Indapamide extended-release tablets

Pharmacology: Diuretic effect acting on the dilute segment of the renal cortex Indapamide is a sulfonamide derivative with an indole ring structure. It is pharmacologically related to thiazide diuretics and achieves a diuretic effect by inhibiting the reabsorption of sodium in the dilute segment of the renal cortex. This drug increases the excretion of urinary sodium and urinary chloride, and to a lesser extent increases the excretion of potassium and magnesium, thereby increasing urine volume and exerting an antihypertensive effect. Phase II and Phase III studies have shown that the antihypertensive effect of monotherapy can last for 24 hours. When this effect occurs, the dose used has only a mild diuretic effect. The antihypertensive effect of this drug is to improve arterial compliance and reduce arteriolar and entire peripheral circulation resistance. Indapamide can reverse left ventricular hypertrophy caused by hypertension. Beyond a certain dose, the efficacy of thiazide and its related diuretics does not further improve, while the side effects continue to increase. If the treatment is ineffective, the drug dose should not be increased. When indapamide is used in the short-term, medium-term and long-term treatment of hypertensive patients, it is found that indapamide: 1. It does not affect lipid metabolism: such as triglycerides, LDL cholesterol and HDL cholesterol. 2. It does not affect carbohydrate metabolism, even when used to treat diabetic and hypertensive patients.

The main ingredient of this product is: Indapamide.

White round film-coated tablets, about 4.3mm thick and 8mm in diameter.

Essential hypertension.

The usual oral dose for adults is 2.5 mg (1 tablet) once a day.

Most clinical and laboratory adverse reactions are dose-dependent. Thiazides and related diuretics including indapamide may cause the following: 1. Laboratory parameters: (1) Potassium depletion and hypokalemia, which are more severe in certain high-risk groups (see Precautions). In clinical trials, 10% of patients treated for 4-6 weeks developed hypokalemia (blood potassium 3.4mmol/L); 4% of patients had blood potassium 3.2mmol/L. After 12 weeks of treatment, the average decrease in blood potassium was 0.23mmol/L. (2) Hyponatremia with hypovolemia causes dehydration and orthostatic hypotension. Concomitant chloride ion depletion can lead to secondary compensatory metabolic alkalosis: this condition has a very low incidence and is also mild. (3) During treatment, plasma uric acid and blood glucose increase: when using these diuretics in patients with gout and diabetes, their indications must be considered very carefully. (4) Hematological disorders: very rare: thrombocytopenia, leukopenia, agranulocytosis, nutritional anemia, hemolytic anemia. (5) Hypercalcemia: very rare. 2. Clinical parameters: (1) In the case of liver dysfunction, hepatic encephalopathy may occur. (2) Allergic reactions, mainly skin allergies, seen in patients with previous allergies or asthma. (3) Maculopapular rash, purpura, may aggravate the original acute systemic lupus erythematosus. (4) Nausea, constipation, dry mouth, dizziness, fatigue, paresthesia, headache and other symptoms rarely occur, and most of them are relieved with drug reduction. (5) Pancreatitis is very rare.

1. Allergy to sulfonamides. 2. Severe renal failure. 3. Hepatic encephalopathy or severe liver failure. 4. Hypokalemia.

Precautions for children: There is a lack of research data on the use of this product in pediatric patients. Precautions for pregnancy and lactation: Use with caution in pregnant women. Precautions for the elderly: Thiazides and related diuretics can only fully function when kidney function is normal or slightly impaired (adult serum creatinine is less than 25 mg/L, i.e. 220 μmol/L). In the elderly, serum creatinine values must be adjusted based on age, weight and gender.

Incompatible drugs: 1. Lithium: During a sodium-free diet (reduced lithium excretion in urine). Indapamide increases blood lithium concentration and leads to manifestations of lithium overdose. However, if diuretics are used at the same time, blood lithium levels should be strictly monitored and the dosage should be adjusted. 2. Non-antiarrhythmic drugs causing torsades de pointes (including astemizole, bepridil, intravenous erythromycin, halofantrine, pentamidine, sultopride, terfenadine, vincamine): torsades de pointes (hypokalemia, bradycardia, and QT prolongation are inducing factors). If hypokalemia occurs, do not use drugs that can cause torsades de pointes. Cautious combination therapy is required. 3. Nonsteroidal anti-inflammatory drugs (systemic), high doses of sodium salicylate: may weaken the antihypertensive effect of indapamide. Acute renal failure (decreased glomerular filtration) in dehydrated patients. When starting treatment, rehydrate the patient and monitor renal function. 4. Other compounds that lower blood potassium: amphotericin B (intravenous), glucocorticoids and mineralocorticoids (systemic), teicoplanin, stimulant laxatives: increase the risk of hypokalemia (synergistic effect). Monitor blood potassium and correct it if necessary. Be especially careful when using digitalis. Use non-stimulant laxatives. 5. Baclofen: enhances the hypotensive effect. Give the patient fluids; monitor renal function at the beginning of treatment. 6. Digitalis: hypokalemia is likely to induce the toxic effects of digitalis. Monitor blood potassium and electrocardiogram when necessary, and readjust treatment if necessary. Combination medications that need to be considered. 7. Potassium-sparing diuretics (amiloride, spironolactone, triamterene): This combination is beneficial for some patients, but the possibility of hypokalemia or hyperkalemia cannot be ruled out, especially for patients with renal failure and diabetes, who are more likely to develop hyperkalemia. Monitor blood potassium and electrocardiogram when necessary, and readjust treatment if necessary. 8. Angiotensin Converting Enzyme (ACE) Inhibitors: In the case of pre-existing sodium deficiency (especially in cases of renal artery stenosis), the combination of indapamide and ACE inhibitors may cause sudden hypotension and/or acute renal failure. In patients with primary hypertension, previous use of diuretics may lead to sodium deficiency. It is important to note that: (1) Before using ACE inhibitors, stop using diuretics for 3 days; if necessary, restart the use of potassium-wasting diuretics. (2) Or when giving ACE inhibitors, use a low starting dose and gradually increase the dose. In patients with congestive heart failure, the initial dose of ACE inhibitors should be very small and can be started after reducing the dose of potassium-wasting diuretics. For all patients using ACE inhibitors, renal function (serum creatinine) should be monitored in the first week. 9. Antiarrhythmic drugs that cause torsades de pointes: Class Ia antiarrhythmic drugs (quinidine, dihydroquinidine, disopyramide), amiodarone, bretylium, sotalol: torsades de pointes (hypokalemia, bradycardia, and pre-existing QT interval prolongation are inducing factors). Prevent hypokalemia and correct it if necessary; monitor the QT interval. In the event of torsades de pointes, do not use antiarrhythmic drugs (but use pacemakers for treatment). 10. Metformin: Functional renal insufficiency induced by diuretics (especially loop diuretics) can stimulate lactic acidosis caused by metformin. Do not use metformin when the blood creatinine level exceeds 15mg/L (135μmol/L) in men and exceeds 12mg/L (110μmol/L) in women. 11. Iodinated contrast media: In the case of dehydration caused by diuretics, iodinated contrast media increase the risk of acute renal failure, especially when used in large doses. Fluid rehydration can be performed before administering iodinated compounds. 12. Imipramine antidepressants (tricyclic antidepressants), neuroleptics: enhance antihypertensive effects and increase the risk of orthostatic hypotension (synergistic effect). 13. Calcium salts: reduced calcium excretion in urine leads to the risk of hypercalcemia. 14. Cyclosporine: ACE inhibitors still have the risk of increasing blood creatinine without increasing the level of cyclosporine in the circulation, even in the absence of water/sodium loss. 15. Corticosteroids, teicosin (systemic route): reduce the antihypertensive effect of indapamide (due to water/sodium retention caused by corticosteroids).

Store below 30℃.

1.5mg

24 months

Jinan Gaohua Pharmaceutical Co., Ltd.

• Founded in:

  1994-12-22

• Address:

  No. 8 Panwang Road, Mingshui Economic Development Zone, Longshan Street, Zhangqiu District, Jinan City, Shandong Province

• Tax NO.:

  913701812644656618

• Registered Funds:

  2.1 million yuan

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