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Diabetes mellitus is a major health problem in Costa Rica. Its prevalence is increasing and represents a significant burden. Objectives: To determine specific diabetes mortality rates (SDMR) in Costa Rica from 2007 to 2017 and explore it's potential causes. Methods: Death certificates (classification CIE-10) were obtained from the Instituto Nacional de Estadística y Censos. All-cause mortality, SDMR, ischemic heart disease (IHD), cerebrovascular disease (CVD), and peripheral vascular disease mortality were assessed per year, sex, age and province. We evaluated relationships between SDMR and Index of Human Development (IHUD), performed a multivariate regression negative binomial model analysis and compared SDMR with goals of metabolic control in the primary care setting. Results: All-cause mortality and SDMR increased while IHD and CVD mortality rates remained invariable. SDMR was higher in females and in provinces with predominant rural areas. The years of observation, sex, age and province were significant predictors of death at a 5% level in people with diabetes. Reports from primary care setting showed inadequeate public health care coverage and insuficient metabolic control. Conclusions: SDMR increased in elderly patients with specific complications. Age, place of residence and sex predicted SDMR. Unsatisfactory diabetes medical coverage and poorly diabetes management likely explain our findings.

Objective: To report an episode of diabetic ketoacidosis (DKA) in a patient with type 1 diabetes mellitus treated with low doses of neutral protamine Hagedorn insulin. The patient had recently initiated treatment with a sodiumglucose cotransporter-2 inhibitor as well. Methods: We describe the clinical presentation, laboratory data, and management of a diabetic patient with DKA. Results: A 50-year-old diabetic male presented with weight loss, fatigue, nausea, recurrent vomiting, muscle pain, malaise, and shortness of breath 2 weeks after initiation of empagliflozin and reduction in insulin dose. On admission to the emergency department, the glucose concentration was 541 mg/dL, pH 7.087, bicarbonate 4.5 mmol/L, blood urea nitrogen 50 mg/dL, creatinine 2.0 mg/ dL, and beta-hydroxybutirate 4.1 mmol/L. The estimated osmolality was 319.9 mOsm/L and the anion gap was 25.6 mEq/L. Empagliflozin was discontinued; the patient was treated with balanced electrolyte solutions and continuous insulin infusion with resolution of acute kidney injury and metabolic acidosis. C-peptide level was <0.1 ng/mL and anti-glutamic acid decarboxylase-65 was 6 IU/mL (reference range is <5 IU/mL). Conclusion: In this patient, who was misdiagnosed with type 2 diabetes mellitus, the insulin dose reduction provoked DKA. When selecting sodium-glucose cotransporter-2 inhibitors in diabetics, physicians must assure adequate insulin provision as well as strict monitoring of blood glucose and urine ketones. (AACE Clinical Case Rep. 2018;4:e505-e508) Abbreviations: DKA = diabetic ketoacidosis; NPH = neutral protamine Hagedorn; SGLT2 = sodium-glucose cotransporter-2; T1DM = type 1 diabetes mellitus; T2DM = type 2 diabetes mellitus e506 DKA in T1DM with SGLT2 inhibitor, AACE Clinical Case Rep. 2018;4(No. 6)