Hydrochlorothiazide + Captopril tabs 25mg + 50mg #30
- 3 or more $22.89
- Availability:In Stock
Hydrochlorothiazide + Captopril instructionYou can buy tablets Hydrochlorothiazide + Captopril hereComposition of 1 tabletActive ingredients: hydrochlorothiazide - 25 mg, captopril - 50.0 mg;Excipients: lactose monohydrate (milk s..
Hydrochlorothiazide + Captopril instruction
You can buy tablets Hydrochlorothiazide + Captopril here
Composition of 1 tablet
Active ingredients: hydrochlorothiazide - 25 mg, captopril - 50.0 mg;
Excipients: lactose monohydrate (milk sugar) - 169.0 mg, microcrystalline cellulose - 100.0 mg, corn starch - 40.0 mg, croscarmellose sodium - 12.0 mg, magnesium stearate - 4.0 mg.
Round, flat-cylindrical tablets with a risk on one side and chamfers on both sides, white or white with a beige tint, with a characteristic odor, slight marbling is allowed.
Pharmacotherapeutic group: Combination antihypertensive agent (diuretic + ACF inhibitor)
C.09.B.A.01 Captopril in combination with diuretics
Hydrochlorothiazide + Captopril is a combination drug that has antihypertensive and diuretic effects.
Captopril is an inhibitor of angiotensin-converting enzyme (ACE), reduces the formation of angiotensin II from angiotensin I, reduces the release of aldosterone, reduces total peripheral vascular resistance (OPS), blood pressure (BP), post- and preload. Expands arteries to a greater extent than veins. Enhances coronary and renal blood flow. With prolonged use, hypertrophy of the myocardium and the walls of resistive arteries is reduced. Captopril improves blood supply to the ischemic myocardium; reduces platelet aggregation.
Hydrochlorothiazide, a thiazide diuretic of moderate strength, reduces the reabsorption of sodium ions at the level of the cortical segment of the loop of Henle. Does not affect the acid-base state. Decreases blood pressure by changing the reactivity of the vascular wall, reducing the pressure of endogenous vasoconstrictor substances (adrenaline, norepinephrine) and increasing the depressor effect on the vegetative ganglia (to a lesser extent, by reducing the circulating blood volume). Enhances the antihypertensive effect of captopril. The diuretic effect is noted after 2 hours and reaches a maximum 4 hours after ingestion. The action lasts for 6-12 hours.
The efficacy and safety of captopril in children have not been established. The literature describes limited experience with captopril in children. Children, especially newborns, may be more likely to develop hemodynamic side effects. There have been cases of excessive, prolonged and unpredictable increases in blood pressure, as well as related complications, including oliguria and convulsions.
Absorption - fast, makes about 60-70% of the accepted dose. Eating reduces bioavailability by 30-40%. The maximum concentration in blood plasma is noted 1 hour after ingestion.
Associated with plasma proteins - 25-30%, mainly with albumin. Less than 0.002% of the accepted dose of captopril is secreted with breast milk, does not penetrate the blood-brain barrier.
Metabolized in the liver to form disulfide dimer captopril and captopril-cysteine sulfide. Metabolites are pharmacologically inactive.
The half-life (T1 / 2) of captopril is about 2-3 hours. About 95% is excreted by the kidneys during the first day, 40-50% of them unchanged, the rest is in the form of metabolites. 4 hours after a single ingestion in the urine contains about 38% of unchanged captopril and 28% in the form of metabolites, after 6 h, only in the form of metabolites; in daily urine - 38% unchanged captopril and 62% - in the form of metabolites.
As a result of the accumulation of captopril and its metabolites in the kidneys, their function may be impaired. The half-life for renal failure is 3.5-32 hours. It accumulates in chronic renal failure. Therefore, patients with impaired renal function should reduce the dose and / or increase the interval between doses.
After ingestion, the absorption and bioavailability of hydrochlorothiazide is about 70%. Communication with plasma proteins - 60-80%.
When ingestion of 12.5 mg of hydrochlorothiazide, the maximum plasma concentration is reached in 1.5-4 hours and is 70 ng / ml, and when ingested 25 mg of hydrochlorothiazide, the maximum plasma concentration is reached in 2-5 hours and is 142 ng / ml.
In the therapeutic dose range, the average value of the area under the "concentration - time" curve (AUC) increases in direct proportion to the dose increase, with an appointment once a day, the cumulation is insignificant. Penetrates through the hemato-placental barrier and into breast milk. T1 / 2 - 5-15 h.
Hydrochlorothiazide is slightly metabolized in the liver. Hydrochlorothiazide is eliminated almost completely (more than 95%) by the kidneys in unchanged form. 50-70% of the ingested dose is eliminated within 24 hours.
Hypersensitivity to captopril or other ACE inhibitors, thiazide diuretics, and other sulfanilamide derivatives (allergic reactions are possible), any component of the drug; angioedema, hereditary or idiopathic edema, including a history of taking ACE inhibitors; aortic stenosis, mitral stenosis; hypertrophic obstructive cardiomyopathy; bilateral renal artery stenosis, renal artery stenosis of a single kidney, condition after kidney transplantation (in history); chronic heart failure; cardiogenic shock, hypotension, tachycardia; severe liver failure (precoma or coma); severe renal impairment (serum creatinine more than 1.8 mg / 100 ml or creatinine clearance (CC) less than 20-30 ml / min, anuria); primary hyper aldosteronism; pregnancy, breastfeeding period, age up to 18 years (efficacy and safety not established), simultaneous use with aliskiren and aliskiren-containing drugs in patients with diabetes mellitus or impaired renal function (glomerular filtration rate (GFR) less than 60 ml / min / 1.73 m2), lactose intolerance, lactase deficiency and glucose-galactose malabsorption syndrome.
Moderate renal failure (CK 30-60 ml / min), proteinuria (more than 1 g / day), abnormal liver function, progressive liver disease, hypokalemia (not corrected by drugs); hyponatremia, hypovolemia, hypercalcemia, gout, hyperuricemia, systemic connective tissue diseases and other immune diseases (including systemic lupus erythematosus, scleroderma, periarteritis nodosa); old age (over 65 years), simultaneous use of drugs that suppress the body's protective reactions (glucocorticosteroids (GCS), cytostatics, immunosuppressants), allopurinol, procainamide, surgery / general anesthesia, use of high-flow membranes in patients, hemodialysis using high-flow membranes ( for example, AN69®), desensitizing therapy, simultaneous use of potassium-saving diuretics, potassium preparations and potassium-containing food salt substitutes, lithium preparations, acute myopia secondary angle-closure glaucoma.
Pregnancy and lactation
The use of the drug Hydrochlorothiazide + Captopril during pregnancy is contraindicated.
Epidemiological evidence of the risk of teratogenicity after exposure to ACE inhibitors in the first trimester of pregnancy was not conclusive, but a slight increase in risk cannot be ruled out. If the use of an ACE inhibitor is considered necessary, patients planning a pregnancy should be transferred to alternative anti-hypertensive therapy with a proven safety profile during pregnancy.
It is known that prolonged exposure of the ACE inhibitors to the fetus in the second and third trimesters of pregnancy can lead to impaired development (reduced kidney function, oligohydramnion, slowing down ossification of the skull bones) and the development of complications in the newborn (renal failure, arterial hypotension, hyperkalemia).
If the patient received the drug Hydrochlorothiazide + Captopril during the II or III trimester of pregnancy, it is recommended to conduct an ultrasound examination of the fetus to assess the condition of the bones of the skull and kidney function.
The use of hydrochlorothiazide during pregnancy is not recommended, as it can worsen the perfusion of the placenta and cause fetal / newborn jaundice, thrombocytopenia, impaired water-electrolyte balance and, possibly, other undesirable reactions observed in adults.
The use of ACE inhibitors during pregnancy can cause developmental disorders (including arterial hypotension, neonatal hypoplasia of the skull bones, anuria, reversible or irreversible renal failure) and death of the fetus. When diagnosing pregnancy, the use of the drug Hydrochlorothiazide + Captopril should be stopped as soon as possible.
Captogtril and hydrochlorothiazide after ingestion by a nursing woman are found in breast milk. In connection with the risk of serious adverse reactions in the child caused by both active substances, breastfeeding should be stopped or therapy with Hydrochlorothiazide + Captopril in the mother should be discontinued during the breastfeeding period.
Dosage and administration
Inside, regardless of meal times, 1 tablet 1 time per day.
Tablets should be swallowed whole, without chewing, with a small amount of liquid.
The frequency of side effects is set out in accordance with the classification of the World Health Organization: often - ≥ 1/100 - <1/10, rarely - ≥ 1/1000 - <1/100, rarely - ≥ 1/10000 - <1/1000, very rarely - <1/10000.
Since the cardiovascular system:
infrequently - chest pain, stenocardia, "flush" of blood to the skin of the face, tachycardia or tachyarrhythmia, feeling of heartbeat, peripheral edema, marked reduction of blood pressure (including orthostatic) with dizziness, weakness, Raynaud's syndrome, myocardial infarction, fainting; very rarely - cardiac arrest, cardiogenic shock.
On the part of the respiratory system:
often - "dry" non-productive cough, shortness of breath; very rarely - bronchospasm, eosinophilic pneumonitis, sinusitis, rhinitis, laryngitis, pulmonary edema.
often - pruritus, with or without a rash, sometimes accompanied by fever and arthralgia, a rash on the skin, alopecia; infrequently - vascular edema of the skin and subcutaneous tissue; rarely - angioedema - intestines; very rarely - urticaria, Stevens-Johnson syndrome, erythema multiforme, photosensitivity, erythroderma, reversible pemphigoid reactions, exfoliative dermatitis, as well as toxic epidermal necrolysis (Lyell's syndrome), allergic alveolitis, eosinophilic pneumonia, angioneurophritis, angioneurovirus, angiopathy, eosinophilic necrolysis lips, mucous membranes (including fatal), respiratory distress syndrome (including pneumonitis and non-cardiogenic pulmonary edema).
From the central and peripheral nervous system:
often - drowsiness, dizziness, insomnia; rarely - headache, ataxia, paresthesia; very rarely - confusion, depression, disorders of cerebral circulation, including stroke and syncope, blurred vision.
From the hemopoietic system:
very rarely - anemia, including aplastic and hemolytic forms, decrease in hematocrit, thrombocytopenia, leukopenia, neutropenia (up to the development of pancytopenia and agranulocytosis - especially against the background of simultaneous administration of allopurinol, procainamide, as well as immunosuppressants), eosinophilia, lymphadenopathy, elevation, lymphadenopathy, and adhepatopathy, erecinophilia, lymphadenopathy, elevation, lyopaurinol, procainamide, and immunosuppressants; autoimmune diseases.
From the digestive system:
often - reversible and usually self-transient disorder of taste, nausea, vomiting, constipation or diarrhea, discomfort in the stomach, dyspepsia, abdominal pain, dryness of the oral mucosa; rarely - stomatitis, aphthous stomatitis, anorexia; very rarely - glossitis, gastric ulcer, pancreatitis, gingival hyperplasia, abnormal liver function and cholestasis (including jaundice), increased activity of "liver" transaminases, hepatitis (including necrosis), hyperbilirubinemia.
From the musculoskeletal system:
very rarely - myalgia, arthralgia, myasthenia.
From the urinary system:
infrequently - impaired renal function (including renal failure), polyuria, oliguria, frequent urination, nephrotic syndrome.
From the reproductive system:
very often - impotence, gynecomastia.
infrequently - chest pain, fatigue, feeling unwell.
often - eosinophilia;
very rarely - proteinuria, hyperkalemia, hyponatremia (including symptomatic), an increase in the concentration of urea nitrogen, bilirubin and creatinine in the blood, a decrease in hematocrit, hemoglobin, leukocytes, platelets.
very rarely - hyperglycemia; hyperuricemia (up to exacerbation of gout).
Treatment with thiazides may impair glucose tolerance, and latent diabetes mellitus can manifest. At use of high doses concentration of lipids in blood serum can increase.
Disorders of water and electrolyte balance: hypokalemia, hypomagnesemia, hypercalcemia and hypochloremic alkalosis: dryness of the oral mucosa, thirst, irregular heart rhythm, changes in mood or psyche, cramps and muscle pain, nausea, vomiting, unusual fatigue or weakness. Hypochloremic alkalosis can cause hepatic encephalopathy or hepatic coma.
Hyponatremia: confusion, convulsions, lethargy, slow thinking, fatigue, irritability, muscle cramps.
When using ACE inhibitors, including captopril, patients receiving intravenous gold preparation (sodium aurothiomalate), a symptom complex was described, including facial flushing, nausea, vomiting, and hypotension.
Symptoms: pronounced decrease in blood pressure, shock, stupor, bradycardia, impaired water and electrolyte balance, renal failure, lethargy (which can progress to coma within a few hours), not accompanied by impaired water and electrolyte balance and causing only slight suppression of the function of respiration and heart . There may be irritation of the gastric mucosa and an increase in the contractile activity of the gastrointestinal tract.
Treatment: gastric lavage, the introduction of adsorbents and sodium sulfate within 30 minutes after administration, 0.9% solution of sodium chloride or other plasma-substituting solutions, hemodialysis.
For bradycardia or marked vagal reactions, atropine is administered.
The use of an artificial pacemaker may be considered.
Peritoneal dialysis is ineffective for removing captopril from the body.
Simultaneous use is contraindicated (see section "Contraindications")
In patients with diabetes mellitus or impaired renal function (GFR less than 60 ml / min / 1.73 m2), the risk of hyperkalemia, deterioration of renal function and an increase in the incidence of cardiovascular morbidity and mortality increases.
Simultaneous use is not recommended (see the section "Special Instructions")
In patients without diabetes mellitus or impaired renal function, there may be an increased risk of hyperkalemia, deterioration of renal function and an increase in the incidence of cardiovascular morbidity and mortality.
Double blockade of RAAS
In the literature, it was reported that in patients with established atherosclerotic disease, heart failure or diabetes mellitus with target organ damage, concurrent therapy with an ACE inhibitor and angiotensin II receptor antagonists (APAII) is associated with a higher incidence of arterial hypotension, syncope, hyperkalemia and worsening renal function (including acute renal failure) compared with the use of only one drug that affects the RAAS. Double blockade (for example, when combining an ACE inhibitor with APAII) should be limited to individual cases with careful monitoring of kidney function, potassium and blood pressure.
In patients taking diuretics, captopril may potentiate the antihypertensive effect. A similar effect is also exerted by the strict limitation of salt intake in the body (salt-free diets), hemodialysis. Usually, an excessive decrease in blood pressure occurs within the first hour after taking the first dose of captopril.
Vasodilators (for example, nitroglycerin) in combination with captopril should be used in the lowest effective doses due to the risk of an excessive decrease in blood pressure.
Reduces excretion of quinidine, norepinephrine, epinephrine and anti-gout drugs.
Caution must be exercised when simultaneously prescribing captopril (without or with a diuretic) and drugs that affect the sympathetic nervous system (for example, ganglioblokatory, alpha-adrenergic blockers).
With the simultaneous use of captopril and nonsteroidal anti-inflammatory drugs (NSAIDs), a decrease in the antihypertensive effect can be observed, especially in hypertension, accompanied by a low content of renin. In patients with risk factors (elderly patients, patients with hypovolemia, receiving diuretics, with impaired renal function), simultaneous use of NSAIDs (including cyclooxygenase-2 inhibitors (COX-2)) and ACE inhibitors, including captopril, can lead to deterioration of kidney function up to acute renal failure. Kidney damage is usually reversible in such cases. Renal function should be monitored periodically in patients taking captopril and NSAIDs.
In captopril therapy, potassium-sparing diuretics (for example, triamterene, amiloride, spironolactone and its derivative - eplerenone), potassium preparations, potassium supplements, salt substitutes (contain large amounts of potassium) should be prescribed only with proven hypokalemia, since their simultaneous use increases the risk of hyperkalemia.
With the simultaneous use of ACE inhibitors (especially in combination with diuretics) and lithium salts, an increase in plasma lithium concentration, and, consequently, the toxicity of lithium preparations is possible. It should periodically determine the concentration of lithium in the blood plasma.
When prescribing captopril while taking allopurinol or procainamide, it increases the risk of developing neutropenia and / or Stevens-Johnson syndrome.
The use of captopril in patients taking immunosuppressants (for example, cyclophosphacin or azathioprine) increases the risk of hematological disorders.
ACE inhibitors, including captopril, can potentiate the hypoglycemic effect of insulin and hypoglycemic oral agents, for example, sulfonylurea derivatives, which may require lowering the dose of hypoglycemic drugs while using captopril.
Sympathomimetics can reduce the antihypertensive effect of captopril.
Increases the concentration of digoxin in the blood plasma by 15-20%.
Increases the bioavailability of propranolol.
Cimetidine, slowing metabolism in the liver, increases the concentration of captopril in the blood plasma.
With simultaneous use with thiazide diuretics, vasodilators (minoxidil), verapamil, beta-blockers, tricyclic antidepressants or ethanol, the antihypertensive effect is enhanced.
Simultaneous use may increase the risk of side effects such as angioedema.
Enhances the antihypertensive effect of ACE inhibitors. Blood pressure and, if necessary, the dosage of antihypertensive drugs should be carefully monitored.
Glyptin (linagliptin, saxagliptin, sitagliptin, vildagliptin)
Combined use with ACE inhibitors may increase the risk of developing angioedema due to the suppression of dipeptidyl peptidase IV (DPP-IV) activity by glyptines.
When using ACE inhibitors, including captopril, patients receiving intravenous gold preparation (sodium aurothiomalate), a symptom complex was described, including facial flushing, nausea, vomiting, and hypotension.
Tricyclic antidepressants, antipsychotics (antipsychotics) and general anesthetics
Simultaneous use with ACE inhibitors can lead to increased antihypertensive action (see section "Special instructions").
With thiazide diuretics, drugs such as ethanol, barbiturates and narcotics can potentiate the risk of orthostatic hypotension.
Hypoglycemic agents (for oral administration and insulin) - may require dose adjustment of hypoglycemic agents.
Other antihypertensives - additive effect.
Kolestiramin and colestipol - in the presence of anion-exchange resins the absorption of hydrochlorothiazide is broken. Kolestiramine and colestipol in a single dose bind hydrochlorothiazide and reduce its absorption in the gastrointestinal tract by 85% and 43%, respectively.
Corticosteroids, ACTH (adrenocorticotropic hormone) or glycyrrhizic acid (found in licorice root) - a pronounced decrease in the content of electrolytes, in particular, the risk of hypokalemia.
Pressor amines (for example, epinephrine, porepinephrine) - reducing the severity of the response to the reception of pressor amines.
Muscle relaxants of non-depolarizing type of action (for example, tubocurarine) - increased effect of muscle relaxants.
Lithium - diuretics reduce renal clearance of lithium and increase the risk of developing the toxic effect of lithium; simultaneous use is not recommended.
NSAIDs (including COX-2 inhibitors) can reduce the diuretic, natriuretic, and antihypertensive effects of diuretics.
In some patients with impaired renal function (for example, elderly patients or patients with dehydration, including receiving diuretics), receiving NSAIDs, including COX-2 inhibitors, treatment with ARAP or ACE inhibitors may cause further deterioration of kidney function, including the development of acute renal failure. These effects are reversible. The simultaneous use of these drugs should be carried out with caution in patients with impaired renal function.
In connection with the effect on calcium metabolism, their intake may distort the results of the study of the function of the parathyroid glands.
Drugs used to treat gout (probenecid, sulfinpirazon and allopurinol): You may need to adjust the dose of uricosuric drugs, since hydrochlorothiazide may cause an increase in serum uric acid concentration. Thiazide diuretics may increase the incidence of hypersensitivity reactions to allopurinol.
Anticholinergic drugs (for example, atropine, biperiden): increase the bioavailability of thiazide diuretics by reducing the motility of the gastrointestinal tract and the rate of gastric emptying.
Cytotoxic drugs, for example, cyclophosphamide, methotrexate: increases myeloid suppressing effect by slowing down the excretion from the body.
Salicylates - when taking high doses of salicylates, hydrochlorothiazide may increase their toxic effects on the central nervous system.
Methyldopa: isolated cases of hemolytic anemia with simultaneous use of hydrochlorothiazide and methyldopa are described.
The simultaneous use of cyclosporine increases the risk of hyperuricemia and exacerbation of the course of gout.
Cardiac glycosides: hypokalemia and hypomagnesemia caused by the use of thiazide diuretics, increases the risk of arrhythmias in the treatment of cardiac glycosides.
Calcium salts - thiazide diuretics can increase the calcium content in blood serum due to a decrease in its excretion. If necessary, the use of calcium preparations dose is selected under the control of calcium in the serum.
Vitamin D - increases the risk of hypercalcemia.
Impact on laboratory results - due to the effect on calcium excretion, thiazides may distort the results of studies of the function of the parathyroid glands.
Carbamazepine - increases the risk of symptomatic hyponatremia. It is necessary to control the content of sodium in serum.
Iodine-containing contrast agents - with dehydration caused by diuretic intake, the risk of developing acute renal failure increases, especially with the introduction of high doses of iodine-containing drugs. Before the introduction of such funds, the patient should be rehydrated.
Amphotericin B (for intravenous administration), stimulant laxatives - hydrochlorothiazide may exacerbate impaired water and electrolyte balance, especially hypokalemia.
Drugs that bind intensively to proteins enhance the diuretic effect. It may be necessary to adjust the dose of anticoagulants for oral administration, probenecid, and sulfinpyrazone, since hydrochlorothiazide may inhibit their action.
At the beginning of treatment, an excessive decrease in blood pressure may be observed, especially in patients with chronic heart failure, severe hypertension (including kidney origin) and / or kidney failure. Before starting treatment, it is necessary to compensate for the deficiency of sodium ions and BCC (reduce the dose of previously prescribed diuretics or, in some cases, completely cancel them), as well as determine the indicators of kidney function.
There is a need for regular monitoring of the content of potassium and calcium ions in plasma (especially in patients receiving treatment with digitalis, glucocorticosteroids, often using laxatives, as well as in elderly patients), glucose, uric acid, lipids (cholesterol and triglycerides), urea and creatinine, activity of "liver" enzymes.
Especially careful monitoring of blood pressure levels and laboratory parameters is necessary in the following cases: in patients with renal insufficiency; patients with severe arterial hypertension (including kidney genesis); in elderly patients (over 65 years); in patients with impaired water and electrolyte balance and decompensated CHF; as well as receiving simultaneously allopurinol, lithium salts, procainamide, and drugs that reduce immunity.
When taking ACE inhibitors, there is a characteristic non-productive cough, which stops after discontinuation of therapy with ACE inhibitors.
In some patients with kidney disease, especially with severe renal artery stenosis, there is an increase in the concentration of urea nitrogen and creatinine in the blood serum after a decrease in blood pressure. This phenomenon is usually reversible, and there is a decrease in the concentration of urea nitrogen and serum creatinine in the event of withdrawal of the drug. You may need a dose reduction of the drug Hydrochlorothiazide + Captopril and / or diuretic withdrawal.
In some cases, against the background of the use of ACE inhibitors, an increase in serum potassium is observed. The risk of developing hyperkalemia with the use of ACE inhibitors is increased in patients with impaired renal function and diabetes mellitus, as well as taking potassium-saving diuretics, potassium preparations, and other drugs that cause an increase in the content of potassium in the blood (for example, heparin). The simultaneous use of potassium-sparing diuretics and potassium preparations should be avoided.
In addition, when using ACE inhibitors simultaneously with thiazide diuretics, the risk of hypokalemia development is not excluded, therefore in such cases it is necessary to regularly monitor the content of potassium in the blood during therapy.
Care should be taken when taking ACE inhibitors by patients with mitral / aortic stenosis / hypertrophic obstructive cardiomyopathy, in the case of cardiogenic shock and hemodynamically significant obstruction - the technique is not recommended.
The use of double blockade of RAAS caused by the simultaneous use of ACE inhibitors and ARAII or aliskiren and aliskiren-containing drugs is not recommended because it was associated with an increased incidence of side effects such as arterial hypotension, hyperkalemia, reduced renal function (including acute renal failure). If the simultaneous use of ACE inhibitors and APAII (double blockade of the RAAS) is necessary, treatment should be carried out under the supervision of a physician and with the implementation of continuous monitoring of kidney function, blood electrolytes, and blood pressure.
The simultaneous use of ACE inhibitors and APAII in patients with diabetic nephropathy is not recommended.
When conducting hemodialysis in patients receiving ACE inhibitors, the use of high-permeability dialysis membranes (eg, AN®69) should be avoided, since in such cases the risk of anaphylactoid reactions increases. Anaphylactoid reactions were also observed in patients who underwent a procedure for removing low-density lipoproteins (apheresis) by absorption using 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 the development of angioedema, the drug is canceled and careful medical monitoring is carried out until the symptoms disappear. Angioedema of the larynx can be fatal. If the edema is localized on the face, special treatment is usually not required (antihistamines may be used to reduce the severity of symptoms), if the edema spreads to the tongue, throat or larynx and there is a threat of respiratory obstruction, epinephrine should be administered immediately (adrenaline ) subcutaneously (0.3-0.5 ml at a dilution of 1: 1000). In rare cases, patients after taking ACE inhibitors had angioedema of the intestines, which was accompanied by abdominal pain (with or without nausea and vomiting). Sometimes - at normal values of C-1-esterase activity and without previous edema of the face. Intestinal edema should be included in the differential diagnosis of patients with complaints of abdominal pain while taking ACE inhibitors.
In representatives of the Negroid race, cases of development of angioedema were noted with greater frequency compared with representatives of the Caucasoid race.
In two patients undergoing desensitization with hymenoptera poison, life-threatening anaphylactoid reactions were noted while receiving captopril. With the temporary cancellation of an ACE inhibitor, it was possible to avoid anaphylactoid reactions. Care should be taken when conducting desensitization therapy in patients taking ACE inhibitors.
In patients with diabetes mellitus, receiving hypoglycemic preparations for oral administration and insulin, the level of glycemia should be carefully monitored, especially during the first month of therapy with ACE inhibitors.
When conducting extensive surgical interventions or when applying funds for general anesthesia, which have antihypertensive effects, patients taking ACE inhibitors may experience an excessive decrease in blood pressure. In these cases, you can increase the BCC.
In rare cases, when taking ACE inhibitors, there is a syndrome that begins with the onset of cholestatic jaundice, which turns into fulminant hepatonecrosis, sometimes with a fatal outcome. The mechanism of development of this syndrome is unknown. If a patient receiving therapy with ACE inhibitors develops jaundice or there is a temporary increase in the activity of liver transaminases, discontinue treatment with ACE inhibitors and establish patient follow-up.
Neutropenia / agranulocytosis, thrombocytopenia and anemia were observed in patients taking ACE inhibitors. In patients with normal renal function and in the absence of other disorders, neutropenia is rare.
The drug Hydrochlorothiazide + Captopril should be used with caution in patients with autoimmune diseases of the connective tissue, in patients receiving immunosuppressants, allopurinol and procainamide, especially in the presence of previously existing renal dysfunction. Due to the fact that the majority of lethal cases of neutropenia against the background of ACE inhibitors developed in these patients, their leukocyte count should be monitored before starting treatment, in the first 3 months every 2 weeks, then every 2 months.
In all patients, the number of leukocytes in the blood should be monitored monthly in the first 3 months after the start of therapy, then every 2 months. If the number of leukocytes is below 4000 / μl, repeated blood count is shown, below 1000 / μl - the drug is discontinued, continuing to monitor the patient. Usually, the number of neutrophils is restored within 2 weeks after the abolition of captopril. In 13% of cases of neutropenia, death was noted.
In almost all cases, death was noted in patients with connective tissue diseases, renal or heart failure, in patients receiving immunosuppressants, or a combination of both of these factors.
When using ACE inhibitors, proteinuria can occur, mainly in patients with impaired renal function, as well as when using high doses of drugs. In most cases, proteinuria when taking the drug captopril disappeared or its severity decreased within 6 months, regardless of whether the drug was stopped or not. Kidney function indicators (urea nitrogen and creatinine concentrations) in patients with proteinuria were almost always within the normal range. In patients with kidney disease, urine protein levels should be determined before starting treatment and periodically throughout the course of therapy.
When taking thiazide diuretics, there have been cases of the development of agranulocytosis and inhibition of bone marrow function.
Hydrochlorothiazide can cause an idiosyncratic reaction leading to the development of acute myopia and an acute attack of secondary angle-closure glaucoma. Symptoms include: a sudden decrease in visual acuity or eye pain, which usually occurs within a few hours or weeks from the start of hydrochlorothiazide therapy. If untreated, acute angle-closure glaucoma can lead to permanent loss of vision. Treatment: discontinue hydrochlorothiazide as soon as possible. If intraocular pressure remains uncontrolled, emergency medical treatment or surgery may be required. Risk factors for the development of acute angle-closure glaucoma are: an allergic reaction to a sulfonamide or penicillin in history.
In all patients taking thiazide diuretics, clinical signs of impaired water-electrolyte balance (hyponatremia, hypochloraemic alkalosis, hypokalemia) should be identified. It is especially important to determine the content of electrolytes in the serum and urine with a strong vomiting or with the introduction of infusion solutions. Symptoms of impaired water and electrolyte balance can be dryness of the oral mucosa, thirst, weakness, lethargy, confusion, anxiety, pain or muscle cramps, muscle weakness, excessive decrease in blood pressure, oliguria, tachycardia, nausea, vomiting.
Hypokalemia may provoke or enhance the cardiotoxic effect of cardiac glycosides. Patients with edema during hot weather may experience hyponatremia caused by an increase in BCC. Limit fluid intake. In cases of life-threatening hyponatremia, salt is prescribed. During therapy with thiazide diuretics, hyperuricemia or exacerbation of the course of gout may occur; latent diabetes mellitus may also appear.
Thiazide diuretics can cause a decrease in the concentration of bound iodine in the serum without signs of dysfunction of the thyroid gland.
On the background of taking thiazide diuretics, the degree of calcium excretion decreases; there have been cases of pathological changes in the parathyroid glands, accompanied by hypercalcemia and hypophosphatemia. Before examining the function of the parathyroid glands, discontinue the use of thiazide diuretics. While receiving thiazide diuretics, an increase in magnesium excretion was noted, which can lead to hypomagnesemia.
The drug can cause false positives in the analysis of urine for acetone and distort the results of the test with benthromide.
When fever, swollen lymph nodes and / or signs of laryngitis and / or pharyngitis appear, the number of leukocytes should be immediately determined.
Athletes should be informed that the drug contains hydrochlorothiazide, which can give false positive results during doping control.
Impact on the ability to drive trans. Wed and fur .:
While taking the drug, care should be taken when driving vehicles, working with mechanisms and engaging in other potentially hazardous activities that require increased concentration of attention and quickness of psychomotor reactions.
Form release / dosage
Tablets, 25 mg + 50 mg.
On 7, 10, 30 tablets in a blister strip packaging from a film of polyvinyl chloride and aluminum foil printed lacquered.
10, 20, 28, 30, 40, 50 or 100 tablets in polyethylene terephthalate cans for drugs, sealed with screw-on caps with first opening control or a push-turn system made of polypropylene or polyethylene or polypropylene cans for drugs, sealed with caps tightened with the control of the first opening of polyethylene or polypropylene cans for medicines, sealed with lids tightened with the control of the first opening of high-pressure polyethylene.
One can or 1, 2, 3, 4, 5 or 10 blister packs together with the instructions for use are placed in a carton (pack).
In the dark place at a temperature of no higher than 25 ° C.
Keep out of the reach of children.
Shelf life - 3 years.
Do not use after the expiration date.
Pharmacy Sale Conditions
You don't need a prescription to buy Hydrochlorothiazide + Captopril.