Antiplatelet and Antithrombotic Therapy in Type I Diabetes Mellitus: Update on Current Data.

Diabetes mellitus type 1 (T1DM) is an autoimmune disease characterized by a markedly elevated cardiovascular (CV) risk due to premature atherosclerosis. Previous studies have shown that intense glycemic control reduces the incidence of CV disease. Antiplatelet therapy is considered to be a very important therapy for secondary prevention of recurrent atherothrombotic events in patients with DM, while it may be considered for primary prevention in individuals with T1DM with additional CV risk factors.The aim of the present review is to summarize existing literature data regarding the thrombotic risk in T1DM patients and discuss current treatment strategies.

Potential Therapeutic Application of Regulatory T Cells in Diabetes Mellitus Type 1

The autoimmune reaction against the beta cells of the pancreatic islets in type 1 diabetes mellitus (T1DM) patients is active in prediabetes and during the development of the clinical manifestation of T1DM, but it decreases within a few years of the clinical manifestation of this disease. A key role in the pathogenesis of T1DM is played by regulatory T cell (Treg) deficiency or dysfunction. Immune interventions, such as potential therapeutic applications or the induction of the Treg-cell population in T1DM, will be important in the development of new types of treatment. The aim of this study was to evaluate innovative immune interventions as treatments for T1DM. After an evaluation of full-length papers from the PubMed database from 2010 to 2021, 20 trials were included for the final analysis. The analysis led to the following conclusions: Treg cells play an important role in the limitation of the development of T1DM, the activation or application of Tregs may be more effective in the early stages of T1DM development, and the therapeutic use of Treg cells in T1DM is promising but requires long-term observation in a large group of patients.

Eurythrematosis as a developmental model of the Diabetes Mellitus type 1 pathological condition: pathophysiological parameters and oxidative stress / Eurytrematose como modelo de desenvolvimento da patologia da Diabetes Mellitus tipo 1: parâmetros fisiopatológicos e stress oxidativo

Eurytrematosis is a helminthic disease caused by trematodes belonging to the genus Eurytrema spp. that parasitize the pancreas of many animals and humans. This parasitosis causes chronic fibrosing pancreatitis, fat infiltration in the pancreatic parenchyma, besides damaging the exocrine pancreas, which is similar to that found in patients with Diabetes Mellitus type 1 (DM1). The current work aimed to evaluate the use of bovine pancreas infected with E. coelomaticum as a model to study DM1 pathophysiology. It was carried out macroscopic analyses, parasite identification, total pancreatic lipid determination and oxidative damage biomarkers levels of pancreas naturally infected with E. coelomaticum. Macroscopically, we observed that the infected pancreas had duct obstruction, organ stiffness due to the visible presence of fibrosis, increased adipose tissue deposition, increased protein and lipid damage, as well as increased antioxidant biomarkers (GSH, CAT and VIT C). Thus, it is possible to show that DM1 may have pancreatic parasitism as a possible primary origin. However, more studies are needed to better investigate this possible primary origin; the results obtained here suggest that the use of pancreas parasitized by E. coelomaticum could be a model to investigate DM1 pathophysiology.

Comprehensive Review on Neuro-Degenerative Type 3DM

: Alzheimer disease (AD) is thought to be the metabolic illness raised by defective insulin signaling, insulin resistance, and low insulin levels in the brain, according to a growing body of research. The "Type 3 diabetes" has been postulated for AD because reduced insulin signalling has molecular and physiological consequences that are comparable to Type I and Type 2 diabetes mellitus (Type 1 DM and Type 2 DM, respectively). The similarities between type 2 diabetes and Alzheimer's disease suggest that these clinical trials might yield therapeutic benefits. However, it's important to note that lowering your risk of Alzheimer's dementia, whether you have diabetes or not, is still a multidimensional process involving factors like exercise, smoking, alcohol, food, and mental challenge. The current aim is to show the relationship between T3D and AD being based on both the processing of amyloid-β (Aβ) precursor protein toxicity and the clearance of Aβ are the result of an impaired insulin signaling. The brain's metabolism with its high lipid content and energy needs, places excess demands on mitochondria and appears more susceptible to oxidative damage than the rest of the body. Current data suggests that increased oxidative stress relates to amyloid-β (Aβ) pathology and onset of AD.

Clinical guidelines «Children with diabetes mellitus type 1, 2020”: what a pediatrician needs to know

A group of experts, leading Russian specialists in the field of pediatric endocrinology prepared updated clinical guidelines for the diagnosis and treatment of type 1 diabetes mellitus in children. The article presents the main provisions of clinical guidelines for diagnosis and differential diagnosis, treatment, organization of medical care, specific and acute complications in children with type 1 diabetes mellitus. These clinical recommendations and concerted actions in practical work will allow pediatricians and pediatric endocrinologists to improve the diagnosis, treatment and quality of medical care for children with type 1 diabetes.

Re – print- An Adjunct Treatment Reverses Chronic Insulin-dependent (Type 1) Diabetes in a Teenager

Globally, more than 30 million people suffer from diabetes mellitus type 1 (T1DM) characterized by pancreas producing little or no insulin hormone to facilitate glucose entering cells for energy production. T1DM patients tend to suffer a higher overall rate of atherosclerosis, cancer, and end-stage renal failure. No drug or surgical therapy seems to halt its annual upward trend amongst children and young adults. Consequently, a significant number of sufferers turn to complementary or alternative therapies for help to arrest this chronic endocrine condition. This paper discusses how a well-designed evidence-based dietary and nutritional therapy with some lifestyle modifications might offer a solution for this highly complex autoimmune disorder. The treatment outcome demonstrated a partial regeneration of pancreatic islet beta cells with substantial improvement for all relevant serum and urine markers tested.

Evaluation of Vascular Endothelial Function in Children with Type 1 Diabetes Mellitus

Diabetic kidney disease belongs to the major complications of diabetes mellitus. Here, hyperglycaemia is a key metabolic factor that causes endothelial dysfunction and vascular changes within the renal glomerulus. The aim of the present study was to assess the function of the vascular endothelium in children with type 1 diabetes mellitus (type 1 diabetes) by measuring selected endothelial lesion markers in blood serum. The selected markers of endothelial lesions (sVCAM-1, sICAM-1, sE-SELECTIN, PAI-1, ADMA and RAGE) were assayed by the immunoenzymatic ELISA method. The study involved 66 patients (age: 5–18 years) with type 1 diabetes and 21 healthy controls (age: 5–16 years). In the type 1 diabetes patients, significantly higher concentrations of all of the assayed markers were observed compared to the healthy controls (p < 0.001). All of the evaluated markers positively correlated with the disease duration, the age, and BMI of the patients, while only PAI-1 and sE-SELECTIN were characteristic of linear correlations with the estimated glomerular filtration rate (eGFR). It can be concluded that endothelial inflammatory disease occurs in the early stages of type 1 diabetes mellitus in children. The correlations between PAI-1, sE-SELECTIN, and eGFR suggest an advantage of these markers over other markers of endothelial dysfunction as prognostic factors for kidney dysfunction in children with type 1 diabetes.