Before the beginning of treatment it is required to conduct an analysis of the previously conducted antihypertensive therapy, the degree of increase in blood pressure, limitations ration on cookery salt and / or fluid and other clinical circumstances. If possible should stop the previous antihypertensive therapy a few days before the start treatment with fosinopril.
Patients with malignant hypertension or concomitant decompensation of chronic heart failure should begin treatment in a hospital.
To reduce the likelihood of arterial hypotension, diuretics should be discontinued 2-3 days before the start of treatment with the drug Fosinopril.
Prior to treatment and during therapy, it is necessary to monitor blood pressure, kidney function, creatinine, urea, control the content of electrolytes, especially potassium and the activity of "liver" enzymes in the blood.
Angioedema. The development of angioedema of the extremities, face, lips, mucous membranes, tongue, throat or larynx in patients with fosinopril 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 (with nausea and vomiting may not be), in some cases, the edema of the intestinal mucosa appeared without edema of the face, the activity of C1-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 (for example, AN®69), 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 Hepaticoptera with the use of an ACE inhibitor enalapril, life-threatening anaphylactoid reaction. Those the same patients were able to avoid these reactions with the timely suspension of the ACE inhibitor; but they appeared again after the involuntary resumption of the ACE inhibitor. Special care should be exercised in carrying out desensitization in patients taking ACE inhibitors.
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 the treatment, the leukocytes and leukocyte formula are determined (once a month, during 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 Fosinopril.
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 taking measures to restore the volume of circulating blood.
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, fosinopril should carefully monitor patients, especially during the first 2 weeks of treatment, as well as with any increase in the dose of fosinopril 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 as such is not a contraindication for the further use of the drug 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. When there is a noticeable icterus and a marked increase in the activity of liver enzymes, treatment with fosinopril should be discontinued and appropriate treatment prescribed.
In patients with impaired liver function, there may be an increased concentration of fosinopril in the blood plasma. With liver cirrhosis (including alcoholic), the apparent overall clearance of fosinoprilat is reduced, and the area under the curve AUC approximately 2 times higher than in patients without violations of 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 kidney function in such patients in the first weeks of treatment. In some patients, an increase in the concentration of blood urea nitrogen and blood serum creatinine (usually small and transient) can be observed even without an obvious impairment of kidney function with simultaneous use of the drug and diuretics.You may need to reduce the dose of Fosinopril.
In patients with severe chronic heart failure, kidney function may depend on the activity of RAAS, so treatment with ACE inhibitors may be accompanied by oliguria and / or progressive azotemia, and in rare cases lead to acute renal failure and death.
Hyperkalemia. There have been cases of increased potassium levels 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, and also taking potassium-sparing diuretics, potassium-containing dietary supplements, or other drugs that increase serum potassium (for example, 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 a 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 exercising or in hot weather due to the risk of dehydration and arterial hypotension and reduce volume of the circulating fluid.
Based on the results of epidemiological studies, it is assumed that the simultaneous administration of ACE inhibitors and insulin, as well as hypoglycemic agents for oral administration may lead to the development of hypoglycemia. The greatest risk of development is observed during the first weeks of combination therapy, as well as in patients with impaired renal function. Patients with diabetes require careful monitoring of glycemia, especially during the first month of therapy with an ACE inhibitor.