Indapamide Tablets

Diuretic effect acting on the dilute segment of the renal cortex (cardiovascular system) Indapamide is a derivative of aminobenzenesulfonamide 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 with this product 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 related to its improvement of arterial compliance and reduction of 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, but 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, medium and long term to treat patients with hypertension, it is found that indapamide: - does not affect lipid metabolism: such as triglycerides, LDL-cholesterol and HDL-cholesterol. - does not affect carbohydrate metabolism, even when used to treat patients with diabetic hypertension. Preclinical safety data showed that the diuretic effect of indapamide can be enhanced by oral administration of large doses of the drug (40 to 8000 times higher than the therapeutic dose) to animals of different species. Acute toxicity tests showed that the main symptoms caused by intravenous or intraperitoneal injection of indapamide were related to the pharmacological effects of indapamide, manifested as bradypnea and peripheral vasodilation. Indapamide mutagenicity and carcinogenicity tests were negative.

Indapamide, N-(2-methyl-2,3-dihydro-1H-indolyl)-3-sulfamoyl-4-chlorobenzamide. [Molecular formula] C16H16ClN3O3S [Molecular weight] 365.8 [Structural formula]

This product is a film-coated tablet, which appears white after removing the coating.

Essential hypertension

Oral. Take 1 tablet every 24 hours, preferably in the morning. Swallow the tablet whole with water and do not chew it. Increasing the dose does not improve the antihypertensive effect of indapamide, but only increases the diuretic effect. [Overdose] Indapamide has no toxic reaction when the dose reaches 40 mg, which is equivalent to 27 times the therapeutic dose. Acute poisoning is mainly manifested by water and electrolyte imbalance (hyponatremia and hypokalemia). Clinical symptoms may be nausea, vomiting, hypotension, painful cramps, dizziness, drowsiness, confusion, polyuria or oliguria or even anuria (due to hypovolemia). The initial treatment method used in specialized medical centers is to remove the ingested drug as soon as possible by gastric lavage and/or administration of activated charcoal. Afterwards, water and electrolytes should be supplemented to restore water and electrolyte balance.

Most clinical and laboratory adverse reactions are dose-dependent. Thiazides and related diuretics including indapamide may cause the following: Effects on the blood and lymphatic circulatory system - Rare: thrombocytopenia, leukopenia, agranulocytosis, aplastic anemia, hemolytic anemia Effects on the nervous system - Rare: dizziness, fatigue, headache, paresthesia Effects on the heart - Rare: arrhythmia, hypotension Effects on the gastrointestinal tract - Rare: nausea, constipation, dry mouth - Rare: pancreatitis Effects on the liver and gallbladder - Patients with liver failure may develop hepatic encephalopathy. (See [Contraindications] and [Precautions]) - Rare: Changes in liver function Effects on the skin and tissues - Allergic reactions, mainly skin allergies, (usually maculopapular rashes, a few appear

[Use in pregnant and lactating women] Diuretics during pregnancy can cause placental ischemia and fetal malnutrition. The general principle is that pregnant women should avoid the use of thiazide and related diuretics, and they must not be used to treat physiological edema of pregnancy. Because the drug may enter the breast milk during lactation, lactating women should avoid taking this product. [Use in children] There is a lack of research data on the use of this product in pediatric patients. [Use in the elderly] See [Precautions]. [Overdose] There is no toxic reaction when the dose of indapamide reaches 40 mg, which is equivalent to 27 times the therapeutic dose. Acute poisoning is mainly manifested by water and electrolyte disorders (hyponatremia and hypokalemia). Clinical symptoms may be nausea, vomiting, hypotension, painful cramps, dizziness, drowsiness, confusion, polyuria or oliguria or even anuria (hypoxia).

Precautions for children: This experiment has not been conducted and there is no reliable reference. Precautions for pregnancy and lactation: Women who are pregnant or lactating should avoid taking this product. Precautions for the elderly: The elderly are more sensitive to antihypertensive effects and electrolyte changes, and often have changes in renal function, so they should be careful when using this product.

Inappropriate co-administration of lithium When a sodium-free diet is used (which reduces lithium excretion in the urine), indapamide increases blood lithium concentrations and can lead to manifestations of lithium overdose. However, if a diuretic is used simultaneously, blood lithium levels should be carefully monitored and the dosage adjusted. Drugs to watch out for when used in combination Drugs that cause torsades de pointes ● Class Ia antiarrhythmics (quinidine, dihydroquinidine, disopyramide) ● Class III antiarrhythmics (amiodarone, sotalol, dofetilide, ibutilide) ● Some antipsychotics: Phenothiazines (chlorpromazine, cyanomemazine, levomepromazine, thioridazine, trifluoperazine) Benzamides (amisulpride, sulpride, sultopride, sulpride) Butyrophenones (droperidol, haloperidol) Others: bepridil, cisapride, diphenylmanil, intravenous erythromycin, halofantrine, mizolastine, pentamidine, sparfloxacin, moxifloxacin, intravenous vincamine. Combination therapy increases the risk of ventricular arrhythmias, especially torsades de pointes (hypokalemia is a risk factor). Hypokalemia should be monitored before combined use and corrected if necessary. Clinical signs, plasma electrolyte levels, and electrocardiograms should be monitored. If hypokalemia occurs, choose a drug that does not cause torsades de pointes. Nonsteroidal anti-inflammatory drugs (systemic), including selective COX-2 inhibitors, and high doses of salicylates (greater than 3 g per day) may reduce the antihypertensive effect of indapamide. Dehydrated patients are at risk of acute renal failure (decreased glomerular filtration rate). Rehydrate patients before treatment and monitor their renal function. Angiotensin-converting enzyme (ACE) inhibitors In the presence of preexisting sodium deficiency (especially in renal artery stenosis), the combination of indapamide and ACE inhibitors carries the risk of sudden hypotension and/or acute renal failure. For essential hypertension, previous diuretic treatment may lead to sodium deficiency. It is important to note that: (1) diuretics should be discontinued 3 days before ACE inhibitors are used, and potassium-wasting diuretics can be restarted if necessary; (2) or when ACE inhibitors are given, a low initial dose should be used and the dose should be increased gradually. In patients with congestive heart failure, the initial dose of ACE inhibitors should be very low and can be started after the dose of potassium-wasting diuretics has been reduced. For all patients, monitor renal function (serum creatinine) during the first week of ACE inhibitor use. Other compounds that lower serum potassium: amphotericin B (IV), glucocorticoids and mineralocorticoids (oral), teicoplanin, stimulant laxatives: increase the risk of hypokalemia (synergistic effect). Special attention should be paid when using digitalis. Monitor serum potassium and correct it if necessary. Use non-stimulant laxatives. Baclofen: enhances the hypotensive effect. Give the patient fluids; monitor renal function at the beginning of treatment. Digitalis: Hypokalemia is likely to induce the toxic effects of digitalis. Serum potassium and electrocardiogram should be monitored carefully and treatment should be readjusted if necessary. Potassium-sparing diuretics (amiloride, spironolactone, triamterene) are 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 prone to hyperkalemia. Serum potassium and electrocardiogram need to be monitored and treatment readjusted if necessary. Functional renal insufficiency induced by metformin diuretics (especially loop diuretics) can increase the risk of metformin-induced lactic acidosis. Do not use metformin when the serum creatinine level exceeds 15 mg/L (135 μmol/L) in men and 12 mg/L (110 μmol/L) in women. Iodinated contrast media increase the risk of acute renal failure in the presence of dehydration caused by diuretics, especially when used in large doses. Fluid replacement therapy must be performed before the administration of iodine compounds. Imipramine antidepressants (tricyclic antidepressants), neuroleptics have antihypertensive effects and increase the risk of orthostatic hypotension (synergistic effect). Reduced calcium excretion in calciuria leads to the risk of hypercalcemia. Cyclosporine carries the risk of increased serum creatinine without increasing circulating cyclosporine levels, even in the absence of water/sodium depletion. Corticosteroids, teicositide (systemic) reduce the antihypertensive effect of indapamide (due to water/sodium retention caused by corticosteroids).

Seal and store in a cool and dry place (not exceeding 20°C).

2.5mg (sugar-coated tablet); 2.5mg (film-coated tablet)

24 months.

Zhejiang Apeloa Kangyu Pharmaceutical Co., Ltd.

• Founded in:

  1995-08-08

• Address:

  No. 333, Jiangnan Road, Hengdian, Dongyang City, Zhejiang Province

• Tax NO.:

  913307831475538495

• Registered Funds:

  108.75 million yuan

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