Rationale for treatment options for mealtime glucose control in patients with type 2 diabetes.

While glycemic control is routinely assessed using HbA1c and fasting glucose measures, postprandial glucose (PPG) is also an important contributor of overall glycemia. Furthermore, PPG excursions have been linked to complications of diabetes. This review examines the effects of glucose-lowering therapies (including treatments administered at mealtime) on postprandial hyperglycemia in patients with type 2 diabetes. A PubMed search was conducted to identify clinical studies of treatments for mealtime glucose control in type 2 diabetes. Different treatments may have comparable effects on HbA1c but varying effects on PPG control and glucose fluctuations. Older classes of oral glucose-lowering treatments administered at mealtime to lower PPG include meglitinides and α-glucosidase inhibitors. Injectable therapies, including prandial insulin analogs, glucagon-like peptide-1 receptor agonists (GLP-1RAs), and the amylin analog pramlintide, all effectively target postprandial hyperglycemia. Compared with longer-acting GLP-1RAs, short-acting GLP-1RAs, such as exenatide twice daily and lixisenatide once daily, have a greater effect on PPG control, which is primarily mediated by a more pronounced effect on delayed gastric emptying. Dipeptidyl peptidase-4 inhibitors and sodium-glucose cotransporter 2 inhibitors also reduce postprandial hyperglycemia. To achieve more physiologically normal glycemic control, choice of therapy should ideally aim to address daily glucose fluctuations, including hyperglycemic peaks and hypoglycemic troughs, and long-term glycemic control.

Anatabine supplementation decreases thyroglobulin antibodies in patients with chronic lymphocytic autoimmune (Hashimoto's) thyroiditis: a randomized controlled clinical trial.

CONTEXT: Hashimoto's thyroiditis is less prevalent in tobacco smokers. Anatabine, an alkaloid found in Solanaceae plants including tobacco, has been reported to ameliorate a mouse model of Hashimoto's thyroiditis. OBJECTIVE: The effects of anatabine in patients with Hashimoto's thyroiditis were studied. DESIGN, SETTING, PATIENTS, AND INTERVENTION: This was a double-blind, randomized, placebo-controlled multisite study. A total of 146 patients (70 treated with anatabine and 76 with placebo) completed the study. Approximately 50% of patients in each group were taking levothyroxine. Anatabine lozenges (9-24 mg/d) or placebo, each containing vitamins A and D3, were administered orally 3 times a day for 3 months. MAIN OUTCOME MEASURES: Serum thyroperoxidase antibody (TPOAb) and thyroglobulin antibody (TgAb) levels were assessed. Safety was assessed through adverse events, clinical laboratory evaluations, and vital sign measurements. RESULTS: Anatabine-treated patients had a significant reduction in absolute serum TgAb levels from baseline by study end relative to those receiving placebo (P=.027); however, there were no significant changes or differences in treatment group means for TPOAb or TgAb levels. Mean±SD TgAb values decreased by 46.2±101.1 and 3.9±83.9 World Health Organization units for the anatabine and placebo groups, respectively. Significantly more patients had a >20% drop in TgAb levels in the anatabine than placebo group (P=.023). Overall, the anatabine supplement was safe and well tolerated, although significantly (P<.05) more patients in the anatabine group reported adverse events. CONCLUSIONS: These results demonstrate an immunological effect of anatabine on TgAb levels. Further studies are warranted to determine the longer-term effects and possible actions of anatabine on the course of Hashimoto's thyroiditis.

The prevalence of anemia in patients with chronic kidney disease.

OBJECTIVE: Anemia is a complication of chronic kidney disease and may contribute to adverse clinical outcomes. Early identification and treatment of anemia may improve cardiovascular morbidity and mortality. No large-scale population data are available specifically for patients with chronic kidney disease regarding prevalence of anemia, subpopulations at risk, and relationships between anemia and kidney function. This study was undertaken to address these questions in patients with chronic kidney disease, and investigate the relationship between anemia and glomerular filtration rate. RESEARCH DESIGN AND METHODS: Large-scale, cross-sectional, US multicenter survey; 5222 patients (mean age, 68.2 years; 46.6% male); 237 physician practices. Eligible patients: > or = 18 years of age; serum creatinine: 1.5 mg/dL-6.0 mg/dL (females), 2.0 mg/dL-6.0 mg/dL (males). MAIN OUTCOME MEASURES: Primary study end point: prevalence and severity of anemia (hemoglobin < or = 12 g/dL). Data further stratified by hemoglobin (< or = 12 g/dL, < or = 10 g/dL). RESULTS: Primary etiologies of chronic kidney disease (5222 evaluable patients): diabetes (49.5%); hypertension (33.0%). Glomerular filtration rate: < 60 mL/min/1.73 m2 for 97.7% of evaluable patients. Mean +/- SD serum creatinine level: 2.2 mg/dL +/- 0.9 mg/dL; 2.5 mg/dL +/- 1.0 mg/dL for males, 2.0 mg/dL +/- 0.8 mg/dL for females. Mean +/- SD hemoglobin: 12.2 g/dL +/- 1.6 g/dL (47.7% had hemoglobin < or = 12 g/dL; 8.9% had hemoglobin < or = 10 g/dL). Prevalence of anemia was strongly associated with declining glomerular filtration rate. Percentage of patients with hemoglobin < or = 12 g/dL increased from 26.7% to 75.5% when glomerular filtration rate decreased from > or = 60 mL/min/1.73 m2 to < 15 mL/min/1.73 m2. Prevalence of hemoglobin < or = 10 g/dL increased substantially from 5.2% to 27.2% when glomerular filtration rate diminished from > or = 60 mL/min/1.73 m2 to < 15 mL/min/1.73 m2. After controlling for other patient characteristics associated with increased prevalence of anemia, the prevalence odds ratio for hemoglobin < or = 10 g/dL was 0.54 (0.49-0.60) and for hemoglobin < or = 12 g/dL was 0.68 (0.65-0.72), with each 10-mL/min/1.73 m2 increase in glomerular filtration rate. Predictors of anemia: diabetes, female sex, and race/ethnicity. CONCLUSIONS: Anemia was present in 47.7% of 5222 predialysis patients with chronic kidney disease. Prevalence of anemia increased as kidney function decreased. Certain subgroups are at increased risk for anemia.