In some countries, this medicine may only be approved for veterinary use.
Ingredient matches for Havaspan
Sulfadimidine
Sulfadimidine is reported as an ingredient of Havaspan in the following countries:
- United States
International Drug Name Search
Thursday 27 May 2010
Wednesday 26 May 2010
Enalapril plus-1A Pharma
Enalapril plus-1A Pharma may be available in the countries listed below.
Ingredient matches for Enalapril plus-1A Pharma
Enalapril
Enalapril maleate (a derivative of Enalapril) is reported as an ingredient of Enalapril plus-1A Pharma in the following countries:
- Germany
Hydrochlorothiazide
Hydrochlorothiazide is reported as an ingredient of Enalapril plus-1A Pharma in the following countries:
- Germany
International Drug Name Search
Tuesday 25 May 2010
Eff-Pha Vitamin C
Eff-Pha Vitamin C may be available in the countries listed below.
Ingredient matches for Eff-Pha Vitamin C
Ascorbic Acid
Ascorbic Acid is reported as an ingredient of Eff-Pha Vitamin C in the following countries:
- Vietnam
International Drug Name Search
Friday 21 May 2010
Salbumol Chrono
Salbumol Chrono may be available in the countries listed below.
Ingredient matches for Salbumol Chrono
Salbutamol
Salbutamol sulfate (a derivative of Salbutamol) is reported as an ingredient of Salbumol Chrono in the following countries:
- Greece
International Drug Name Search
Monday 17 May 2010
Tobrom
Tobrom may be available in the countries listed below.
Ingredient matches for Tobrom
Tobramycin
Tobramycin is reported as an ingredient of Tobrom in the following countries:
- Georgia
International Drug Name Search
Sunday 16 May 2010
Mictonetten
Mictonetten may be available in the countries listed below.
Ingredient matches for Mictonetten
Propiverine
Propiverine hydrochloride (a derivative of Propiverine) is reported as an ingredient of Mictonetten in the following countries:
- Czech Republic
- Germany
- Slovakia
International Drug Name Search
Thursday 13 May 2010
Riomet
Riomet (metformin hydrochloride oral solution) is an oral antihyperglycemic drug used in the management of type 2 diabetes. Metformin hydrochloride, USP (N,N- dimethylimidodicarbonimidic diamide hydrochloride) is not chemically or pharmacologically related to any other classes of oral antihyperglycemic agents. The structural formula is as shown:
Metformin hydrochloride, USP is a white crystalline powder with a molecular formula of C4H11N5•HCl and a molecular weight of 165.63. Metformin hydrochloride, USP 2.0 g is soluble in 20 mL of water. The pKa of metformin is 12.4. The pH of a 1% aqueous solution of metformin hydrochloride is 6.68.
Riomet contains 500 mg of metformin hydrochloride, USP per 5 mL and the following inactive ingredients: Cherry flavor, hydrochloric acid, potassium bicarbonate, purified water, saccharin calcium, and xylitol.
Riomet - Clinical Pharmacology
Mechanism of Action
Metformin is an antihyperglycemic agent which improves glucose tolerance in patients with type 2 diabetes, lowering both basal and postprandial plasma glucose. Its pharmacologic mechanisms of action are different from other classes of oral antihyperglycemic agents. Metformin decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization. Unlike sulfonylureas, metformin does not produce hypoglycemia in either patients with type 2 diabetes or normal subjects (except in special circumstances, see PRECAUTIONS) and does not cause hyperinsulinemia. With metformin therapy, insulin secretion remains unchanged while fasting insulin levels and day-long plasma insulin response may actually decrease.
Pharmacokinetics
Absorption and Bioavailability
Two pharmacokinetic studies have been performed in healthy volunteers to evaluate the bioavailability of Riomet in comparison with the commercially available metformin tablets under fasting and fed conditions (study 1 and study 2). A third pharmacokinetic study (study 3) assessed effects of food on absorption of Riomet.
The rate and extent of absorption of Riomet was found to be comparable to that of Metformin tablets under fasting or fed conditions (see Table 1).
The food-effect study (study 3) assessed the effects of a high fat/high calorie meal and a low fat/low calorie meal on the bioavailability of Riomet in comparison with administration in the fasted state, in healthy volunteers. The extent of absorption was increased by 21% and 17% with the low fat/low calorie meal and the high fat/high calorie meal, respectively, compared with the administration in the fasted state. The rate and extent of absorption with high fat/high calorie and low fat/low calorie meal were similar. The mean t max was 2.5 hours under fasting conditions as compared to 3.9 hours with both low fat/ low calorie meal and high fat/high calorie meals (see Table 2).
| Meal type | Cmax(ng/mL) | AUC0-∞ (ng.h/mL) | tmax (h) |
| Fasting (F) | 1641.5 ± 551.8 | 9982.9 ± 2544.5 | 2.5 ± 0.9 |
| Low fat/ low calorie meal (L) | 1525.8 ± 396.7 | 11542.0 ± 2947.5 | 3.9 ± 0.6 |
| High fat/high calorie meal (H) | 1432.5 ± 346.8 | 11184.5 ± 2446.1 | 3.9 ± 0.8 |
| L/F Ratio X 100 (90% confidence interval) | 94.6 (84.0-106.5) | 115.6 (103.6-128.9) | - |
| H/F Ratio X 100 (90% confidence interval) | 89.4 (79.4-100.6) | 112.6 (100.9-125.6) | - |
| L/H Ratio X 100 (90% confidence interval) | 105.8 (94.0-119.2) | 102.7 (92.0-114.6) | - |
Studies using single oral doses of metformin tablet formulations 500 mg to 1500 mg, and 850 mg to 2550 mg, indicate that there is a lack of dose proportionality with increasing doses, which is due to decreased absorption rather than an alteration in elimination.
Distribution
The apparent volume of distribution (V/F) of metformin following single oral doses of metformin 850 mg averaged 654 ± 358 L. Metformin is negligibly bound to plasma proteins, in contrast to sulfonylureas, which are more than 90% protein bound. Metformin partitions into erythrocytes, most likely as a function of time. At usual clinical doses and dosing schedules of metformin, steady state plasma concentrations of metformin are reached within 24 to 48 hours and are generally < 1 µg/mL. During controlled clinical trials of metformin, maximum metformin plasma levels did not exceed 5 mg/mL, even at maximum doses.
Metabolism and Elimination
Intravenous single-dose studies in normal subjects demonstrate that metformin is excreted unchanged in the urine and does not undergo hepatic metabolism (no metabolites have been identified in humans) nor biliary excretion. Renal clearance (see Table 3) is approximately 3.5 times greater than creatinine clearance, which indicates that tubular secretion is the major route of metformin elimination. Following oral administration, approximately 90% of the absorbed drug is eliminated via the renal route within the first 24 hours, with a plasma elimination half-life of approximately 6.2 hours. In blood, the elimination half-life is approximately 17.6 hours, suggesting that the erythrocyte mass may be a compartment of distribution.
Special Populations
Patients with Type 2 Diabetes
In the presence of normal renal function, there are no differences between single- or multiple-dose pharmacokinetics of metformin between patients with type 2 diabetes and normal subjects (see Table 3), nor is there any accumulation of metformin in either group at usual clinical doses.
Renal Insufficiency
In patients with decreased renal function (based on measured creatinine clearance), the plasma and blood half-life of metformin is prolonged and the renal clearance is decreased in proportion to the decrease in creatinine clearance (see Table 3; also see WARNINGS).
Hepatic Insufficiency
No pharmacokinetic studies of metformin have been conducted in patients with hepatic insufficiency.
Geriatrics
Limited data from controlled pharmacokinetic studies of metformin in healthy elderly subjects suggest that total plasma clearance of metformin is decreased, the half-life is prolonged, and Cmax is increased, compared to healthy young subjects. From these data, it appears that the change in metformin pharmacokinetics with aging is primarily accounted for by a change in renal function (see Table 3). Riomet (metformin hydrochloride oral solution) treatment should not be initiated in patients ≥ 80 years of age unless measurement of creatinine clearance demonstrates that renal function is not reduced. (See WARNINGS and DOSAGE AND ADMINISTRATION).
Pediatrics
After administration of a single oral metformin 500 mg dose with food, geometric mean metformin Cmax and AUC differed less than 5% between pediatric type 2 diabetic patients (12 to 16 years of age) and gender- and weight-matched healthy adults (20 to 45 years of age), all with normal renal function.
Gender
Metformin pharmacokinetic parameters did not differ significantly between normal subjects and patients with type 2 diabetes when analyzed according to gender (males = 19, females = 16). Similarly, in controlled clinical studies in patients with type 2 diabetes, the antihyperglycemic effect of metformin was comparable in males and females.
Race
No studies of metformin pharmacokinetic parameters according to race have been performed. In controlled clinical studies of metformin in patients with type 2 diabetes, the antihyperglycemic effect was comparable in whites (n = 249), blacks (n = 51), and Hispanics (n= 24).
Clinical Studies
In a double-blind, placebo-controlled, multicenter U.S. clinical trial involving obese patients with type 2 diabetes whose hyperglycemia was not adequately controlled with dietary management alone (baseline fasting plasma glucose [FPG] of approximately 240 mg/dL), treatment with metformin (up to 2550 mg/day) for 29 weeks resulted in significant mean net reductions in fasting and postprandial plasma glucose (PPG) and hemoglobin A1c (HbA1c) of 59 mg/dL, 83 mg/dL, and 1.8%, respectively, compared to the placebo group (see Table 4).
A 29-week, double-blind, placebo-controlled study of metformin and glyburide, alone and in combination, was conducted in obese patients with type 2 diabetes who had failed to achieve adequate glycemic control while on maximum doses of glyburide (baseline FPG of approximately 250 mg/dL) (see Table 5). Patients randomized to the combination arm started therapy with metformin 500 mg and glyburide 20 mg. At the end of each week of the first four weeks of the trial, these patients had their dosages of metformin increased by 500 mg if they had failed to reach target fasting plasma glucose. After week four, such dosage adjustments were made monthly, although no patient was allowed to exceed metformin 2500 mg. Patients in the metformin only arm (metformin plus placebo) followed the same titration schedule. At the end of the trial, approximately 70% of the patients in the combination group were taking metformin 2000 mg/glyburide 20 mg or metformin 2500 mg/glyburide 20 mg. Patients randomized to continue on glyburide experienced worsening of glycemic control, with mean increases in FPG, PPG, and HbA1c of 14 mg/dL, 3 mg/dL, and 0.2%, respectively. In contrast, those randomized to metformin (up to 2500 mg/day) experienced a slight improvement, with mean reductions in FPG, PPG, and HbA1c of 1 mg/dL, 6 mg/dL, and 0.4%, respectively. The combination of metformin and glyburide was effective in reducing FPG, PPG, and HbA1c levels by 63 mg/dL, 65 mg/dL, and 1.7%, respectively. Compared to results of glyburide treatment alone, the net differences with combination treatment were -77 mg/dL, -68 mg/dL, and -1.9%, respectively (see Table 5).
The magnitude of the decline in fasting blood glucose concentration following the institution of metformin therapy was proportional to the level of fasting hyperglycemia. Patients with type 2 diabetes with higher fasting glucose concentrations experienced greater declines in plasma glucose and glycosylated hemoglobin.
In clinical studies, metformin, alone or in combination with a sulfonylurea, lowered mean fasting serum triglycerides, total cholesterol, and LDL cholesterol levels and had no adverse effects on other lipid levels (see Table 6).
| Metformin vs Placebo | Combined Metformin/Glyburide vs Monotherapy | ||||
| Metformin (n = 141) | Placebo (n = 145) | Metformin (n = 210) | Metformin/Glyburide (n = 213) | Glyburide (n = 209) | |
| Total Cholesterol (mg/dL) | |||||
| Baseline | 211.0 | 212.3 | 213.1 | 215.6 | 219.6 |
| Mean % Change at FINAL VISIT | -5% | 1% | -2% | -4% | 1% |
| Total Triglycerides (mg/dL) | |||||
| Baseline | 236.1 | 203.5 | 242.5 | 215.0 | 266.1 |
| Mean % Change at FINAL VISIT | -16% | 1% | -3% | -8% | 4% |
| LDL-Cholesterol (mg/dL) | |||||
| Baseline | 135.4 | 138.5 | 134.3 | 136.0 | 137.5 |
| Mean % Change at FINAL VISIT | -8% | 1% | -4% | -6% | 3% |
| HDL-Cholesterol (mg/dL) | |||||
| Baseline | 39.0 | 40.5 | 37.2 | 39.0 | 37.0 |
| Mean % Change at FINAL VISIT | 2% | -1% | 5% | 3% | 1% |
In contrast to sulfonylureas, body weight of individuals on metformin tended to remain stable or even decrease somewhat (see Tables 4 and 5).
A 24-week, double-blind, placebo-controlled study of metformin plus insulin versus insulin plus placebo was conducted in patients with type 2 diabetes who failed to achieve adequate glycemic control on insulin alone (see Table 7). Patients randomized to receive metformin plus insulin achieved a reduction in HbA1c of 2.10%, compared to a 1.56% reduction in HbA1c achieved by insulin plus placebo. The improvement in glycemic control was achieved at the final study visit with 16% less insulin, 93.0 U/day vs. 110.6 U/day, metformin plus insulin versus insulin plus placebo, respectively, p = 0.04.
A second double-blind, placebo-controlled study (n = 51), with 16 weeks of randomized treatment, demonstrated that in patients with type 2 diabetes controlled on insulin for 8 weeks with an average HbA1c of 7.46 ± 0.97%, the addition of metformin maintained similar glycemic control (HbA1c 7.15 ± 0.61 versus 6.97 ± 0.62 for metformin plus insulin and placebo plus insulin, respectively) with 19% less insulin versus baseline (reduction of 23.68 ± 30.22 versus an increase of 0.43 ± 25.20 units for metformin plus insulin and placebo plus insulin, p < 0.01). In addition, this study demonstrated that the combination of metformin plus insulin resulted in reduction in body weight of 3.11 ± 4.30 lbs, compared to an increase of 1.30 ± 6.08 lbs for placebo plus insulin, p = 0.01.
Pediatric Clinical Studies
In a double-blind, placebo-controlled study in pediatric patients aged 10 to 16 years with type 2 diabetes (mean FPG 182.2 mg/dL), treatment with metformin (up to 2000 mg/day) for up to 16 weeks (mean duration of treatment 11 weeks) resulted in a significant mean net reduction in FPG of 64.3 mg/dL, compared with placebo (see Table 8).
Indications and Usage for Riomet
Riomet (metformin hydrochloride oral solution) is indicated as an adjunct to diet and exercise to improve glycemic control in adults and children with type 2 diabetes mellitus.
Contraindications
Riomet is contraindicated in patients with:
1. Renal disease or renal dysfunction (e.g., as suggested by serum creatinine levels ≥ 1.5 mg/dL [males], ≥ 1.4 mg/dL [females] or abnormal creatinine clearance) which may also result from conditions such as cardiovascular collapse (shock), acute myocardial infarction, and septicemia (see WARNINGS and PRECAUTIONS).
2. Known hypersensitivity to metformin hydrochloride.
3. Acute or chronic metabolic acidosis, including diabetic ketoacidosis, with or without coma. Diabetic ketoacidosis should be treated with insulin.
Riomet should be temporarily discontinued in patients undergoing radiologic studies involving intravascular administration of iodinated contrast materials, because use of such products may result in acute alteration of renal function. (See also PRECAUTIONS).
Warnings
Lactic Acidosis:
Lactic acidosis is a rare, but serious, metabolic complication that can occur due to metformin accumulation during treatment with Riomet; when it occurs, it is fatal in approximately 50% of cases. Lactic acidosis may also occur in association with a number of pathophysiologic conditions, including diabetes mellitus, and whenever there is significant tissue hypoperfusion and hypoxemia. Lactic acidosis is characterized by elevated blood lactate levels (> 5 mmol/L), decreased blood pH, electrolyte disturbances with an increased anion gap, and an increased lactate/pyruvate ratio. When metformin is implicated as the cause of lactic acidosis, metformin plasma levels > 5 µg/mL are generally found.
The reported incidence of lactic acidosis in patients receiving metformin hydrochloride is very low (approximately 0.03 cases/1000 patient-years, with approximately 0.015 fatal cases/1000 patient-years). In more than 20,000 patient-years exposure to metformin in clinical trials, there were no reports of lactic acidosis. Reported cases have occurred primarily in diabetic patients with significant renal insufficiency, including both intrinsic renal disease and renal hypoperfusion, often in the setting of multiple concomitant medical/surgical problems and multiple concomitant medications. Patients with congestive heart failure requiring pharmacologic management, in particular those with unstable or acute congestive heart failure who are at risk of hypoperfusion and hypoxemia, are at increased risk of lactic acidosis. The risk of lactic acidosis increases with the degree of renal dysfunction and the patient’s age. The risk of lactic acidosis may, therefore, be significantly decreased by regular monitoring of renal function in patients taking Riomet and by use of the minimum effective dose of Riomet. In particular, treatment of the elderly should be accompanied by careful monitoring of renal function. Riomet treatment should not be initiated in patients ≥ 80 years of age unless measurement of creatinine clearance demonstrates that renal function is not reduced, as these patients are more susceptible to developing lactic acidosis. In addition, Riomet should be promptly withheld in the presence of any condition associated with hypoxemia, dehydration, or sepsis. Because impaired hepatic function may significantly limit the ability to clear lactate, Riomet should generally be avoided in patients with clinical or laboratory evidence of hepatic disease. Patients should be cautioned against excessive alcohol intake, either acute or chronic, when taking Riomet, since alcohol potentiates the effects of metformin hydrochloride on lactate metabolism. In addition, Riomet should be temporarily discontinued prior to any intravascular radiocontrast study and for any surgical procedure (see also PRECAUTIONS).
The onset of lactic acidosis often is subtle, and accompanied only by nonspecific symptoms such as malaise, myalgias, respiratory distress, increasing somnolence, and nonspecific abdominal distress. There may be associated hypothermia, hypotension, and resistant bradyarrhythmias with more marked acidosis. The patient and the patient’s physician must be aware of the possible importance of such symptoms and the patient should be instructed to notify the physician immediately if they occur (see also PRECAUTIONS). Riomet should be withdrawn until the situation is clarified. Serum electrolytes, ketones, blood glucose and, if indicated, blood pH, lactate levels, and even blood metformin levels may be useful. Once a patient is stabilized on any dose level of Riomet, gastrointestinal symptoms, which are common during initiation of therapy, are unlikely to be drug related. Later occurrence of gastrointestinal symptoms could be due to lactic acidosis or other serious disease.
Levels of fasting venous plasma lactate above the upper limit of normal but less than 5 mmol/L in patients taking Riomet do not necessarily indicate impending lactic acidosis and may be explainable by other mechanisms, such as poorly controlled diabetes or obesity, vigorous physical activity, or technical problems in sample handling. (See also PRECAUTIONS).
Lactic acidosis should be suspected in any diabetic patient with metabolic acidosis lacking evidence of ketoacidosis (ketonuria and ketonemia).
Lactic acidosis is a medical emergency that must be treated in a hospital setting. In a patient with lactic acidosis who is taking Riomet, the drug should be discontinued immediately and general supportive measures promptly instituted. Because metformin hydrochloride is dialyzable (with a clearance of up to 170 mL/min under good hemodynamic conditions), prompt hemodialysis is recommended to correct the acidosis and remove the accumulated metformin. Such management often results in prompt reversal of symptoms and recovery. (See also CONTRAINDICATIONS and PRECAUTIONS).
Precautions
There have been no clinical studies establishing conclusive evidence of macrovascular risk reduction with Riomet or any other oral anti-diabetic drug.
Monitoring of renal function — Metformin is known to be substantially excreted by the kidney, and the risk of metformin accumulation and lactic acidosis increases with the degree of impairment of renal function. Thus, patients with serum creatinine levels above the upper limit of normal for their age should not receive Riomet. In patients with advanced age, Riomet should be carefully titrated to establish the minimum dose for adequate glycemic effect, because aging is associated with reduced renal function. In elderly patients, particularly those ≥80 years of age, renal function should be monitored regularly and, generally, Riomet should not be titrated to the maximum dose (see WARNINGS and DOSAGE AND ADMINISTRATION).
Before initiation of Riomet therapy and at least annually thereafter, renal function should be assessed and verified as normal. In patients in whom development of renal dysfunction is anticipated, renal function should be assessed more frequently and Riomet discontinued if evidence of renal impairment is present.
Use of concomitant medications that may affect renal function or metformin disposition — Concomitant medication(s) that may affect renal function or result in significant hemodynamic change or may interfere with the disposition of metformin, such as cationic drugs that are eliminated by renal tubular secretion (see PRECAUTIONS: Drug Interactions), should be used with caution.
Radiologic studies involving the use of intravascular iodinated contrast materials (for example, intravenous urogram, intravenous cholangiography, angiography, and computed tomography (CT) scans with intravascular contrast materials) — Intravascular contrast studies with iodinated materials can lead to acute alteration of renal function and have been associated with lactic acidosis in patients receiving metformin (see CONTRAINDICATIONS). Therefore, in patients in whom any such study is planned, Riomet should be temporarily discontinued at the time of or prior to the procedure, and withheld for 48 hours subsequent to the procedure and reinstituted only after renal function has been re-evaluated and found to be normal.
Hypoxic states — Cardiovascular collapse (shock) from whatever cause, acute congestive heart failure, acute myocardial infarction and other conditions characterized by hypoxemia have been associated with lactic acidosis and may also cause prerenal azotemia. When such events occur in patients on Riomet therapy, the drug should be promptly discontinued.
Surgical procedures — Riomet therapy should be temporarily suspended for any surgical procedure (except minor procedures not associated with restricted intake of food and fluids) and should not be restarted until the patient’s oral intake has resumed and renal function has been evaluated as normal.
Alcohol intake — Alcohol is known to potentiate the effect of metformin on lactate metabolism. Patients, therefore, should be warned against excessive alcohol intake, acute or chronic, while receiving Riomet.
Impaired hepatic function — Since impaired hepatic function has been associated with some cases of lactic acidosis, Riomet should generally be avoided in patients with clinical or laboratory evidence of hepatic disease.
Vitamin B12 levels — In controlled clinical trials of metformin of 29 weeks duration, a decrease to subnormal levels of previously normal serum Vitamin B12 levels, without clinical manifestations, was observed in approximately 7% of patients. Such decrease, possibly due to interference with B12 absorption from the B12-intrinsic factor complex, is, however, very rarely associated with anemia and appears to be rapidly reversible with discontinuation of metformin or Vitamin B12 supplementation. Measurement of hematologic parameters on an annual basis is advised in patients on Riomet and any apparent abnormalities should be appropriately investigated and managed (see PRECAUTIONS: Laboratory Tests).
Certain individuals (those with inadequate Vitamin B12 or calcium intake or absorption) appear to be predisposed to developing subnormal Vitamin B12 levels. In these patients, routine serum Vitamin B12 measurements at two- to three-year intervals may be useful.
Change in clinical status of patients with previously controlled type 2 diabetes — A patient with type 2 diabetes previously well controlled on Riomet who develops laboratory abnormalities or clinical illness (especially vague and poorly defined illness) should be evaluated promptly for evidence of ketoacidosis or lactic acidosis. Evaluation should include serum electrolytes and ketones, blood glucose and, if indicated, blood pH, lactate, pyruvate, and metformin levels. If acidosis of either form occurs, Riomet must be stopped immediately and other appropriate corrective measures initiated (see also WARNINGS).
Hypoglycemia — Hypoglycemia does not occur in patients receiving metformin alone under usual circumstances of use, but could occur when caloric intake is deficient, when strenuous exercise is not compensated by caloric supplementation, or during concomitant use with other glucose-lowering agents (such as sulfonylureas and insulin) or ethanol.
Elderly, debilitated, or malnourished patients, and those with adrenal or pituitary insufficiency or alcohol intoxication are particularly susceptible to hypoglycemic effects. Hypoglycemia may be difficult to recognize in the elderly, and in people who are taking beta-adrenergic blocking drugs.
Loss of control of blood glucose — When a patient stabilized on any diabetic regimen is exposed to stress such as fever, trauma, infection, or surgery, a temporary loss of glycemic control may occur. At such times, it may be necessary to withhold Riomet and temporarily administer insulin. Riomet may be reinstituted after the acute episode is resolved.
The effectiveness of oral antidiabetic drugs in lowering blood glucose to a targeted level decreases in many patients over a period of time. This phenomenon, which may be due to progression of the underlying disease or to diminished responsiveness to the drug, is known as secondary failure, to distinguish it from primary failure in which the drug is ineffective during initial therapy. Should secondary failure occur with either Riomet or sulfonylurea monotherapy, combined therapy with Riomet and sulfonylurea may result in a response. Should secondary failure occur with combined Riomet/sulfonylurea therapy, it may be necessary to consider therapeutic alternatives including initiation of insulin therapy.
Patients should be informed of the potential risks and benefits of Riomet and of alternative modes of therapy. They should also be informed about the importance of adherence to dietary instructions, of a regular exercise program, and of regular testing of blood glucose, glycosylated hemoglobin, renal function, and hematologic parameters.
The risks of lactic acidosis, its symptoms, and conditions that predispose to its development, as noted in the WARNINGS and PRECAUTIONS sections, should be explained to patients. Patients should be advised to discontinue Riomet immediately and to promptly notify their health practitioner if unexplained hyperventilation, myalgia, malaise, unusual somnolence, or other nonspecific symptoms occur. Once a patient is stabilized on any dose level of Riomet, gastrointestinal symptoms, which are common during initiation
Tuesday 11 May 2010
Keppra
In the US, Keppra (levetiracetam systemic) is a member of the drug class pyrrolidine anticonvulsants and is used to treat Bipolar Disorder, Epilepsy, Neuralgia, New Daily Persistent Headache and Seizures.
US matches:
- Keppra
- Keppra Solution
- Keppra Tablets
- Keppra XR Extended-Release Tablets
- Keppra XR
- Keppra Intravenous
- Keppra Injection
- Keppra-XR
UK matches:
- Keppra (SPC)
- Keppra 250,500,750 and 1000 mg film-coated Tablets, 100 mg/ml oral solution and 100 mg/ml concentrate for solution for infusion (SPC)
- Keppra film-coated Tablets 250mg, 500mg, 750mg, 1000mg, Keppra 100mg/ml oral solution, Keppra 100mg/ml concentrate for solution for infusion (SPC)
Ingredient matches for Keppra
Levetiracetam
Levetiracetam is reported as an ingredient of Keppra in the following countries:
- Australia
- Austria
- Bahrain
- Belgium
- Benin
- Bulgaria
- Burkina Faso
- Canada
- Central African Republic
- Chad
- Colombia
- Congo
- Croatia (Hrvatska)
- Czech Republic
- Denmark
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- France
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- Germany
- Greece
- Guinea
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- Mauritania
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- Netherlands
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- Niger
- Norway
- Oman
- Philippines
- Poland
- Portugal
- Romania
- Russian Federation
- Singapore
- Slovakia
- Slovenia
- South Africa
- Spain
- Sweden
- Switzerland
- Taiwan
- Thailand
- Togo
- Turkey
- United Kingdom
- United States
- Vietnam
- Zaire
International Drug Name Search
Glossary
| SPC | Summary of Product Characteristics (UK) |
Click for further information on drug naming conventions and International Nonproprietary Names.
Monday 10 May 2010
Neophedan
Neophedan may be available in the countries listed below.
Ingredient matches for Neophedan
Tamoxifen
Tamoxifen is reported as an ingredient of Neophedan in the following countries:
- South Africa
International Drug Name Search
Salamol Easi-Breathe
Salamol Easi-Breathe may be available in the countries listed below.
Ingredient matches for Salamol Easi-Breathe
Salbutamol
Salbutamol is reported as an ingredient of Salamol Easi-Breathe in the following countries:
- Ireland
Salbutamol sulfate (a derivative of Salbutamol) is reported as an ingredient of Salamol Easi-Breathe in the following countries:
- Malta
International Drug Name Search
Sunday 9 May 2010
Cortancyl
Cortancyl may be available in the countries listed below.
Ingredient matches for Cortancyl
Prednisone
Prednisone is reported as an ingredient of Cortancyl in the following countries:
- France
International Drug Name Search
Friday 7 May 2010
Mébévérine Teva
Mébévérine Teva may be available in the countries listed below.
Ingredient matches for Mébévérine Teva
Mebeverine
Mebeverine hydrochloride (a derivative of Mebeverine) is reported as an ingredient of Mébévérine Teva in the following countries:
- France
International Drug Name Search
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