Glime - instructions for use, dose, side effects, contraindications

Excipients: lactose monohydrate - 70.0 mg, microcrystalline cellulose, type 101 - 12.5 mg, sodium carboxymethyl starch (type A) 4.0 mg, povidone-K29-32 - 1.0 mg, a mixture of pigments RV-24880 (lactose monohydrate 0.81 mg, dye red iron oxide 0.09 mg) 0.9 mg magnesium stearate 0.6 mg.

Each tablet with a dosage of 3 mg contains:

active substance: glimepiride - 3.0 mg;

Excipients: lactose monohydrate - 139.0 mg, cellulose microcrystalline, type 101 25.0 mg, sodium carboxymethyl starch (type A) 8.0 mg, povidone-K29-32 - 2.0 mg, a mixture of pigments RV-22865 (lactose monohydrate - 1.71 mg, dye iron oxide yellow - 0.09 mg) - 1.8 mg, magnesium stearate - 1.2 mg.

Each tablet with a dosage of 4 mg contains:

active substance: glimepiride - 4.0 mg;

Excipients: lactose monohydrate - 138.0 mg, cellulose microcrystalline, tin 101 - 25.0 mg, sodium carboxymethyl starch (type A) - 8.0 mg, povidone-K29-32 2.0 mg, a mixture of pigments PB-20978 (lactose monohydrate - 1.60 mg, indigocarmia - 0.20 mg) - 1.8 mg, magnesium stearate - 1.2 mg.

Description:

Tablets 1 mg

Oblong, flat pills of pink color with a bevel, with an engraving "G" on one side of the pill and risk on the other side of the pill.

Tablets 3 mg

Oblong, flat pills of a pale yellow color with a bevel, with an engraving "G" on one side of the pill and risk on the other side of the pill.

Tablets 4 mg

Oblong, flat blue tablets with a bevel, with an engraving "G" on one side of the pill and risk on the other side of the pill.

Pharmacotherapeutic group:Hypoglycemic agent for oral use of the sulfonylurea group of the third generation

ATX: & nbsp

A.10.B.B.12 Glimepiride

Pharmacodynamics:

Glimepiride reduces the concentration of glucose in the blood, mainly by stimulating the release of insulin from βcells of the pancreas. Its effect is mainly associated with improving the ability β-cells of the pancreas respond to physiological stimulation with glucose. Compared to glibenclamide, taking low doses of glimepiride causes the release of less insulin when the blood glucose concentration is approximately the same. This fact testifies in favor of the presence in glimepiride of extrapancreatic hypoglycemic effects (increase of sensitivity of tissues to insulin and insulinomimetic effect).

Secretion of insulin. Like all other sulfonylureas, glimepiride regulates insulin secretion by interaction with the ATP-sensitive potassium channels in the membranes of β-cells. Unlike other derivatives of sulfonylureas glimepiride selectively binds to a protein with a molecular weight of 65 kilodaltons located in membranes β-cells of the pancreas. This interaction of glimepiride with the protein binding it regulates the opening or closing of ATP-sensitive potassium channels.

Glimepiride covers potassium channels. This causes depolarization β-cells and leads to the discovery of voltage-sensitive calcium channels and the entry calcium inside the cell. As a result, an increase in intracellular calcium activates the insulin secretion by exocytosis.

Glimepiride is much faster and, accordingly, more often enters into a bond and is released from the bond with the protein that binds it, than glibenclamide. It is assumed that the property of a high rate of exchange of glimepiride with the protein binding to it causes its pronounced effect of sensitization β-cells to glucose and their protection against desensitization and premature exhaustion.

The effect of increasing the sensitivity of tissues to insulin. Glimepiride enhances insulin effects on glucose uptake by peripheral tissues.

Insulinomimetichesky effect. Glimepiride has effects similar to insulin effects on glucose uptake by peripheral tissues and glucose output from the liver. Absorption of glucose by peripheral tissues is carried out by its transport inside the muscle cells and adipocytes. Glimepiride directly increases the amount of glucose-transporting molecules in the plasma membranes of muscle cells and adipocytes. Increasing the intake of glucose in the cells leads to the activation of glycosylphosphatidylinositol-specific phospholipase C. As a result, the intracellular calcium content decreases, causing a decrease in the activity of protein kinase A, which in turn leads to stimulation of glucose metabolism. Glimepiride inhibits glucose output from the liver by increasing the concentration of fructose-2,6-bisphosphate, which inhibits gluconeogenesis.

Effect on platelet aggregation. Glimepiride reduces platelet aggregation in vitro and in vivo. This effect appears to be due to the selective inhibition of cyclooxygenase, which is responsible for the formation of thromboxane A, an important endogenous platelet aggregation factor.

Anti-atherogenic action. Glimepiride promotes the normalization of lipid content, reduces the concentration of malonic aldehyde in the blood, which leads to a significant decrease in lipid peroxidation. In animals glimepiride leads to a significant decrease in the formation of atherosclerotic plaques.

Reducing the severity of oxidative stress, which is constantly present in patients with type 2 diabetes mellitus. Glimepiride increases the level of endogenous α-tocopherol, catalase activity, glutathione peroxidase and superoxide dismutase.

Cardiovascular effects. Through ATP-sensitive potassium channels, the sulfonylureas derivatives also affect the cardiovascular system. Compared with the traditional derivatives of sulfonylurea, glimepiride has a significantly lower effect on the cardiovascular system, which can be explained by the specific nature of its interaction with the ATP-sensitive protein binding to itpotassium channels.

In healthy volunteers, the minimum effective dose of glimepiride is 0.6 mg. The effect of glimepiride is dose-dependent and reproducible. Physiological response to physical activity (reduced secretion of insulin) with the intake of glimepiride is preserved.

There are no significant differences in the effect, depending on whether the drug was taken 30 minutes before meals or just before meals. In patients with diabetes mellitus, sufficient metabolic control can be achieved within 24 hours with a single administration of the drug. In addition, in a clinical trial, sufficient metabolic control was also achieved in 12 of 16 patients with renal insufficiency (creatinine clearance 4-79 ml / min).

Combination therapy with metformin. In patients who do not achieve sufficient metabolic control with the maximum dose of glimepiride, combined therapy with glimepiride and metformin may be initiated. In two studies, combined therapy has been shown to improve metabolic control compared to that in each of these drugs alone.

Combination therapy with insulin. In patients with the achievement of insufficient metabolic control with the intake of glimepiride in maximum doses, simultaneous therapy with insulin can be started. Based on the results of two studies using this combination, the same improvement in metabolic control is achieved as with the use of only one insulin. However, combined therapy requires a lower dose of insulin.

Use in children

There is insufficient data on the long-term efficacy and safety of glimepiride in children.

Pharmacokinetics:

When comparing the data obtained with a single and multiple (once-a-day) intake of glimepiride, there were no significant differences in pharmacokinetic parameters, and their variability between different patients was very low. There is no significant accumulation of the drug.

Suction

When administered, the bioavailability of glimepiride is complete. The intake of food does not have a significant effect on absorption, with the exception of a slight slowing of its absorption speed. With multiple administration of glimepiride inside at a daily dose of 4 mg, the maximum concentration (C_max) in the blood serum is reached after about 2.5 hours and averages 309 ng / ml. There is a linear relationship between dose and C_maxglimepiride in blood plasma, as well as between the dose and the area under the pharmacokinetic curve "concentratetion-time "(A UC).

Distribution

Glimepiride is characterized by a low volume of distribution (V_d) (about 8.8 liters), approximately equal V_d albumin, a high degree of binding to plasma proteins (more than 99%) and low clearance (about 48 ml / min).

Glimepiride penetrates into breast milk and through the placental barrier, and also in small amounts - through the blood-brain barrier.

Metabolism

Glimepiride is metabolized in the liver (mainly with the participation of isoenzyme CYP2C9) with the formation of 2 metabolites - hydroxylated and carboxylated derivatives, which are excreted by the kidneys and through the intestine.

Excretion

Period nolovevyvedepiya (T_1/2) at plasma serum glimepiride concentrations corresponding to a multiple dosing regimen is approximately 5-8 hours. PAfter taking glimepiride in high doses T_1/2 slightly increases.

After a single glimepiride intake, labeled with a radioactive label, 58% of glimepiride is excreted by the kidneys and 35% by the intestine.Unchanged glimepiride in the urine is not found.

T_1/2 hydroxylated and carboxylated metabolites of glimepiride in the final phase were respectively about 3-5 hours and 5-6 hours, respectively.

Pharmacokinetics in special clinical cases

Pharmacokinetic parameters are similar in patients of different sex and different age groups.

In patients with impaired renal function (with a low CC), there is a tendency to increase the clearance of glimepiride and to reduce its average serum concentrations, which, but most likely, is due to the faster elimination of glimepiride due to its lower binding to proteins. Thus, in this category of patients there is no additional risk of glimepiride cumulation.

Indications:Diabetes mellitus type 2 (as a monotherapy or as part of a combination therapy with metformin or insulin).

Contraindications:

hypersensitivity to glimepiride or to some inactive component of nthe drug;
hypersensitivity to other sulfonylurea derivatives or sulfonamide preparations (risk of hypersensitivity reactions);
type 1 diabetes mellitus;
diabetic ketoacidosis, diabetic precoma and coma;
severe liver dysfunction (lack of clinical experience);
severe renal dysfunction, including among the Nazis on hemodialysis (lack of clinical experience);
pregnancy and the period of breastfeeding;
children under 18 years of age (lack of clinical experience);
rare hereditary diseases, such as galactose intolerance, lactase deficiency or glucose-galactosia malabsorption (contains lactose monohydrate).

Carefully:

in the first weeks of treatment (increased risk of hypoglycemia);
in the presence of risk factors for the development of hypoglycemia (see section Special instructions, it may be necessary to adjust the dose of glimepiride or the whole therapy);
with intercurrent diseases during treatment (for example, severe injuries, surgical interventions, infectious diseases accompanied by high body temperature, and the recovery period of the body after other stressful conditions);
when changing the lifestyle of patients (changing the diet and time of taking a niche, increasing or decreasing physical activity);
with insufficiency of glucose-6-phosphate dehydrohease;
when malabsorption of the nurse and drugs from the gastrointestinal tract (intestinal obstruction, intestinal paresis).

Pregnancy and lactation:

Glime is contraindicated in pregnancy. In the case of a planned pregnancy or at the onset of pregnancy, the patient should be transferred to insulin therapy.

Glimepiride penetrates into breast milk. Because of the possible risk of developing hypoglycemia in a newborn, breastfeeding should be discontinued when taking Glime or taking the patient to insulin therapy.

Dosing and Administration:

Inside.

As a rule, the dose of the drug is determined by the target concentration of glucose in the blood. The drug should be used in a minimum dose sufficient to achieve the necessary metabolic control.

During treatment with the drug, it is necessary to regularly determine the concentration of glucose in the blood. In addition, regular monitoring of the concentration of glycosylated hemoglobin is recommended.

Violation of the regimen of taking the drug, for example, skipping the next dose, should not be replenished by subsequent taking the drug at a higher dose.

The physician should instruct the patient in advance about the actions to be taken when mistakes are made in taking the drug (in particular, if you miss a regular dose or when you miss a meal), or in situations where it is not possible to take the drug.

Reception of the drug

Tablets should be taken whole, not liquid, squeezed with enough liquid (about 0.5 cup). If necessary, Gliema tablets can be divided along the risks into 2 equal parts.

Initial dose and dose selection

The initial dose of the drug is 1 mg 1 time per day. If necessary (in case of insufficient control of blood glucose concentration), the daily dose can be gradually increased (at intervals of 1-2 weeks between periods of dose increase) under regular control of blood glucose concentration. It is recommended to increase the dose with the following interval: I mg - 2 mg - 3 mg - 4 mg - 6 mg (-8 mg) per day. Usually the daily dose of glimepiride in patients with good glycemic control is 1 mg - 4 mg. The recommended maximum daily dose is 6 mg, since a daily dose of more than 6 mg is more effective only in a small number of patients.

Dosing regimen

The doctor determines the burden and multiplicity of the drug taking into account the patient's lifestyle (meal time, number of physical exertions). The daily dose is prescribed in one session immediately before or during a hearty breakfast or the first main meal. It is very important after taking the drug not to miss the intake of the poor in order to avoid the development of hypoglycemia.

As the improvement in metabolic control is associated with an increase in insulin sensitivity, a reduction in the requirement for glimepiride is possible during treatment. In order to avoid the development of hypoglycemia, it is necessary to reduce the dose in time or stop taking the drug.

Conditions in which glimepiride dose adjustment may also be required:

weight loss in the patient;
changes in the lifestyle of the patient (changing diet, meal time, amount of exercise);
the occurrence of other factors that lead to a predisposition to the development of hypoglycemia or hyperglycemia.

Duration of treatment

Treatment with glimepiride is usually carried out for a long time.

Transfer of a patient from another oral hypoglycemic preparation to glimepiride There is no exact correlation between doses of glimsniride and other oral hypoglycemic agents. When transferring from such drugs to glimepiride the recommended initial daily dose of the latter is 1 mg (even if the patient is transferred to glimepiride with a maximum dose of another oral hypoglycemic drug). Any increase in the dose of glimepiride should be carried out in stages, taking into account the response to glimepiride in accordance with the above recommendations. It is necessary to take into account the intensity and duration of the effect of the previous hypoglycemic agent. It may be necessary to interrupt treatment to avoid an additive effect that increases the risk of developing hypoglycemia.

Use in combination with metformin

In patients with insufficiently controlled diabetes mellitus, when taking glimepiride or metformin at the maximum daily doses, a combination of these two drugs can be started. In this case, the previous treatment with either glimepiride or metformin continues in the same doses, and an additional intake of metformin or glimepiride begins with a low dose,which is then titrated depending on the target value of the gl and by any control, up to the maximum daily vine. Combination therapy should be started under strict medical supervision.

Use in combination with insulin

Patients with insufficiently controlled diabetes mellitus while taking glimepiride in the maximum daily dose can be simultaneously assigned to insulin. In this case, the last dose of glimepiride prescribed to the patient remains unchanged. In this case, treatment with insulin begins with low doses, which gradually increase under the control of the concentration of glucose in the blood. Combined treatment is conducted under close medical supervision.

Patients with impaired renal function may be more sensitive to the hypoglycemic effect of glimepiride. Data on the use of the drug in patients with renal insufficiency are limited (sections Pharmacokinetics, PContraindications).

Data on the use of the drug in patients with hepatic insufficiency are limited (see section Contraindications).

Use of the drug in children

Data on the use of the drug in children is not enough

Side effects:

The incidence of adverse reactions with glimepiride is distributed as follows: very frequent (≥10%); frequent (≥1% and <10%); infrequent (≥0.1% and <1%); rare (≥0.01% and <0.1%); very rare (<0.01%); the frequency is unknown (can not be determined from the available data).

From the side of the blood and lymphatic system: rare - thrombocytopenia, leukopenia, granulocytopenia, agranulocytosis, erythrocytopenia, hemolytic anemia and pancytopenia¹); frequency unknown - severe thrombocytopenia with a platelet count of less than 10,000 / μL and thrombocytopenic purpura.

From the immune system: very rare - leukocytoclastic vasculitis, mild hypersensitivity reactions that can progress to serious reactions accompanied by dyspnea, a sharp decrease in blood pressure and in some cases anaphylactic shock; frequency is unknown - cross-allergic reactions with other sulfonylurea derivatives, sulfonylamides or other related compounds.

From the side of metabolism and nutrition: rare - hypoglycemia²) (see section Overdose).

From the side of the organ-vision: frequency unknown - impaired vision³).

From the gastrointestinal tract: very rare - nausea, vomiting, diarrhea, a feeling of heaviness or overflow in the epigastrium, abdominal pain⁴).

From the liver and bile ducts: very rare - a violation of the liver (for example, cholestasis and jaundice), hepatitis and liver failure; frequency unknown - increased activity of "liver" enzymes.

From the skin and subcutaneous tissues: frequency is unknown - reactions hypersensitivity in the form of skin itching, rash, urticaria and photosensitivity reactions.

When symptoms of urticaria appear, consult a doctor immediately.

Laboratory and instrumental data: very rare - hyponatrine.

¹⁾ These violations are usually reversible after discontinuation of treatment.

²⁾These hypoglycemic reactions mainly occur immediately after taking the drug, can be severe and difficult to adjust. The frequency of these reactions depends on the intake of other hypoglycemic drugs and other individual risk factors, such as the characteristics of the diet and the dose of the drug (see section Special instructions).

³⁾These disorders are transient and, as a rule, occur at the beginning of treatment due to changes in the concentration of glucose in the blood. Their cause is a temporary change in the swelling of the lens, depending on the concentration of glucose in the blood, and due to this the change in the refractive index of the lens.

⁴⁾These reactions in rare cases lead to withdrawal of treatment with glimepiride.

Overdose:

Acute overdose, as well as long-term treatment with high doses of glimepiride, can lead to the development of severe life-threatening hypoglycemia.

Symptoms of hypoglycemia - headache, hunger, nausea, vomiting, tiredness, sleepiness, sleep disturbances, restlessness, aggressiveness, impaired concentration, alertness and speed of reactions, depression, confusion, speech disorders, aphasia, visual disorders, tremor, paresis, sensory disturbances , dizziness, loss of self-control, delirium, cerebral convulsions, disturbance of consciousness or loss of consciousness up to coma, shallow breathing, bradycardia. In addition, there may occur manifestations of adrenergic counterregulation in response to hypoglycemia,such as the appearance of cold sticky sweat, anxiety, tachycardia, arterial hypertension, angina pectoris, palpitations and heart rhythm disturbances. The clinical picture of severe hypoglycemia may resemble a stroke. Symptoms of hypoglycemia almost always disappear after its elimination.

Treatment

As soon as an overdose is detected, the doctor should be informed immediately. If the patient is conscious, hypoglycemia can almost always be quickly stopped by the immediate intake of carbohydrates (glucose, a piece of sugar, sweet fruit juice or tea). In this regard, the patient should always have at least 20 grams of glucose (not less than 4 pieces of sugar). Sugary substitutes are ineffective in the treatment of hypoglycemia.

If the reception of carbohydrates has not removed the symptoms of hypoglycemia, then this should be reported to the doctor and to stop it in a hospital. Until the doctor decides that the patient is out of danger, the patient needs careful medical supervision. It should be remembered that hypoglycemia may resume after initial recovery of blood glucose.

When taking high doses of glimepiride, you may need to wash the stomach and take activated charcoal.

In cases of severe overdose, it is recommended that the patient be transferred to the intensive care unit.

As soon as possible, start the injection of dextrose, if necessary in the form of intravenous spraying 50 ml of a 40% solution, followed by the introduction of a 10% solution, with careful monitoring of the concentration of glucose in the blood. An alternative treatment for severe hypoglycemia can be a subcutaneous or intramuscular injection of a solution of glucagon in a dose of 0.5-1 ml (administered by a relative of the patient). Further treatment should be symptomatic. After a rapid recovery of the blood glucose concentration, an intravenous infusion of dextrose solution at a lower concentration is necessary to prevent the resumption of hypoglycemia. The concentration of blood glucose in these patients should be constantly monitored within 24 hours. In severe cases, prolonged course of hypoglycemia may persist for several days.

In the treatment of hypoglycemia due to accidental intake of the drug by infants or young children, the dose of dextrose should be carefully adjusted to avoid the development of hyperglycemia.The administration of dextrose should be carried out under constant control of the concentration of glucose in the blood.

Interaction:

With the joint administration of glimepiride with other medicines, both its hypoglycemic effect may increase or decrease. For this reason, joint intake of other drugs can be started only after the doctor's recommendation.

Glimepiride is metabolized by cytochrome P4502C9 (isoenzyme CYP2C9), which should be taken into account when it is used simultaneously with inductors (for example, rifampicin) or inhibitors (e.g., fluconazole) isoenzyme CYP2C9. Results of the study of interaction in vivo showed an increase AUC glimepiride approximately in 2 times at joint reception with one of the strongest inhibitors of isoenzyme CYP2C9 fluconazole.

Potentiation of hypoglycemic action and in some cases associated with this possible development of hypoglycemia can be observed with the simultaneous use of glimepiride with:

phenylbutazone, azapropane, oxyphenbutazone,
insulin, other hypoglycemic agents for oral administration,
salicylates and para-aminosalicylic acid,
anabolic steroids and male sex hormones,
chloramphenicol, prolonged-action sulfanilamides, tetracyclines, quinolone antibiotics and clarithromycin,
derivatives of coumarin,
fenfluramine,
disopyramide,
fibrates,
inhibitors of the angiotensin converting enzyme,
fluoxetine, monoamine oxidase inhibitors,
allopurinol, probenecid, sulfinpyrazone,
sympatholytic (including guapetidine),
cyclophosphamide, trophosphamide and ifosfamide,
miconazole, fluconazole,
pentoxifylline (with parenteral administration in high doses),
tritvaline.

Reduction of hypoglycemic action and the associated increase in the concentration of glucose in the blood is possible with simultaneous application with:

estrogens and progestogens,
saluretics, thiazide diuretics,
iodine-containing hormones of the thyroid gland, glucocorticosteroids,
phenothiazines, chloromarosine,
sympathomimetic agents (including epinephrine),
nicotinic acid (in high doses) and its derivatives,
laxatives (with prolonged use),
phenytoin, diazoxide,
glucagon, barbiturates and rifampicin,
acetazolamide.

BlockersH₂-gistaminovyh receptors, beta-adrenoblockers, clonidine and reserpine are able to both enhance and reduce the hypoglycemic effect of glimepiride.

Under the influence of sympatholytic agents, such as beta-blockers, clonidine, guanethidine and reserpine, signs of adrenergic counterregulation in response to hypoglycemia may decrease or be absent.

Against the background of glimepiride, it is possible to enhance or weaken the action of coumarin derivatives.

A single or chronic use of alcohol can both enhance and weaken the hypoglycemic effect of glimepiride.

Colesveum binds to glimepiride and reduces its absorption from the gastrointestinal tract. In the case of glimepiride, no interaction is observed at least 4 hours before the administration of colezevelam. therefore glimepiride should be taken, but at least 4 hours before the intake of Wheelsewell.

Special instructions:

It is known that drugs of the sulfonylurea group can cause hypoglycemia, despite compliance with all recommendations for its prevention.

If a patient with diabetes is treated by different doctors (for example, during a hospital stay after an accident, with a disease on a weekend), he must necessarily inform them about his illness and about the previous treatment.

The key to successful treatment of diabetes is compliance with diet, regular exercise, as well as routine monitoring of blood and urine tests. It is also recommended to additionally determine the concentration of glycosylated hemoglobin.

Perhaps the lack of treatment results by oral hypoglycemic agents, as well as with insulin therapy, if the patient does not follow the recommended diet.

If a patient experiences hypoglycemia after taking 1 mg of glimepiride, this indicates that the concentration of glucose in the blood can be controlled by diet.

In stressful conditions such as trauma, surgical interventions, infections with febrile temperature, metabolic control may be impaired in patients with diabetes mellitus, therefore, a temporary transfer to insulin therapy may be required to maintain adequate metabolic control.In the first weeks of treatment, there may be an increased risk of developing hypoglycemia, which requires a particularly careful control of the concentration of glucose in the blood.

Factors that contribute to the risk of developing hypoglycemia include:

unwillingness or inability of the patient (more often observed in elderly patients) to cooperate with a doctor;
malnutrition, irregular intake of food or skipping meals;
an imbalance between exercise and carbohydrate intake;
changing diet;
alcohol consumption, especially when combined with meals;
severe violations of the function of the nights;
severe violations of liver function (in patients with severe impairment of liver function, a transfer to insulin therapy is indicated, at least until metabolic control is achieved);
an overdose of glimepiride;
some uncompensated endocrine disorders that disrupt carbohydrate metabolism or adrenergic counterregulation in response to hypoglycemia (for example, certain disorders of the thyroid gland and anterior pituitary gland, insufficiency of the adrenal cortex);
concurrent administration of certain medicines (see section Interaction with other drugs).

Treatment with derivatives of sulfonylurea, which includes glimepiride, Can lead to hemolytic anemia, however in patients with deficiency of glucose-6-phosphate must be particularly careful when assigning glimepiride, preferably used hypoglycemic agents are not sulfonylureas.

In the case of the above risk factors for hypoglycemia, as well as in the event of intercurrent diseases but the treatment or changing patient's lifestyle, may require correction vines glimepiride or the entire therapy.

Symptoms of hypoglycemia arising from adrenergic kontrregulyatsii the body in response to hypoglycemia may be mild or absent at the gradual development of hypoglycemia in elderly patients, in patients with disorders of the autonomic nervous system, or in patients receiving beta-blockers, clonidine, reserpine, guanethidine and other sympatholytic agents.

Hypoglycemia can be quickly eliminated by immediate intake of rapidly digesting carbohydrates (glucose or sucrose). As with the administration of other sulfonylureas, despite initial successful reduction of hypoglycemia, hypoglycemia may resume. Therefore, patients should remain under constant supervision. Severe or prolonged hypoglycemia can only be temporarily treated with carbohydrate intake, these conditions require hospitalization and drug therapy.

During treatment with glimepiride, regular monitoring of liver function and peripheral blood pattern (especially the number of leukocytes and platelets) is required.

Such side effects as severe hypoglycemia, severe changes in the blood picture, severe allergic reactions, liver failure may under certain circumstances pose a threat to life, therefore, if such reactions develop, the patient should immediately inform the attending physician about them, stop taking the drug and not resume taking without the advice of a doctor.

Effect on the ability to drive transp.cf. and fur:

At the beginning of treatment, after a change in treatment or with an irregular intake of glimepiride, there may be a decrease in the concentration of attention and speed of psychomotor reactions caused by hypo- or hyperglycemia. This can adversely affect the ability to manage various vehicles and mechanisms.

Form release / dosage:

Tablets, 1 mg, 3 mg, 4 mg.

Packaging:For 15 tablets in a PVC blister / Aluminum foil. For 1, 2, 3, 4, 5, 6, 8 or 13 blisters with instructions for use in a cardboard box.

Storage conditions:

At a temperature of no higher than 30 ° C. Keep out of the reach of children!

Shelf life:

3 years. Do not apply but the expiration date.

Terms of leave from pharmacies:On prescription

Registration number:LP-003334

Date of registration:24.11.2015

Expiration Date:24.11.2020

The owner of the registration certificate:AKTAVIS GROUP, AO AKTAVIS GROUP, AO Iceland

Manufacturer: & nbsp

FHI ZDRAVLJE AD LESKOVAC Serbia

Representation: & nbspAktavis, Open Company Aktavis, Open Company

Information update date: & nbsp25.04.2017

Illustrated instructions

Instructions

Glime (Glaym)