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l quantified; determining this impact will be essential to lessen the future impact. Expanding epidemiologic studies of the relationship of diabetes to COVID-19 beyond few high-income countries will also be essential to limit the burden in low- and middle-income countries where 80% of individuals with diabetes reside and where the COVID-19 pandemic has been so damaging.

Type 2 diabetes all-cause mortality (ACM) and myocardial infarction (MI) glycemic legacy effects have not been explained. We examined their relationships with prior individual HbA

values and explored the potential impact of instituting earlier, compared with delayed, glucose-lowering therapy.

Twenty-year ACM and MI hazard functions were estimated from diagnosis of type 2 diabetes in 3,802 UK Prospective Diabetes Study participants. Impact of HbA

values over time was analyzed by weighting them according to their influence on downstream ACM and MI risks.

Hazard ratios for a one percentage unit higher HbA

for ACM were 1.08 (95% CI 1.07-1.09), 1.18 (1.15-1.21), and 1.36 (1.30-1.42) at 5, 10, and 20 years, respectively, and for MI was 1.13 (1.11-1.15) at 5 years, increasing to 1.31 (1.25-1.36) at 20 years. Imposing a one percentage unit lower HbA

from diagnosis generated an 18.8% (95% CI 21.1-16.0) ACM risk reduction 10-15 years later, whereas delaying this reduction until 10 years after diagnosis showed a sevenfold lower 2.7% (3.1-2.3) risk reduction. Corresponding MI risk reductions were 19.7% (22.4-16.5) when lowering HbA

at diagnosis, and threefold lower 6.5% (7.4-5.3%) when imposed 10 years later.

The glycemic legacy effects seen in type 2 diabetes are explained largely by historical HbA

values having a greater impact than recent values on clinical outcomes. Early detection of diabetes and intensive glucose control from the time of diagnosis is essential to maximize reduction of the long-term risk of glycemic complications.

The glycemic legacy effects seen in type 2 diabetes are explained largely by historical HbA1c values having a greater impact than recent values on clinical outcomes. Early detection of diabetes and intensive glucose control from the time of diagnosis is essential to maximize reduction of the long-term risk of glycemic complications.Coronavirus disease 2019 (COVID-19) viral infection, like other infections, triggers an inflammatory response that is usually confined to the respiratory system. However, there is evidence that in a full-blown case, almost all systems of the body may be involved. In addition, there is the syndrome of cytokine storm, characterized by severe systemic inflammation and a massive release of proinflammatory cytokines (1). It is well established that obesity and diabetes are major risk factors for COVID-19 infections and that the morbidity and mortality in association with these conditions is markedly increased. Since both obesity and diabetes are associated with chronic inflammation, it is likely that the inflammatory response to COVID-19 in such patients is affected by the background of chronic inflammation. This review aims to elucidate some of these processes and potential strategies to combat them.

Whether advances in the management of type 1 diabetes are reducing rates of diabetic ketoacidosis (DKA) is unclear. VX-680 solubility dmso We investigated time trends in DKA rates in a national cohort of individuals with type 1 diabetes monitored for 14 years, overall and by socioeconomic characteristics.

All individuals in Scotland with type 1 diabetes who were alive and at least 1 year old between 1 January 2004 and 31 December 2018 were identified using the national register (

= 37,939). DKA deaths and hospital admissions were obtained through linkage to Scottish national death and morbidity records. Bayesian regression was used to test for DKA time trends and association with risk markers, including socioeconomic deprivation.

There were 30,427 DKA admissions and 472 DKA deaths observed over 393,223 person-years at risk. DKA event rates increased over the study period (incidence rate ratio [IRR] per year 1.058 [95% credibility interval 1.054-1.061]). Males had lower rates than females (IRR male-to-female 0.814 [0.776-0.855]). DKA incidence rose in all age-groups other than 10- to 19-year-olds, in whom rates were the highest, but fell over the study. There was a large socioeconomic differential (IRR least-to-most deprived quintile 0.446 [0.406-0.490]), which increased during follow-up. Insulin pump use or completion of structured education were associated with lower DKA rates, and antidepressant and methadone prescription were associated with higher DKA rates.

DKA incidence has risen since 2004, except in 10- to 19-year-olds. Of particular concern are the strong and widening socioeconomic disparities in DKA outcomes. Efforts to prevent DKA, especially in vulnerable groups, require strengthening.

DKA incidence has risen since 2004, except in 10- to 19-year-olds. Of particular concern are the strong and widening socioeconomic disparities in DKA outcomes. Efforts to prevent DKA, especially in vulnerable groups, require strengthening.

Patients with type 1 diabetes (T1D) exhibit modest lipid abnormalities as measured by traditional metrics. This study aimed to identify lipidomic predictors of rapid decline of kidney function in T1D.

In a case-control study, 817 patients with T1D from three large cohorts were randomly split into training and validation subsets. Case was defined as >3 mL/min/1.73 m

per year decline in estimated glomerular filtration rate (eGFR), while control was defined as <1 mL/min/1.73 m

per year decline over a minimum 4-year follow-up. Lipids were quantified in baseline serum samples using a targeted mass spectrometry lipidomic platform.

At individual lipids, free fatty acid (FFA)202 was directly and phosphatidylcholine (PC)160/226 was inversely and independently associated with rapid eGFR decline. When examined by lipid class, rapid eGFR decline was characterized by higher abundance of unsaturated FFAs, phosphatidylethanolamine (PE)-Ps, and PCs with an unsaturated acyl chain at the sn1 carbon, and by lower abundance of saturated FFAs, longer triacylglycerols, and PCs, PEs, PE-Ps, and PE-Os with an unsaturated acyl chain at the sn1 carbon at eGFR ≥90 mL/min/1.