At the beginning of treatment, there may be an excessive decrease in blood pressure, especially in patients with chronic heart failure, severe arterial hypertension (including renal genesis), and / or renal insufficiency. Before the start of treatment, it is necessary to compensate for the deficiency of sodium ions and to normalize the volume of circulating blood (reduce the dose of previously prescribed diuretics or, in some cases, completely cancel them), as well as determine the indicators of kidney function.
It is necessary to regularly monitor the content of potassium and calcium ions in the blood plasma (especially in patients receiving cardiac glycosides, glucocorticosteroids, often using laxatives,as well as in elderly patients), glucose, uric acid, lipids (cholesterol and triglycerides), urea and creatinine, the activity of "hepatic" enzymes.
Especially regular monitoring of blood pressure and laboratory indicators is necessary in the following cases: in patients with renal insufficiency; patients with arterial hypertension of severe course (including renal genesis); in elderly patients (over 65 years); in patients with disturbances of water-electrolyte balance and decompensated chronic renal insufficiency; as well as receiving at the same time allopurinol, preparations of lithium, procainamide and drugs that reduce immunity.
When taking PSA inhibitors, a characteristic non-productive cough is observed, which stops after the abolition of therapy by PSL inhibitors.
In some patients with kidney disease, especially with severe renal artery stenosis, there is an increase in the concentrations of urea nitrogen and creatinine in the blood serum after lowering blood pressure. This phenomenon is usually reversible, and there is a decrease in the concentration of urea nitrogen and creatinine in the blood serum if the drug is discontinued. It may be necessary to reduce the dose of Kapozid® and / or to cancel the diuretic.In some cases, against the background of the use of PSA inhibitors, an increase in serum potassium is observed. The risk of developing hyperkalemia with the use of inhibitors of LPP is increased in patients with renal insufficiency and diabetes mellitus, and also taking potassium-sparing diuretics, potassium preparations or other drugs that cause an increase in the potassium content in the blood (for example, heparin). You should avoid the simultaneous use of potassium-sparing diuretics and potassium preparations.
In addition, with the use of ACE inhibitors concomitantly with thiazide diuretics, the risk of hypokalemia is not ruled out, so in such cases regular monitoring of the potassium content in the blood during therapy should be carried out.
Care should be taken when taking ACE inhibitors in patients with mitral / aortic stenosis /hypertrophic obstructive cardiomyopathy; in the case of cardiogenic shock and hemodynamically significant obstruction - the technique is not recommended.
It is not recommended to use the double blockade of the renin-angiotensin-aldosterone system (RAAS) caused by simultaneous administration of ACE inhibitors and antagonists of the receptors to angiotensin II or aliskiren and aliskiren-containing drugs,because it was associated with an increased incidence of side effects, such as hypotension. gperkalemia, decreased renal function (including acute renal failure). If simultaneous use of ACE inhibitors and ARAII (double blockade of RAAS) is necessary, the treatment should be carried out under the supervision of a doctor and with the constant monitoring of kidney function, the level of electrolytes in the blood, and blood pressure.
It is not recommended joint use of ACE inhibitors and receptor antagonists for angiotensin II in patients with diabetic nephropathy. When hemodialysis in patients receiving ACE inhibitors should avoid the use of dialysis membranes with high permeability (for example, AN69), because in such cases the risk of anaphylactoid reactions increases. Anaphylactoid reactions were also observed in patients undergoing low-density lipoprotein (apheresis) removal by absorption with dextran sulfate. Consideration should be given to the use of either antihypertensive drugs of another class, or another type of dialysis membrane.
In the case of angioedema, the drug is withdrawn and carefully monitored until the symptoms disappear completely. Angioneurotic edema of the larynx can lead to death. If the edema is localized on the face, special treatment is usually not required (to reduce the severity of symptoms can be used antihistamines); if the swelling spreads to the tongue, throat or larynx and there is a threat of development of airway obstruction, theenter immediately epinephrine (epinephrine) subcutaneously (0.3-0.5 ml in a dilution of 1: 1000). In rare cases, angiotoneurotic edema of the intestine was observed in patients after receiving PSA inhibitors, which was accompanied by pains in the abdominal cavity (with or without nausea and vomiting), sometimes with normal values of C-1-esterase activity and without previous edema of the face. Bowel edema should be included in the spectrum of differential diagnosis of patients with complaints of abdominal pain when taking ACE inhibitors.
In representatives of the Negroid race, cases of angioedema development were noted with greater frequency in comparison with representatives of the European race.
Life-threatening anaphylactoid reactions were noted in two patients under the procedure of desensitization by Hymenoptera venom against the background of captopril administration. With the temporary abolition of the inhibitor of PSA in the same patients, anaphylactoid reactions were avoided. Care should be taken when carrying out desensitization in patients taking ACE inhibitors.
In patients with diabetes mellitus receiving hypoglycemic drugs (hypoglycemic agents for ingestion or insulin), the level of glycemia should be carefully monitored, especially during the first month of therapy with ACE inhibitors.
ACE inhibitors are less effective in representatives of the Negroid than in the patients of the European race, which may be due to the greater prevalence of low renin activity in representatives of the Negroid race.
In carrying out extensive surgical interventions or using general anesthetic agents that have an antihypertensive effect, patients who take ACE inhibitors may experience an excessive reduction in blood pressure. In these cases, the volume of circulating blood can be increased.
In rare cases, with the intake of ACE inhibitors, a syndrome begins, which begins with the appearance of cholestatic jaundice, which changes into lightning-fast hepatonecrosis, sometimes with a lethal outcome. The mechanism of development of this syndrome is unknown. If a patient receiving ACE inhibitor therapy develops jaundice or a marked increase in activity of hepatic enzymes, discontinue treatment with ACE inhibitors and establish patient monitoring.
In patients taking ACE inhibitors, there was neutropenia / agranulocytosis, thrombocytopenia and anemia. In patients with normal renal function and in the absence of other disorders, neutropenia is rare.
The preparation Kapozid® should be used very carefully in patients with autoimmune connective tissue diseases, in those taking immunosuppressors, allopurinol and procainamide, especially if there is a previously existing renal dysfunction. Due to the fact that the majority of lethal cases of neutropenia against the background of ACE inhibitors developed in such patients, it is necessary to monitor the number of blood leukocytes before treatment, in the first 3 months.- every 2 weeks, then every 2 months.
All patients should be monitored monthly for the number of leukocytes in the blood in the first 3 months after the start of therapy, then every 2 months. If the number of white blood cells is less than 4000 / μl, a repeated blood test is shown, below 1000 / μl, the drug is discontinued while continuing to monitor the patient. Usually, the recovery of the number of neutrophils occurs within 2 weeks after the withdrawal of captopril. In 13% of cases, neutropenia was fatal. Practically in all cases, lethal outcome was noted in patients with connective tissue diseases, renal or heart failure, against the background of immunosuppressive medication or a combination of both.
With the use of PSA inhibitors, proteinuria can be noted, mainly in patients with impaired renal function, as well as in the application of high doses of drugs. In most cases, proteinuria with the use of the drug captopril disappeared or the degree of its severity decreased within 6 months, regardless of whether the drug was stopped or not. Indices of kidney function (concentration of urea nitrogen in the blood and creatinine) in patients with proteinuria almost always were within normal limits.Patients with kidney diseases should determine the protein content in the urine before starting treatment and periodically during the course of therapy. When receiving thiazide diuretics, rare cases of agranulocytosis and oppression of bone marrow function were noted. Sulfonamide derivatives (including hydrochlorothiazide) can cause transient myopia and acute closed-angle glaucoma, risk factors are allergy to sulfonylureas or penicillin in history. Symptoms (sharp reduction in visual acuity, pain in the eyeball) are usually observed in a few hours - a few weeks after the start of treatment. If symptoms appear, stop taking the medication immediately; if necessary, appoint medications to correct intraocular pressure.
All patients taking thiazide diuretics should identify clinical signs of a disturbance of the water-electrolyte balance (hyponatremia, hypochloraemic alkalosis, hypokalemia). It is especially important to determine the content of electrolytes in blood serum and urine with strong vomiting or with the introduction of infusion solutions.Signs of violations of water-electrolyte balance may be dryness of the oral mucosa, thirst, weakness, lethargy, confusion, anxiety, pain or muscle cramps, muscle weakness, excessive lowering of arterial pressure, oliguria, tachycardia, nausea, vomiting. HypocaLyme can trigger or exacerbate the cardiotoxic effect of cardiac glucosides. The lack of chloride ions is usually poorly expressed and does not require correction. In patients with edema in hot weather, there may be hyponatremia caused by an increase in the volume of circulating blood. Limit fluid intake. In cases of life-threatening hyponatremia, the intake of edible salt is prescribed. During therapy with thiazide diuretics, hyperuricemia or exacerbation of the gout current may occur; can also manifest a latent diabetes mellitus.
Thiazide diuretics can cause a decrease in the concentration of bound iodine in the serum without signs of thyroid dysfunction. Against the background of taking thiazide drugs, the level of calcium excretion decreases; cases of pathological changes of parathyroid glands accompanied by hypercalcemia and hypophosphatemia were noted.Before controlling the function of the parathyroid glands, you should stop taking the thiazide diuretic. Against the background of taking thiazide drugs, magnesium excretion increased, which can lead to hypomagnesemia.
The preparation Kapozid® can cause a false-positive reaction in the analysis of urine for acetone and distort the results of the test with bentiromide.
When fever, enlargement of lymph nodes and / or signs of laryngitis and / or pharyngitis occur, the number of white blood cells must be determined immediately. The use of thiazide diuretics may be the cause of a positive result in doping control.