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Telmisartan-N STADA (Telmisartan-N STADA)

Hydrochlorothiazide

Renal dysfunction

In patients with impaired renal function, hydrochlorothiazide may cause azotemia. In case of renal failure, accumulation of hydrochlorothiazide is possible.

In patients with reduced renal function, periodic monitoring of creatinine clearance is necessary. If renal dysfunction progresses and/or oliguria (anuria) occurs, hydrochlorothiazide should be discontinued.

Liver dysfunction

When using thiazide diuretics in patients with impaired liver function, hepatic encephalopathy may develop. In patients with severe liver failure or hepatic encephalopathy, the use of thiazides is contraindicated. In patients with mild to moderate hepatic impairment and/or progressive liver disease, hydrochlorothiazide should be used with caution, since even a slight change in fluid and electrolyte balance and the accumulation of ammonium in the blood serum can cause hepatic coma. If symptoms of encephalopathy occur, diuretics should be discontinued immediately.

Water-electrolyte balance and metabolic disorders

Thiazide diuretics (including hydrochlorothiazide) can cause a decrease in the volume of circulating fluid (hypovolemia) and disturbances in water and electrolyte balance (including hypokalemia, hyponatremia, hypochloremic alkalosis).

Clinical symptoms of fluid and electrolyte imbalance are dry mouth, thirst, weakness, lethargy, fatigue, drowsiness, restlessness, muscle pain or cramps, muscle weakness, marked decrease in blood pressure, oliguria, tachycardia, arrhythmia and gastrointestinal disorders (such as nausea and vomiting). In patients receiving hydrochlorothiazide therapy (especially with long-term course treatment), clinical symptoms of water-electrolyte imbalance should be identified and blood electrolyte levels should be regularly monitored.

Sodium

All diuretics can cause hyponatremia, sometimes leading to severe complications.

Hyponatremia and hypovolemia can lead to dehydration and orthostatic hypotension. A concomitant decrease in chlorine ions can lead to secondary compensatory metabolic alkalosis, but the frequency and severity of this effect are insignificant. It is recommended to determine the content of sodium ions in the blood plasma before starting treatment and regularly monitor this indicator while taking hydrochlorothiazide.

Potassium

When using thiazide and thiazide-like diuretics, there is a risk of a sharp decrease in the potassium content in the blood plasma and the development of hypokalemia (potassium concentration less than 3.4 mmol/l).

Hypokalemia increases the risk of developing heart rhythm disturbances (including severe arrhythmias) and enhances the toxic effect of cardiac glycosides. In addition, hypokalemia (as well as bradycardia) is a condition that contributes to the development of polymorphic ventricular tachycardia of the “pirouette” type, which can be fatal.

Hypokalemia poses the greatest danger to the following groups of patients: elderly people, patients simultaneously receiving therapy with antiarrhythmic and non-antiarrhythmic drugs that can cause polymorphic ventricular tachycardia of the "pirouette" type or increase the duration of the QT interval on the ECG, patients with impaired liver function, coronary heart disease , chronic heart failure. In addition, patients with an increased QT interval are at increased risk. It does not matter whether this increase is caused by congenital causes or the effect of drugs.

In all the cases described above, it is necessary to avoid the risk of developing hypokalemia and regularly monitor the potassium content in the blood plasma. The first measurement of the content of potassium ions in the blood must be carried out within the first week from the start of treatment. If hypokalemia occurs, appropriate treatment should be prescribed. Hypokalemia can be corrected by using potassium-containing medications or eating foods rich in potassium (dried fruits, fruits, vegetables).

Calcium

Thiazide diuretics may reduce the excretion of calcium ions by the kidneys, leading to a slight and temporary increase in plasma calcium levels. In some patients, with long-term use of thiazide diuretics, pathological changes in the parathyroid glands were observed with hypercalcemia and hyperphosphatemia, but without the typical complications of hyperparathyroidism (nephrolithiasis, decreased bone mineral density, peptic ulcer). Severe hypercalcemia may be a manifestation of previously undiagnosed hyperparathyroidism.

Because of their effect on calcium metabolism, thiazides may interfere with laboratory parameters of parathyroid function. Thiazide diuretics (including hydrochlorothiazide) should be discontinued before testing parathyroid function.

Magnesium

Thiazides have been found to increase renal excretion of magnesium, which can lead to hypomagnesemia. The clinical significance of hypomagnesemia remains unclear.

Glucose

Treatment with thiazide diuretics may impair glucose tolerance. When using hydrochlorothiazide in patients with manifest or latent diabetes mellitus, it is necessary to regularly monitor the concentration of glucose in the blood. Dosage adjustment of hypoglycemic drugs may be required.

Uric acid

In patients with gout, the frequency of attacks may increase or the course of gout may worsen. Careful monitoring of patients with gout and impaired uric acid metabolism (hyperuricemia) is necessary.

Lipids

When using hydrochlorothiazide, the concentration of cholesterol and triglycerides in the blood plasma may increase.

Choroidal exudate / acute myopia / secondary angle-closure glaucoma

Hydrochlorothiazide can cause an idiosyncratic reaction leading to the development of choroidal exudate with visual field defect, acute myopia and an acute attack of secondary angle-closure glaucoma.

Symptoms include: sudden loss of visual acuity or eye pain, usually occurring within hours to weeks of starting hydrochlorothiazide therapy. If left untreated, acute angle-closure glaucoma can lead to irreversible vision loss. If symptoms appear, you should stop taking 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: a history of an allergic reaction to sulfonamides or penicillin.

Immune system disorders

There are reports that thiazide diuretics (including hydrochlorothiazide) may cause exacerbation or progression of systemic lupus erythematosus, as well as lupus-like reactions.

In patients receiving thiazide diuretics, hypersensitivity reactions may occur even in the absence of a history of allergic reactions or bronchial asthma.

Photosensitivity

There is information about cases of the development of photosensitivity reactions when taking thiazide diuretics. If photosensitivity occurs while taking hydrochlorothiazide, treatment should be discontinued. If continued use of the diuretic is necessary, the skin should be protected from exposure to sunlight or artificial ultraviolet rays.

Non-melanoma skin cancer

Two pharmacoepidemiological studies using data from the Danish National Cancer Registry demonstrated an association between hydrochlorothiazide use and an increased risk of non-melanoma skin cancer (NMSC) basal cell carcinoma and squamous cell carcinoma. The risk of developing NMSC increased with increasing total (cumulative) dose of hydrochlorothiazide. A possible mechanism for the development of NMSC is the photosensitizing effect of hydrochlorothiazide.

Patients taking hydrochlorothiazide as monotherapy or in combination with other drugs should be aware of the risk of developing NMSC. It is recommended that such patients undergo regular skin examination to identify any new suspicious lesions as well as changes in existing skin lesions.

Any suspicious skin changes should be reported to your doctor immediately. Suspicious areas of skin should be examined by a specialist. To clarify the diagnosis, histological examination of skin biopsies may be required.

To minimize the risk of developing NMSC, patients should be advised to follow preventive measures, such as limiting exposure to sunlight and UV rays, and using appropriate protective equipment.

In patients with a history of non-melanoma skin cancer, it is recommended to reconsider the use of hydrochlorothiazide.

Other

In patients with severe atherosclerosis of the cerebral and coronary arteries, hydrochlorothiazide should be used with extreme caution.

Thiazide diuretics can reduce the amount of iodine bound to plasma proteins without causing signs of thyroid dysfunction.

Telmisartan

Liver failure

Telmisartan should not be used in patients with cholestasis, biliary obstruction or severe hepatic impairment (Child-Pugh class C), since telmisartan is excreted primarily in the bile. It is assumed that in such patients the hepatic clearance of telmisartan is reduced.

Renovascular hypertension

When treated with drugs that act on the RAAS, the risk of severe arterial hypotension and renal failure increases in patients with bilateral renal artery stenosis or stenosis of the artery of a solitary kidney.

Double blockade of the RAAS

Data on the simultaneous use of ACE inhibitors with ARB II or drugs containing aliskiren confirm an increased risk of a sharp decrease in blood pressure, the development of hyperkalemia and impaired renal function (including acute renal failure). Concomitant use of ARB II, including telmisartan, with drugs containing aliskiren is contraindicated in patients with diabetes mellitus and/or with moderate or severe renal impairment (GFR less than 60 ml/min/1.73 m2 body surface area) and is not recommended in others patients. Concomitant use of II receptor antagonists, including telmisartan, with ACE inhibitors is contraindicated in patients with diabetic nephropathy and is not recommended in other patients.

If it is necessary to carry out double blockade of the RAAS, each case should be considered individually and carefully monitor renal function, water-electrolyte balance and blood pressure.

Other diseases characterized by stimulation of the RAAS

In patients whose vascular tone and renal function depend primarily on the activity of the RAAS (for example, patients with chronic heart failure or kidney disease, including renal artery stenosis), the use of drugs acting on this system, such as telmisartan, has been associated with the occurrence of acute arterial hypotension, hyperazotemia, oliguria, or rarely - acute renal failure.

Primary hyperaldosteronism

Patients with primary hyperaldosteronism generally do not respond to treatment with antihypertensive drugs that act by inhibiting the RAAS. In this regard, the use of telmisartan in these cases is not recommended.

Kidney failure and kidney transplantation

There is no clinical experience with the use of telmisartan in patients who have recently undergone kidney transplantation.

Decrease in circulating blood volume (CBV)

In patients with a decrease in blood volume and/or sodium content due to previous diuretic therapy, restriction of salt intake, diarrhea or vomiting, symptomatic arterial hypotension may occur, especially after the first dose of telmisartan.

Aortic and mitral valve stenosis, hypertrophic obstructive cardiomyopathy As with other vasodilators, caution should be exercised when prescribing the drug to patients with aortic or mitral valve stenosis or hypertrophic obstructive cardiomyopathy.

Hyperkalemia

Telmisartan may cause hyperkalemia due to antagonism of angiotensin II receptors (AT1 subtype). For elderly patients, patients with renal failure, patients with diabetes mellitus and also with arterial hypertension and coronary artery disease (CHD), patients receiving concomitant therapy with drugs that may cause an increase in potassium levels, and/or patients with concomitant disease, hyperkalemia can be fatal. Before considering the possibility of concomitant use of drugs acting on the RAAS, it is necessary to assess the benefit-risk ratio.

The main risk factors to consider are:

-diabetes mellitus, renal failure, heart failure, old age (patients over 70 years old);

- combination with one or more drugs acting on the RAAS and/or nutritional supplements containing potassium. Medicines that can cause hyperkalemia are potassium-sparing diuretics, ACE inhibitors, ARB II, NSAIDs, including selective COX-2 inhibitors, heparin, immunosuppressants (cyclosporine or tacrolimus), trimethoprim, and salt substitutes containing potassium;

- associated diseases or conditions, especially dehydration, acute heart failure, metabolic acidosis, renal dysfunction, acute renal failure (for example, in infectious diseases), cytolysis syndrome (for example, acute limb ischemia, rhabdomyolysis, major trauma). Patients at risk are advised to carefully monitor plasma potassium levels.

Heart failure

As with other drugs that affect the RAAS, patients with heart failure (with or without renal impairment) are at risk of developing a significant decrease in blood pressure, as well as renal dysfunction, including acute renal failure.

Ethnic differences Liver dysfunction when prescribed telmisartan was observed in most cases in Japanese residents.

Hydrochlorothiazide + telmisartan

Liver failure

Telmisartan-N STADA should be used with extreme caution in patients with mild to moderate hepatic impairment (Child-Pugh class A and B), since even minor changes in water and electrolyte balance can contribute to the development of hepatic coma.

Kidney failure

The use of Telmisartan-N STADA is contraindicated in patients with severe renal impairment (CrCl - 30 ml/min). When using the drug in patients with mild to moderate renal impairment, it is recommended to periodically monitor the content of potassium, creatinine and uric acid in the blood plasma, as well as indicators of renal function.

Decrease in circulating blood volume (CBV)

Effect on metabolism and function of endocrine glands

The use of hydrochlorothiazide may impair glucose tolerance, and in patients with diabetes mellitus hypoglycemia may develop during the simultaneous use of insulin or hypoglycemic agents and telmisartan. Dosage adjustment of hypoglycemic agents, including insulin, may be required.

Treatment with thiazide diuretics is associated with an increase in the concentration of cholesterol and triglycerides in the blood plasma. However, when using a drug containing 12.5 mg of hydrochlorothiazide, this effect is minimal or absent.

Water-electrolyte imbalance

When using the drug Telmisartan-N STADA, as in the case of diuretic therapy, periodic monitoring of the content of electrolytes in the blood plasma is necessary.

Hypokalemia

When using thiazide diuretics, hypokalemia may develop, but concomitantly used telmisartan may increase the potassium level in the blood. The risk of hypokalemia increases most in patients with liver cirrhosis, with increased diuresis, while following a salt-free diet, as well as in the case of simultaneous use of gluco- and mineralocorticosteroids or corticotropin.

Hyperkalemia

When using a combination drug containing telmisartan and hydrochlorothiazide, clinically significant hyperkalemia was not recorded. However, risk factors for its development should be taken into account (see section “Special instructions”, subsection “Telmisartan”, Hyperkalemia).

Patients at risk are advised to carefully monitor plasma potassium levels.

Hyponatremia and hypochloremia

There is no evidence that a combination drug containing telmisartan and hydrochlorothiazide can reduce or prevent diuretic-induced hyponatremia. Hypochloremia is usually minor and does not require treatment.

Coronary heart disease and cerebrovascular disease

As with the use of other antihypertensive drugs, an excessive decrease in blood pressure in patients with coronary heart disease or cerebrovascular disease can lead to the development of myocardial infarction or stroke.

Other

If a photosensitivity reaction occurs, it is recommended to stop taking Telmisartan-N STADA. If the use of diuretics is still necessary, it is recommended to protect exposed skin from exposure to sunlight or artificial ultraviolet irradiation. A combination drug containing telmisartan and hydrochlorothiazide is less effective in black patients.

Instructions for use TELSARTAN®

Telsartan®, like other drugs acting on the RAAS, can cause hyperkalemia. The risk of developing hyperkalemia increases when used simultaneously with other drugs that cause hyperkalemia, incl. with potassium-sparing diuretics, potassium supplements, potassium-containing nutritional supplements and other drugs and substances that can increase potassium levels in the blood serum (for example, heparin), ACE inhibitors, angiotensin II receptor antagonists, NSAIDs, including selective COX-2 inhibitors, immunosuppressive drugs (cyclosporine or tacrolimus) and trimethoprim. The incidence of hyperkalemia depends on the presence of risk factors. With the simultaneous use of potassium-sparing diuretics and potassium-containing salt substitutes, the risk of developing hyperkalemia is especially high. Concomitant use with ACE inhibitors or NSAIDs is accompanied by a lower risk of hyperkalemia, provided careful precautions are taken.

Data obtained from clinical studies indicate an increased incidence of adverse events such as hypotension, hyperkalemia and decreased renal function (including the development of renal failure) with dual blockade of the RAAS due to the simultaneous use of ACE inhibitors, angiotensin II receptor antagonists or aliskiren compared with the use of only one drug that affects the RAAS.

Concomitant use with aliskiren in patients with diabetes mellitus or moderate/severe renal failure (GFR <60 ml/min/1.73 m2) is contraindicated.

Concomitant use is not recommended

Potassium-sparing diuretics, potassium supplements, or potassium-containing salt substitutes

Angiotensin II receptor antagonists, such as telmisartan, reduce potassium loss caused by diuretics. Potassium-sparing diuretics such as spironolactone, eplerenone, triamterene or amiloride, potassium supplements, or potassium-containing salt substitutes may cause a significant increase in serum potassium levels. If their simultaneous use is necessary due to the presence of proven hypokalemia, treatment should be carried out with caution and frequent monitoring of serum potassium levels.

Lithium

With the simultaneous use of lithium preparations with ACE inhibitors, a reversible increase in the concentration of lithium in the blood plasma was observed with the development of toxic effects. Similar changes have been observed in rare cases with the use of angiotensin II receptor antagonists. If necessary, simultaneous use of lithium preparations and angiotensin II receptor antagonists, incl. telmisartan, monitoring of lithium levels in the blood plasma is recommended.

Concomitant use with caution

NSAIDs, incl. selective COX-2 inhibitors, acetylsalicylic acid and non-selective NSAIDs

In patients with impaired renal function (eg, dehydrated or elderly patients), concomitant use may result in further deterioration of renal function, including the development of reversible acute renal failure. This combination should be used with caution, especially in elderly patients. Therefore, before using telmisartan, it is recommended to evaluate renal function, as well as correct water and electrolyte imbalances; In the future, it is advisable to monitor renal function. NSAIDs reduce the hypotensive effect of telmisartan.

Ramipril

Concomitant use with ramipril leads to an increase in AUC0-24 and Cmax of ramipril and ramiprilat by 2.5 times. The clinical significance of this effect has not been established.

Diuretics (thiazide and loop)

Previous therapy with diuretics in high doses, incl. furosemide (“loop” diuretic) and hydrochlorothiazide (thiazide diuretic), can lead to a decrease in blood volume and an increased risk of arterial hypotension at the beginning of therapy with telmisartan.

Concomitant use requiring attention

Telmisartan enhances the effect of other antihypertensive drugs.

Considering the pharmacological properties, it is possible to potentiate the antihypertensive effect when used simultaneously with baclofen and amifostine.

Ethanol, barbiturates, anesthetics and antidepressants

may contribute to the development of orthostatic hypotension.

GKS

reduce the antihypertensive effect of telmisartan.

When taking telmisartan with digoxin

There is a median increase in the maximum and residual concentrations of digoxin in the blood plasma (49% and 20%, respectively). During initiation, adjustment, and discontinuation of telmisartan, digoxin concentrations must be monitored to maintain them within the therapeutic range.

Academpharm

Pharmacodynamics

Telmisartan is a specific angiotensin II receptor antagonist (AT1 type), effective when taken orally. Telmisartan displaces angiotensin II from the AT1 receptor binding site, which is responsible for the known mechanisms of action of angiotensin, and exhibits very high affinity for this site. Telmisartan does not demonstrate partial agonism at the AT1 receptor. Telmisartan selectively and long-lastingly binds to the AT1 receptor. Telmisartan has no affinity for other receptors, including AT2 and other less studied angiotensin receptors. The functional role of these receptors is unknown, as is the effect of their possible excessive stimulation by angiotensin II, the concentration of which increases with the administration of telmisartan. Telmisartan reduces plasma aldosterone levels, does not inhibit human plasma renin, and does not block ion channels. Telmisartan does not inhibit angiotensin-converting enzyme (kininase II), an enzyme that breaks down bradykinin. Therefore, an increase in bradykinin-mediated side effects is not expected.

In humans, an 80 mg dose of telmisartan almost completely suppresses the increase in blood pressure caused by angiotensin II. The inhibitory effect persists for 24 hours and remains significant for up to 48 hours.

Clinical efficacy and safety

Treatment of essential arterial hypertension

After taking the first dose of telmisartan, the onset of antihypertensive action is observed within 3 hours. The greatest reduction in blood pressure is usually achieved 4-8 weeks after the start of treatment and persists with long-term treatment.

The antihypertensive effect persists continuously for 24 hours after dosing, including 4 hours before the next dose, as shown by ambulatory blood pressure measurements. This is confirmed by the ratio of maximum and minimum drug levels, which exceeded 80% after taking 40 and 80 mg of telmisartan in placebo-controlled clinical studies. There was a clear tendency for the time to return systolic blood pressure (SBP) to baseline to depend on the dose taken. Data for diastolic blood pressure (DBP) did not show such a clear relationship.

In patients with arterial hypertension, telmisartan reduces SBP and DBP without affecting pulse rate. The contribution of the diuretic and natriuretic effect to the antihypertensive activity of the drug has not yet been determined. The antihypertensive effectiveness of telmisartan is comparable to that of other classes of antihypertensive drugs (shown in clinical studies comparing telmisartan with amlodipine, atenolol, enalapril, hydrochlorothiazide and lisinopril).

After abrupt cessation of treatment with telmisartan, blood pressure gradually (over several days) returns to its original level without the development of withdrawal syndrome.

The incidence of dry cough was significantly lower in patients treated with telmisartan compared with patients treated with angiotensin-converting enzyme inhibitors in clinical studies directly comparing these two antihypertensive therapy regimens.

Prevention of cardiovascular events

The clinical trial compared the effects of telmisartan, ramipril, and their combination on cardiovascular outcomes in patients over 55 years of age at risk for cardiovascular events. Telmisartan had a similar effect to ramipril for the primary outcome of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for congestive heart failure. Telmisartan was noninferior to ramipril in the total incidence of cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke.

Patients treated with telmisartan were less likely to develop cough or angioedema compared to patients treated with ramipril. Co-administration of telmisartan and ramipril did not provide additional benefits compared with taking either drug alone. Cardiovascular and all-cause mortality were higher with combination treatment. In addition, the incidence of hyperkalemia, renal failure, hypotension, and syncope was significantly higher in the combination treatment group. Therefore, the use of a combination of telmisartan and ramipril in this population is not recommended.

so that a slight decrease in AUC reduces therapeutic efficacy. There is no linear relationship between the dose taken and the plasma level of telmisartan. When taking doses above 40 mg, there is a disproportionate increase in maximum plasma concentration (Cmax) and, to a lesser extent, AUC.

Distribution

Telmisartan is highly bound to plasma proteins (>99.5%), predominantly to albumin and α-1 acid glycoprotein. The average apparent volume of distribution at equilibrium (Vdss) is about 500 l.

Metabolism

Telmisartan is metabolized by conjugation of the parent compound with a glucuronide. This conjugate has not been shown to have pharmacological activity.

Removal

Telmisartan exhibits biexponential disintegration pharmacokinetics with a terminal half-life of >20 hours. Cmax and, to a lesser extent, AUC increase disproportionately with increasing dose. There are no data on clinically significant accumulation of telmisartan when taken at the recommended dose. Plasma concentrations were higher in women than in men, which did not have a significant effect on the effectiveness of treatment.

Following oral or intravenous administration, telmisartan is excreted almost exclusively in the feces, predominantly as unchanged substance. Total urinary excretion is <1% of the dose taken. The total plasma clearance (Cltot approximately 1000 ml/min) is high compared to the blood flow in the liver (about 1500 ml/min).

Pharmacokinetics in special groups of patients

Influence of gender

Differences in plasma concentrations of telmisartan were noted: in women, Cmax and AUC were, respectively, approximately 3 and 2 times higher than in men.

Elderly patients

The pharmacokinetics of telmisartan in elderly people does not differ from that in patients under 65 years of age.

Renal dysfunction

In patients with mild to moderate renal impairment and severe renal failure, a twofold increase in plasma concentrations was observed. However, lower plasma concentrations were observed in patients with renal failure on hemodialysis. Telmisartan is highly bound to plasma proteins in patients with renal failure and is not excreted during dialysis. The half-life does not change in patients with impaired renal function.

Liver dysfunction

Pharmacokinetic studies in patients with impaired liver function showed an increase in absolute bioavailability of almost 100%. The half-life does not change in patients with impaired liver function.