Data regarding improvement in glycemic control with glucagon-like peptide-1 receptor agonists have been inconsistent. In 2013, canagliflozin was the 1st SGLT-2 inhibitor therapy to be authorized for use in the United States after early results from the CANVAS trial showed significant improvement in cardiovascular end result in individuals with DM2. changes in blood pressure or lipid profiles were seen except for a slight increase in low-density lipoprotein (= .049). No individual developed euglycemic diabetic ketoacidosis. Three individuals discontinued therapy due lorcaserin hydrochloride (APD-356) to uncontrolled genital yeast infections. Summary: SGLT-2 inhibitors can be a useful adjunctive therapy in individuals with DM1 to improve glycemic control and excess weight. Although our study did not display any significant changes in the metabolic profile and insulin requirements in these individuals, a larger sample size may yield different results. = .032) with therapy. Improvement in glycemic control was seen as early as one month posttherapy and was managed with continued SGLT-2 inhibitor use. There was a slight increase in LDL level with therapy, from mean of 93 mg/dL (SD 29) to 98 mg/dL (SD 32); = .049. No significant changes lorcaserin hydrochloride (APD-356) were seen with regard to excess weight (= .518), systolic BP (= .95), diastolic BP (= .273), triglycerides (= .84), high-density lipoprotein (HDL; = .094), or cholesterol (= .60). Changes in the metabolic profile are demonstrated table 3. There was a nonsignificant poor negative correlation between HbA1c switch and Goserelin Acetate duration of SGLT-2 inhibitor therapy (rho -0.2, p=0.35) indicating that the switch in HbA1c may not be solely associated with the latter; limitation may be due to low power to detect variations. Table 2. Characteristics of the Individuals Who Either Experienced No Improvement or Worsening of Glycemic Control With SGLT-2 Inhibitor Therapy. thead th align=”remaining” rowspan=”1″ colspan=”1″ HbA1c Switch (%) /th th align=”center” rowspan=”1″ colspan=”1″ Insulin Routine /th th align=”center” rowspan=”1″ colspan=”1″ SGLT-2 Inhibitor Prescribed /th th align=”center” rowspan=”1″ colspan=”1″ Duration of SGLT-2 Inhibitor Therapy (Weeks) /th th align=”center” rowspan=”1″ colspan=”1″ Reason for SGLT-2 Inhibitor Discontinuation /th th align=”center” rowspan=”1″ colspan=”1″ Age (Years) /th th align=”center” rowspan=”1″ colspan=”1″ BMI (kg/m2) /th th align=”center” rowspan=”1″ colspan=”1″ Gender /th th align=”center” rowspan=”1″ colspan=”1″ Duration of DM1 Prior to Initiation of SGLT-2 Inhibitor Therapy (Weeks) /th /thead No changeInsulin pumpCanagliflozin 300 mg daily146830MaleNew diagnosisIncrease by 0.4Insulin pumpEmpagliflozin 25 mg daily122422Male12Increase by 1Insulin pumpEmpagliflozin 10 mg daily117327Female5Increase by 1.3Basal/BolusCanagliflozin 100 mg daily12422Male24Increase by 0.2Basal/BolusCanagliflozin 100 mg daily4Fatigue5425Male3Increase by 0.7Basal/BolusCanagliflozin 300 mg daily3Cost4829Female1 Open in a separate window Abbreviations: SGLT-2 inhibitor, sodium-glucose cotransporter 2 inhibitor; DM1, diabetes mellitus type 1. Table 3. Changes in the Metabolic Profile Seen With SGLT-2 Inhibitor Therapy in Individuals With DM1. thead th align=”remaining” rowspan=”1″ colspan=”1″ Characteristics /th th align=”center” rowspan=”1″ colspan=”1″ Pretherapy Mean /th th align=”center” rowspan=”1″ colspan=”1″ Posttherapy Mean /th th align=”center” rowspan=”1″ colspan=”1″ SD /th th align=”center” rowspan=”1″ colspan=”1″ em lorcaserin hydrochloride (APD-356) P /em /th /thead HbA1c (%)8.277.91.2.032Weight (kg)88.48810.1.518Systolic BP (mm Hg)121.5121.813.9.951Diastolic BP (mm Hg)73719.9.273TG (mg/dL)839555.841Cholesterol (mg/dL)16916546.603HDL (mg/dL)606119.094LDL (mg/dL)929832.034 Open in a separate window Abbreviations: SGLT-2 inhibitor, sodium-glucose cotransporter 2 inhibitor; DM1, diabetes mellitus type 1; BP, blood pressure; TG, triglycerides; LDL, low-density lipoprotein; HDL, high-density lipoprotein; SD, standard deviation. Adverse Events No individuals developed euglycemic diabetic ketoacidosis. The medication was discontinued in 3 individuals due to uncontrolled genital yeast infections. Cost was a limiting factor in most individuals as the cost can range up to several hundred dollars for a month supply if not covered by the insurance Conversation DM1 is definitely a lifelong disease requiring continuous insulin therapy. Glycemic control is essential in these individuals to help decrease the development of microvascular and macrovascular complications. Intensification of therapy is usually limited out of lorcaserin hydrochloride (APD-356) concern for hypoglycemic episodes. Insulin is also associated with weight gain and worsening of blood pressure due to its anabolic effects, which in turn may exacerbate cardiovascular complications. The part of oral medications to target the metabolic profile of these individuals is currently becoming investigated. To day, pramlintide is the only oral medication authorized for use in individuals with DM1. Its use may be limited by multiple daily dosing and gastrointestinal side effects. Metformin has not been shown to improve HbA1c levels in individuals with DM1 despite the significant improvement in excess weight and insulin requirements seen. Similarly, dipeptidyl peptidase-4 inhibitors have been shown to reduce insulin requirements without a significant switch in the HbA1c level. Data concerning improvement in glycemic control with glucagon-like peptide-1 receptor agonists have been inconsistent. In 2013, canagliflozin was the 1st SGLT-2 inhibitor therapy to be authorized for use in the United States after early results from the CANVAS trial showed significant improvement in cardiovascular end result in individuals with DM2. Studies possess since demonstrated significant cardiovascular and renal benefit in individuals with DM2 on the various SGLT-2 inhibitor therapy. The significant improvement in excess weight, insulin.
Data regarding improvement in glycemic control with glucagon-like peptide-1 receptor agonists have been inconsistent