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PubMed2005

Comparative outcomes study of metformin intervention versus conventional approach the COSMIC Approach Study.

OBJECTIVE: Metformin was approved by the Food and Drug Administration in 1995 subject to the conduct of a randomized trial to evaluate the risk of lactic acidosis or other serious adverse events (SAEs) with this agent, under usual care conditions. RESEARCH DESIGN AND METHODS: The Comparative Outcomes Study of Metformin Intervention versus Conventional (COSMIC) Approach Study was a randomized, open-label, active-comparator, parallel-group, 1-year trial in type 2 diabetic patients suboptimally controlled on diet or sulfonylurea. Patients received metformin (n = 7,227) or other usual care treatments (n = 1,505). The primary end point was the incidence of SAEs, death, and hospitalization. RESULTS: SAEs occurred in 10.3% (95% CI 9.6-11.1%) of the metformin group and in 11.0% (9.5-12.7%) of the usual care group (P = 0.431). Lactic acidosis did not occur. All-cause mortality (1.1% [0.9-1.4%] vs. 1.3% [0.8-2.0%], P = 0.596) and hospitalization (9.4% [8.8-10.1%] vs. 10.4% [8.9-12.1%], P = 0.229) were similar between groups. CONCLUSIONS: The incidence of SAEs was similar between groups. Lactic acidosis was not observed. Metformin may be safely prescribed for type 2 diabetes if contraindications and warnings are respected. This study demonstrates the utility of large, simple trials for risk evaluation of treatments for common diseases.

Acidosis, Lactic↗
PubMed1979

Treatment of diabetic ketoacidosis with a computer-controlled bedside monitoring and infusion system.

A metabolic monitoring system is described that allows the simultaneous and automatic in vivo analysis of the metabolic parameters glucose, pH, and pCO2 as well as the computer-controlled automation of the possible necessary infusion therapy. This bedside system has proved to be useful in treating acidotically and non-acidotically decompensated diabetes mellitus. Our experience with this system is as follows: 1. quick correction of the acidosis without danger of alkalosis, 2. shorter period of treatment, 3. considerably reduced insulin requirement, 4. no danger of hypoglycemia, and 5. minimum net blood withdrawal (1.2 ml/h). The efficiency of this system is demonstrated by examples.

Adult↗
PubMed2004

Evaluation of a bedside blood ketone sensor: the effects of acidosis, hyperglycaemia and acetoacetate on sensor performance.

AIMS: To assess the performance of a handheld bedside ketone sensor in the face of likely metabolic disturbances in diabetic ketoacidosis, namely: pH, glucose and acetoacetate. METHODS: The effects of pH (7.44-6.83), glucose (5-50 mmol/l) and acetoacetate (0-5 mmol/l) were examined in venous blood to investigate the accuracy of betahydroxybutyrate measurement (0-5 mmol/l) by a handheld ketone sensor. Sensor results were compared with a reference method. Linear regression models were fitted to the difference between the methods with the concentration of metabolite as the explanatory factor. RESULTS: Decreasing pH and increasing glucose had no effect on the accuracy of the handheld ketone sensor; the gradients of the fitted lines were -0.14 and -0.003, respectively. The 95% confidence intervals were -0.7-0.4 and -0.01-0.004, respectively (P = 0.59 and 0.4, respectively). In the acetoacetate study, a positive relationship between the sensor and reference method results was found, the gradient was 0.09. The 95% confidence interval was 0.05-0.14 (P < or = 0.001), indicating that high concentrations of acetoacetate interfere with the sensor performance. CONCLUSIONS: Acidosis and hyperglycaemia have minimal effects on the sensor performance. However, high concentrations of acetoacetate result in some overestimation of betahydroxybutyrate. This bedside ketone sensor provides useful data over a broad range of conditions likely to be encountered during moderate to severe diabetic ketoacidosis.

Acetoacetates↗
PubMedDate not supplied

Evaluation of plasma-ionized magnesium concentration in 122 dogs with diabetes mellitus: a retrospective study.

The goal of this study was to evaluate plasma-ionized magnesium (iMg2+) concentration in a large group of dogs with naturally occurring diabetes mellitus and to determine whether dogs with diabetes mellitus have hypomagnesemia, as reported in diabetic humans and cats. Plasma iMg2+ concentrations were retrospectively evaluated at the time of initial examination of 122 diabetic dogs at the Matthew J. Ryan Veterinary Hospital of the University of Pennsylvania. Diabetic dogs were defined as having uncomplicated diabetes mellitus (DM, 78 dogs) diabetic ketoacidosis (DKA, 32 dogs), or ketotic nonacidotic diabetes mellitus (DK, 12 dogs) on the basis of presence or absence of metabolic acidosis or ketonuria. Twenty-two control dogs were used to determine reference values for plasma iMg2+ concentration in healthy dogs. Plasma iMg2+ concentration also was evaluated in 19 nondiabetic dogs with acute pancreatitis because many of the dogs with DKA had concurrent acute pancreatitis. Plasma iMg2+ concentration was significantly higher in dogs with DKA (median 0.41 mmol/L, reference range 0.14-0.72 mmol/L) than in dogs with DM (0.33 mmol/L, 0.17-0.65 mmol/L; P = .0002) or the control group (0.32 mmol/L, 0.26-0.41 mmol/L; P = .006). There were no significant differences between plasma iMg2+ concentrations in dogs with DM or DK compared with control dogs. We conclude that dogs with naturally occurring diabetes mellitus do not have marked hypomagnesemia on initial examination at a tertiary care center.

Animals↗
PubMed1998

Oral antidiabetic agents. A guide to selection.

Type 2 diabetes mellitus (formerly named non-insulin-dependent diabetes mellitus or NIDDM) is a heterogeneous disease resulting from a dynamic interaction between defects in insulin secretion and insulin action. Various pharmacological approaches can be used to improve glucose homeostasis via different modes of action: sulphonylureas essentially stimulate insulin secretion, biguanides (metformin) act by promoting glucose utilisation and reducing hepatic-glucose production, alpha-glucosidase inhibitors (acarbose) slow down carbohydrate absorption from the gut and thiazolidinediones (troglitazone) enhance cellular insulin action on glucose and lipid metabolism. These pharmacological treatments may be used individually for certain types of patients, or may be combined in a stepwise fashion to provide more ideal glycaemic control for most patients. Selection of oral antihyperglycaemic agents as first-line drug or combined therapy should be based on both the pharmacological properties of the compounds (efficacy and safety, profile) and the clinical characteristics of the patient (stage of disease, bodyweight, etc.). Mildly hyperglycaemic patients should preferably be treated with metformin, acarbose or thiazolidinediones (which are not associated with any hypoglycaemic risk), while more severely hyperglycaemic individuals should receive a sulphonylurea. In moderately hyperglycaemic patients, sulphonylureas should be preferred in nonobese patients while metformin, and probably also thiazolidinediones, should have priority in obese insulin-resistant type 2 diabetic patients. Acarbose is mainly indicated to reduce post-prandial glucose fluctuations and improve glycaemic stability. Each antihyperglycaemic agent may also be combined with insulin therapy to improve glycaemic control and/or reduce the insulin requirement of diabetic patients after secondary failure to oral treatment. Finally, safety should be taken into account in elderly patients and/or those with renal impairment, especially as far as the use of sulphonylureas (higher risk of hypoglycaemia) and metformin (higher risk of lactic acidosis) is concerned.

Administration, Oral↗
PubMed1998

Epidemiology of A3243G, the mutation for mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes: prevalence of the mutation in an adult population.

Mitochondrial diseases are characterized by considerable clinical variability and are most often caused by mutations in mtDNA. Because of the phenotypic variability, epidemiological studies of the frequency of these disorders have been difficult to perform. We studied the prevalence of the mtDNA mutation at nucleotide 3243 in an adult population of 245,201 individuals. This mutation is the most common molecular etiology of MELAS syndrome (mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes), one of the clinical entities among the mitochondrial disorders. Patients with diabetes mellitus, sensorineural hearing impairment, epilepsy, occipital brain infarct, ophthalmoplegia, cerebral white-matter disease, basal-ganglia calcifications, hypertrophic cardiomyopathy, or ataxia were ascertained on the basis of defined clinical criteria and family-history data. A total of 615 patients were identified, and 480 samples were examined for the mutation. The mutation was found in 11 pedigrees, and its frequency was calculated to be >=16. 3/100,000 in the adult population (95% confidence interval 11.3-21. 4/100,000). The mutation had arisen in the population at least nine times, as determined by mtDNA haplotyping. Clinical evaluation of the probands revealed a syndrome that most frequently consisted of hearing impairment, cognitive decline, and short stature. The high prevalence of the common MELAS mutation in the adult population suggests that mitochondrial disorders constitute one of the largest diagnostic categories of neurogenetic diseases.

Acidosis, Lactic↗
PubMed1997

[Severe ketoacidosis because of delayed diagnosis of diabetes in children. 4 cases to alert physicians].

BACKGROUND: In France, 48% of children with insulin-dependent diabetes mellitus (IDDM) are seen for the first time at the stage of keto-acidosis (DKA), a figure far higher than in other countries. The four consecutive cases reported in this paper suggest that severity at presentation is directly related to the delay of diagnosis. CASE REPORTS: All children, aged 6 to 11, presented with severe clinical and metabolic conditions: coma, hemodynamic failure, severe dehydration and acidosis (pH = 6.86 to 7.06). However, clinical symptoms were a present from 2 to 4 months, parents did not worry about them. Family practitioners visited 2-21 days before admission failed to immediately make the diagnosis of IDDM. True DKA was however present in all cases 48 hours prior to admission. CONCLUSIONS: Earlier diagnosis of IDDM in children is necessary to reduce morbidity and mortality of DKA. General practitioners, pediatricians and emergency care practitioners must be made fully aware to consider diabetes in children and to use more extensively glucose-tests based on urine and blood strips.

Child↗
PubMed2006

[Perinatal morbidity in pregnancies of women with preconceptional and gestational diabetes mellitus in comparison with pregnancies of non-diabetic women. Results of the perinatal registry of Lower Saxony, Germany].

OBJECTIVE: Pregnancies of women with glucose tolerance disorders are still associated with high maternal and perinatal morbidity. In the present population-based study, we investigated the fetal and neonatal risks and complications in pregnancies of women with preconceptional and gestational diabetes in comparison with pregnancies of non-diabetic women. METHODS: A total of 913,255 pregnancies with 926,685 newborns documented by the Perinatal Registry of Lower Saxony, Germany, between 1987 and 1999 was retrospectively evaluated. In particular, the obstetric parameters of 3439 women with preconceptional diabetes mellitus (PDM, n = 3485 neonates), 4051 women with gestational diabetes mellitus (GDM, n = 4155 neonates) and 905,765 non-diabetic women (NDM, n = 919.053 neonates) were analysed. RESULTS: The diabetes groups had a higher rate of preterm birth < 31st week of gestation (PDM vs. NDM odds ratio [OR] 2.341; GDM vs. NDM OR 1.483) and between the 32nd and 37th weeks of gestation (OR 3.688 and 2.418, respectively). The incidences of pathological cardiotocograms (OR 1.519 and 1.258, respectively) and acidosis as indication for operative delivery (OR 5,015 and 2,102, respectively) were increased in the diabetes groups. There was a higher prevalence of birth weight > 4500 g (OR 2.775 and 2.742, respectively) and >95. percentile (OR 4.268 and 3.610, respectively) in newborns of diabetic women. The higher rate of umbilical arterial pH < 7.00 (OR 2.481 and 1.195, respectively) as well as Apgar score at 1 minute <7 (OR 2.971 and 1.897, respectively) indicated a poorer neonatal outcome in pregnancies of women with diabetes mellitus. The frequency of necessary intubation of the infants was significantly higher in the diabetes group (OR 3.384 and 1.317, respectively). There also was an increased prevalence of intrauterine fetal death in pregnancies of diabetic women (OR 4.197 and 2.511, respectively). CONCLUSION: Pregnancies of women with diabetes mellitus are still correlated with higher perinatal risks and complications. The neonatal morbidity in pregnancies with gestational diabetes mellitus was more similar to that of pregnancies with preconceptional diabetes mellitus than to the morbidity in the group of non-diabetic women. Changes of the parameters within the observation period were the same in all three groups and therefore cannot be attributed to a primary more intensive prenatal care of diabetic women.

Adult↗
PubMed1987

The maximal activity of phosphate-dependent glutaminase and glutamine metabolism in the colon and the small intestine of streptozotocin-diabetic rats.

The effects of short- and long-term diabetes on the maximal activities of phosphate-dependent glutaminase and glutamine metabolism were studied in the colon and the small intestine of streptozotocin-diabetic rats. The maximal activity of colonic phosphate-dependent glutaminase was decreased [44% in mucosal scrapings (p less than 0.01); 29% in whole colon (p less than 0.001)] or unchanged in short- or long-term diabetes respectively. That of the small intestine was increased in both short- (110%) and long-term (200%-500%) diabetes; insulin treatment corrected this increase. Acute insulin-deficiency (using anti-insulin serum) resulted in the increase (18%, p less than 0.05) of the activity of only intestinal glutaminase. Chemically-induced acidosis and alkalosis decreased (46%, p less than 0.001) and increased (24%, p less than 0.001), respectively, the activity of intestinal glutaminase, but had no effect on the colonic enzyme. Changes in glutaminase of the enlarged colon and small intestine were only detectable when activities were measured in whole organ. Arteriovenous-difference measurements showed diminished metabolism of plasma glutamine by the gut which correlated with the duration of the state of diabetes, and was accompanied by enhanced release by skeletal muscle and increased uptake by both kidney and liver. It is concluded that insulin is directly or indirectly involved in the regulation of glutamine metabolism of the gut.

Acidosis↗
PubMed2000

Diabetic ketoacidosis associated with Guillain-Barré syndrome with autonomic dysfunction.

A 37-year-old woman was admitted in a comatose state, after exhibiting fever and diarrhea. Diabetic ketoacidosis was diagnosed due to an increased blood glucose level (672 mg/dl), metabolic acidosis, and positive urinary ketone bodies. On the fifth hospital day, despite recovery from the critical state of ketoacidosis, the patient suffered from dysphagia, hypesthesia and motor weakness, followed by respiratory failure. Cerebrospinal fluid analysis was suggestive of Guillain-Barre syndrome (GBS). Autonomic dysfunction was manifested as tachycardia and mild hypertension in the acute stage. Marked orthostatic hypotension persisted long after paresis was improved, indicating an atypical clinical course of GBS.

Adult↗
PubMedDate not supplied

Non-insulin dependent diabetes mellitus in a prepubertal child with Prader-Willi syndrome.

Diabetes mellitus has only rarely been reported in prepubertal children with Prader-Willi syndrome. All reported children have required insulin therapy. We report the development of a previously unrecognized association of non-insulin dependent diabetes mellitus in an obese 6 year-old child with Prader-Willi syndrome. She has never developed ketosis or acidosis, and she has been treated with oral hypoglycemic medication.

Child↗
PubMed2007

Admissions for diabetic ketoacidosis in ethnic minority groups in a city hospital.

Hospitalization for diabetic ketoacidosis (DKA) is increasing, perhaps due to the rising incidence of DKA in patients with type 2 diabetes mellitus (T2DM). Ethnic minority groups are at increased risk for T2DM. This study aimed at elucidating the characteristics of patients with ketosis-prone diabetes in a predominantly ethnic minority population. We performed a retrospective analysis of adults admitted with DKA at the Bronx Lebanon Hospital Center, Bronx, NY over 3 years. The patients were divided into cohorts based on type of diabetes and ethnicity. The cohorts were described and compared using statistical methods. We recorded 219 cases of DKA in 168 patients, 97% of whom were African American or Hispanic. Fifty-three (32%) patients had T2DM. New-onset diabetes, which was more common in T2DM (P < .0001), and African Americans (P = .008), occurred in 42 patients (25%). Readmission with DKA was more common in the Hispanic patients with type 1 diabetes mellitus (T1DM) (P = .0001). Type 2 diabetes mellitus was more prevalent in the African Americans (P = .04). Patients with T1DM had more severe acidosis than patients with T2DM (lower pH and bicarbonate and larger anion gap; P = .03, .02, and .005, respectively). Creatinine level was higher in patients with T2DM (P = .04) who were also less likely to have identifiable precipitating causes (P = .02). Hemoglobin A(1c) level was higher in patients with new-onset diabetes (P < .05), but did not differ between those with T1DM and T2DM. Mortality, which was 2%, occurred only in the African Americans with T2DM. We conclude that DKA is an important mode of initial presentation of T2DM, with new-onset T2DM accounting for about 60% of all new cases of DKA. African American patients with T2DM, in comparison with the Hispanic patients, are more susceptible to developing DKA. Diabetic ketoacidosis could occur in T2DM without any identifiable precipitant. The rising incidence of DKA may be attributable to its increasing occurrence in T2DM; therefore, measures aimed at primary prevention of T2DM are worthwhile.

Adult↗
PubMedDate not supplied

[Simultaneous onset of steroid-sensitive nephrotic syndrome and type 1 diabetes].

OBJECTIVE: We describe the case of a boy with steroid-sensitive nephrotic syndrome coexisting with type-1 diabetes mellitus. DESCRIPTION: Nephrotic syndrome was diagnosed in a boy (age 3 years and 11 months) with generalized edema. Marked weight loss (23 to 16 kg), polyuria, polydipsia and weakness were observed after three weeks of treatment with prednisone 2 mg/kg/day. Diabetic ketoacidosis was confirmed by laboratory tests: hyperglycemia (glucose 657 mg/dl), glycosuria without proteinuria, acidosis and ketonuria. Therapy with insulin and prednisone was started. He was then maintained on a daily dose of NPH insulin. At age 4 years and 1 month a new episode of ketoacidosis without proteinuria occurred in association with a viral infection of the upper airways. At age 4 years and 4 months nephrotic syndrome relapsed, but the child responded well to steroid therapy. There was another relapse three months later, when prednisone treatment was interrupted. This led to the introduction of cyclophosphamide, with good results. Since then, the patient (now 5 years and 6 months old) has been taking insulin daily and nephrotic syndrome has not relapsed. Plasma levels of C3 and C4 and renal function are normal. Hematuria is occasionally present. Anti-GAD antibodies (glutamic decarboxilase) are normal and anti-islet cell antibodies are positive. HLA antigens: A2; B44; B52; DR4; DR8; DR53. COMMENTS: The simultaneous occurrence of steroid-sensitive nephrotic syndrome and type-1 diabetes mellitus is rare.

Child, Preschool↗
PubMed2003

Metformin hydrochloride in the treatment of type 2 diabetes mellitus: a clinical review with a focus on dual therapy.

BACKGROUND: Type 2 diabetes mellitus typically involves abnormal beta-cell function that results in relative insulin deficiency, insulin resistance accompanied by decreased glucose transport into muscle and fat cells, and increased hepatic glucose output, all of which contribute to hyperglycemia. OBJECTIVE: This review examines the pharmacology, pharmacokinetics, drug-interaction potential, adverse effects, and dosing guidelines for metformin hydrochloride, a biguanide agent for the treatment of type 2 diabetes. Clinical trial data are reviewed, including efficacy and tolerability information, with a focus on studies of dual metformin therapy (metformin plus another oral agent or insulin) published from 1998 to the present. Pharmacoeconomic considerations are also discussed. METHODS: Primary research and review articles were identified through a search of MEDLINE (1966-May 2003) and International Pharmaceutical Abstracts (1970-May 2003) using the terms metformin and/or Glucophage. Web of Science (1995-May 2003) was used to search for additional abstracts. The package inserts for metformin and metformin combination products were consulted. All identified articles and abstracts were assessed for relevance, and all relevant information was included. Priority was given to the primary medical literature and clinical trial reports. RESULTS: Metformin is the only currently available oral antidiabetic/hypoglycemic agent that acts predominantly by inhibiting hepatic glucose release. Because patients with type 2 diabetes often have excess hepatic glucose output, use of metformin is effective in lowering glycosylated hemoglobin (HbA1c) by 1 to 2 percentage points when used as monotherapy or in combination with other blood glucose-lowering agents or insulin. Other metabolic variables (eg, dyslipidemia, fibrinolysis) may be improved with the use of metformin. Body weight is often maintained or slightly reduced from baseline. Metformin is well tolerated and is associated with few clinically deleterious adverse events. The most important and potentially life-threatening adverse event associated with its use is lactic acidosis, which occurs very rarely. CONCLUSIONS: Metformin has multiple benefits in patients with type 2 diabetes. It can effectively lower HbA1c values, positively affect lipid profiles, and improve vascular and hemodynamic indices. Adverse effects are generally tolerable and self-limiting. The availability of products combining metformin with a sulfonylurea or rosiglitazone has expanded the array of therapies for the management of type 2 diabetes.

Clinical Trials as Topic↗
PubMed1993

Fetal pancreatic beta-cell function in pregnancies complicated by maternal diabetes mellitus: relationship to fetal acidemia and macrosomia.

OBJECTIVE: Our purpose was to investigate the relationship between fetal pancreatic beta-cell function and fetal acidemia and macrosomia in pregnancies complicated by maternal diabetes mellitus. STUDY DESIGN: A cross-sectional study at the Harris Birthright Research Centre for Fetal Medicine, London, was performed. In 32 pregnancies complicated by maternal diabetes mellitus cordocentesis was performed at 36 to 39 weeks' gestation for the measurement of umbilical venous blood pH, PO2, PCO2, lactate, and glucose concentration; plasma insulin immunoreactivity; and insulin/glucose ratio. A reference range for plasma insulin and insulin/glucose ratio was constructed by studying fetal blood samples from 80 women who did not have diabetes mellitus. RESULTS: Mean umbilical venous blood pH was significantly lower and plasma insulin immunoreactivity and insulin/glucose ratio were significantly higher than the appropriate normal mean for gestation. There were significant associations between (1) maternal and fetal blood glucose concentrations (r = 0.95, p < 0.0001), (2) fetal blood glucose and plasma insulin immunoreactivity (r = 0.57, p < 0.01), (3) fetal plasma insulin immunoreactivity and blood pH (r = -0.39, p < 0.05), and (4) fetal insulin/glucose ratio and degree of macrosomia (r = 0.76, p < 0.0001). CONCLUSION: Fetal pancreatic beta-cell hyperplasia is implicated in the pathogenesis of both fetal acidemia and macrosomia.

Acidosis↗
PubMedDate not supplied

Repeated hypoglycemia and cognitive decline. A case report.

OBJECTIVE: Diabetes mellitus has a high incidence in general population and goes by high morbidity by specific micro vascular pathology in the retina, renal glomerul and peripheral nerves. In type 1 DM, intensive therapy can prevent or delay the development of long-term complications associated with DM but hypoglycaemia especially severe hypoglycaemia defined, as a low blood glucose resulting in stupor, seizure, or unconsciousness that precludes self-treatment is a serious threat. Hypoglycaemia that may preferentially harm neurons in the medial temporal region, specifically the hippocampus, is a potential danger for the brain cognitive function which several studies failed to detect any significant effects, whereas others indicated an influence on it. A young diabetic case presented here with severe cognitive defect. Great number of severe hypoglycaemic or hyperglycaemic attacks and convulsion episodes were described in his medical history. RESULTS AND CONCLUSION: Neuroradiologic findings on CT and MRI, pointed that global cerebral atrophy that is incompatible with his age. Brain perfusion studies (SPECT, (99m)Tc-labeled HMPAO) also showed that there were severe perfusion defects at superior temporal region and less perfusion defects at gyrus cingulum in frontal region. These regions are related with memory processing. Severe cognitive defect in this patient seems to be closely related these changes and no another reason was found to explain except the repeated severe hypoglycaemic episodes.

Acidosis↗
PubMed1978

Disposition of metformin (N,N-dimethylbiguanide) in man.

Kinetic parameters of metformin (N,N-dimethylbiguanide), an anti-diabetic reported to be associated with a lower number of episodes of lactic acidosis than phenformin, were determined in volunteers with normal renal function and in patients with different degrees of renal impairment. Drug in body fluids was measured by a highly specific and sensitive mass fragmentographic method, after the formation of a triazine derivative, obtained with heptafluorobutyric anhydride. The half-life (t 1/2) for the elimination of drug from plasma after intravenous injection in 5 normal subjects (1.52 +/- 0.3 hr) (mean +/- SD) was shorter than that reported for phenformin by a similar assay method (7 to 15 hr). The mean t 1/2 in 5 renal patients was 4.94 +/- 1.11 hr, and a correlation was observed between t 1/2 of drug from plasma and creatinine clearance. After oral administration of metformin tablets, drug recovery in urines was only 37.6%, possibly not as a consequence of low bioavailability (a similar low recovery was found after oral administration of the metformin solution used for the intravenous studies), but of binding to the intestinal wall, as shown in animal and clinical studies with metformin and other biguanides. Metformin is rapidly eliminated through active secretion by the kidney (mean renal clearance, 440.8 ml/min)--it is neither metabolized nor protein bound in plasma. The very brief plasma t 1/2 makes significant cumulation, with a standard tid regimen, unlikely. These findings may help explain the lower incidence of toxic effects, particularly lactic acidosis, than after phenformin.

Administration, Oral↗
PubMed1989

Fluid and electrolyte balance in critical patients.

Recognition and appropriate management of fluid and electrolyte disorders in critical patients is extremely important. In many cases, these secondary problems are more complicated and more serious than the initiating disease process. A severely ill diabetic patient, for example, is more likely to die from dehydration, hyperosmolality, metabolic acidosis, hypokalemia or hypophosphatemia than from hyperglycemia or lack of insulin therapy. Proper fluid therapy and treatment of electrolyte abnormalities make a major difference in the survival rate of critically ill animals.

Animals↗