For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
22
views
30
references
 Top references
cited by
6
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      387
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Metformin Treatment in Hyperglycemic Critically Ill Patients: Another Challenge on the Control of Adverse Outcomes

      research-article

      Read this article at

      ScienceOpenPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          New-onset hyperglycemia in patients admitted to intensive care units increases the risk of morbidity and mortality. Insulin resistance is frequently seen in the treatment of stress-induced hyperglycemia. Metformin, an oral anti-hyperglycemic agent, may introduce a new treatment protocol in critically ill patients with insulin-resistance hyperglycemia.

          Fifty-one non-diabetic traumatized patients with blood sugar (BS) levels more than 130 mg/dLwere introducedto three days of treatment with intensive insulin (50 IU) or metformin (1000 mg, twice daily) therapy. Clinical evaluationsincluded acute physiological and chronic health evaluation (APACHE II) and Glasgow Coma Scale (GCS). Experimental tests included BS level, mean arterial pressure (MAP), pH, HCO 3, and lactate.

          Eight patients were excluded and 21 of remained patients treated with insulin and 23 with metformin. There was no significant difference in terms of the evaluated factors between the two groups at the time of admission. Although desirable BS level (BS < 130 mg/dL) was reached by three days of metformin treatment (p < 0.01),there was no significant difference in BS, MAP, pH and HCO 3of insulin treated groupin comparison with metformin treated patients. The findings weresimilar for APACHE II and GCS as well.

          Although obvious studies are required, these findings may lead to effective therapies against stress-induced hyperglycemia.

          Related collections

          Most cited references30

          • Record: found
          • Abstract: found
          • Article: not found

          Glucose metabolism in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus: a prospective study.

          Anna Norhammar, Ake Tenerz, Göran Nilsson … (2002)
          Glycometabolic state at hospital admission is an important risk marker for long-term mortality in patients with acute myocardial infarction, whether or not they have known diabetes mellitus. Our aim was to ascertain the prevalence of impaired glucose metabolism in patients without diagnosed diabetes but with myocardial infarction, and to assess whether such abnormalities can be identified in the early course of a myocardial infarction. We did a prospective study, in which we enrolled 181 consecutive patients admitted to the coronary care units of two hospitals in Sweden with acute myocardial infarction, no diagnosis of diabetes, and a blood glucose concentration of less than 11.1 mmol/L. We recorded glucose concentrations during the hospital stay, and did standardised oral glucose tolerance tests with 75 g of glucose at discharge and again 3 months later. The mean age of our cohort was 63.5 years (SD 9) and the mean blood glucose concentration at admission was 6.5 mmol/L (1.4). The mean 2-h postload blood glucose concentration was 9.2 mmol/L (2.9) at hospital discharge, and 9.0 mmol/L (3.0) 3 months later. 58 of 164 (35%, 95% CI 28-43) and 58 of 144 (40%, 32-48) individuals had impaired glucose tolerance at discharge and after 3 months, respectively, and 51 of 164 (31%, 24-38) and 36 of 144 (25%, 18-32) had previously undiagnosed diabetes mellitus. Independent predictors of abnormal glucose tolerance at 3 months were concentrations of HbA(1c) at admission (p=0.024) and fasting blood glucose concentrations on day 4 (p=0.044). Previously undiagnosed diabetes and impaired glucose tolerance are common in patients with an acute myocardial infarction. These abnormalities can be detected early in the postinfarction period. Our results suggest that fasting and postchallenge hyperglycaemia in the early phase of an acute myocardial infarction could be used as early markers of high-risk individuals.
          Article 0 comments Cited 166 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Effect of glucose-insulin-potassium infusion on mortality in patients with acute ST-segment elevation myocardial infarction: the CREATE-ECLA randomized controlled trial.

            Shamir R Mehta, Salim Yusuf, Rafael Diaz … (2005)
            Glucose-insulin-potassium (GIK) infusion is a widely applicable, low-cost therapy that has been postulated to improve mortality in patients with acute ST-segment elevation myocardial infarction (STEMI). Given the potential global importance of GIK infusion, a large, adequately powered randomized trial is required to determine the effect of GIK on mortality in patients with STEMI. To determine the effect of high-dose GIK infusion on mortality in patients with STEMI. Randomized controlled trial conducted in 470 centers worldwide among 20,201 patients with STEMI who presented within 12 hours of symptom onset. The mean age of patients was 58.6 years, and evidence-based therapies were commonly used. Patients were randomly assigned to receive GIK intravenous infusion for 24 hours plus usual care (n = 10,091) or to receive usual care alone (controls; n = 10,110). Mortality, cardiac arrest, cardiogenic shock, and reinfarction at 30 days after randomization. At 30 days, 976 control patients (9.7%) and 1004 GIK infusion patients (10.0%) died (hazard ratio [HR], 1.03; 95% confidence interval [CI], 0.95-1.13; P = .45). There were no significant differences in the rates of cardiac arrest (1.5% [151/10 107] in control and 1.4% [139/10,088] in GIK infusion; HR, 0.93; 95% CI, 0.74-1.17; P = .51), cardiogenic shock (6.3% [640/10 107] vs 6.6% [667/10 088]; HR, 1.05; 95% CI, 0.94-1.17; P = .38), or reinfarction (2.4% [246/10,107] vs 2.3% [236/10,088]; HR, 0.98; 95% CI, 0.82-1.17; P = .81). The rates of heart failure at 7 days after randomization were also similar between the groups (16.9% [1711/10,107] vs 17.1% [1721/10,088]; HR, 1.01; 95% CI, 0.95-1.08; P = .72). The lack of benefit of GIK infusion on mortality was consistent in prespecified subgroups, including in those with and without diabetes, in those presenting with and without heart failure, in those presenting early and later after symptom onset, and in those receiving and not receiving reperfusion therapy (thrombolysis or primary percutaneous coronary intervention). In this large, international randomized trial, high-dose GIK infusion had a neutral effect on mortality, cardiac arrest, and cardiogenic shock in patients with acute STEMI.
            Article 0 comments Cited 84 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Metabolic effects of metformin on glucose and lactate metabolism in noninsulin-dependent diabetes mellitus.

              K Cusi, R A Consoli, R. DeFronzo (1996)
              Metformin is a biguanide that has been shown to effectively lower plasma glucose levels in subjects with noninsulin-dependent diabetes mellitus (NIDDM). However, its mechanism of action remains unknown. Studies that have examined the effect of metformin on hepatic glucose production (HGP) and muscle glucose utilization in NIDDM have yielded conflicting results, and little information is available about the action of metformin on lactate turnover and gluconeogenesis from lactate in humans. We studied 20 NIDDM subjects and 8 nondiabetic controls in a randomized, double blind, placebo-controlled trial to determine the effect of 15 weeks of treatment with metformin or placebo on glucose and lactate metabolism. Before and after treatment, all participants received a 7-h infusion of [6-3H]glucose and [3-14C]lactate in combination with indirect calorimetry and estimation of lactate central vein specific activity. A euglycemic insulin clamp (20 mU/m2.min) was performed during the last 3 h of the tracer infusions. The study design allowed us to evaluate the effects of metformin vs. placebo treatment on glycemic control, plasma lipid profile, HGP, insulin-mediated glucose uptake, oxidative and nonoxidative glucose metabolism, and lactate turnover. Metformin treatment significantly reduced fasting plasma glucose (196 +/- 18 vs. 152 +/- 12 mg/dL; P < 0.01), hemoglobin A1 (12.5 +/- 0.6 vs. 9.2 +/- 0.3%; P < 0.01), and plasma triglyceride and low density lipoprotein cholesterol concentrations. When diabetics were compared to nondiabetic controls, basal HGP was higher (12.9 +/- 1.0 vs. 9.8 +/- 1.2 mumol/kg.min; P < 0.01) despite the presence of fasting hyperinsulinemia and insulin-mediated total body glucose disposal (10.9 +/- 0.9 vs. 20.2 +/- 3.3 mumol/kg.min; P < 0.01) was decreased. Metformin significantly reduced fasting HGP (from 12.9 +/- 0.7 to 11.0 +/- 0.5 mumol/kg.min; P < 0.01), but did not enhance total body glucose disposal during insulin stimulation (10.9 +/- 0.9 vs. 11.0 +/- 0.5 mumol/kg.min; P = NS). Neither oxidative nor nonoxidative glucose disposal was improved by metformin treatment. The fasting plasma lactate concentration (1.1 +/- 0.1 vs. 0.6 +/- 0.1 mmol/L) and lactate turnover (14.0 +/- 0.8 vs. 10.3 +/- 0.6 mumol/kg.min) were significantly increased in diabetics and strongly correlated (r = 0.68; P < 0.001). The percent gluconeogenesis derived from lactate was similar in diabetic and control subjects (17 +/- 2% vs. 15 +/- 2%; P = NS), but the estimated rate of gluconeogenesis from lactate was increased in the diabetic group (P < 0.01). Despite the significant reduction in HGP after metformin treatment, the percentage of gluconeogenesis from lactate and the rate of lactate-derived gluconeogenesis were unchanged from baseline. Basal lactate turnover (15.4 +/- 1.4 vs. 14.8 +/- 1.4 mumol/kg.min) and lactate oxidation (7.9 +/- 0.7 vs. 8.1 +/- 0.9 mumol/ kg.min) as well as total lactate turnover and lactate oxidation during the insulin clamp were similar before and after metformin treatment. There were no changes in any of the above metabolic parameters in the placebo-treated group. In poorly controlled NIDDM subjects, the primary mechanism by which metformin improves glycemic control is related to the suppression of accelerated basal HGP, and this most likely is secondary to an inhibition of hepatic glycogenolysis. Metformin has no effect on the rate of lactate turnover or gluconeogenesis from lactate in either the basal or insulin-stimulated states.
              Article 0 comments Cited 71 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Iran J Pharm Res
                Journal ID (iso-abbrev): Iran J Pharm Res
                Journal ID (publisher-id): IJPR
                Title: Iranian Journal of Pharmaceutical Research : IJPR
                Publisher: Shaheed Beheshti University of Medical Sciences (Tehran, Iran )
                ISSN (Print): 1735-0328
                ISSN (Electronic): 1726-6890
                Publication date (Print): Autumn 2011
                Volume: 10
                Issue: 4
                Pages: 913-919
                Affiliations
                [a ] Chemical Injuries Research Center, Baqiyatallah Medical Sciences University, Tehran, Iran.
                [b ] Pharmaceutical Research Center, Tehran University of Medical Sciences, Tehran, Iran.
                [c ] Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
                [d ] Nephrology and Urology Research Center, Baqiyatallah Medical Sciences University, Tehran, Iran.
                [e ] ICU, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran
                [f ] Trauma Research Center, Tehran University of Medical Sciences, Tehran, Iran.
                Author notes
                [* ]Corresponding author: E-mail: mmojtahedzadeh@tums.ac.ir
                Article
                Publisher ID: ijpr-10-913
                PMC ID: 3813075
                PubMed ID: 24250430
                SO-VID: 1c4cd023-fbc4-4145-90a1-8798696adbfb
                Copyright © © 2011 by School of Pharmacy, Shaheed Beheshti University of Medical Sciences and Health Services
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License, ( http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : December 2009
                Date accepted : July 2010
                Categories
                Subject: Original Article

                Keywords: metformin,hyperglycemic,ill patients,insulin.
                Data availability:
                Keywords: metformin, hyperglycemic, ill patients, insulin.

                Comments

                Comment on this article

                Similar content387

                See all similar

                Cited by6

                See all cited by

                Most referenced authors757

                See all reference authors