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Glucotrol

Glucotrol is a medication consists in a class of drugs called sulfonylureas. Glucotrol is used to treat type 2 diabetes. Glucotrol may be used along with diet, exercise and insulin therapy. Glucotrol works by controlling blood sugar levels in your organism.

Other names for this medication:
Actine, Antidiab, Beapizide, Diactin, Diasef, Dipazide, Euglizip, Gabaz, Glibenese, Glide, Glidiab, Glimerol, Glipicontin, Glipizid, Glipizida, Glipizidum, Glipom, Gluco-rite, Glucolip, Glucopress, Glucotrol, Glutrol, Glynase, Glyzip, Luditec, Melizid, Melizide, Mindiab, Minodiab, Ozidia, Singloben, Sucrazide, Xiprine, Zitrol xr

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Also known as:  Glipizide.

Description

Glucotrol is a medication consists in a class of drugs called sulfonylureas.

Glucotrol is used to treat type 2 diabetes. Glucotrol may be used along with diet, exercise and insulin therapy.

Glucotrol is also known as Glipizide, Glytop SR.

Glucotrol works by controlling blood sugar levels in your organism.

Generic name of Glucotrol is Glipizide.

Brand names of Glucotrol are Glucotrol, Glucotrol XL.

Dosage

Take Glucotrol orally.

Do not chew, divide or crush the tablet. Swallow it whole.

Glucotrol is usually taken before breakfast if it is taken once a day, or before meals if it is taken several times each day.

Take each dose of Glucotrol with a full glass of water.

The dosage and the kind of tablets depend on the disease and its prescribed treatment.

While taking Glucotrol follow diet, medication and exercise routines closely.

If you want to achieve most effective results do not stop taking Glucotrol suddenly.

Overdose

If you overdose Glucotrol and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Glucotrol overdosage: hunger, nausea, anxiety, cold sweats, weakness, drowsiness, unconsciousness, coma.

Storage

Store at room temperature below 30 degrees C (86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Glucotrol are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Glucotrol if you are allergic to Glucotrol components.

Be careful with Glucotrol if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Glucotrol if you have kidney disease, liver disease, thyroid disease, type 1 diabetes, serious infection, illness, or injury.

Be careful with Glucotrol if you take aspirin or another salicylate such as magnesium/choline salicylate (Trilisate), salsalate (Disalcid, others), choline salicylate (Arthropan), magnesium salicylate (Magan) or bismuth subsalicylate (Pepto-Bismol); nonsteroidal anti-inflammatory drug (NSAID) such as ibuprofen (Motrin, Advil, Nuprin, others), ketoprofen (Orudis, Orudis KT, Oruvail), diclofenac (Voltaren, Cataflam), etodolac (Lodine), indomethacin (Indocin), nabumetone (Relafen), oxaprozin (Daypro), naproxen (Anaprox, Naprosyn, Aleve) and others; sulfa-based drug such as sulfamethoxazole-trimethoprim (Bactrim, Septra), sulfisoxazole (Gantrisin), or sulfasalazine (Azulfidine); monoamine oxidase inhibitor (MAOI) such as isocarboxazid (Marplan), tranylcypromine (Parnate) or phenelzine (Nardil); beta-blocker such as propranolol (Inderal), atenolol (Tenormin), acebutolol (Sectral), metoprolol (Lopressor) and others; diuretic (water pill) such as hydrochlorothiazide (HCTZ, Hydrodiuril), chlorothiazide (Diuril) and others; steroid medicine such as prednisone (Deltasone, Orasone, others), methylprednisolone (Medrol, others), prednisolone (Prelone, Pediapred, others) and others; phenothiazine such as chlorpromazine (Thorazine), fluphenazine (Prolixin, Permitil), prochlorperazine (Compazine), promethazine (Phenergan) and others; phenytoin (Dilantin); isoniazid (Nydrazid); prescription, over-the-counter, or herbal cough, cold, allergy or weight loss medications.

Avoid alcohol.

Do not stop taking Glucotrol suddenly.

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Saxagliptin + metformin was associated with fewer patients reporting hypoglycemia and fewer and less severe hypoglycemic events in those experiencing hypoglycemia compared with glipizide + metformin. ClinicalTrials.gov registration number: NCT00575588.

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The anti-diabetics were isolated from equine plasma and urine by liquid-liquid extraction with 1,2-dichloroethane at acidic pH, and analysed by LC-MS-MS in the positive electrospray ionisation mode. Separation of 10 anti-diabetic drugs was achieved with a reversed phase C8 column using a mixture of aqueous ammonium formate (pH 3.0, 10 mM) and methanol as the mobile phase.

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The emerging new fixed dose combination of metformin hydrocholride (HCl) as sustained release and glipizide as immediate release were formulated as a bilayer matrix tablet using hydroxy propyl methyl cellulose (HPMC) as the matrix-forming polymer, and the tablets were evaluated via in vitro studies. Three different grades of HPMC (HPMC K 4M, HPMC K 15M, and HPMC K 100M) were used. All tablet formulations yielded quality matrix preparations with satisfactory tableting properties. In vitro release studies were carried out at a phosphate buffer of pH 6.8 with 0.75% sodium lauryl sulphate w/v using the apparatus I (basket) as described in the United States Pharmacopeia (2000). The release kinetics of metformin were evaluated using the regression coefficient analysis. There was no significant difference in drug release for different viscosity grade of HPMC with the same concentration. Tablet thus formulated provided sustained release of metformin HCl over a period of 8 hours and glipizide as immediate release.

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Simultaneously administered magnesium hydroxide or sodium bicarbonate can increase the rate and extent of absorption of non-micronized glibenclamide and glipizide. To clarify the mechanism of this interaction we have studied the effect of pH on the dissolution of two different formulations of glibenclamide (micronized and non-micronized) and one formulation of glipizide. One tablet of each sulphonylurea preparation was placed in a dissolution chamber containing continuously mixed dissolution medium at pH 2, pH 6 or pH 9; 5 mL of the medium was replaced every 2 min. The amount of glibenclamide dissolved from the non-micronized formulation within 2 h, was 1.2, 4.5 and 76% at pH 2, pH 6 and pH 9, respectively (P < 0.01), whereas 21, 29 and 100% was dissolved from the micronized formulation (P < 0.01). The amount of glipizide dissolved within 2 h at pH 2, pH 6 and pH 9 was 3.9, 24 and 92%, respectively (P < 0.01). We conclude that the elevated pH of the gastric contents is the most likely explanation for the interactions previously demonstrated between antacids and sulphonylureas after their concomitant ingestion.

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To examine whether initiation of fibrates or statins in sulfonylurea users is associated with hypoglycaemia, and examine in vitro inhibition of cytochrome P450 (CYP) enzymes by statins, fenofibrate and glipizide.

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The Tmax (time to maximal plasma concentration) of LA administered as CRLA was 1.25 hours and was approximately 2.5-fold longer in comparison with the Tmax for QRLA (Tn,5X = 0.5 hour; P<0.02). No severe side effects or changes in either liver or kidney function or hematologic profiles were noted after the administration of CRLA. In 15 patients, the mean plasma fructosamine concentration was reduced from 313 to 283 micromol/L(P<0.05) after 12 weeks of treatment with CRLA.

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Rheological studies were made on the blood of 12 diabetic patients after a period of poor diabetic control (HbA1 12.6 +/- 0.7% (mean +/- SD); mean home capillary blood glucose level 11.7 +/- 1.2 mmol/l), and after at least three months of improved control (HbA1 9.1 +/- 0.4%, p < 0.01; mean home capillary blood glucose level 9.2 +/- 0.6 mmol/l). There were significant decreases in plasma fibrinogen levels (4.1 +/- 0.6 to 3.7 +/- 0.6 g/l, p < 0.01), plasma viscosity (1.31 +/- 0.1 to 1.25 +/- 0.04, p < 0.001), and whole blood viscosity at low (22.8 +/- 2.7 to 20.2 +/- 2.9, p < 0.01) and high shear rates (3.4 +/- 0.2 to 3.1 +/- 0.2, p < 0.01). Ten diabetics with clinically evident complications were matched with diabetics of similar age, sex, duration and current control of diabetes. There were no significant differences in plasma or whole blood viscosities between the two groups. Hyperviscosity in diabetes seems strongly related to hyperglycaemia and to be influenced by the quality of diabetic control.

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The present study was aimed to investigate the role of plasma glucose concentration as a phenotypic marker and to study the frequency distribution of CYP2C9 genetic variants in Gujarat state diabetic population. One hundred and nine unrelated diabetes mellitus patients treated with sulfonylureas were genotyped for CYP2C9*2 and CYP2C9*3 alleles. Their pre- and posttreatment postprandial blood glucose levels were recorded and mean glucose drop per milligram of drug values were calculated and further used as an index for phenotypic correlation. The frequencies of CYP2C9*1, CYP2C9*2 and CYP2C9*3 alleles in the Gujarat state diabetic population were 0.84, 0.07 and 0.09, respectively. The distribution of CYP2C9*1/*1, CYP2C9*1/*2, CYP2C9*1/*3, CYP2C9*2/*2, CYP2C9*2/*3 and CYP2C9*3/*3 genotypes were 0.73, 0.08, 0.13, 0.0, 0.06 and 0.0, respectively. Patients with CYP2C9*1/*2 genotype did not show any significant difference in the mean glucose drop per milligram of drug values when compared with wild-type patients in glipizide-treatment group. Patients with CYP2C9*1/*3 genotype showed greater mean glucose drop per milligram of drug values than patients with CYP2C9*1/*1 wild-type genotype for both glipizide and glimepiride while patients with CYP2C9*2/*3 genotype showed greater drop than patients with CYP2C9*1/*1 genotype only in the glipizide-treatment group. The presence of CYP2C9*3 allele significantly affected plasma glucose drop per milligram of drug values in patients taking glipizide and glimepiride, while effects of CYP2C9*2 allele were insignificant. Further studies are needed to confirm the effects of CYP2C9*2 allele on plasma glucose drop per milligram of drug values. However, plasma glucose concentration is a complex physiological marker that cannot be used to establish perfect genotype-phenotype correlation. Hence studies exploring robust phenotypic markers must be initiated.

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A total of 900 patients with T2DM were enrolled in the study from four community health service centers in Beijing and followed up for one year. The following data were collected and analyzed, including patients characteristics, the proportion of patients with glycosylated hemoglobin A1c (HbA1c) less than 7% and the coverage rate of the hypoglycemic agents.

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We searched Medline and Embase from inception to June 11, 2014, to identify controlled studies reporting the risk of all-cause mortality, cardiovascular-related mortality, or myocardial infarction for at least two sulfonylureas. We examined differences in cardiovascular event risk among sulfonylureas with random effects models for direct pairwise comparisons and network meta-analyses to incorporate direct and indirect data.

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The objective of this study was to measure the serum insulin and C-peptide concentrations among diabetic patients known to be taking sulfonylurea agents who presented to the emergency department with hypoglycemia thought to be due to therapeutic usage as opposed to overdose. A recently published systematic review of 22 articles involving 76 patients with sulfonylurea-induced hypoglycemia (glucose <49 mg/dL) resulting from accidental ingestion or intentional overdose found that patients had an average serum insulin concentration of 3.9 μIU/mL or higher and an average serum C-peptide concentration of 1.4 ng/mL or higher.

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Compression coating, which presents some advantages like short manufacturing process and non-solvent residue over liquid coating, has been introduced to the oral administration systems for decades. The purpose of this study was to design a zero-order release of compression-coated tablets using hydroxypropylcellulose (HPC) as the coating layer and glipizide which was solubilized by manufacturing the inclusion complex of β-cyclodextrin as a model drug. The effects of the weight ratio of drug and the viscosity of HPC on the release profile were investigated by "f2" factor with Glucotrol XL(®). The uptake and erosion study, the correlation coefficient (R) and the exponent (n) were used as indicators to justify drug release mechanism. Bioavailability in vivo was determined by administering the compression-coated tablets to rabbits in contrast with Glucotrol XL(®). It was found that the formulation presented a well zero-order behavior at the weight ratio of drug 11:14 (core:layer) and the combination of HPC-L (8.0 mPa s) and HPC-M (350 mPa s) (8:9), with the "f2" of 66.90. The mechanism for zero-order release of these compression-coated tablets was solvent penetration into the dosage form and drug dissolution from the erosion of the gelled HPC matrix. The parameter AUC0-∞ of the compression coated tablets and the market tablets were 37,255.93±1474.08 h ng/ml and 43265.40±1015.28 h ng/ml, while the relative bioavailability was 87.66±1.56%. These studies demonstrate that the designed compression-coated tablets may be a promising strategy for peroral controlled release delivery system of water-insoluble drugs.

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Glipizide is an oral antidiabetic drug that has been used in the treatment of post-transplant diabetes mellitus (PTDM). However, a published case report has indicated a possible interaction of glipizide with cyclosporine (CsA) pharmacokinetics in two renal transplant (tx) patients. The aim of this open prospective study was to investigate whether glipizide interacts with CsA pharmacokinetics in renal tx patients with PTDM.

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glucotrol 5 mg 2016-11-05

Forty-three patients with type 2 diabetes and glycosylated haemoglobin (HbA1c) > 8.9% were randomized to either improved glycaemic control (IC) n = 21 or usual glycaemic Glucovance 850 Mg control (UC) n = 22 for 20 weeks. Using high-resolution B-mode ultrasound, brachial artery flow-mediated dilatation (FMD) and glyceryl trinitrate-mediated dilatation (GTN-D) were measured at baseline and 20 weeks later.

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Initiation of OD pharmacotherapy results in better adherence and persistence compared with a BID regimen, despite a greater daily pill burden in the OD cohort. These data suggest that dosing Inderal Generic frequency exerts a greater impact on patient adherence and persistence than number of tablets per dose.

glucotrol medicine 2017-01-25

The detection of diabetic metabolism disorders raises problems in forensic practice and sudden death with a subsequent negative autopsy finding is a common problem. In the case of an unclear hypoglycaemia, the detection of oral antidiabetics allows the differentiation of hypoglycaemia due to oral antidiabetics from that due to other reasons (insulin-induced, insulinoma). The development of an electrospray ionisation (ESI) liquid chromatography-tandem mass spectrometry (LC-MS/MS) procedure for the simultaneous identification and quantification of oral antidiabetics of the sulfonylurea, the glinide, the thiazolidinedione and the gliptin types in human plasma is desired. The following analytes were included: glimepiride, glibenclamide, gliquidone, glibornuride, glisoxepide, glipizide and gliclazide (sulfonylurea type), nateglinide and repaglinide (glinide type), rosiglitazone and pioglitazone (thiazolidinedione type) and the dipeptidyl peptidase Avapro Prices inhibitors vildagliptin, sitagliptin and saxagliptin. After a liquid-liquid extraction with tert-butyl methyl ether at two pHs, the oral antidiabetics were separated with fast gradient elution over a C(8) column. Identification of the oral antidiabetics was achieved by two specific ion transitions of each analyte in multiple reaction monitoring mode. Quantification was performed by referring the most intense ion transition peak areas to peak areas of the ion transitions of deuterated oral antidiabetics (hydroxytolbutamide-d(9) for the sulfonylureas, repaglinide-ethyl-d(5) for the glinides, pioglitazone-d(4) for the thiazolidinediones and vildagliptin-d(3) for the gliptins). The assay was validated according to international guidelines. The LC-MS/MS assay allows the simultaneous identification of 14 oral antidiabetics and quantification of 11 oral antidiabetics in plasma in the ESI mode in a single run. Linearity is shown up to overdose concentrations. The limits of detection with a signal-noise-ratio greater than 3 were below 1 ng/ml for all analytes. Recoveries ranged from 78 to 105%; for vildagliptin and saxagliptin recoveries were worse (45%) owing to their hydrophilic character. Intraday and interday precision and accuracy were below 20% for 11 drugs at three concentrations. For the gliptins, several validation parameters were out of range and, therefore, quantitatively this method is inappropriate.

generic glucotrol xl 2016-08-20

We found elevated adjusted overall ORs for glyburide-fenofibrate (OR 1.84, 95% CI 1.37, 2.47) and glyburide-gemfibrozil (OR 1.57, 95 Omnicef With Alcohol % CI 1.25, 1.96). The apparent risk did decline over time as might be expected from a pharmacokinetic mechanism. Fenofibrate was a potent in vitro inhibitor of CYP2C19 (IC50 = 0.2 μm) and CYP2B6 (IC50 = 0.7 μm) and a moderate inhibitor of CYP2C9 (IC50 = 9.7 μm). The predicted CYP-based AUCRs for fenofibrate-glyburide and gemfibrozil-glyburide interactions were only 1.09 and 1.04, suggesting that CYP inhibition is unlikely to explain such an interaction.

glucotrol dosage administration 2015-01-05

We have previously shown that brain adenosine A1 receptors and nitric oxide (NO) play an important role in ethanol (EtOH)-induced cerebellar ataxia (EICA Imodium Dosage Directions ) through glutamate/NO/cGMP pathway. I now report possible modulation of EICA by the cerebellar NO/cGMP/K(ATP) pathway.

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To determine the risk of hypoglycemia and associated costs in older patients prescribed glipizide or glyburide Shallaki Tablets Himalaya who fill a prescription for an antimicrobial drug.

glucotrol xl dosage 2016-07-20

The mechanism by which glibenclamide regulates mechanically activated atrial natriuretic peptide (ANP) secretion was investigated using isolated perfused rat atria. A reduction in atrial pressure from an experimentally imposed distending pressure stimulated the secretion of ANP and caused concomitant translocation of extracellular fluid (ECF) into the atrial lumen. The activation of ANP secretion and ECF translocation were closely correlated with atrial volume changes and the increase in ANP secretion was a function of the ECF translocation. Glibenclamide (1, 10, 100 microM), an ATP-sensitive K+ (K+ATP) channel blocker, had no effect on the basal secretion of ANP, suppressed the stimulation of stretch-activated ANP secretion in a dose-dependent manner, but not the translocation of the ECF. Glipizide (100 microM) and tolbutamide (100 microM), other K+ATP channel blockers, had similar effects to those of glibenclamide. Suppression by glibenclamide (100 microM) of the stretch-induced ANP secretion was not observed in atria that had been pretreated with pinacidil (200 microM), an ATP-sensitive K+ channel opener: pinacidil alone had no effect on ECF translocation and ANP secretion. Furthermore, blocking Ca2+ influx by using the Viagra Typical Dosage Ca2+ channel blocker diltiazem (10 nM), or a Ca2+-depleted medium prevented the suppression of stretch-induced ANP secretion by glibenclamide. In other experiments, atrial distension produced a slight membrane depolarization of cardiomyocytes; this was accentuated in the presence of glibenclamide. Furthermore, in single cardiomyocytes, glibenclamide increased the intracellular Ca2+ concentration ([Ca2+]i) in a dose-dependent manner. From these results, we suggest that glibenclamide suppresses atrial release of ANP by blocking K+ATP channels and increasing Ca2+ influx and that the K+ATP channels are associated with the regulation of the mechanically activated ANP secretion from the atria.

glucotrol drug 2016-08-04

We screened 400 drugs frequently co-prescribed with the secretagogues as candidate interacting precipitants. We first predicted the drug-drug interaction potential based on the pharmacokinetics of each secretagogue-precipitant pair. We then performed pharmacoepidemiologic screening for each secretagogue of interest, and for metformin as a negative control, using an administrative claims database and the self-controlled case series design. The overall rate ratios (RRs) and those for four predefined risk periods were estimated Periactin Migraine Reviews using Poisson regression. The RRs were adjusted for multiple estimation using semi-Bayes method, and then adjusted for metformin results to distinguish native effects of the precipitant from a drug-drug interaction.

glucotrol glipizide dose 2016-06-19

To review the efficacy and safety of sitagliptin in combined therapies (as add on or initial combination treatment) in type 2 diabetes Duricef Generic .

glucotrol drug class 2017-07-16

Significantly higher mortality was associated with glibenclamide, glipizide and rosiglitazone use compared with metformin, and with glipizide use compared with rosiglitazone or glibenclamide. The potential for residual confounding by indication should be considered in interpreting these results.