Practice Update: DIABETES

AACE 2017 13

consistent with diabetic ketoacidosis. Records were reviewed on 224 patients with diabetic ketoacidosis and 151 individuals with diabetes but not diabetic ketoacidosis (beta-hydroxybutyrate <3.8 mmoL/L). Among patients with diabetic ketoacido- sis, serum bicarbonate was >18 mEq/L in 17%, consistent with previous reports. Urine ketones were negative to trace in 21%, and glucose was <250 mg/dL in 4%. Urine ketones and serum bicarbonate were both negative for diabetic ketoacidosis in 7%. Among individuals who did not experience diabetic ketoacidosis, 17% harbored small to large urine ketones, 18% serum bicarbo- nate ≤18 mEq/L, and 4%, both. Thus, 35% of patients who experienced diabetic ketoac- idosis as defined by beta-hydroxybutyrate lacked one or more American Diabetic Association diagnostic laboratory criteria. Thirty-one percent who did not experi- ence diabetic ketoacidosis fulfilled criteria for diabetic ketoacidosis with respect to serum bicarbonate, ketonuria, or both. When patients with diabetes who are admitted to the hospital are characterized as suffering from diabetic ketoacidosis or not based on admission beta- hydroxybutyrate, substantial discordance with American Diabetes Association diagnostic criteria is observed. Specifically, serum bicarbonate and urine ketones were often at odds with beta-hydroxybutyrate results. This is not surprising, considering the limitations of the urine ketone test and the fact that a serum bicarbonate ≤18 mEq/L is not specific for diabetic ketoacidosis. The results argue in favor of the use of serum beta-hydroxybutyrate to diagnose diabetic ketoacidosis, at least in hospi- tals with sufficient admissions for diabetic ketoacidosis to justify test availability. Dr Miles concluded that beta-hydroxybu- tyrate measurement should not supersede clinical judgment in the care of patients with diabetic ketoacidosis, but the meas- urement does add diagnostic rigor. If validated in other studies, interventions may be designed to reduce hospital readmissions in this population. Such interventions could help save the healthcare system billions of dollars.

Heart failure deserves more scrutiny as a complication of type 2 diabetes While much attention is given to the microvascular effects of type 2 diabetes, such as diabetic retinopathy, nephropathy, neuropathy; and macrovascular consequences such as stroke, myocardial infarction, and peripheral vascular disease, heart failure is a seventh and more sinister

complication that raises mortality. T his conclusion was based on an in-depth session entitled, “Heart Failure: The Frequent, Forgotten and Often Fatal Complication of Type 2 Diabetes”. David S.H. Bell, MD, of the University of Ala- bama at Birmingham School of Medicine, has performed clinical trials on the effects of angiotensin II receptor blockers in patients with diabetes and diastolic dysfunction. He suggested that the evidence should pro- pel endocrinologists to screen symptomatic patients more rigorously and to consider treating heart failure to mitigate the poor outcomes often seen in these patients. Anti-heart failure therapies such as angiotensin- converting-enzyme inhibitors and others work similarly well in individuals with diabetes as in those without diabetes. He said, “It’s not widely realized how common this condition is. Between 40 and 45% percent of US patients with diabetes suffer heart failure vs 12% of nondiabetics. Mortality depends on the degree of glycemic control.” Dr Bell highlighted studies that examined

has been found to increase heart failure in patients with diabetes. An expert in kidney disease and diabetes as major, independent risk factors for the development of heart failure, Dr Gilbert highlighted the relation between gly- cemic control and heart failure risk. He focused on evidence of the detrimental and beneficial effects of various types of hypoglycemic drugs. Aaron I. Vinik, PhD, FCP, MACP, FACE, of Eastern Virginia Medical School, Norfolk, presented his research on autonomic neuropathy, one of the most overlooked complications of type 2 diabetes, contrib- uting to the high incidence of heart failure. Vascular damage extends to involuntary nerves that stimulate the heart and blood vessels, resulting in heart rate and vascu- lar abnormalities. Dr Vinik noted that autonomic system dysfunction is a predictor of cardiovas- cular risk and sudden death in patients with type 2 diabetes. Autonomic dysfunc- tion also occurs in prediabetes, offering opportunities for early intervention. Impor- tant technological advances in technology during the past decade allow for identi- fication of early stages of autonomic dysfunction using objective, standardized measurements.

the complex effect of diabetes and contributing factors to the three causes of the heart fail- ure, including coronary artery disease, left ventricular hyper- trophy (approximately 65% of patients with type 2 diabetes), and diabetic cardiomyopathy. Richard E. Gilbert, MD, PhD, FRCPC, of the University of Toronto, Canada, noted that anti-heart failure therapies such as angiotensin-converting- enzyme inhibitors and others work similarly well in individuals with diabetes as in thosewithout diabetes. The glucose-lowering drug dipeptidylpeptidase-4 inhibitor saxagliptin, however,

PracticeUpdate Editorial Team

PracticeUpdate Editorial Team

© Photo by Jean Whiteside/AACE 2017

VOL. 1 • NO. 1 • 2017