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Amaryl (Glimepiride)
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Amaryl

Generic Amaryl is the medication of high quality, which is taken in treatment of type 2 diabetes. Generic Amaryl is acting by stimulating the pancreas to produce more insulin. It is sulfonylureas.

Other names for this medication:

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Glucophage, Actos, Avandia, Glucovance, Precose, Micronase, Glycomet

 

Also known as:  Glimepiride.

Description

Generic Amaryl is the medication of high quality, which is taken in treatment of type 2 diabetes.

The target of this perfect remedy is struggle against type 2 diabetes.

Amaryl is also known as Glimepiride, Diapride, Amyline, Euglim.

Generic Amaryl is acting by stimulating the pancreas to produce more insulin. It is sulfonylureas.

Generic name of Generic Amaryl is Glimepiride.

Brand name of Generic Amaryl is Amaryl.

Dosage

Take Generic Amaryl tablets orally with breakfast or the first big meal of the day.

Do not crush or chew it.

Take Generic Amaryl at the same time once a day with water.

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

Overdose

If you overdose Generic Amaryl and you don't feel good you should visit your doctor or health care provider immediately.

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 Amaryl 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 Generic Amaryl if you are allergic to Generic Amaryl components.

Do not take Generic Amaryl if you're pregnant or you plan to have a baby, or you are a nursing mother. Generic Amaryl can ham your baby.

It can be dangerous to use Generic Amaryl if you suffer from or have a history of heart disease.

Avoid alcohol.

Do not stop taking Generic Amaryl suddenly.

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Sulfonylureas are widely used to stimulate insulin secretion in type 2 diabetic patients because they close adenosine triphosphate-sensitive potassium (K(ATP)) channels in the pancreatic beta-cell membrane. This action is mediated by binding of the drug to the sulfonylurea receptor (SUR1) subunit of the channel. K(ATP) channels are also present in a range of extrapancreatic tissues, but many of these contain an alternative type of SUR subunit (SUR2A in heart and SUR2B in smooth muscle). The sulfonylurea-sensitivity of K(ATP) channels containing the different types of SUR is variable: gliclazide and tolbutamide block the beta cell, but not the cardiac or smooth muscle types of K(ATP) channels with high affinity. Glibenclamide and glimepiride, on the other hand, block channels containing SUR1 and SUR2 with similar affinity. The reversibility of the different sulfonylureas also varies. Tolbutamide and gliclazide produce a reversible inhibition of Kir6.2/SUR1 and Kir6.2/SUR2 channels, whereas glibenclamide has a reversible effect on cardiac, but not beta-cell, K(ATP) channels. In this article, we summarize current knowledge of how sulfonylureas act on K(ATP) channels containing the different types of sulfonylurea receptor, and discuss the implications of these findings for the use of sulfonylureas in the treatment of diabetes mellitus.

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Eight Phase III clinical studies compared the efficacy and safety of liraglutide to other monotherapies or combinations. Liraglutide as monotherapy in doses of 0.9 mg or above showed a significantly superior reduction in HbA1C compared to monotherapies with glimepiride or glyburide. When liraglutide was used as add-on therapy to glimepiride in doses of 1.2 mg or above, the reduction of HbA1C was greater than that in the combination therapy of glimepiride and rosiglitazone. However, liraglutide as add-on therapy to metformin failed to show benefit over combination of metformin and glimepiride. Triple therapy of using liraglutide in addition to metformin plus either glimepiride or rosiglitazone resulted in additional benefit in HbA1C reduction. Most common adverse events were gastrointestinal disturbance such as nausea, vomit, diarrhea, and constipation. During the eight clinical studies, six cases of pancreatitis and five cases of cancer were reported in liraglutide arm, whereas there was one case of each of pancreatitis in exenatide and glimepiride arms, respectively, and one case of cancer in metformin plus sitagliptin arm.

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Eight hearts underwent IPC consisting of two cycles of 5 min global ischemia and reperfusion. Six hearts received a 5-min infusion of 10 microM glimepiride, six hearts received a 5-min infusion of 50 microM glimepiride, and seven hearts received a 5-min infusion of 10 microM glibenclamide before IPC. Seven hearts received a 5-min infusion of the selective mitochondrial K(ATP) channel opener diazoxide (50 microM). Other hearts received a 5-min infusion of 10 microM glimepiride (n = 6), 50 microM glimepiride (n = 6), or 10 microM glibenclamide (n = 7) before diazoxide. Seven hearts served as a control. All groups then were subjected to 1 h of regional ischemia, followed by 1 h of reperfusion. LV pressures, monophasic action potential duration (APD(50)), and infarct size were measured.

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Baseline HbA1c correlated to Δ HbA1c (r (2) = 0.36, slope = -0.54 [95% CI -0.55, -0.53; p < 0.0001]) for both treatments. With sulfonylureas, the slope of the correlation was steeper in the observational study than in RCTs (interaction coefficient = -0.327, p < 0.001), whereas for vildagliptin, the slope was virtually identical in the observational study and the RCTs (interaction coefficient = 0.024, p = 0.175). For any given baseline HbA1c, Δ HbA1c with sulfonylureas was smaller in real life than in RCTs, whereas Δ HbA1c with vildagliptin was the same.

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We demonstrate that glibenclamide and glimepiride modulate FXR activation in a reporter-gene assay and induce FXR target genes in HepG2 cells. Within the docking experiments and molecular dynamics simulation, we found glibenclamide interacting with the ligand-binding domain of FXR and with helix 12.

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DPP-4-i are an additional choice in the group of anti-hyperglycemics. Their principal advantage is a low incidence of hypoglycemia, making these agents desirable in patients such as the elderly and those with cardiac disease. Several large trials have hinted at less cardiac risk with DPP-4-i than with sulfonylureas. The CAROLINA Trial comparing linagliptin and glimepiride may provide a conclusive answer to this question.

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Two review authors independently selected trials, assessed risk of bias, extracted data and evaluated overall quality of the evidence using GRADE. We summarised data statistically if they were available, sufficiently similar and of sufficient quality. We performed statistical analyses according to the statistical guidelines in the Cochrane Handbook for Systematic Reviews of Interventions.

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To examine comparative efficacies of adjunctive therapy with insulin in subjects with type 2 diabetes manifesting lapse of glycemic control while receiving various individual sulfonylurea drugs.

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Altogether, 93 episodes of SH were registered, 37 on glimepiride and 56 on glibenclamide. The characteristics of the glimepiride- versus glibenclamide-induced SH were as follows: initial blood glucose 1.9+/-0.66 mmol/l versus 1.8+/-0.89 mmol/l, P=0.17; age 77+/-11.2 years versus 78+/-9.6 years, P=0.35; HbA1c 5.4+/-0.7% versus 5.2+/-0.9%, P=0.18; creatinine clearance 38+/-23 ml/min versus 54+/-32 ml/min, P=0.005; co-medication 6.2.+/-3 versus 3.6+/-3 preparations, P< 0.0001. Even very low doses of glimepiride (0.5 mg) and glibenclamide (0.88 mg) were associated with SH. Prolonged hypoglycaemia requiring more than 12 h i.v. glucose administration occurred in 8 of 37 of the glimepiride-treated subjects and 5 of 56 of those on glibenclamide. Prolonged hypoglycaemia necessitated infusion of 308+/-256 g (104-862 g) i.v. glucose over 43+/-16 h (24-64 h) in glimepiride-treated patients compared with 168+/-98 g (66-300 g) over 33+/-28 h (14-80 h) in glibenclamide-treated patients. Impaired renal function was present in 11 of 13 of all patients with prolonged hypoglycaemia and impaired liver function in 1 of 13.

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The studies were performed on healthy male Wistar rats with a body mass of 220+/-30 g, fed with LSM-type standard chow, and given water ad libitum. Transient or prolonged hyperglycemia was induced by intraperitoneal administration of streptozotocin. Blood samples were taken from the right heart ventricle to heparinized test tubes and centrifuged for 10 minutes at 700 i. g. Plasma was collected and the glucose level was determined. From each animal 1 g of skeletal muscle and 1 g of liver were collected as well, placed in liquid nitrogen and stored until determination of the affinity and number of receptors.

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Despite the current guideline's recommendation of a timely stepwise intensification therapy, the "clinical inertia", termed as the delayed treatment intensification, commonly exists in the real world, which may be partly due to the relatively little substantial evidence and no clear consensus regarding the efficacy and safety of triple oral agents in patients inadequately controlled with dual therapy. In this clinical trial performed in 237 centers in China, 5,535 type 2 diabetic patients inadequately controlled by previous therapies were treated with a stable metformin/sitagliptin dual therapy for 20 weeks. The patients who did not reach the glycated hemoglobin A1c (HbA1c) goal were then further randomized into glimepiride, gliclazide, repaglinide, or acarbose group for an additional 24-week triple therapy. A mean HbA1c reduction of 0.85% was observed when sitagliptin was added to the patients inadequately controlled with metformin in 16 weeks. Further HbA1c reductions in the 24-week triple therapy stage were 0.65% in glimepiride group, 0.70% in gliclazide group, 0.61% in repaglinide group, and 0.45% in acarbose group. The non-inferiority criterion for primary hypotheses was met for gliclazide and repaglinide, but not for acarbose, compared with glimepiride, when added to metformin/sitagliptin dual therapy. The incidences of adverse events (AEs) were 29.2% in the dual therapy stage and 30.3% in the triple therapy stage. Metformin/sitagliptin as baseline therapy, with the addition of a third oral antihyperglycemic agent, including glimepiride, gliclazide, repaglinide, or acarbose, was effective, safe and well-tolerated for achieving an HbA1c <7.0% goal in type 2 diabetic patients inadequately controlled with previous therapies. The timely augmentation of up to three oral antihyperglycemic agents is valid and of important clinical benefit to prevent patients from exposure to unnecessarily prolonged hyperglycemia.

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Improved efficacy and greater compliance were observed in response to treatment with glimepiride compared with acarbose, in patients with Type 2 diabetes.

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This large-scale study, conducted under conditions approximating to current medical practice, confirms that glimepiride has a favourable risk-benefit ratio in type 2 diabetes mellitus. Diabetes duration and previous treatment with OADs reduced the likelihood of being a responder to treatment.

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The development and progress of antidiabetic drugs (e.g., insulin preparations and hypoglycemic drugs) are retrospectively investigated in Japan. Their influences on the treatment of diabetes mellitus (DM) and its epidemiological aspects are also discussed. 1) Insulin preparations: Insulin was introduced for DM therapy in 1925, two or three years after its discovery in Canada. The preparations were raw extracts of bovine or porcine pancreas. These did not prevail widely in Japan because of the low incidence of DM before World Wan II. After the war, a shortage of mammalian materials compelled the use of fish pancreatic tissues such as bonito and/or tuna for insulin production. Insulin infection, so-called regular insulin, was first promoted in the 6th "Pharmacopoeia Japonica" (JP6) in 1951 and has been maintained to the present edition (JP14, 2001). Although depot-type insulin preparations were developed in the USA and Europe during the war, the introduction of those preparations to Japan was delayed until 1951, when Protamine zinc insulin appeared. Globin zinc insulin and Isophane insulin were introduced for clinical use in 1952 and 1955, respectively. These were also adopted for JP7 (1961). Biphasic-type insulin, which has a rapid onset and long duration of activity, appeared in 1965. Purified preparations from bovine or porcine sources have been available since 1980, which might be a strong reason for the decrease in insulin allergy. Insulin from animal origin has been supplied for almost 60 years since its discovery. Amino acid sequences of insulins from various species of animals were determined by the pioneering studies of Sanger and his associates. Human insulin, which differs from porcine insulin by only one amino acid, was produced by Novo researchers in 1982 using a semi-synthetic method. Then the Lilly group soon succeeded in obtaining human insulin by recombinant DNA technology in the same year. Both products were introduced to Japan in 1985, and the recombinant products prevailed throughout the 1990s. Human insulin analogues (i.e., Insulin lispro and Insulin aspart) appeared in 2001. These are applied for after-meal glycosmia owing to their ultrarapid onset of activity. Self-injection by DM patients was legalized in 1981. To make the infection technique sure and easy, cartridge (pen-type) and disposable kit-type needles were devised in the 1990s. 2) Oral hypoglycemic drugs: Instead of the exclusive parenteral usage of insulins, there was also demand for oral dosage forms. The first of the sulfonyrlurea (SU) group, BZ-55, was used for DM clinically in 1955 in Germany. But it was soon withdrawn because of its antibacterial action. This led to the development of various SU groups. Tolbutamide (1956), chlorpropamide (1959), acetohexamide (1964) and tolazamide (1961) were introduced to Japan as first-generation SUs. Then glyclopyramide (Kyorin, 1965), glybenclamide (1971), gliclazide (1984) and glimepiride (1999) appeared as the second-generation SUs. These were used orally for Type 2 diabetes. Biguanide (BG) group, phenformin HC1 (1959), metformin HC1 (1961) and buformin HC1 (1961) had also been in use by oral treatment of Type 2 diabetes. SU appears to act by increasing the sensitivity of b-cells, which secrete insulin. BG probably exerts by increasing glucose transport across the membranes of target organs. 3) New types of antidiabetic drugs: a-Glucosidase inhibitors (i.e., acarbose: Bayer, 1993; and voglibose: Takeda, 1994) act on hyperglycemia after meals by decreasing glucose absorption. Thiazolidinedione compounds, such as troglitazone (Sankyo, 1995) and pioglitazone HC1 (Takeda, 1994) act by increasing the insulin sensitivity of the target tissues. These are useful for Type 2 DM patients when SUs are ineffective. Nevertheless, troglitazone was discontinued in 2000 due to severe liver damage. Nateglinide (Ajinomoto Co., 1999), which is a D-phenylalanine derivative acting similar to SUs, is useful orally for after-meal hyperglycemia of Type 2 diabetes. Epalrestat (Ono Yakuhin Co., 1992) is effective for diabetic neuropathy by reducing the formation of sorbitol. These anti-DM drugs were recently studied and developed in Japan. 4) The Japan Diabetes Society proposed a guideline on diagnostic criteria and treatment of diabetes mellitus (DM) in 1999 and revised it in 2002. DM is classified as insulin-dependent DM (Type l) and non-insulin dependent DM (Type 2). Type 1, juvenile onset DM, requires insulin therapy to prevent ketosis and to sustain life. Treatment of type 2, adult onset DM, is recommended as a step-by-step method, starting with dietary-exercise therapy, followed by oral hypoglycemic drugs and then insulin therapy. DM patients with complications should have a therapy devised to match their circumstances. 5) Epidemiological aspects: The mortality rate of DM compared to the time of drug appearance was traced from 1920 to 2000. The curve goes down slowly in the time frame of World War II, but rises from 1950 to 1970. The elevation could not be suppressed by the appearance of SUs, BGs or improved insulin preparations. The curve runs flat from 1980 to 1990, which might be related to the use of purified insulin or human insulin therapy. The mortality rate of DM indicates that death by hyperglycemic coma and other deaths resulting from complications are excluded. The survey of the principal cause of death by DM during the period of 1981-1990 indicates that the death rate due to hyperglycemic coma is only 1.7% of the total deaths caused by DM. The effect of drug therapy on all of the death resulting from DM is not detected. Hospital visitation and admission rates of the DM patients have been recorded since 1952 in Japan. This curve is rising continuously, and none of the antidiabetic drugs has been able to suppress it. These data show that the antidiabetic drugs relieve DM symptoms through their effective hypoglycemic actions, but that they cannot suppress the mortality rate of DM. It is possible that none of the drugs currently available can suppress the increasing tendency of DM patients.

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Canagliflozin 100 and 300 mg provided durable glycemic improvements and body weight reductions compared with glimepiride over 104 weeks. At Week 52, the proportion of patients who achieved reductions in both HbA1c and body weight was 72.4% with canagliflozin 100 mg, 78.5% with canagliflozin 300 mg, and 26.8% with glimepiride; similar results were observed at Week 104 (65.5%, 71.1%, and 26.8% with canagliflozin 100 and 300 mg and glimepiride, respectively). The AE profile of canagliflozin was comparable to that observed in previous studies, with increased incidence of AEs related to the mechanism of SGLT2 inhibition (e.g., genital mycotic infections, urinary tract infections, and osmotic diuresis-related AEs) and a low risk of hypoglycemia.

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As assessed by the composite outcome of HbA1c <7%, no hypoglycaemia and no weight gain, liraglutide was clearly superior to the other commonly used therapies. However, the long-term clinical impact of this observation remains to be shown.

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The addition of sitagliptin 100 mg/day produced a statistically significant reduction in mean HbA1c level (mean HbA1c reduction of 0.99±0.85%, P<0.01). In the group taking a combination of sitagliptin and metformin (n=143, initial mean HbA1c level=7.48%), the reductions in HbA1c, 2-hour postprandial glucose, and fasting glucose levels were 0.72±0.76% (P<0.01), 47±65 mg/dL (P<0.01), and 15±44 mg/dL (P<0.01), respectively. In the group taking a combination of sitagliptin, glimepiride, and metformin (n=125, initial mean HbA1c level=8.42%), the reductions in HbA1c, 2-hour postprandial glucose, and fasting glucose levels were 1.09±0.86% (P<0.01), 62±64 mg/dL (P<0.01), and 31±45 mg/dL (P<0.01), respectively. In the group taking a combination of sitagliptin, glimepiride, metformin, and α-glucosidase inhibitor (n=63, initial mean HbA1c level=9.19%), the reductions in HbA1c, 2-hour postprandial glucose, and fasting glucose levels were 1.27±0.70% (P<0.01), 72±65 mg/dL (P<0.01), and 35±51 mg/dL (P<0.01), respectively. In the group that had previous hypoglycemic events and that changed from glimepiride to sitagliptin, HbA1c level did not change but fasting glucose increased significantly (14±29 mg/dL, P<0.01).

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Pharmacodynamic profiles for plasma glucose and insulin showed no statistically significant differences among genotype groups, and parameters were not different from one another. There were no association of the KCNJ11, NOS1AP, TCF7L2 and ABCC8 gene polymorphisms and the efficacy of glimepiride.

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To observe the intervention effects of electroacupuncture at "Yishu" (EX-B 3) on rats with type-2 diabetes mellitus (T2DM), so as to provide experiment references for acupuncture to treat T2DM.

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We used the indirect method for estimating the rate of prevalence of diabetes based on antidiabetic drug in the Madrid Community. We studied the consumption or oral antidiabetics (OH) and insulin (IN) in all the Madrid Community Area from 1996 to 2002. To make consumption uniform we used the daily doses/1,000 inhabitants/day (DHD). The total consumption was obtained using the official billing data and the annual population data provided by the "Institute Madrileño de Salud".

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These results confirm earlier reports that insulin glargine provides superior glycemic control with less hypoglycemia and demonstrates that these benefits are consistent between different ethnicities.

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The GAME regimen provides long-term glycaemic control as well as stabilization of body weight in about 60% of type 2 patients presenting with secondary failure.

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Genotyping for the CYP2C9*2 and CYP2C9*3 alleles currently appears to have no clinical implications for dosing of sulfonylureas in primary care patients with Type 2 diabetes mellitus.

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HbA (1c) change was significantly greater in the BIAsp 30 plus met group than the glarg plus glim group (between-group difference: -0.5% (95% CI: -0.8; -0.2); P=0.0002). Mean prandial plasma glucose increment was significantly lower for BIAsp 30 plus met compared with glarg plus glim: 1.4+/-1.4 mmol/l vs. 2.2+/-1.8 mmol/l; P=0.0002. During the maintenance phase (weeks 6-26), one major hypoglycemic episode occurred in each group; 20.3% and 9% of patients experienced minor hypoglycemic episodes in the BIAsp 30 plus met and glarg plus glim groups, respectively ( P=0.0124). At end-of-trial, mean daily insulin doses were 0.40 U/kg BIAsp 30 and 0.39 U/kg glarg. Glarg plus glim-treated patients experienced significant weight gain of 1.5 kg (95% CI: 0.84; 2.19; P<0.0001). Weight change with BIAsp 30 plus met of +0.7 kg was not statistically significant (95% CI: -0.07; 1.42; P=0.0762).

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There was no significant difference between the 2 patient groups for glimepiride in terms of mean peak concentration (C(max)) (p = 0.0807), time to reach C(max) (t(max)) (p = 0.9916), AUC(0-24) (p = 0.2609), AUC(0- infinity ) (p = 0.1275), or terminal half-life (p = 0.3076). Mean t(max) values and relative total clearances for the 2 groups were also equivalent. Some differences were noted with respect to the pharmacokinetics of metabolites between the groups. In particular, over a 24-hour period, the morbidly obese group excreted statistically significantly greater amounts of MI (p = 0.0430) and MII (p = 0.0051) compared with the normal-weight group. However, none of the differences was considered clinically significant since these metabolites do not have meaningful pharmacologic activity.

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The aim of the study was to determine the influence of glimepiride on the binding kinetics of insulin with its skeletal muscle receptor in rats with transient and prolonged hyperglycemia induced by streptozotocin.

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Rg, Gm and Gli can all decrease blood glucose effectively in newly diagnosed T2DM patients, while Rg performs outstandingly in the aspects of improving early-phase insulin secretion, glucose excursion, postprandial lipids and 8-iso PGF(2alpha).

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The present study was undertaken to evaluate the antihyperglycemic, antihyperlipidemic and hepatoprotective effect of a traditional unani formulation "Qurs Tabasheer" in streptozotocin (STZ) induced diabetic wistar rats. Up till now no study was undertaken to appraise the efficacy of "Qurs Tabasheer" in the diabetic rats. Qurs Tabasheer is a unani formulation restraining preparations from five various herbs namely Tukhme Khurfa (Portulaca oleracea seed), Gule Surkh (Rosa damascena flower), Gulnar (Punica granatum flower), Tabasheer (Bambusa arundinasia dried exudate on node), Tukhme Kahu (Lactuca sativa Linn seed).

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amaryl 2mg tablet 2017-09-05

To compare mortality risks among type 2 diabetes (T2D) patients being treated with buy amaryl glibenclamide, gliclazide, or glimepiride.

glimepiride amaryl generic 2017-12-16

Serum IGF-I levels decrease in diabetes and insulin treatment restores IGF-I depletion significantly. And although less effective, treatment with glimepiride restores IGF- buy amaryl I levels significantly.

amaryl brand 2015-10-02

Liraglutide reduces bodyweight in patients with type 2 diabetes mellitus (T2DM buy amaryl ). This study aimed to investigate the mechanisms underlying this effect.

amaryl reviews 2016-10-31

The objective buy amaryl of the study was to estimate the most successful way of treating patients with type 2 diabetes mellitus.

amaryl overdose 2017-06-01

A 54-year-old Asian woman weighing 77 kg developed massive bilateral pleural effusion after receiving pioglitazone (30 mg QD) in combination with glimepiride 2 mg BID and metformin 500 mg TID. Despite treatment with furosemide (20 mg intravenously at 12-hour intervals for 4 days) and a decrease in weight from 77 to 72 kg, the effusion persisted. However, it began to decrease after pioglitazone was discontinued, and it had resolved completely when the patient was buy amaryl evaluated on follow-up 1 month later in the outpatient department.

amaryl pills 2017-06-14

The human transcription factor pregnane X receptor (hPXR) is a key regulator of enzyme expression, especially cytochrome P450 3A4 (CYP3A4). Due to the prominence of CYP3A4 in the elimination of many drugs, the development of high throughput in vitro models to predict the effect of drugs on CYP3A4 expression have increased. To better interpret and predict potential drug-drug interactions due to buy amaryl CYP3A4 enzyme induction, we evaluated 170 xenobiotics in a hPXR transactivation assay and compared these results to known clinical drug-drug interactions. Of the 170 xenobiotics tested, 54% of them demonstrated some level of hPXR transactivation. By taking into consideration cell culture conditions (solubility, cytotoxicity, appropriate drug concentration in media), as well as in vivo pharmacokinetics (therapeutic plasma C(max), distribution, route of administration, dosing regimen, liver exposure, potential to inhibit CYP3A4), the risk potential of CYP3A4 enzyme induction for most compounds reduced dramatically. By employing this overall interpretation strategy, the final percentage of compounds predicted to significantly induce CYP3A4 reduced to 5%, all of which are known to cause drug-drug interactions. Also, this is the first report that identifies several potent compounds that have the ability to transactivate hPXR that previously have not been identified, such as terbinafine, diclofenac, sildenafil, glimepiride, montelukast, and ticlopidine.

amaryl drug class 2016-10-25

Liraglutide has been shown to offer effective glycaemic control for patients with type 2 diabetes and is appropriate for use across the conventional continuum of care. Despite the sustained reductions in HbA(1c) , FPG and PPG levels achieved with liraglutide, rates of minor hypoglycaemia were generally low, although the risk increased when combined with buy amaryl a sulfonylurea. Liraglutide is therefore a promising new option for the treatment of type 2 diabetes.

amaryl tablets 2017-06-21

Our objective was to investigate the effects of genetic polymorphisms of cytochrome buy amaryl P450 (CYP) 2C9 on the pharmacokinetics of glyburide (INN, glibenclamide) and glimepiride, two widely used sulfonylurea antidiabetic drugs.

amaryl generic equivalent 2017-05-01

Since endogenous insulin secretion is more buy amaryl physiological than subcutaneous insulin injection, continuing glimepiride may remain beneficial, partly through enhancing insulin secretion, in individuals with a long duration of diabetes and basal-prandial insulin therapy.

amaryl dosage form 2017-12-27

Willingness to pay (WTP) for diabetes drug treatment was assessed by combining results from a recent WTP study with analysis of results from the Liraglutide Effect and Action in Diabetes (LEAD) programme. The LEAD programme included six randomised clinical trials with 3967 participants analysing efficacy and safety of liraglutide 1.2 mg (LEAD 1-6 trials), buy amaryl rosiglitazone (LEAD 1 trial), glimepiride (LEAD 2-3 trials), insulin glargine (LEAD 5 trial), and exenatide (LEAD 6 trial). The WTP survey used discrete choice experimental (DCE) methodology to evaluate the convenience and clinical effects of glucose lowering treatments.

amaryl buy online 2017-06-06

Glimepiride treatment as initial mono-therapy could effectively improve blood glucose control in type 2 diabetic patients, with a buy amaryl favorable safety profile. Lack of control group was the major limitation of this study. ClinicalTrial.gov identifier: NCT00908921.

amaryl tabs 2016-08-03

Considering the cost of acquiring a buy amaryl liquid chromatographic instrument in underdeveloped economies, the rising incidence of diabetes mellitus, the need to evaluate the quality performance of glimepiride generics, and the need for less toxic processes, this research is an imperative.

amaryl 30 mg 2016-05-26

Non-diabetic volunteers (age 38±2years, BMI 26±1kg/m(2)) were studied in a single-blind fashion during separate 2day randomized protocols consisting of 2h hyperinsulinemic (9pmol/kg/min) euglycemic (4.9±0.1mmol) and hypoglycemic (2.9±0.1mmol/L) clamps. Individuals received biologically equivalent doses of glimepiride (4mg) or glyburide (10mg) 1h prior to Cozaar 40 Mg each glucose clamp (n=11) as well as a control group of placebo studies. Glucose kinetics were calculated using D-Glucose-6-6d2.

amaryl 1mg tablets 2017-02-04

The overall incidence of non-fatal cardiovascular events was the highest for patients taking glyburide (169.1 per 1000 person-years Asacol Alcohol ), followed by for those taking glimepiride and metformin (95.2 and 49.1 per 1000 person-years, respectively). Compared with the adjusted hazard ratio for patients taking glyburide, the adjusted hazard ratio for those taking glimepiride was 0.52 (95% CI 0.40-0.69) and for those taking metformin was 0.31 (95% CI 0.24-0.40).

amaryl drug classification 2016-05-05

In patients with T2DM, Buy Kemadrin inadequately controlled on OADs, once-daily insulin glargine plus glimepiride is effective in improving metabolic control with a reduced incidence of nocturnal hypoglycemia compared with NPH insulin.

amaryl 40 mg 2016-07-20

This meta-analysis will include the randomized controlled trials (RCT) evaluating the efficacy of dapagliflozin as an add-on drug in treating T2D for >8 weeks with the outcome measures glycosylated hemoglobin (HbA1c), fasting plasma glucose (FPG) and body weight. Information of relevant RCTs will be retrieved from major databases including PubMed, Cochrane Library, Embase, ClinicalTrials.gov, and Google Scholar according to a pre-specified search strategy. Google and manual search will find other unpublished reports and supplementary data. Eligible RCTs will be selected according to pre-specified inclusion and exclusion criteria. Data will be extracted and input Coumadin 5 Pill into a pre-formatted spreadsheet. The Cochrane risk of bias tool will be used to assess the quality of the eligible RCTs. Meta-analysis based on the random-effects model will be conducted to compare the changes of HbA1c (%), FPG (mmol/L), and body weight (kg) between dapagliflozin arm and placebo arm. Publication bias will be evaluated with a funnel plot and the Egger's test. Heterogeneity will be assessed with the I2 statistics. Sensitivity analysis will be conducted on follow-up periods. The evidential quality of the findings will be assessed with the GRADE profiler.

amaryl 500 mg 2016-01-01

The incidence of type 2 diabetes mellitus (T2DM) among children and adolescents has been rising. This condition is associated with obesity, and it's prevalence is higher among minority or female youth. Lifestyle modification including diet and exercise is only successful in a small proportion of patients; therefore, pharmacotherapy approaches are needed to treat T2DM among youth. Currently, in the USA, only metformin and insulin are approved for the treatment of T2DM in children. However, several antihyperglycemic agents including exenatide, glimepiride, glyburide, liraglutide, pioglitazone, and rosiglitazone are also used off-label in this population. Moreover, a number of clinical trials are ongoing that are aimed at addressing the safety and efficacy of newer antihyperglycemic agents in this population. Little is known about the safety, efficacy, or pharmacokinetics of antihyperglycemic agents in children or adolescents. Our ability to predict the pharmacokinetics of these agents in youth is hampered first by the lack of information about the expression and activity of drug-metabolizing enzymes and transporters in this population and second by the Depression Medication Desyrel presence of comorbid conditions such as obesity and fatty liver disease. This article reviews the prevalence of obesity and T2DM in children and adolescents (youth). We then summarize published studies on safety and effectiveness of antihyperglycemic medications in youth. Drug disposition may be affected by age or puberty and thus the expression and activity of different pathways for drug metabolism and xenobiotic transporters are compared between youth and adults followed by a summary of pharmacokinetics studies of antihyperglycemic agents currently used in this population.

amaryl oral medication 2017-06-01

To examine the options for add-on therapy in patients with type 2 diabetes whose disease is no longer adequately controlled by lifestyle interventions and oral antidiabetic drug ( Protonix Drug Interactions OAD)monotherapy.

amaryl tab use 2015-03-22

In the Cymbalta 30mg Cost present study, sulphonylureas with greater selectivity for beta-cell receptors, such as glimepiride and gliclazide, were associated with a lower mortality when used in combination with metformin in comparison with glibenclamide. Safety of such combinations deserves further investigation.

amaryl 50 mg 2015-10-03

A prospective and case-control study was conducted. Ninty-four patients with Type 2 diabetes mellitus (35-70 year-old) were divided into 3 groups T Augmentin Dose : glimepiride treated group (n=33), metformin treated group (n=29) and glimepiride plus metformin treated group (n=32). These patients were followed up for 6 months. Free fatty acids were measured by using an enzymatic colorimetry.

amaryl starting dose 2017-06-17

This analysis included a subset of patients receiving prior OAD monotherapy from 2 phase 3, 26-week, randomized, double-blind, double-dummy, active-control, parallel-group, multicenter, multinational trials. Prior to randomization, patients not already receiving either metformin or glimepiride were switched to monotherapy with one of these drugs, and the dose was titrated to defined targets. Patients were then randomized to liraglutide (1.8 mg, 1.2 mg, or 0.6 mg once daily), placebo (OAD monotherapy plus placebo), or active comparator (rosiglitazone or glimepiride). For this analysis, only the liraglutide 1.8-mg dose was included. The primary outcome measure was change in glycosylated hemoglobin (HbA1c) from baseline. Secondary endpoints included in this analysis are percentage of patients achieving HbA1c < 7%, change in fasting plasma glucose, systolic blood pressure, body weight, beta-cell function, hypoglycemic episodes, and nausea.

amaryl 6 mg 2016-01-07

Excess adiposity contributes to cardiometabolic disease. Although adipose depots can be measured using imaging, implementation remains limited in practice. Data comparing surrogate indices of total and visceral adiposity with gold standard measurements in the context of a clinical trial population are lacking. We explored the relationships between adipose distribution indices and imaging assessments of body composition using baseline data from the EMPA-REG H2H SU™ trial.