ObjectiveThe primary aim was to evaluate the extent to which persons with type 1 diabetes perform self-monitoring of blood glucose (SMBG) according to guidelines. Secondary objectives were to investigate predictors for good SMBG adherence, reasons for non-adherence, and association between SMBG frequency and hemoglobin A1c (HbA1c).MethodsThis was a survey-based cross-sectional study. Questionnaires were sent out to 600 random patients at five sites. Patients were included if they were diagnosed with type 1 diabetes and ≥18 years old and excluded if they were currently using continuous glucose monitoring (CGM). Analysis of data was performed separately for the three sites where the answer frequency was ≥70%.ResultsIn total, 138 of 314 study participants, 43.9% (95% CI 38.5% to 49.4%) performed SMBG ≥4 times per day. For the three clinics where ≥70% of surveyed patients were included in the analysis, results were similar, 41.3% (95% CI 34.7% to 47.8%). Top three reported reasons for not performing more frequent SMBG were lack of time, not remembering, and self-consciousness. Frequency of SMBG was associated with HbA1c levels (p<0.0001). 30% of patients believed that ≤3 SMBG/day was recommended by healthcare providers.ConclusionsLess than 50% of patients in Sweden follow guidelines of SMBG ≥4 times per day, despite glucose meters and strips being generally available at no cost. This indicates a need for further support in performing SMBG and increased availability of other tools for glucose monitoring.

BackgroundNeurodegeneration occurs during the early stages of multiple sclerosis. It is an essential, devastating part of the pathophysiology. Tools for measuring the degree of neurodegeneration could improve diagnostics and patient characterization.ObjectiveThis study aimed to determine the diagnostic value of biomarkers of degeneration in patients with recent clinical onset of suspected multiple sclerosis, and to evaluate these biomarkers for characterizing disease course.MethodsThis cross-sectional study included 271 patients with clinical features of suspected multiple sclerosis onset and was the baseline of a prospective study. After diagnostic investigations, the patients were classified into the following disease groups: patients with clinically isolated syndrome (n = 4) or early relapsing remitting multiple sclerosis (early RRMS; n = 93); patients with relapsing remitting multiple sclerosis with disease durations ≥2 years (established RRMS; n = 39); patients without multiple sclerosis, but showing symptoms (symptomatic controls; n = 89); and patients diagnosed with other diseases (n = 46). In addition, we included healthy controls (n = 51) and patients with progressive multiple sclerosis (n = 23). We analyzed six biomarkers of neurodegeneration: cerebrospinal fluid neurofilament light chain levels; cerebral spinal fluid glial fibrillary acidic protein; cerebral spinal fluid tau; retinal nerve fiber layer thickness; macula volume; and the brain parenchymal fraction.ResultsExcept for increased cerebral spinal fluid neurofilament light chain levels, median 670 ng/L (IQR 400–2110), we could not find signs of early degeneration in the early disease group with recent clinical onset. However, the intrathecal immunoglobin G production and cerebral spinal fluid neurofilament light chain levels showed diagnostic value. Moreover, elevated levels of cerebral spinal fluid glial fibrillary acidic protein, thin retinal nerve fiber layers, and low brain parenchymal fractions were associated with progressive disease, but not with the other phenotypes. Thin retinal nerve fiber layers and low brain parenchymal fractions, which indicated neurodegeneration, were associated with longer disease duration.ConclusionsIn clinically suspected multiple sclerosis, intrathecal immunoglobin G production and neurofilament light chain levels had diagnostic value. Therefore, these biomarkers could be included in diagnostic work-ups for multiple sclerosis. We found that the thickness of the retinal nerve fiber layer and the brain parenchymal fraction were not different between individuals that were healthy, symptomatic, or newly diagnosed with multiple sclerosis. This finding suggested that neurodegeneration had not reached a significant magnitude in patients with a recent clinical onset of multiple sclerosis.

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 1c values and explored the potential impact of instituting earlier, compared with delayed, glucose-lowering therapy. RESEARCH DESIGN AND METHODSTwenty-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 1c values over time was analyzed by weighting them according to their influence on downstream ACM and MI risks. RESULTS