Euglycemic diabetic ketoacidosis (eu-DKA) is an uncommon and serious adverse event associated with the use of sodium-glucose cotransporter (SGLT-2) inhibitors. It is a state of increased anion gap metabolic acidosis with ketosis but in the setting of normal serum glucose levels. Diagnosis of this serious entity could easily be missed given the non-specific symptoms and the normal glucose measurements. This ketogenic state can be triggered by various stressors including infection, surgery, myocardial infarctions, omission of insulin dosage, as well as low carbohydrate diet. In this report, we present a case of eu-DKA in a 68-year-old woman with type 2 diabetes that occurred in the postoperative period of glaucoma surgery. She was started shortly before surgery on SGLT-2 inhibitor (ertugliflozin). While the diagnosis was initially missed, it was subsequently confirmed when she presented with reduced appetite, generalized fatigue, and constipation. Ertugliflozin was discontinued, and she was successfully treated with conservative management and without insulin drip. This case highlights the need to consider the diagnosis of eu-DKA in patients treated with SGLT-2 inhibitors since the diagnosis could easily be missed especially in the postoperative period with the non-characteristic symptomatology and normoglycemia.
With its alarmingly rising prevalence worldwide, type 2 diabetes has become a leading cause of morbidity and mortality around the planet. Efforts to prevent progression to diabetes in individuals at risk could have a significant positive public health impact. Multiple trials examining cardiovascular outcomes of Renin-Angiotensin-Aldosterone System (RAAS) inhibitors revealed, in secondary analysis, a significantly reduced risk of new onset diabetes in participants receiving these agents. This glycemic protective effect is attributed to the known implication of RAAS in the development of insulin resistance and type 2 diabetes. The DREAM trial and the NAVIGATOR trial were two large randomized controlled studies examining, as primary outcome, the effect of Ramipril and Valsartan respectively on the incidence of diabetes in patients with prediabetes. Their results confirmed a favorable glycemic effect of RAAS inhibition agents and suggested a possible added benefit of diabetes prevention to their other several cardiovascular and blood pressure benefits.
IntroductionAlthough the association between gout and cardiovascular disease (CVD) has been extensively studied, scarce data are available for the Black population. We aimed to assess the association between gout and CVD in a predominantly Black urban population with gout.MethodsA cross-sectional analysis was performed between a gout cohort and an age-/sex-matched control group. Clinical parameters and 2D echocardiograms were reviewed for the patients with gout and heart failure (HF). The primary outcome studied includes the prevalence and strength of association between gout and CVD. Secondary outcomes studied includes strength of association of gout and HF categorized by ejection fraction, mortality, and HF readmissions.ResultsFour hundred seventy-one patients with gout had a mean age of 63.7 ± 0.5 years; 89% were Black, 63% were men, and mean body mass index was 31.3 ± 0.4 kg/m2. Hypertension, diabetes mellitus, and dyslipidemia were present in 89%, 46%, and 52%, respectively. Compared with controls, patients with gout had significantly higher rates of angina, arrhythmia, coronary artery disease/stents, myocardial infarction, coronary artery bypass graft surgery, cerebrovascular accident, and peripheral vascular disease. The adjusted odds ratio for CVD was 2.9 (95% confidence interval, 1.9–4.5; p < 0.001). Gout patients had a higher prevalence of HF with 45% (n = 212) compared with controls with 9.4% (n = 44). Adjusted odds ratio for HF risk was 7.1 (95% confidence interval, 4.7–10.6; p < 0.01).ConclusionsGout in a predominantly Black population confers 3 times the CVD risk and 7 times HF-specific risk compared with age- and sex-matched cohort. Further research is needed to confirm our findings and to develop interventions to reduce morbidity associated with gout.
Background: Pseudohypoglycemia is a condition where the measured glucose level is falsely lower than the actual level. It can be due to impaired circulation or in vitro glycolysis. Clinical Case: Patient 1: A 58-year-old male with a past medical history of sickle cell trait was admitted for alcohol intoxication. Low blood glucose levels were found on finger stick point-of-care testing (POCT). Fasting and postprandial glucose levels were between 17 and 60 mg/dL. The patient was asymptomatic, alert with no tremor, palpitation, or sweating. Glucose POCT was repeated from the earlobe each time a low finger stick level was found, showing normal glucose levels ranging between 85 to 115 mg/dL, confirmed with venous blood glucose measurement. On examination, the patient had mild skin thickening of the hands, with no acrocyanosis, calcinosis, or finger ulceration—normal peripheral pulses with no signs of heart failure. Lab results showed macrocytic anemia, otherwise normal metabolic panel. ANA, anti-Scl-70, and anticentromere antibodies were negative. Patient 2: A 91-year-old female admitted for decompensated heart failure was incidentally found to have fasting glucose levels on finger stick POCT ranging between 30–50 mg/dL. Postprandial glucose on finger stick POCT was ranging between 55–120 mg/dL. Venous glucose levels were ranging between 90 and 180 mg/dL. The patient was alert and asymptomatic. Examination showed bilateral acrocyanosis, poor peripheral circulation with capillary refill > 5 seconds, pitting pedal edema, elevated JVP, and crackles on chest auscultation. Labs showed BNP levels of 1130 pg/mL (n < 100 pg/mL), with ejection fraction of about 35% on echocardiography. Heart failure management was optimized, and warming of the hands with blankets improved peripheral circulation, with capillary refill < 2 seconds, and resolution of cyanosis coinciding with matching of finger stick POCT glucose levels to that of venous blood. Both patients were asymptomatic at the time of low POCT glucose and thus did not fulfill Whipple’s triad (measured hypoglycemia, symptomatic, a reversal of symptoms on glucose administration). Furthermore, they had no history of diabetes or the use of any hypoglycemic agents. Thus, normal venous blood glucose levels documented at the time of low POCT glucose lead to a diagnosis of pseudohypoglycemia. The etiology in patient 1 was likely due to peripheral vascular disease. In patient 2, the cause was likely due to congestive heart failure, with poor peripheral perfusion. Clinical Lesson: Low glucose levels are frequently encountered in clinical practice. It is essential to check if the non-diabetic patient is symptomatic or not. It is worth checking glucose levels from other sites in asymptomatic patients who do not fulfill Whipple’s triad before preceding into an elaborate hypoglycemia work-up.
Introduction: While the association between gout and cardiovascular disease (CVD) has been extensively studied, scarce data is available for the Black population. We aimed to assess, in a predominantly Black urban population with gout, the prevalence of traditional CVD risk factors, CV outcomes, and the strength of the association between gout and CVD after adjusting for CVD risk factors. Hypothesis: Black patients with gout have higher CVD rates compared to a matched cohort without gout. Methods: Cross-sectional analysis of data obtained from the EMR of gout patients followed at our primary care clinics. Patients were identified by ICD codes and compared to age, sex and race matched non- gout cohort. Descriptive data was obtained, and logistic regression used to assess the strength of association between gout and CVD, before and after adjustment for CVD risk factors including obesity, DM, HTN, dyslipidemia and smoking. Results: There were 471 patients with gout with a mean age of 63.7 ± 0.5 years (mean ±SEM); 89% were Black, 63% were men, mean BMI was 31.3 ± 0.4 Kg/m 2 . HTN, DM and dyslipidemia were present in 89%, 46% and 52% respectively.Compared to controls, patients with gout had significantly higher rates of angina, arrythmia, CAD/stents, MI, CABG, CVA, and PVD. The odds ratio (OR) for CVD = 4.5 (3.3-6.2) (95% CI), p<0.001 and OR =2.9 (1.9-4.5), p<0.001 before and after adjustment for CVD risk factors respectively. There was a significantly higher mortality rate of 6.2 in gout vs 2.6 in the non- gout cohort, p <0.01. Conclusion: Gout in a predominantly Black population confers three times the CVD risk and overall mortality compared to a race, age and sex-matched cohort.This risk appears greater compared to previously published data in whites (OR 1.25-1.55) (Choi HK et al Circulation 2007;116:894-900). Further research is needed to confirm our findings and to develop interventions to reduce morbidity and mortality among these vulnerable patients.
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