1,721,039 research outputs found
Covid-19 and diabetes mellitus: unveiling the interaction of two pandemics
A novel RNA betacoronavirus causing coronavirus disease 2019 (Covid-19) has now been declared pandemic disease by WHO. Guo et al published the first report of biochemical features in patients with diabetes and the further risk that this disease can determine to the progression of Covid-19. Among different cytokines found significantly higher in patients with diabetes compared to those without, Interleukin-6 (IL-6), which is already increased in conditions of chronic inflammation, may play a more deleterious role in Covid-19 infection. Targeting the overexpression of Il-6 effects with a monoclonal antibody against IL-6 receptor or using Janus Kinase inhibitors may be particularly helpful for treatment of Covid-19 pneumonia in diabetes
Comment on: "Early insulin treatment in type 2 diabetes: ORIGINal sin or valuable choice as ORIGINal treatment? An open debate on the ORIGIN study results"
Editorial: The Changing Panorama of Diabetes Outcomes: Novel Complications and Novelties in Classical Complication
Il ruolo del biostatistico nella preparazione conduzione e monitoraggio delle sperimentazioni cliniche
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The complex combination of COVID-19 and diabetes: pleiotropic changes in glucose metabolism
Purpose: Angiotensin converting enzyme 2 (ACE2) is the door for SARS-CoV-2, expressed in critical metabolic tissues. So, it is rational that the new virus causes pleiotropic alterations in glucose metabolism, resulting in the complication of pre-existing diabetes’s pathophysiology or creating new disease mechanisms. However, it seems that less attention has been paid to this issue. This review aimed to highlight the importance of long-term consequences and pleiotropic alterations in glucose metabolism following COVID-19 and emphasize the need for basic and clinical research in metabolism and endocrinology. Results: SARS-CoV-2 shifts cellular metabolism from oxidative phosphorylation to glycolysis, which leads to a decrease in ATP generation. Together with metabolic imbalance, the impaired immune system elevates the susceptibility of patients with diabetes to this deadly virus. SARS-CoV-2-induced metabolic alterations in immune cells can result in hyper inflammation and a cytokine storm. Metabolic dysfunction may affect therapies against SARS-CoV-2 infection. The effective control of metabolic complications could prove useful therapeutic targets for combating COVID-19. It is also necessary to understand the long-term consequences that will affect patients with diabetes who survived COVID-19. Conclusions: Since the pathophysiology of COVID-19 is still mostly unknown, identifying the metabolic mechanisms contributing to its progression is essential to provide specific ways to prevent and improve this dangerous virus’s detrimental effects. The findings show that the new virus may induce new-onset diabetes with uncertain metabolic and clinical features, supporting a potential role of COVID-19 in the development of diabetes
Long-term Risk of Cardiovascular Disease in Individuals with Latent Autoimmune Diabetes of Adults (UKPDS 85)
AIMS:
Latent Autoimmune Diabetes of Adults (LADA) is diagnosed in up to 12% of adults with clinically-diagnosed type 2 diabetes (T2D). LADA tend to have healthier cardiovascular (CV) risk profiles than T2D, but it remains uncertain whether their risk of CV events differ. We examined the risk of CV events in patients enrolled in the United Kingdom Prospective Diabetes Study (UKPDS), according to their LADA status.
MATERIALS AND METHODS:
Diabetes autoantibodies (AAb) were measured in 5,062 UKPDS participants. The incidence of major adverse CV events (MACE), defined as CV death, nonfatal myocardial infarction or nonfatal stroke, was compared in those with LADA (≥1 AAb test positive) and those without LADA (AAb negative).
RESULTS:
There were 567 LADA participants (11.2%). Compared with T2D, they were younger, with higher mean HbA1c and HDL-cholesterol values but lower body mass index, total cholesterol and systolic blood pressure values (all p<0.01). After median (IQR) 17.3 (12.6-20.7) years follow-up, MACE occurred in 157 (17.4 per 1000 person-years) LADA and 1544 (23.5 per 1000 person-years) T2D participants respectively (HR 0.73, 95% Confidence Interval [CI] 0.62-0.86, p<0.001). However, after adjustment for confounders, this difference was no longer significant (HRadj 0.90, 95% CI 0.76-1.07, p=0.22).
CONCLUSIONS:
In adults thought to have newly-diagnosed T2D the long-term risk of MACE was lower in those with LADA. However, this did not differ after adjustment for conventional CV risk factors suggesting that measurement of AAb in addition to traditional CV risk factors will not aid CV risk stratification in clinically-diagnosed T2D.
FUNDING:
EFSD Mentorship Programm
Investigational therapies targeting CD3 for prevention and treatment of type 1 diabetes
Introduction: Immunotherapies for type 1 diabetes mellitus (T1D) have been the focus of intense research over the past few decades. Nevertheless, the results of clinical trials have not matched expectations. However, thanks to the recent and promising results on T1D prevention, among all the different immune-intervention strategies, clinical evidence on anti-CD3 monoclonal antibodies (mAb) deserves particular attention and in-depth evaluation. In this narrative review, we introduce the role of T-cells and their co-receptor CD3 in the pathogenesis of T1D and examine the potential of anti-CD3 mAbs as a treatment for preventing or curing T1D. We discuss pre-clinical studies and phase II/III clinical trials testing the anti-CD3 mAb teplizumab in subjects at T1D high risk, and testing teplizumab and otelixizumab in T1D recent onset patients. In this work, we discuss the current evidence gathered on anti-CD3 therapy to offer insights on the treatment strengths, limitations, and unmet needs. Recent phase II clinical trials with teplizumab in individuals at high-risk of developing T1D seem encouraging, but benefits associated with the use of anti-CD3 mAb in recent-onset T1D are still controversial. A better patient selection, based on immunological profiles and specific biomarkers, is crucial to improve clinical outcomes in T1D immunotherapies
Going Beyond Counting First Authors in Author Co-citation Analysis
The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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