Before the start of treatment, it is required to conduct an analysis of previous antihypertensive therapy, the degree of increase in blood pressure, the restriction of ration for salt and / or fluid and other clinical circumstances. If possible, the previous antihypertensive therapy should be discontinued several days before the start of treatment with MONOPRIL®.
To reduce the likelihood of arterial hypotension, diuretics should be discontinued 2-3 days before treatment with MONOPRIL®.
Before treatment and during therapy, it is necessary to monitor blood pressure, kidney function, potassium ion, creatinine, urea, electrolyte content and activity of "hepatic" enzymes in the blood.
Angioedema. The development of angioedema of the extremities, face, lips, mucous membranes, tongue, pharynx or larynx in patients with the use of the drug MONOPRIL® has been reported.When swelling of the tongue, throat or larynx, airway obstruction may develop with possible fatal outcome. In such cases, it is necessary to stop taking the drug and carry out emergency measures, including subcutaneous injection of epinephrine (adrenaline) solution (1: 1000), as well as taking other measures of emergency therapy. In most cases, edema of the face, oral mucosa, lips and extremities discontinuation of the drug led to the normalization of the condition; However, sometimes an appropriate therapy was required.
Edema of the intestinal mucosa. During the administration of ACE inhibitors, edema of the intestinal mucosa was rarely observed. Patients complained of abdominal pain (there could be no nausea and vomiting), in some cases, the edema of the intestinal mucosa appeared without edema of the face, the activity of Cl-esterase was normal. Symptoms disappeared after the cessation of the use of ACE inhibitors. Swelling of the intestinal mucosa should be included in the differential diagnosis of patients taking ACE inhibitors who complain of abdominal pain.
Anaphylactic reactions during dialysis using high permeability membranes. Anaphylactic reactions can develop in patients taking ACE inhibitors during hemodialysis with high permeability membranes, as well as during apheresis of low-density lipoproteins with adsorption to dextran sulfate. In these cases, the use of dialysis membranes of a different type or the use of antihypertensive drugs of another class should be considered.
Anaphylactic reactions during desensitization. In two patients, during the desensitization of the Hymenoptera with the use of an ACE inhibitor enalapril, life-threatening anaphylactoid reactions were noted. In the same patients, these reactions were avoided by the timely suspension of the ACE inhibitor; however, they appeared again after the involuntary resumption of the ACE inhibitor. Care should be taken when desensitizing patients taking inhibitors: ACE.
Neutropenia / agranulocytosis. Perhaps the development of agranulocytosis and suppression of bone marrow function during treatment with ACE inhibitors.These cases are more common in patients with impaired renal function, especially in the presence of systemic connective tissue diseases (systemic lupus erythematosus or scleroderma). Before the beginning of therapy with ACE inhibitors and during treatment, the leukocytes and leukocyte formula are determined (once a month for the first 3-6 months of treatment and in the first year of use in patients with an increased risk of neutropenia).
Arterial hypotension. Patients with uncomplicated form of hypertension may develop arterial hypotension due to the use of the drug MONOPRIL®.
Symptomatic arterial hypotension with the use of ACE inhibitors often develops in patients on the background of intensive treatment with diuretics, a diet associated with (restriction of table salt, or during dialysis.) Transient arterial hypotension is not a contraindication for the use of the drug after (measures to restore the volume of circulating blood (BCC).
In patients with chronic heart failure, treatment with ACE inhibitors can cause an excessive antihypertensive effect, which can lead to oliguria or azotemia and, in rare cases, to acute renal failure with a fatal outcome.Therefore, in the treatment of chronic heart failure with the drug MONOPRIL®, patients should be closely monitored, especially during the first 2 weeks of treatment, as well as with any increase in the dose of MONOPRIL® or diuretic.
It may be necessary to reduce the dose of a diuretic in patients with normal or low blood pressure who were previously treated with diuretics or who have hyponatraemia. Arterial hypotension per se is not a contraindication for the further use of the drug MONOPRIL® in chronic heart failure.
Some reduction in systemic BP is a common and desirable effect at the beginning of the drug in chronic heart failure. The degree of this decrease is maximal at early stages of treatment and stabilizes within one or two weeks from the start of treatment. BP usually returns to baseline without reducing therapeutic effectiveness.
Violation of the function of the liver. In rare cases, with the use of ACE inhibitors, there is a syndrome, the first manifestation of which is cholestatic jaundice. Then follows the fulminant necrosis of the liver, sometimes with a fatal outcome.The mechanism of development of this syndrome has not been studied. If there is noticeable icterus and a marked increase in the activity of liver enzymes, treatment with MONOPRIL® should be discontinued and appropriate treatment should be prescribed.
In patients with impaired liver function, there may be an increased concentration of fosinopril in the blood plasma. With cirrhosis of the liver (including alcohol), the apparent overall clearance of fosinoprilat is reduced, and the area under the curve is approximately 2 times higher than in patients without violations of the liver function.
Impaired renal function. In patients with arterial hypertension with unilateral or bilateral stenosis of the renal arteries or stenosis of the artery of a single kidney during treatment with ACE inhibitors, the concentration of blood urea nitrogen and serum creatinine may increase. These effects are usually reversible and pass after discontinuation of treatment. It is necessary to monitor the kidney function in such patients in the first weeks of treatment. In some patients, an increase in the concentrations of blood urea nitrogen and blood serum creatinine (usually small and transient) can occur even without an obvious impairment of kidney function, while simultaneously using the drug MONOPRIL® and diuretics. It may be necessary to reduce the dose of Monopril®.
In patients with severe chronic heart failure, kidney function may depend on the activity of the renin-angiotensin-aldosterone system, therefore treatment with ACE inhibitors may be accompanied by oliguria and / or progressive azotemia, and in rare cases acute renal failure and death. Tipercalemia. There have been cases of an increase in the content of potassium ions in the blood serum of patients taking ACE inhibitors, including fosinopril. The risk group in this respect is patients with renal insufficiency, type 1 diabetes mellitus, and also taking potassium-sparing diuretics, potassium-containing dietary supplements, or other drugs that increase the potassium ion content in the blood serum (eg, heparin).
Cough. With the use of ACE inhibitors, including fosinopril, there was an unproductive, persistent cough, which occurs after the abolition of therapy. When cough occurs in patients taking ACE inhibitors, this therapy should be considered as a possible cause in the context of differential diagnosis.
Surgical interventions / general anesthesia.ACE inhibitors can enhance the antihypertensive effect of agents used for general anesthesia.
Before surgery (including dentistry), a physician / anesthesiologist should be warned about the use of ACE inhibitors.
Caution should be exercised when performing physical exercises or roasting weather because of the risk of dehydration and arterial hypotension due to a decrease in the volume of the circulating fluid.