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Metformin And Dka

New Diabetes Drugs May Bring On Ketoacidosis

New Diabetes Drugs May Bring On Ketoacidosis

SGLT2 inhibitors, which are some of the newest diabetes drugs on the market, may increase the risk of a serious condition. A new study concludes that these medications actually double the likelihood of developing diabetic ketoacidosis. Because diabetes is becoming more prevalent in the United States, the hunt for new and more effective medication is in full flow. Sodium-glucose cotransporter-2 (SGLT2) inhibitors are the most recent additions to the list of available medicines. SGLT2 inhibitors reduce blood glucose levels by encouraging the kidneys to increase sugar excretion in urine. These drugs are often given in combination with other diabetes medications, such as metformin and insulin. The new class of drugs has become relatively popular, but the latest research finds that they could increase the risk of a serious diabetes-related complication. Rare but dangerous Diabetic ketoacidosis is relatively uncommon but potentially life-threatening. It occurs when acids called ketones build up in the body, increasing the acidity of the blood, or when the body does not produce enough insulin. When insulin is absent, glucose cannot enter cells and provide them with the energy they need. Therefore, the body falls back on its secondary fuel source: fat. Ketones are byproducts of burning fat. Symptoms of diabetic ketoacidosis include increased thirst, abdominal pain, nausea and vomiting, and confusion. It can also cause swelling in the brain, and, if left unchecked, can be fatal. Although diabetic ketoacidosis is more likely to occur in people with type 1 diabetes, it does occasionally appear in individuals with type 2 diabetes. Examining the interaction The new study, carried out by Dr. Michael Fralick and a team from Brigham and Women’s Hospital in Boston, set out to examine Continue reading >>

Sglt2 Inhibitors: Updated Advice On The Risk Of Diabetic Ketoacidosis

Sglt2 Inhibitors: Updated Advice On The Risk Of Diabetic Ketoacidosis

Advice for healthcare professionals: When treating patients who are taking a sodium-glucose co-transporter 2 (SGLT2) inhibitor (canagliflozin, dapagliflozin, or empagliflozin): inform them of the signs and symptoms of diabetic ketoacidosis (DKA) – see below – and advise them to seek immediate medical advice if they develop any of these discuss the risk factors for DKA with patients (see below) discontinue treatment with the SGLT2 inhibitor immediately if DKA is suspected or diagnosed do not restart treatment with any SGLT2 inhibitor in patients who experienced DKA during use, unless another cause for DKA was identified and resolved interrupt treatment with the SGLT2 inhibitor in patients who are hospitalised for major surgery or acute serious illnesses; treatment may be restarted once the patient’s condition has stabilised Reports of diabetic acidosis EU medicines regulators have completed a review of DKA associated with SGLT2 inhibitor treatment; this article summarises the review’s recommendations. We published preliminary advice on this in June 2015. SGLT2 inhibitors are licensed for use in adults with type 2 diabetes to improve glycaemic control. Serious, life-threatening, and fatal cases of DKA have been reported in patients taking an SGLT2 inhibitor (canagliflozin, dapagliflozin, or empagliflozin). The EU review concluded that this side effect is rare (affecting between 1 in 1000 and 1 in 10,000 patients). Up to 26 February 2016, we had received 118 Yellow Card reports of DKA and associated reactions in patients taking an SGLT2 inhibitor in the UK. In several cases, blood glucose levels were only moderately elevated (eg <14mmol/L)—representing an atypical presentation for DKA, which could delay diagnosis and treatment. Therefore inform patients of the si Continue reading >>

Apo-metformin

Apo-metformin

NOTICE: This Consumer Medicine Information (CMI) is intended for persons living in Australia. What is in this leaflet This leaflet answers some common questions about metformin It does not contain all the available information. It does not take the place of talking to your doctor or pharmacist or diabetes educator. The information in this leaflet was last updated on the date listed on the last page. More recent information on this medicine may be available. You can also download the most up to date leaflet from www.apotex.com.au. All medicines have risks and benefits. Your doctor has weighed the risks of you using this medicine against the benefits they expect it will have for you. Pharmaceutical companies cannot give you medical advice or an individual diagnosis. Keep this leaflet with your medicine. You may want to read it again. What this medicine is used for The name of your medicine is APO-Metformin 500, 850 or 1000 tablets. It contains the active ingredient metformin (as metformin hydrochloride). It is used to treat type 2 diabetes (also called non-insulin dependent diabetes mellitus or maturity onset diabetes) in adults and children over 10 years of age. It is especially useful in those who are overweight, when diet and exercise are not enough to lower high blood glucose levels (hyperglycaemia). For adult patients, metformin can be used alone, or in combination with other oral diabetic medicines or in combination with insulin in insulin requiring type 2 diabetes. Ask your doctor if you have any questions about why this medicine has been prescribed for you. Your doctor may have prescribed this medicine for another reason. This medicine is available only with a doctor's prescription. How it works Metformin lowers high blood glucose by helping your body make better Continue reading >>

Sglt2 Inhibitors And Diabetic Ketoacidosis: What's Behind The Fda Warning

Sglt2 Inhibitors And Diabetic Ketoacidosis: What's Behind The Fda Warning

With commentary by Yehuda Handelsman, MD, FACP, FACE, FNLA, an endocrinologist in private practice in Tarzana, CA, Medical Director and Principal Investigator of the Metabolic Institute of America and President of the American College of Endocrinology People with diabetes who take blood sugar-lowering drugs called SGLT2 inhibitors were recently warned by the U.S. Food and Drug Administration (FDA) that they should watch for signs of a life-threatening condition called diabetic ketoacidosis. canagliflozin (Invokana) dapagliflozin (Farxiga) empagliflozin (Jardiance) as well as the combination pills: canagliflozin plus metformin (Invokamet) dapagliflozin plus metformin extended-release (Xigduo XR) empagliflozin plus linagliptin (Glyxambi). “Diabetic ketoacidosis (DKA) can be deadly,” says Amy Hess-Fischl, MS, RD, LDN, BC-ADM, CDE, an advanced practice dietitian at the University of Chicago Kovler Diabetes Center and a member of EndocrineWeb’s advisory board. “DKA is usually more of a concern for people with type 1 diabetes, but this warning is for people with type 2 diabetes who are taking the SGLT2 inhibitors, as well as people with type 1 diabetes who take these medications off label. DKA — dangerously high acid levels in the bloodstream — happens when your body breaks down fat instead of glucose for energy, releasing acidic compounds called ketones. Early symptoms include thirst, frequent urination and sweet, fruity breath, Hess-Fischl says. You may feel tired and confused, and develop nausea, stomach pain, vomiting and difficulty breathing. “If you notice symptoms, call your doctor immediately. But if you’re vomiting, can’t catch your breath or are concerned, go to the emergency room,” she says. Putting the Risk in Perspective The FDA warning, relea Continue reading >>

Hyperglycaemic Crises And Lactic Acidosis In Diabetes Mellitus

Hyperglycaemic Crises And Lactic Acidosis In Diabetes Mellitus

Hyperglycaemic crises are discussed together followed by a separate section on lactic acidosis. DIABETIC KETOACIDOSIS (DKA) AND HYPERGLYCAEMIC HYPEROSMOLAR STATE (HHS) Definitions DKA has no universally agreed definition. Alberti proposed the working definition of “severe uncontrolled diabetes requiring emergency treatment with insulin and intravenous fluids and with a blood ketone body concentration of >5 mmol/l”.1 Given the limited availability of blood ketone body assays, a more pragmatic definition comprising a metabolic acidosis (pH <7.3), plasma bicarbonate <15 mmol/l, plasma glucose >13.9 mmol/l, and urine ketostix reaction ++ or plasma ketostix ⩾ + may be more workable in clinical practice.2 Classifying the severity of diabetic ketoacidosis is desirable, since it may assist in determining the management and monitoring of the patient. Such a classification is based on the severity of acidosis (table 1). A caveat to this approach is that the presence of an intercurrent illness, that may not necessarily affect the level of acidosis, may markedly affect outcome: a recent study showed that the two most important factors predicting mortality in DKA were severe intercurrent illness and pH <7.0.3 HHS replaces the older terms, “hyperglycaemic hyperosmolar non-ketotic coma” and “hyperglycaemic hyperosmolar non-ketotic state”, because alterations of sensoria may be present without coma, and mild to moderate ketosis is commonly present in this state.4,5 Definitions vary according to the degree of hyperglycaemia and elevation of osmolality required. Table 1 summarises the definition of Kitabchi et al.5 Epidemiology The annual incidence of DKA among subjects with type 1 diabetes is between 1% and 5% in European and American series6–10 and this incidence appear Continue reading >>

Chapter 220. Diabetic Ketoacidosis

Chapter 220. Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus. The incidence and prevalence of diabetes are rising; as of 2005, an estimated 7% of the U.S. population had diabetes. In patients age 60 or older, the prevalence is estimated to be 20.9%.1 DKA occurs predominately in patients with type 1 (insulin-dependent) diabetes mellitus, but unprovoked DKA can occur in newly diagnosed type 2 (non–insulin-dependent) diabetes mellitus, especially in blacks and Hispanics.2 Between 1993 and 2003, the yearly rate of ED visits for DKA per 10,000 U.S. population with diabetes was 64, with a trend toward an increased rate of visits among the black population compared with the white population.3 Europe has a comparable incidence. A better understanding of pathophysiology and an aggressive, uniform approach to diagnosis and management have reduced mortality to <5% of reported episodes in experienced centers.4 However, mortality is higher in the elderly due to underlying renal disease or coexisting infection and in the presence of coma or hypotension. DKA is a response to cellular starvation brought on by relative insulin deficiency and counterregulatory or catabolic hormone excess (Figure 220-1). Insulin is the only anabolic hormone produced by the endocrine pancreas and is responsible for the metabolism and storage of carbohydrates, fat, and protein. Counterregulatory hormones include glucagon, catecholamines, cortisol, and growth hormone. Complete or relative absence of insulin and the excess counterregulatory hormones result in hyperglycemia (due to excess production and underutilization of glucose), osmotic diuresis, prerenal azotemia, worsening hyperglycemia, ketone formation, and a wide-anion gap metabolic acidosis.4 Insulin deficiency. Patho Continue reading >>

Sglt2 Inhibitors [invokana (canagliflozin), Forxiga (dapagliflozin), Xigduo (dapagliflozin/metformin), Jardiance (empagliflozin)] - Risk Of Diabetic Ketoacidosis

Sglt2 Inhibitors [invokana (canagliflozin), Forxiga (dapagliflozin), Xigduo (dapagliflozin/metformin), Jardiance (empagliflozin)] - Risk Of Diabetic Ketoacidosis

Report a Concern Audience Healthcare professionals including internal medicine specialists, endocrinologists, cardiologists, nephrologists, general or family practitioners, emergency healthcare professionals, critical care physicians, certified diabetes educators and pharmacists. Key messages Serious, sometimes life-threatening and fatal cases of diabetic ketoacidosis (DKA) have been reported in patients on sodium glucose co-transporter 2 (SGLT2) inhibitors for type 1 and type 2 diabetes. In a number of these cases, the presentation of the condition was atypical with only moderately increased blood glucose levels observed. SGLT2 inhibitors are NOT indicated for treatment of type 1 diabetes mellitus and should not be used in type 1 diabetes. It is recommended that: if DKA is suspected or diagnosed, treatment with SGLT2 inhibitors should be discontinued immediately. SGLT2 inhibitors should not be used in patients with a history of DKA. in clinical situations known to predispose to ketoacidosis (e.g. major surgical procedures, serious infections and acute serious illness), consideration be given to temporarily discontinuing SGLT2 inhibitor therapy. patients be informed of the signs and symptoms of DKA and be advised to immediately seek medical attention if they develop them. caution be used before initiating SGLT2 inhibitor treatment in patients with risk factors for DKA. The Canadian Product Monographs of these products will be updated to reflect this safety information. Issue Clinical trial and post-market cases of DKA, a serious, life-threatening condition requiring urgent hospitalization have been reported in patients with type 1 and type 2 diabetes mellitus on SGLT2 inhibitor treatment. In a number of these reports, the presentation of the condition was atypical with Continue reading >>

Ketoacidosis In A Patient With Type 2 Diabetes – Flatbush Diabetes

Ketoacidosis In A Patient With Type 2 Diabetes – Flatbush Diabetes

There is increasing recognition of a group of patients with type 2 diabetes who can present with ketoacidosis. Most reports have been of patients of African descent; however, the condition has been reported in other groups. This is a case of a Caucasian patient who has had three presentations with ketoacidosis and whose diabetes is not usually insulin-dependent. A patient, aged 48 years, presented with diabetic ketoacidosis (DKA) in a semi-comatose condition. She had a 3-day history of vomiting and loss of appetite. In the previous weeks she had undergone radiotherapy for metastatic squamous cell carcinoma (skin primary). The patient had two similar episodes of DKA, one 20 months and another 3 months earlier. Two of the patient’s brothers had type 2 diabetes. The patient was not abusing alcohol and did not have a history of pancreatitis. Three years prior to this admission the patient had been diagnosed elsewhere with type 2 diabetes, for which she had been on metformin and a small dose of insulin glargine. Two months after stopping her insulin glargine she developed her first episode of DKA while visiting our town. DKA, was diagnosed on the basis of arterial pH 7.03, blood glucose level 25.9 mmol/L, bicarbonate level of 5 mmol/L and positive urinary ketones. It was felt that infected skin lesions may have precipitated the DKA. Eleven days later, she was discharged on metformin 250 mg twice daily and a falling dose of insulin glargine (26 units a day). She was then lost to follow-up in our centre, but apparently soon after did not require insulin and maintained adequate gylcaemic control for 18 months until just prior to her next admission solely on metformin 1 g twice daily. The next admission for DKA occurred while living in a city. She was discharged on insulin but Continue reading >>

Dka Vs Hhns Nclex Questions

Dka Vs Hhns Nclex Questions

This quiz on DKA vs HHNS (Diabetic Ketoacidosis vs Hyperglycemic Hyperosmolar Nonketotic Syndrome) will test you on how to care for the diabetic patient who is experiencing these conditions. As the nurse, you must know typical signs and symptoms of DKA and HHNS, patient teaching, and expected medical treatments. Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS) are both complication of diabetes mellitus, but there are differences between the two complications that you must know as a nurse. This endocrine teaching series will test your knowledge on how to differentiate between the two conditions, along with a video lecture. This quiz will test you on the following for the NCLEX exam: Signs and Symptoms of Diabetic Ketoacidosis vs Hyperglycemic Hyperosmolar Nonketotic Syndrome Causes of Diabetic Ketoacidosis vs Hyperglycemic Hyperosmolar Nonketotic Syndrome Patient education for DKA vs HHNS Treatments of Diabetic Ketoacidosis vs Hyperglycemic Hyperosmolar Nonketotic Syndrome Lecture on DKA vs HHS (NOTE: When you hit submit, it will refresh this same page. Scroll down to see your results.) DKA vs HHS Quiz 1. This complication is found mainly in Type 2 diabetics? 2. A patient is found to have a blood glucose of 375 mg/dL, positive ketones in the urine, and blood pH of 7.25. Which condition is this? 3. Hyperglycemic Hyperosmolar Nonketotic Syndrome would have all of the following signs and symptoms EXPECT? A. Dry mucous membranes B. Polyuria C. Blood glucose >600 mg/dL D. Kussmaul breathing 4. This condition happens gradually and is more likely to affect older adults? 5. A patient has an infection and reports not checking their blood glucose or regularly taking Metformin. What condition is this patient MOST at risk for? A. DKA B. HHNS C. Metabol Continue reading >>

(sitagliptin And Metformin Hcl) Tablets Or

(sitagliptin And Metformin Hcl) Tablets Or

JANUMET tablets contain 2 prescription medicines: sitagliptin (JANUVIA®) and metformin. Once-daily prescription JANUMET XR tablets contain sitagliptin (the medicine in JANUVIA®) and extended-release metformin. JANUMET or JANUMET XR can be used along with diet and exercise to lower blood sugar in adults with type 2 diabetes. JANUMET or JANUMET XR should not be used in patients with type 1 diabetes or with diabetic ketoacidosis (increased ketones in the blood or urine). If you have had pancreatitis (inflammation of the pancreas), it is not known if you have a higher chance of getting it while taking JANUMET or JANUMET XR. Selected Risk Information About JANUMET and JANUMET XR Metformin, one of the medicines in JANUMET and JANUMET XR, can cause a rare but serious side effect called lactic acidosis (a buildup of lactic acid in the blood), which can cause death. Lactic acidosis is a medical emergency that must be treated in a hospital. Call your doctor right away if you get any of the following symptoms, which could be signs of lactic acidosis: feel cold in your hands or feet; feel dizzy or lightheaded; have a slow or irregular heartbeat; feel very weak or tired; have unusual (not normal) muscle pain; have trouble breathing; feel sleepy or drowsy; have stomach pains, nausea, or vomiting. Most people who have had lactic acidosis with metformin have other things that, combined with the metformin, led to the lactic acidosis. Tell your doctor if you have any of the following, because you have a higher chance of getting lactic acidosis with JANUMET or JANUMET XR if you: have severe kidney problems or your kidneys are affected by certain x-ray tests that use injectable dye; have liver problems; drink alcohol very often, or drink a lot of alcohol in short-term “binge” drinkin Continue reading >>

Glyburide / Metformin Disease Interactions

Glyburide / Metformin Disease Interactions

Major Metformin (Includes Glyburide/metformin) ↔ Lactic Acidosis Severe Potential Hazard, High plausibility Applies to: Renal Dysfunction, Liver Disease, Congestive Heart Failure, Dehydration, Shock, Myocardial Infarction, Asphyxia, Acidosis, Diarrhea, Vomiting, Anemia, Alcoholism The use of metformin is contraindicated in patients with renal dysfunction (serum creatinine >= 1.5 mg/dL in males and 1.4 mg/dL in females, or above the upper limit of normal for age); congestive heart failure requiring pharmacologic treatment (especially unstable or acute CHF where there is risk of hypoperfusion and hypoxemia); and any condition associated with hypoxemia (e.g., severe anemia, myocardial infarction, asphyxia, shock), dehydration (e.g., severe diarrhea or vomiting), or sepsis. Patients with these conditions may be at increased risk for the development of lactic acidosis, which is a rare but serious metabolic complication associated with metformin accumulation in plasma usually at levels exceeding 5 mcg/mL. Metformin should also not be administered to patients with acute or chronic metabolic acidosis. In addition, metformin should generally be avoided in alcoholics and patients with clinical or laboratory evidence of hepatic disease, since alcohol potentiates the effects of metformin on lactate metabolism and impaired hepatic function may significantly limit the ability to clear lactate. All patients treated with metformin should have renal function monitored regularly (at least annually or more frequently if necessary) and be advised of the significance of nonspecific symptoms such as malaise, myalgias, respiratory distress, increasing somnolence, and gastrointestinal disturbances that arise after stabilization of metformin dosage. More marked acidosis may be associated with Continue reading >>

Metformin, Sitagliptin Prolong Normoglycemia Remission In Dka

Metformin, Sitagliptin Prolong Normoglycemia Remission In Dka

(HealthDay)—For patients with new-onset diabetic ketoacidosis (DKA) and severe hyperglycemia, metformin and sitagliptin treatment after normoglycemia remission correlate with increased relapse-free survival and prolonged remission, according to a study published online Aug. 29 in Diabetes Care. Priyathama Vellanki, M.D., from the Emory University School of Medicine in Atlanta, and colleagues conducted a prospective four-year study involving 48 African-American subjects with DKA and severe hyperglycemia. Participants were randomized to metformin (17 participants), sitagliptin (16 participants), or placebo (15 participants) after normoglycemia remission. Oral glucose tolerance tests were conducted at randomization, at three months, and every six months for a median of 331 days. The researchers found that the metformin and sitagliptin groups had significantly higher relapse-free survival compared with placebo (P = 0.015), and significantly prolonged mean time to relapse (480 versus 305 days; P = 0.004). Compared with placebo, the probability of relapse was significantly lower for metformin and sitagliptin (hazard ratios, 0.28 and 0.31, respectively). Compared with those with hyperglycemia relapse, individuals who remained in remission had a higher disposition index and incremental area under the curve for insulin, with no significant changes in insulin sensitivity. "This study shows that near-normoglycemia remission was similarly prolonged by treatment with sitagliptin and metformin," the authors write. "The prolongation of remission was due to improvement in β-cell function." Several authors disclosed financial ties to pharmaceutical companies, including Merck, which manufactures sitagliptin. More information: Full Text (subscription or payment may be required) Continue reading >>

Causes Of Lactic Acidosis

Causes Of Lactic Acidosis

INTRODUCTION AND DEFINITION Lactate levels greater than 2 mmol/L represent hyperlactatemia, whereas lactic acidosis is generally defined as a serum lactate concentration above 4 mmol/L. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Although the acidosis is usually associated with an elevated anion gap, moderately increased lactate levels can be observed with a normal anion gap (especially if hypoalbuminemia exists and the anion gap is not appropriately corrected). When lactic acidosis exists as an isolated acid-base disturbance, the arterial pH is reduced. However, other coexisting disorders can raise the pH into the normal range or even generate an elevated pH. (See "Approach to the adult with metabolic acidosis", section on 'Assessment of the serum anion gap' and "Simple and mixed acid-base disorders".) Lactic acidosis occurs when lactic acid production exceeds lactic acid clearance. The increase in lactate production is usually caused by impaired tissue oxygenation, either from decreased oxygen delivery or a defect in mitochondrial oxygen utilization. (See "Approach to the adult with metabolic acidosis".) The pathophysiology and causes of lactic acidosis will be reviewed here. The possible role of bicarbonate therapy in such patients is discussed separately. (See "Bicarbonate therapy in lactic acidosis".) PATHOPHYSIOLOGY A review of the biochemistry of lactate generation and metabolism is important in understanding the pathogenesis of lactic acidosis [1]. Both overproduction and reduced metabolism of lactate appear to be operative in most patients. Cellular lactate generation is influenced by the "redox state" of the cell. The redox state in the cellular cytoplasm is reflected by the ratio of oxidized and reduced nicotine ad Continue reading >>

Hyperglycemic Crises

Hyperglycemic Crises

What They Are and How to Avoid Them One type results in about 100,000 hospitalizations a year with a mortality rate of under 5%. The other is thought to cause fewer hospitalizations, yet the mortality rate is about 15%. Severe hyperglycemic conditions, known as diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS), involve very serious imbalances in blood chemistry and usually require that a person be hospitalized until normal blood chemistry is restored. Because they can occur in anyone with diabetes, everyone should know what causes them, how to prevent them, how they are treated, and when to seek medical attention. The body in balance Glucose metabolism is a complex balancing act. In people who don’t have diabetes, a number of interconnected processes help the body to use glucose and keep blood glucose levels in the normal range. The body constantly balances glucose extracted from foods and produced by the liver with glucose utilization by the body’s tissues. When there is ample glucose in the bloodstream, the liver converts some of it into glycogen for storage. When the body needs more energy, such as during a prolonged period of fasting or activity, the liver converts stored glycogen back into glucose so that it can be used by the body’s tissues. The liver also can create glucose from amino acids and fats. Insulin lowers blood glucose levels both by slowing down the liver’s glucose production and by helping the body’s tissues to use glucose for energy. If the blood glucose level goes too low, other hormones, called counterregulatory hormones, work against the action of insulin to raise blood glucose levels. These hormones include glucagon, epinephrine, growth hormone, and cortisol. All work by prodding the liver to release glucose and by Continue reading >>

Metformin In Type 1 Diabetes

Metformin In Type 1 Diabetes

Is this a good or bad idea? The article by Meyer et al. (1) revives a debate regarding the appropriateness of metformin use for people with type 1 diabetes. Given the potential for coexisting lactic acidosis and diabetic ketoacidosis, how can one justify its use? Indeed, there was little reason to expect a benefit in patients who were studied: nonobese type 1 diabetic subjects with HbA1c <9.0% who were taking ∼0.7 units · kg insulin−1 · day−1. A modest average reduction of daily insulin requirements, 4.3 units, as compared with an increase of 1.7 units for placebo, does not seem to be worth the trade-off of increased risk for severe hypoglycemia (19 events in metformin group vs. 8 events in placebo group). There was no differential effect in terms of HbA1c. Only 7 of 31 patients (23%) treated with metformin responded in terms of a significant (20%) reduction in insulin requirement. Furthermore, it is likely that the incidence of hypoglycemia would be much greater if more aggressive metabolic targets of HbA1c had been applied. Despite the failure to observe diabetic ketoacidosis, the limited number and short period of observation does not permit the conclusion that metformin is safe in ketosis-prone diabetic subjects. We have seen a number of type 1 diabetic patients who have received metformin prescriptions by other practitioners. It appears that these prescriptions were given because of a failure to identify latent autoimmune diabetes in adults or because the physician believed that the potential for insulin dose reduction and lipid improvement justified a putative small risk for diabetic ketoacidosis and lactic acidosis. The temptation to prescribe metformin is increased because of the high prevalence of metabolic syndrome among U.S. adults (2). Indeed, the di Continue reading >>

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