:

Angioedema of the face, extremities, lips, tongue, glottis and/or larynx, including some fatal reactions, have occurred in patients treated with angiotensin converting enzyme inhibitors, including lisinopril, at any time during treatment. Patients with involvement of the tongue, glottis or larynx are likely to experience airway obstruction, especially those with a history of airway surgery. Lisinopril should be promptly discontinued and appropriate therapy and monitoring should be provided until complete and sustained resolution of signs and symptoms of angioedema has occurred.

Patients with a history of angioedema unrelated to ACE inhibitor therapy may be at increased risk of angioedema while receiving an ACE inhibitor [see CONTRAINDICATIONS (4)]. ACE inhibitors have been associated with a higher rate of angioedema in black than in non-black patients.

Intestinal Angioedema:

Intestinal angioedema has occurred 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. In some cases, the angioedema was diagnosed by procedures including abdominal CT scan or ultrasound, or at surgery, and symptoms resolved after stopping the ACE inhibitor.

Anaphylactoid Reactions

Anaphylactoid Reactions During Desensitization:

Two patients undergoing desensitizing treatment with hymenoptera venom while receiving ACE inhibitors sustained life-threatening anaphylactoid reactions.

Anaphylactoid Reactions During Dialysis :

Sudden and potentially life threatening anaphylactoid reactions have occurred in some patients dialyzed with high-flux membranes and treated concomitantly with an ACE inhibitor. In such patients, dialysis must be stopped immediately, and aggressive therapy for anaphylactoid reactions must be initiated. Symptoms have not been relieved by antihistamines in these situations. In these patients, consideration should be given to using a different type of dialysis membrane or a different class of antihypertensive agent. Anaphylactoid reactions have also been reported in patients undergoing low-density lipoprotein apheresis with dextran sulfate absorption.

5.3 Impaired Renal Function

Monitor renal function periodically in patients treated with lisinopril. Changes in renal function including acute renal failure can be caused by drugs that inhibit the renin-angiotensin system. Patients whose renal function may depend in part on the activity of the renin-angiotensin system (e.g., patients with renal artery stenosis, chronic kidney disease, severe congestive heart failure, post-myocardial infarction or volume depletion) may be at particular risk of developing acute renal failure on lisinopril. Consider withholding or discontinuing therapy in patients who develop a clinically significant decrease in renal function on lisinopril [see ADVERSE REACTIONS ( 6.1), DRUG INTERACTIONS ( 7.4)] .

5.4 Hypotension

Lisinopril can cause symptomatic hypotension, sometimes complicated by oliguria, progressive azotemia, acute renal failure or death. Patients at risk of excessive hypotension include those with the following conditions or characteristics: heart failure with systolic blood pressure below 100 mmHg, ischemic heart disease, cerebrovascular disease, hyponatremia, high dose diuretic therapy, renal dialysis, or severe volume and/or salt depletion of any etiology.

In these patients, lisinopril should be started under very close medical supervision and such patients should be followed closely for the first two weeks of treatment and whenever the dose of lisinopril and/or diuretic is increased. Avoid use of lisinopril in patients who are hemodynamically unstable after acute MI.

Symptomatic hypotension is also possible in patients with severe aortic stenosis or hypertrophic cardiomyopathy.

Surgery/Anesthesia

In patients undergoing major surgery or during anesthesia with agents that produce hypotension, lisinopril may block angiotensin II formation secondary to compensatory renin release. If hypotension occurs and is considered to be due to this mechanism, it can be corrected by volume expansion.

5.5 Hyperkalemia

Serum potassium should be monitored periodically in patients receiving lisinopril. Drugs that inhibit the renin angiotensin system can cause hyperkalemia. Risk factors for the development of hyperkalemia include renal insufficiency, diabetes mellitus, and the concomitant use of potassium-sparing diuretics, potassium supplements and/or potassium-containing salt substitutes [see DRUG INTERACTIONS ( 7.1)] .

5.6 Hepatic Failure

ACE inhibitors have been associated with a syndrome that starts with cholestatic jaundice or hepatitis 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 treatment.

6 ADVERSE REACTIONS

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