XI. STRATEGIES FOR IMPROVING DIABETES CARE D iabetes is a chronic illness that requires continuing medical care and patient self-management education to prevent acute complications and to reduce the risk of long-term complications. Diabetes care is complex and requires that many issues, beyond glycemic control, be addressed. A large body of evidence exists that supports a range of interventions to improve diabetes outcomes. These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care. While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided. These standards are not intended to preclude more extensive evaluation and management of the patient by other specialists as needed. For more detailed information, refer to Bode (Ed.): Medical Management of Type 1 Diabetes (1), Burant (Ed): Medical Management of Type 2 Diabetes (2), and Klingensmith (Ed): Intensive Diabetes Management (3). The recommendations included are diagnostic and therapeutic actions that are known or believed to favorably affect health outcomes of patients with diabetes. A grading system (Table 1), developed by the American Diabetes Association (ADA) and modeled after existing methods, was utilized to clarify and codify the evidence that forms the basis for the recommendations. The level of evidence that supports each recommendation is listed after each recommendation using the letters A, B, C, or E.

Standards of Medical Care in Diabetes

Summary Background Since December, 2019, Wuhan, China, has experienced an outbreak of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Epidemiological and clinical characteristics of patients with COVID-19 have been reported but risk factors for mortality and a detailed clinical course of illness, including viral shedding, have not been well described. Methods In this retrospective, multicentre cohort study, we included all adult inpatients (≥18 years old) with laboratory-confirmed COVID-19 from Jinyintan Hospital and Wuhan Pulmonary Hospital (Wuhan, China) who had been discharged or had died by Jan 31, 2020. Demographic, clinical, treatment, and laboratory data, including serial samples for viral RNA detection, were extracted from electronic medical records and compared between survivors and non-survivors. We used univariable and multivariable logistic regression methods to explore the risk factors associated with in-hospital death. Findings 191 patients (135 from Jinyintan Hospital and 56 from Wuhan Pulmonary Hospital) were included in this study, of whom 137 were discharged and 54 died in hospital. 91 (48%) patients had a comorbidity, with hypertension being the most common (58 [30%] patients), followed by diabetes (36 [19%] patients) and coronary heart disease (15 [8%] patients). Multivariable regression showed increasing odds of in-hospital death associated with older age (odds ratio 1·10, 95% CI 1·03–1·17, per year increase; p=0·0043), higher Sequential Organ Failure Assessment (SOFA) score (5·65, 2·61–12·23; p Interpretation The potential risk factors of older age, high SOFA score, and d-dimer greater than 1 μg/mL could help clinicians to identify patients with poor prognosis at an early stage. Prolonged viral shedding provides the rationale for a strategy of isolation of infected patients and optimal antiviral interventions in the future. Funding Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences; National Science Grant for Distinguished Young Scholars; National Key Research and Development Program of China; The Beijing Science and Technology Project; and Major Projects of National Science and Technology on New Drug Creation and Development.

Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study

In the past decade, extracellular vesicles (EVs) have been recognized as potent vehicles of intercellular communication, both in prokaryotes and eukaryotes. This is due to their capacity to transfer proteins, lipids and nucleic acids, thereby influencing various physiological and pathological functions of both recipient and parent cells. While intensive investigation has targeted the role of EVs in different pathological processes, for example, in cancer and autoimmune diseases, the EV-mediated maintenance of homeostasis and the regulation of physiological functions have remained less explored. Here, we provide a comprehensive overview of the current understanding of the physiological roles of EVs, which has been written by crowd-sourcing, drawing on the unique EV expertise of academia-based scientists, clinicians and industry based in 27 European countries, the United States and Australia. This review is intended to be of relevance to both researchers already working on EV biology and to newcomers who will encounter this universal cell biological system. Therefore, here we address the molecular contents and functions of EVs in various tissues and body fluids from cell systems to organs. We also review the physiological mechanisms of EVs in bacteria, lower eukaryotes and plants to highlight the functional uniformity of this emerging communication system.

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Biological properties of extracellular vesicles and their physiological functions

1. Type 1 diabetes (due to b-cell destruction, usually leading to absolute insulin deficiency) 2. Type 2 diabetes (due to a progressive insulin secretory defect on the background of insulin resistance) 3. Gestational diabetes mellitus (GDM) (diabetes diagnosed in the second or third trimester of pregnancy that is not clearly overt diabetes) 4. Specific types of diabetes due to other causes, e.g., monogenic diabetes syndromes (such as neonatal diabetes and maturity-onset diabetes of the young [MODY]), diseases of the exocrine pancreas (such as cystic fibrosis), and drugor chemical-induced diabetes (such as in the treatment of HIV/AIDS or after organ transplantation)

Classification and diagnosis of diabetes

https://academicworks.medicine.hofstra.edu/cgi/viewcontent.cgi?article=7158&context=articles

COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-up

Should women with abnormal serum thyroid stimulating hormone undergo screening for anemia

A specific subset of micro RNAs (miRs), including miR-133 and miR-206, is specifically expressed in muscle tissue, so that they are currently defined as muscular miRs (myomiRs). To further elucidate the role of myomiRs in muscle biology, we measured miR-133a and miR-206 in plasma of 28 middle-age recreational athletes. The study population consisted of 28 middle aged, recreation athletes (11 women and 17 men; mean age, 46 years) who completed a 21.1 km, half-marathon. The plasma concentration of miR-133a and miR-206, the serum concentration of creatine kinase (CK) and high-sensitivity (HS) cardiac troponin T (cTnT), as well as capillary lactate, were measured before and immediately after the run. The median serum concentration of total CK (257 versus 175 U/L; p < .001), cTnT (17.8 versus 5.6 ng/L; p < .001), and the plasma values of both miR-133a (4.22 versus 0.64 × 10-4; p < .001) and miR-206 (1.36 versus 0.63 × 10-4; p = .001) were considerably increased immediately after the half-marathon run. In multivariate analysis only post-exercise capillary lactate was found to be independently associated with running time. A significant and independent correlation was observed between plasma variations of the two miRs, but not with other physiological or laboratory parameters. The results of this study suggest that the biological significance of miR-133a and 206 variation after middle-distance running parallels but not overlaps the release of biomarkers of nonspecific tissue damage. Enhanced plasma values of these myomiRs may hence reflect a physiological response to high-intensity and/or prolonged exercise rather than tissue injury.

Influence of middle-distance running on muscular micro RNAs.

BACKGROUND Although it is known that glucose concentration exhibits a time-dependent decay in uncentrifuged serum and lithium-heparin blood tubes, no evidence exists on how this variation may depend on blood cell counts (CBC) and volumes. METHODS Venous blood was drawn from 30 non fasting healthy volunteers into three serum and three lithium-heparin tubes. One serum and lithium-heparin tubes were centrifuged within 15 min after collection and glucose was measured with a hexokinase assay. The second and third serum and lithium-heparin tubes were maintained at room temperature for 1 and 2 h after the first tubes were centrifuged. These other tubes were then centrifuged and glucose was measured. CBC was performed in the first lithium-heparin tube, before centrifugation. RESULTS The mean decrease of glucose was higher in lithium-heparin plasma than in serum (0.33 vs. 0.24 mmol/L/h; p<0.001). Glucose concentration decreased by 7% and 5% per hour in lithium-heparin plasma and serum, respectively. In univariate analysis, the absolute decrease of glucose concentration was associated with sex (higher in men than in women), red blood cell (RBC) count, hematocrit, white blood cell (WBC) count, neutrophils and monocytes in both lithium-heparin plasma and serum. In multivariate analysis, the decrease of glucose concentration remained independently associated with RBC, WBC, neutrophils and monocytes in both sample matrices. No significant association was found with platelet number and erythrocyte or platelet volume. CONCLUSIONS Glucose concentration decrease in uncentrifuged lithium-heparin and serum tubes depends on the baseline number of RBC, WBC, neutrophils and monocytes within the tubes.

Impact of blood cell counts and volumes on glucose concentration in uncentrifuged serum and lithium-heparin blood tubes

Cardiac troponin T during sickle cell crisis.

Haemochromatosis, a disease characterised by an increase in iron storage which may cause pathological changes1, is divided into primary or secondary forms. While primary (or genetic) haemochromatosis, the most common autosomal recessive disorder, is due in the majority of cases to mutations in the HFE gene, secondary haemochromatosis can have several causes including ineffective erythropoiesis and multiple red blood cell transfusions1,2.

A number of studies have documented that subjects carrying mutations in the haemochoromatosis gene have significantly increased peripheral blood erythrocyte indices (haematocrit, haemoglobin and mean corpuscular haemoglobin concentrations), compared with wild-type individuals, thus suggesting an evolutionary sex-related protecting role against iron deficiency3–7. By contrast, no studies have so far analysed the relationship between serum ferritin, a widely accepted measurement of iron storage, and haemoglobin concentration.

We, therefore, performed a retrospective analysis on the database of the Laboratory Information System of the Clinical Chemistry Institute of the University Hospital of Verona on outpatients referred by the general practitioner to our laboratory for routine blood testing. Between May 2004 and May 2007, 1,907 consecutive subjects underwent routine blood tests including measurement of serum ferritin levels and inflammatory indices (C-reactive protein) and blood cell count.

After the exclusion of women, duplicate tests from the same person and individuals with abnormal inflammatory indices or low serum ferritin levels ( 350 μg/L, mean 658.4 ± 341.8 μg/L). The mean age and haemoglobin concentration were then compared between these two groups (Table I).



Table I

Characteristics of the 589 patients enrolled in the study



There were statistically significant differences in age (36.3 ± 26.1 years in the first group versus 51.6 ± 16.4 years in the second group, p <0.0001) and haemoglobin concentration (14.4 ± 1.7 g/dL in the first group versus 15.5 ± 1.6 g/dL in the second, p < 0.0001).

In conclusion, the results of our study document a positive correlation between serum ferritin level and haemoglobin concentration, thus confirming the previous data from studies on patients with primary iron overload. The different mean age between the two groups is also an interesting finding of our study and testifies that iron accumulation is an age-dependent process which happens regardless of the underlying cause.

Gian Luca Salvagno

Papers

Should women with abnormal serum thyroid stimulating hormone undergo screening for anemia

Influence of middle-distance running on muscular micro RNAs.

Impact of blood cell counts and volumes on glucose concentration in uncentrifuged serum and lithium-heparin blood tubes

Cardiac troponin T during sickle cell crisis.

Serum ferritin levels correlate with haemoglobin concentration: a report on 589 outpatients from a single centre.