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Some side effects of lisinopril may not be reported. Always consult your doctor or healthcare specialist for medical advice. You may also report side effects to the FDA.
Get emergency medical help if you have any of these signs of an allergic reaction while taking lisinopril: hives; severe stomach pain, difficult breathing; swelling of your face, lips, tongue, or throat.
Call your doctor at once if you have a serious side effect such as:
· feeling like you might pass out;
· urinating less than usual or not at all;
· swelling, rapid weight gain;
· fever, chills, body aches, flu symptoms;
· tired feeling, muscle weakness, and pounding or uneven heartbeats;
· psoriasis (raised, silvery flaking of the skin);
· chest pain; or
· high potassium (slow heart rate, weak pulse, muscle weakness, tingly feeling);
Less serious side effects of lisinopril may include:
· dizziness, drowsiness, headache;
· depressed mood;
· nausea, vomiting, diarrhea, upset stomach; or
· mild skin itching or rash.
This is not a complete list of side effects and others may occur. Call your doctor for medical advice about side effects.
Hypotension is most likely in patients who are sodium and intravascular volume depleted. In large studies, patients have reported "heart pounding" and chest pain, although the relationship to lisinopril is questionable.
A possible relationship between lisinopril use and a case of penile angioedema has been published. After six days of lisinopril therapy, a 74-year-old patient complained of penile "swelling". Lisinopril was suspected as the cause of the angioedema and was discontinued. The localized angioedema resolved within a few days following discontinuation.
Cardiovascular side effects have included hypotension (0.6% to 1.0% of patients) and angioneurotic edema (0.2% of patients). Angina pectoris, orthostatic hypotension, and palpitations are each reported in approximately 1% of patients. Patients with heart failure are more likely to experience hypotension. In one study the incidence of hypotension-related undesirable side effects was only 0.6% compared to 4% in patients with CHF.
Renal side effects have included new (usually mild) or worsened renal insufficiency which has rarely developed during ACE inhibitor therapy. Patients with renal artery stenosis should not receive lisinopril or any other ACE inhibitor. Proteinuria has also been reported.
Patients with renal artery stenosis maintain glomerular filtration by efferent arteriolar vasoconstriction, which is blocked by lisinopril.
Although lisinopril may be associated with a rise in serum creatinine and BUN, GFR has been shown to remain unchanged or improve in most patients.
Nervous system side effects have included dizziness in up to 13% and headache in up to 6% of patients. Paresthesias are reported in 1% of patients.
A retrospective study has revealed a significantly higher incidence of discontinuation of angiotensin converting enzyme inhibitor therapy due to cough among black patients compared with non-black patients (9.6% vs. 2.4%).
Several agents have been studied for treating cough with ACE inhibitors. No long term trials exist to allow a definitive treatment option. Cromolyn has the most data showing some benefit. Other agents studied include baclofen, theophylline, sulindac, and benzonatate.
Respiratory side effects have included a reversible dry cough in up to 3% of patients. Cough has appeared as common in women as men, but in some reviews women have reported cough more often than men. Other respiratory system side effects are limited to stridor secondary to hypersensitivity to lisinopril.
A rise in serum potassium is due to a mild reduction in serum aldosterone concentrations.
Metabolic side effects are unusual and have included a moderate, often clinically insignificant rise in serum potassium. Lisinopril and other ACE inhibitors appear to have a beneficial effect on plasma insulin levels. Cases of hypoglycemia have been reported in diabetic patients receiving ACE inhibitors when concurrently treated with oral antidiabetic agents or insulin.
Gastrointestinal side effects have included diarrhea (4%), nausea (3%), and vomiting (1%). Taste disturbances and constipation are reported in less than 1% of patients. Acute pancreatitis has been associated with lisinopril.
In at least two cases of lisinopril-associated angioedema of the face and neck, the affected patients did not have a history of reactive airways disease. Patients with intestinal angioedema generally present with abdominal pain (with or without nausea or vomiting) and in some cases there was no prior history of facial angioedema, and C-1 esterase levels were normal. These symptoms resolve after stopping the ACE inhibitor.
Hypersensitivity reactions to lisinopril, as with some other angiotensin converting enzyme (ACE) inhibitors, may be life-threatening. Angioedema occurs in approximately 0.2% of patients. Angioedema of the face, extremities, lips, tongue, glottis and/or pharynx have been reported rarely in patients receiving ACE inhibitors. Obstructive laryngeal and glossal angioedema due to lisinopril is a rare, but potentially fatal reaction. In addition, intestinal angioedema has been reported in patients treated with ACE inhibitors. It is recommended that any patient with dyspnea, dysphagia, or significant facial angioedema stop therapy immediately and avoid ACE inhibitor therapy in general.
Dermatologic side effects have included rare instances of urticaria, alopecia, herpes zoster, photosensitivity, skin lesions, skin infections, pemphigus, erythema, psoriasis, and rare cases of other severe skin reactions, including toxic epidermal necrolysis and Stevens-Johnson Syndrome, (causal relationship has not been established).
Hematologic side effects, including neutropenia and fatal aplastic anemia, have rarely been associated with lisinopril or other ACE inhibitors. A case of Henoch-Schonlein purpura complicated by polyarthritis has been associated with lisinopril.
A 64-year-old woman with aortic insufficiency, coronary artery disease, and atrial fibrillation developed fever and anorexia associated with pancytopenia within seven days after starting furosemide, digoxin, warfarin, and lisinopril. She died despite intensive supportive measures. Autopsy revealed bone marrow aplasia and changes consistent with hepatorenal failure. There was no evidence of infection or autoantibody disease. At least one other (reversible) case has been reported.
Although angiotensin converting enzymes are found in many areas of the central nervous system, the mechanism for ACE inhibitor-induced mania is unclear. They are lipophilic and are not known to cross the blood-brain barrier. ACE inhibitors have been shown to alter the metabolism of enkephalins and modulate cholinergic activity. Interestingly, one case of captopril-induced hallucinations was successfully treated with naloxone.
Psychiatric complications have rarely been attributed to use of ACE inhibitors, including memory impairment, confusion, somnolence, irritability, and nervousness. A single case of mania has been associated with the use of lisinopril in an elderly woman who had previously tolerated enalapril.
Hepatic side effects associated with the use of ACE inhibitors have included a rare syndrome that begins with cholestatic jaundice and progresses to fulminant hepatic necrosis and (sometimes) death. Experts recommend discontinuation of therapy with this drug if jaundice or markedly elevated hepatic serum enzymes develop.
Endocrine side effects including case reports indicating development of the syndrome of inappropriate secretion of antidiuretic hormone have been reported.
Other side effects have included olfactory disturbance.
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