The Experts below are selected from a list of 10500 Experts worldwide ranked by ideXlab platform
Maria E Craig - One of the best experts on this subject based on the ideXlab platform.
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blood β hydroxybutyrate vs urine acetoacetate testing for the prevention and management of Ketoacidosis in type 1 diabetes a systematic review
Diabetic Medicine, 2013Co-Authors: A A Klocker, Helen Phelan, Stephen M Twigg, Maria E CraigAbstract:AbstactAim Diabetic Ketoacidosis is a life-threatening complication of Type 1 diabetes. Blood β-hydroxybutyrate testing is now widely available as an alternative to urine acetoacetate testing for detecting ketosis. The aim of this study was to review the effectiveness of capillary or serum β-hydroxybutyrate compared with urine acetoacetate testing in prevention and management of diabetic Ketoacidosis. Methods MEDLINE, EMBASE, EBM Reviews, The Cochrane Library and CINAHL (until April 2012, no language restrictions, studies in humans) were searched for experimental and observational studies comparing the effectiveness of blood β-hydroxybutyrate and urine acetoacetate testing. Outcomes examined were prevention of diabetic Ketoacidosis, time to recovery from diabetic Ketoacidosis, healthcare costs and patient or caregiver satisfaction. Additional sources included reference lists, conference proceedings and contact with experts in the field. Results Four studies (two randomized controlled trials and two cohort studies) met eligibility criteria, including 299 participants across 11 centres. Risk of bias was low to moderate. Blood ketone testing compared with urine testing was associated with reduced frequency of hospitalization (one study), reduced time to recovery from diabetic Ketoacidosis (three studies), cost benefits (one study) and greater satisfaction (one study, intervention group only). No study assessed prevention of diabetic Ketoacidosis. Meta-analysis could not be performed because of heterogeneity in study design and published data. Conclusions There is evidence suggesting that blood β-hydroxybutyrate testing is more effective than urine acetoacetate testing in reducing emergency department assessment, hospitalization and time to recovery from diabetic Ketoacidosis, as well as potentially lowering healthcare expenditure. Further research in both young people and adults is needed.
Larry A Weinrauch - One of the best experts on this subject based on the ideXlab platform.
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sodium glucose cotransporter 2 inhibition and acidosis in patients with type 2 diabetes a review of us fda data and possible conclusions
International Journal of Nephrology and Renovascular Disease, 2017Co-Authors: John A Delia, Alissa R Segal, George Bayliss, Larry A WeinrauchAbstract:OBJECTIVE To evaluate whether adverse event reports to the US Food and Drug Administration on incidents of Ketoacidosis from use of sodium glucose cotransport inhibitors (SGLT2 inhibitors) provide insight into ways this new class of drugs is being prescribed with other antihyperglycemic agents; to examine possible mechanisms to explain Ketoacidosis. DESIGN AND METHODS Reports of adverse events concerned to SGLT2 inhibitors, namely, empagliflozin, dapagliflozin, and canagliflozin were obtained under the Freedom of Information Act for 5 years ending in August 31, 2015. The data were evaluated for incidents of Ketoacidosis by looking for keywords such as diabetic Ketoacidosis, Ketoacidosis, lactic acidosis, acidosis, and metabolic acidosis. Results were tabulated individually for empagliflozin (n=260 adverse event reports), dapagliflozin (n=520), and canagliflozin (n=2159). Adverse events were categorized according to age, gender, and insulin use. RESULTS There were 46, 144, and 450 reports of Ketoacidosis concerned with the use of empagliflozin, dapagliflozin, and canagliflozin, respectively. The use of SGLT2 inhibitors was not strictly limited to patients with type 2 diabetes but was cut across categories of insulin use, including a total of 172 cases of SGLT2-related Ketoacidosis in individuals above the age of 40 who were not on insulin. CONCLUSION Further studies should focus to detect pleiotropic effects of SGLT2 inhibitors, particularly with other oral antihyperglycemic drugs or insulin. A review of the literature suggests that patients with type 2 diabetes with low C-peptide level may be at increased risk of Ketoacidosis, particularly if they are on statins and diuretics due to hypokalemia and impaired release of insulin. More studies are warranted to further clarify these mechanisms.
Kitchen Anthony - One of the best experts on this subject based on the ideXlab platform.
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Euglycemic Diabetic Ketoacidosis in Type 1 Diabetes on Insulin Pump, with Acute Appendicitis: A Case Report
'Western Journal of Emergency Medicine', 2021Co-Authors: Brian Thompson, Kitchen AnthonyAbstract:Introduction: Recently, euglycemic diabetic Ketoacidosis has been an increasing topic of discussion within emergency medicine literature. Euglycemic diabetic Ketoacidosis can easily be missed, as a normal point-of-care glucose often mistakenly precludes the work-up of diabetic Ketoacidosis. Case report: A 16-year-old female with a past medical history of type 1 diabetes presented to the emergency department with altered mental status, vomiting, and abdominal pain. She was diagnosed with euglycemic diabetic Ketoacidosis. Conclusion: Reported cases of euglycemic diabetic Ketoacidosis are most frequently attributed to sodium glucose cotransporter-2 inhibitors, but other potential causes have been discussed in the literature. In this patient, a starvation state with continued insulin use in the setting of acute appendicitis led to her condition
Simeon I Taylor - One of the best experts on this subject based on the ideXlab platform.
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sglt2 inhibitors may predispose to Ketoacidosis
The Journal of Clinical Endocrinology and Metabolism, 2015Co-Authors: Simeon I Taylor, Jenny E Blau, Kristina I RotherAbstract:Context: Sodium glucose cotransporter 2 (SGLT2) inhibitors are antidiabetic drugs that increase urinary excretion of glucose, thereby improving glycemic control and promoting weight loss. Since approval of the first-in-class drug in 2013, data have emerged suggesting that these drugs increase the risk of diabetic Ketoacidosis. In May 2015, the Food and Drug Administration issued a warning that SGLT2 inhibitors may lead to Ketoacidosis. Evidence Acquisition: Using PubMed and Google, we conducted Boolean searches including terms related to ketone bodies or Ketoacidosis with terms for SGLT2 inhibitors or phlorizin. Priority was assigned to publications that shed light on molecular mechanisms whereby SGLT2 inhibitors could affect ketone body metabolism. Evidence Synthesis: SGLT2 inhibitors trigger multiple mechanisms that could predispose to diabetic Ketoacidosis. When SGLT2 inhibitors are combined with insulin, it is often necessary to decrease the insulin dose to avoid hypoglycemia. The lower dose of insuli...
Edoardo Mannucci - One of the best experts on this subject based on the ideXlab platform.
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effects of sglt 2 inhibitors on diabetic Ketoacidosis a meta analysis of randomised controlled trials
Diabetes Research and Clinical Practice, 2017Co-Authors: Matteo Monami, Besmir Nreu, S Zannoni, Carlotta Lualdi, Edoardo MannucciAbstract:Abstract Aims Diabetic Ketoacidosis (DKA) associated with SGLT-2 inhibitors (SGLT-2i) is a possible adverse event. In fact, SGLT-2i are capable of stimulating the release of glucagon and ketone re-absorption in the renal tubuli, thus increasing the concentration of ketone bodies. Methods A Medline search for SGLT2i (dapagliflozin, empagliflozin, canagliflozin, ipragliflozin, ertugliflozin, luseogliflozin) was performed, collecting all randomized trials with a duration of treatment ≥ 12 weeks, enrolling patients with type 2 diabetes, and comparing a SGLT2i with placebo or other comparators. The principal outcome was the effect of SGLT2i on Ketoacidosis as serious adverse event. Results Out of 72 trials reporting information on DKA, 9 reported at least one event of Ketoacidosis; those eight trials enrolled 10,157 and 5396 in SGLT-2 inhibitors and comparator groups, respectively. No signal of increased risk for Ketoacidosis was observed for SGLT2 inhibitors as a class (MH-OR [95% CI] 1.14 [0.45–2.88], p = 0.78) or as individual molecule. The sensitivity analysis with continuity correction (inputing one event each in drug and comparator arms of each trial with zero events) suggested a reduced incidence of Ketoacidosis in patients treated with SGLT-2 inhibitors (MH-OR 0.65 [0.47–0.90]; p = 0.01). Conclusions The results of clinical trials summarized in the present meta-analysis reassure us that, when the drug is properly prescribed, the risk of DKA is negligible.
