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Defining And Characterising The Progression Of Type 2 Diabetes

The Hyperfiltering Kidney In Diabetes

The Hyperfiltering Kidney In Diabetes

Hyperfiltering kidney is a typical feature of diabetes. Improvement observed with regard to glucose control and blood pressure control reduces the high glomerular filtration rate and may contribute to retard the appearance and the progression of diabetic renal disease. Although the mechanism of hyperfiltration is still unclear, there is mounting evidence that the increased reabsorption of glucose and sodium by sodium glucose transporter-2 (SGLT-2) is involved in this altered renal function. There is a possibility that SGLT-2 inhibition may correct hyperfiltration in diabetes, adding a new therapeutic approach to halt renal disease in patients with diabetes. Hyperfiltration, a Typical Feature of Diabetes in Humans An increased glomerular filtration rate (GFR) is a typical feature of type 1 diabetic patients of short duration and it is also observed in type 2 diabetic patients. Although early elevation of the GFR plays a central role in the pathogenesis and progression of renal disease in experimental diabetes [ 1 ], a clear evidence that glomerular hyperfiltration may contribute to the progression of kidney disease in humans is still lacking. Small cohort studies found that types 1 and 2 diabetes subjects with glomerular hyperfiltration tended to be at increased risk of microalbuminuria, taken as an early marker of nephropathy [ 2 ]. Some studies found an accelerated renal function loss in hyperfiltering patients compared to those with normal or reduced GFR [ 2 ], but these findings were not confirmed in other series [ 3 ]. However, whether hyperfiltration affected the rate of GFR decline and predicted microalbuminuria independent of blood pressure and metabolic control has never been formally addressed in adequately powered studies. Moreover, reported prevalence of hyp Continue reading >>

The Causes And Progression Of Type 2 Diabetes

The Causes And Progression Of Type 2 Diabetes

Many people are born with a genetic predisposition to developing diabetes at some point in life – though this does not necessarily mean that they are destined to develop diabetes. We explore why and how type 2 diabetes develops in some people, and not others. First comes love…then comes marriage…then comes a baby - wait. That's not the progression we are talking about. We're talking about the progression of a disease. A very deadly disease at that, with type 2 diabetes being the 7th leading cause of death, according to the Centers for Disease Control and Prevention. How does Type 2 Diabetes Develop? Many people are born with a genetic predisposition to developing diabetes at some point in life - though this does not necessarily mean that they are destined to develop diabetes. It does, however mean that you they are more likely to develop diabetes than someone who is not genetically predisposed. Even if you don't have diabetes running in your family - you can certainly still develop it. After conception, your genes are all planned out and locked in for life, you might say. After this point, lifestyle takes over and plays the biggest role in whether you will develop type 2 diabetes in your lifetime. It's the classic nature vs. nurture argument, and we must consider both genetics and environment to explain how you get type 2 diabetes. As you grow and develop as toddler, how you eat can begin to influence the progression of type 2 diabetes. If you consume lots of sugary drinks and fruit juices, candy, and simple carbohydrates like crackers, cookies, and chips, then you are already increasing your risk, as a child, for type 2 diabetes. These kinds of foods cause your pancreas to begin working overtime to produce insulin in order to process all that sugar. So when you c Continue reading >>

Pharmacogenomics Of Drug Response In Type 2 Diabetes: Toward The Definition Of Tailored Therapies?

Pharmacogenomics Of Drug Response In Type 2 Diabetes: Toward The Definition Of Tailored Therapies?

Pharmacogenomics of Drug Response in Type 2 Diabetes: Toward the Definition of Tailored Therapies? 1Institute of Genetics and Biophysics Adriano Buzzati-Traverso, National Research Council, Via Pietro Castellino 111, 80131 Naples, Italy 2DiST, Department of Science and Technology, Parthenope University of Naples, Centro Direzionale, Isola C4, 80143 Naples, Italy Received 3 March 2015; Accepted 24 May 2015 Copyright 2015 Carla Pollastro et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Type 2 diabetes is one of the major causes of mortality with rapidly increasing prevalence. Pharmacological treatment is the first recommended approach after failure in lifestyle changes. However, a significant number of patients showsor develops along time and disease progressiondrug resistance. In addition, not all type 2 diabetic patients have the same responsiveness to drug treatment. Despite the presence of nongenetic factors (hepatic, renal, and intestinal), most of such variability is due to genetic causes. Pharmacogenomics studies have described association between single nucleotide variations and drug resistance, even though there are still conflicting results. To date, the most reliable approach to investigate allelic variants is Next-Generation Sequencing that allows the simultaneous analysis, on a genome-wide scale, of nucleotide variants and gene expression. Here, we review the relationship between drug responsiveness and polymorphisms in genes involved in drug metabolism (CYP2C9) and insulin signaling (ABCC8, KCNJ11, and PPARG). We also highlight the advancements in sequencing technologies that to date en Continue reading >>

Classification, Pathophysiology, Diagnosis And Management Of Diabetes Mellitus

Classification, Pathophysiology, Diagnosis And Management Of Diabetes Mellitus

University of Gondar, Ethopia *Corresponding Author: Habtamu Wondifraw Baynes Lecturer Clinical Chemistry University of Gondar, Gondar Amhara 196, Ethiopia Tel: +251910818289 E-mail: [email protected] Citation: Baynes HW (2015) Classification, Pathophysiology, Diagnosis and Management of Diabetes Mellitus. J Diabetes Metab 6:541. doi:10.4172/2155-6156.1000541 Copyright: © 2015 Baynes HW. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Diabetes & Metabolism Abstract Diabetes Mellitus (DM) is a metabolic disorder characterized by the presence of chronic hyperglycemia either immune-mediated (Type 1 diabetes), insulin resistance (Type 2), gestational or others (environment, genetic defects, infections, and certain drugs). According to International Diabetes Federation Report of 2011 an estimated 366 million people had DM, by 2030 this number is estimated to almost around 552 million. There are different approaches to diagnose diabetes among individuals, The 1997 ADA recommendations for diagnosis of DM focus on fasting Plasma Glucose (FPG), while WHO focuses on Oral Glucose Tolerance Test (OGTT). This is importance for regular follow-up of diabetic patients with the health care provider is of great significance in averting any long term complications. Keywords Diabetes mellitus; Epidemiology; Diagnosis; Glycemic management Abbreviations DM: Diabetes Mellitus; FPG: Fasting Plasma Glucose; GAD: Glutamic Acid Decarboxylase; GDM: Gestational Diabetes Mellitus; HDL-cholesterol: High Density Lipoprotein cholesterol; HLA: Human Leucoid Antigen; IDD Continue reading >>

The Natural History Of Type 2 Diabetes: Practical Points To Consider In Developing Prevention And Treatment Strategies

The Natural History Of Type 2 Diabetes: Practical Points To Consider In Developing Prevention And Treatment Strategies

CLINICAL DIABETES VOL. 18 NO. 2 Spring 2000 PRACTICAL POINTERS Type 2 diabetes, previously referred to as adult-onset or non-insulin-dependent diabetes, progresses from an early asymptomatic stage with insulin resistance to mild postprandial hyperglycemia to frank diabetes requiring pharmacological intervention. Understanding this natural history of type 2 diabetes will guide primary care providers in formulating effective treatment regimens that reflect the pathological differences between these stages of the disease. The optimal medication regimen, when used in conjunction with dietary changes and exercise, will require modifications for each patient as the disease progresses. The term impaired glucose tolerance (IGT) or pre-diabetes was first coined in 1979 by the World Health Organization and the National Diabetes Data Group to replace the terms borderline, chemical, and asymptomatic diabetes mellitus. In 1997, an expert committee of the American Diabetes Association recommended the following criteria for IGT: a normal fasting plasma glucose (<126 mg/dl) with a postprandial plasma glucose of >140 mg/dl but <200 mg/dl 2 h after a 75-g oral glucose challenge.1 This stage of mild postprandial hyperglycemia is an extremely useful marker of patients at risk for the eventual development of type 2 diabetes. Patients with IGT may benefit from timely patient education and perhaps even more aggressive forms of intervention, such as diet, exercise, or medication. An estimated 15.7 million Americans have type 2 diabetes, representing 5.9% of the population. Only two-thirds of those affected are diagnosed and are being actively treated. Although these numbers are staggering, there are even more potential diabetic patients waiting in the wings: the prevalence of IGT is estimated Continue reading >>

Defining And Characterizing The Progression Of Type 2 Diabetes

Defining And Characterizing The Progression Of Type 2 Diabetes

Type 2 diabetes is a progressive disease in which the risks of myocardial infarction, stroke, microvascular events, and mortality are all strongly associated with hyperglycemia (1). The disease course is primarily characterized by a decline in β-cell function and worsening of insulin resistance. The process is manifested clinically by deteriorations in multiple parameters, including A1C, fasting plasma glucose (FPG), and postprandial glucose levels. In this review, we will evaluate our current understanding of the role played by deteriorating β-cell function and other abnormalities linked with the progression of type 2 diabetes. An improved understanding of these abnormalities may provide the scientific groundwork for novel therapies that may help achieve and maintain good glycemic control. CHARACTERISTICS OF DISEASE PROGRESSION Progression from pre-diabetes to overt diabetes Because glucose is a continuous variable, the use of thresholds to make a diagnosis is somewhat arbitrary. The term “pre-diabetes” has become well established and implies a risk of progression to overt diabetes. However, although such progression is well studied in prevention trials, little is known about the rate of progression and the characteristics of such progression in the population at large. Table 1 summarizes some of the factors associated with such progression. Nichols et al. (2) studied the progression of pre-diabetes to overt disease and observed that 8.1% of subjects whose initial abnormal fasting glucose was 100–109 mg/dl and 24.3% of subjects whose initial abnormal fasting glucose was 110–125 mg/dl developed diabetes over an average of 29.0 months (1.34 and 5.56% per year, respectively). A steeper rate of increasing fasting glucose; higher BMI, blood pressure, and triglycer Continue reading >>

Type 2 Diabetes

Type 2 Diabetes

Tweet Type 2 diabetes mellitus is a metabolic disorder that results in hyperglycemia (high blood glucose levels) due to the body: Being ineffective at using the insulin it has produced; also known as insulin resistance and/or Being unable to produce enough insulin Type 2 diabetes is characterised by the body being unable to metabolise glucose (a simple sugar). This leads to high levels of blood glucose which over time may damage the organs of the body. From this, it can be understood that for someone with diabetes something that is food for ordinary people can become a sort of metabolic poison. This is why people with diabetes are advised to avoid sources of dietary sugar. The good news is for very many people with type 2 diabetes this is all they have to do to stay well. If you can keep your blood sugar lower by avoiding dietary sugar, likely you will never need long-term medication. Type 2 diabetes was formerly known as non-insulin-dependent or adult-onset diabetes due to its occurrence mainly in people over 40. However, type 2 diabetes is now becoming more common in young adults, teens and children and accounts for roughly 90% of all diabetes cases worldwide. How serious is type 2 diabetes? Type 2 diabetes is a serious medical condition that often requires the use of anti-diabetic medication, or insulin to keep blood sugar levels under control. However, the development of type 2 diabetes and its side effects (complications) can be prevented if detected and treated at an early stage. In recent years, it has become apparent that many people with type 2 diabetes are able to reverse diabetes through methods including low-carb diets, very-low-calorie diets and exercise. For guidance on healthy eating to improve blood glucose levels and weight and to fight back against ins Continue reading >>

Defining And Characterizing The Critical Transition State Prior To The Type 2 Diabetes Disease

Defining And Characterizing The Critical Transition State Prior To The Type 2 Diabetes Disease

Abstract Type 2 diabetes mellitus (T2DM), with increased risk of serious long-term complications, currently represents 8.3% of the adult population. We hypothesized that a critical transition state prior to the new onset T2DM can be revealed through the longitudinal electronic medical record (EMR) analysis. We applied the transition-based network entropy methodology which previously identified a dynamic driver network (DDN) underlying the critical T2DM transition at the tissue molecular biological level. To profile pre-disease phenotypical changes that indicated a critical transition state, a cohort of 7,334 patients was assembled from the Maine State Health Information Exchange (HIE). These patients all had their first confirmative diagnosis of T2DM between January 1, 2013 and June 30, 2013. The cohort’s EMRs from the 24 months preceding their date of first T2DM diagnosis were extracted. Analysis of these patients’ pre-disease clinical history identified a dynamic driver network (DDN) and an associated critical transition state six months prior to their first confirmative T2DM state. This 6-month window before the disease state provides an early warning of the impending T2DM, warranting an opportunity to apply proactive interventions to prevent or delay the new onset of T2DM. Figures Citation: Jin B, Liu R, Hao S, Li Z, Zhu C, Zhou X, et al. (2017) Defining and characterizing the critical transition state prior to the type 2 diabetes disease. PLoS ONE 12(7): e0180937. Editor: Cheng Hu, Shanghai Diabetes Institute, CHINA Received: March 16, 2017; Accepted: June 24, 2017; Published: July 7, 2017 Copyright: © 2017 Jin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribu Continue reading >>

Is Diabetes Mellitus A Continuous Spectrum?

Is Diabetes Mellitus A Continuous Spectrum?

BACKGROUND: Diabetes mellitus has been historically divided into type 1 and type 2 diabetes, with type 1 being an autoimmune disease and type 2 being primarily a metabolic disease. CONTENT: The current diabetes classification scheme needs to be reevaluated because of the accumulating evidence of immune system involvement in the pathophysiology of type 2 diabetes. SUMMARY: There are similarities and differences between type 1 and type 2 diabetes with regard to pathogenesis, pathophysiology, and genetics. We propose a resolution to the dilemma of the current classification scheme. In the pancreas of T1D patients, the immune system selectively destroys β cells in a process known as insulitis (12). Recently, immune cells have also been demonstrated to infiltrate the pancreata of T2D patients (10–14). In T1D, an autoimmune reaction characterizes the insulitis, whereas a more “autoinflammatory” infiltrate appears to characterize the insulitis associated with T2D (10–14). Moreover, islet-reactive T cells responding to multiple islet proteins have been found in both T1D patients (15–18) and phenotypic T2D patients with and without islet autoantibodies, the historical hallmark of islet autoimmunity (19–22). Potential differences between T1D patients and autoimmune phenotypic T2D patients in the islet proteins recognized by T cells have been identified, hinting at potentially different pathogenic mechanisms (21). These studies suggest that T-cell–mediated islet damage may be a component of more than just classic T1D. Recently, we demonstrated in phenotypic T2D patients that the presence of islet-reactive T cells identified patients with a more severe β-cell lesion, compared with assessing islet autoantibodies alone (23). This result thus indicated a potential link Continue reading >>

Recent Advances In Understanding Type 1 Diabetes - F1000research

Recent Advances In Understanding Type 1 Diabetes - F1000research

Type 1 diabetes is a multifactorial disease in which genetic and environmental factors play a key role. The triggering event is still obscure, and so are many of the immune events that follow. In this brief review, we discuss the possible role of potential environmental factors and which triggers are believed to have a role in the disease. In addition, as the disease evolves, beta cells are lost and this occurs in a very heterogeneous fashion. Our knowledge of how beta cell mass declines and our view of the diseases pathogenesis are also debated. We highlight the major hallmarks of disease, among which are MHC-I (major histocompatibility complex class I) expression and insulitis. The dependence versus independence of antigen for the immune infiltrate is also discussed, as both the influence from bystander T cells and the formation of neo-epitopes through post-translational modifications are thought to influence the course of the disease. As human studies are proliferating, our understanding of the diseases pathogenesis will increase exponentially. This article aims to shed light on some of the burning questions in type 1 diabetes research. Corresponding author: Matthias von Herrath How to cite: Christoffersson G, Rodriguez-Calvo T and von Herrath M. Recent advances in understanding Type 1 Diabetes [version 1; referees: 2 approved]. F1000Research 2016, 5(F1000 Faculty Rev):110 (doi: 10.12688/f1000research.7356.1 ) Copyright: 2016 Christoffersson G et al. This is an open access article distributed under the terms of the Creative Commons Attribution Licence , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Competing interests: MGvH is an employee of Novo Nordisk. The other authors declare that the Continue reading >>

Deteriorating Betacell Function In Type 2 Diabetes: A Longterm Model

Deteriorating Betacell Function In Type 2 Diabetes: A Longterm Model

Deteriorating betacell function in type 2 diabetes: a longterm model From the York Health Economics Consortium, University of York, UK Search for other works by this author on: From the York Health Economics Consortium, University of York, UK Search for other works by this author on: QJM: An International Journal of Medicine, Volume 96, Issue 4, 1 April 2003, Pages 281288, A. Bagust, S. Beale; Deteriorating betacell function in type 2 diabetes: a longterm model, QJM: An International Journal of Medicine, Volume 96, Issue 4, 1 April 2003, Pages 281288, Background: Type 2 diabetes is characterized by insulin resistance and the progressive loss of islet betacell function. Although the former is already established at diagnosis and changes little thereafter, betacell function continues to decline, leading to secondary failure of antihyperglycaemic therapies. Aim: To develop a quantitative model of the process of betacell function decay over time, using trial data. Methods: The results of the Belfast Diet Study were reanalysed. Assuming patients are diagnosed at different stages in the disease process, time displacement of data was used to obtain a bipartite spline model describing loss of insulin secretion over a 6year period. Results: The model was developed combining two phases, in which a long slow gradual loss of betacell function leads to a crisis in metabolic regulation, precipitating a much more rapid decay phase. This paradigm was consistent with a previous nonlinear model of betacell mass regulation. Discussion: This model may have important implications for targeting appropriate therapy to patients in each phase: delaying or avoiding full clinical type 2 diabetes in the first phase; and preventing the development of diabetic complications in the second phase. Sev Continue reading >>

Aldehyde Dehydrogenase 1a3 Defines A Subset Of Failing Pancreatic Cells In Diabetic Mice

Aldehyde Dehydrogenase 1a3 Defines A Subset Of Failing Pancreatic Cells In Diabetic Mice

Aldehyde dehydrogenase 1a3 defines a subset of failing pancreatic cells in diabetic mice Nature Communications volume 7, Articlenumber:12631 (2016) Insulin-producing cells become dedifferentiated during diabetes progression. An impaired ability to select substrates for oxidative phosphorylation, or metabolic inflexibility, initiates progression from -cell dysfunction to -cell dedifferentiation. The identification of pathways involved in dedifferentiation may provide clues to its reversal. Here we isolate and functionally characterize failing cells from various experimental models of diabetes and report a striking enrichment in the expression of aldehyde dehydrogenase 1 isoform A3 (ALDH+) as cells become dedifferentiated. Flow-sorted ALDH+ islet cells demonstrate impaired glucose-induced insulin secretion, are depleted of Foxo1 and MafA, and include a Neurogenin3-positive subset. RNA sequencing analysis demonstrates that ALDH+ cells are characterized by: (i) impaired oxidative phosphorylation and mitochondrial complex I, IV and V; (ii) activated RICTOR; and (iii) progenitor cell markers. We propose that impaired mitochondrial function marks the progression from metabolic inflexibility to dedifferentiation in the natural history of -cell failure. Diabetes arises as a consequence of combined abnormalities in insulin production and function 1 . Although alterations in either arm of this homeostatic loop can result in full-blown disease, in most individuals, the two abnormalities coexist. While target organs show an impaired response to insulin (so-called insulin resistance), -cells of diabetics show a blunted and mistimed response to nutrients 2 . During the natural history of the disease, -cell function markedly deteriorates 3 . In fact, an intrinsic susceptibility of the Continue reading >>

Defining And Characterizing The Progression Of Type 2 Diabetes

Defining And Characterizing The Progression Of Type 2 Diabetes

Go to: Progression from pre-diabetes to overt diabetes Because glucose is a continuous variable, the use of thresholds to make a diagnosis is somewhat arbitrary. The term “pre-diabetes” has become well established and implies a risk of progression to overt diabetes. However, although such progression is well studied in prevention trials, little is known about the rate of progression and the characteristics of such progression in the population at large. Table 1 summarizes some of the factors associated with such progression. Nichols et al. (2) studied the progression of pre-diabetes to overt disease and observed that 8.1% of subjects whose initial abnormal fasting glucose was 100–109 mg/dl and 24.3% of subjects whose initial abnormal fasting glucose was 110–125 mg/dl developed diabetes over an average of 29.0 months (1.34 and 5.56% per year, respectively). A steeper rate of increasing fasting glucose; higher BMI, blood pressure, and triglycerides; and lower HDL cholesterol predicted diabetes development. The Baltimore Longitudinal Study of Aging (3) concluded that although phenotypic differences in rates of progression are partly a function of diagnostic thresholds, fasting and postchallenge hyperglycemia may represent phenotypes with distinct natural histories in the evolution of type 2 diabetes. Does hyperglycemia evolve from normoglycemia gradually over time or as a step increase? Ferrannini et al. (4) measured plasma glucose and insulin levels during oral glucose testing at baseline and after 3 and 7 years of follow-up. In subjects with normal glucose tolerance on all three occasions (nonconverters), FPG increased only slightly over 7 years. In contrast, conversion to both impaired glucose tolerance (IGT) and diabetes among normal glucose tolerance subjects Continue reading >>

Daily Patterns Of Physical Activity By Type 2 Diabetes Definition: Comparing Diabetes, Prediabetes, And Participants With Normal Glucose Levels In Nhanes 20032006

Daily Patterns Of Physical Activity By Type 2 Diabetes Definition: Comparing Diabetes, Prediabetes, And Participants With Normal Glucose Levels In Nhanes 20032006

Daily patterns of physical activity by type 2 diabetes definition: Comparing diabetes, prediabetes, and participants with normal glucose levels in NHANES 20032006 Author links open overlay panel Jeremy A.Steevesa Daily patterning of physical activity was similar regardless of diabetes definition. Diabetes participants had significantly less objectively measured physical activity. Those with normal glucose levels and prediabetes had similar activity levels. Diabetes participant's physical activity dropped significantly more in the afternoon. Timing of activity differences can inform interventions to increase activity. Diabetes is associated with low levels of physical activity (PA), but detailed objective information about how PA patterns vary by diabetes definition is lacking. PA was measured with ActiGraph accelerometers in older (60+) adults from the 20032006 National Health and Nutrition Examination Survey (n=1,043) and analyzed in 2014. Diabetes definition (normal glucose levels, prediabetes, and diabetes) was assessed (fasting glucose, hemoglobin A1C, and self-report). Accelerometer data were used to characterize total activity counts (TAC) per day and hour-by-hour activity counts by diabetes definition. Multiple linear regression models explored the relationship between diabetes definition and TAC. Despite similar patterns of PA, diabetes participants had significantly lower TAC compared to participants with normal glucose levels and prediabetes. Diabetes participants' activity counts per hour declined more rapidly after 12p.m., with the biggest differences between the groups occurring at 4:00p.m. Participants with normal glucose levels and prediabetes had similar TAC and daily PA profiles. Our novel methodology provides information about PA patterns by diabetes Continue reading >>

Guasalud. Cpg Diabetes Mellitus. English Full Version. Definition.

Guasalud. Cpg Diabetes Mellitus. English Full Version. Definition.

4. Definition and diagnostic criteria of diabetes mellitus type 1 4.1. Definition of diabetes mellitus type1 Diabetes mellitus (DM) comprises a group of metabolic diseases characterized by secondary hyperglycaemia to an absolute or relative defect in insulin secretion, which is accompanied, to a greater or lesser extent, by alterations in the metabolism of lipids and proteins, which leads to micro- and macro-vascular impairment affecting different organs such as eyes, kidneys, nerves, heart and vessels. Diabetes mellitus type 1 (DM1) corresponds to the entity formerly termed insulin dependent or juvenile diabetes mellitus, in which the destruction of the pancreatic cells leads to an absolute insulin deficiency. In the current classification, the DM1 is divided into two subtypes: DM1 A or autoimmune and DM1 B or idiopathic. DM1 A or autoimmune: T lymphocytes activated in people with predisposing HLA haplotypes. After a preclinical period of variable duration, during which the patient is asymptomatic, when the mass of insulin-producing cells reaches a critical value the patient has classic symptoms: polyuria, polydipsia, polyphagia, weight loss and a progressive ketosis that can lead to ketoacidosis, if not treated with exogenous insulin.. DM1 B or idiopathic: as opposed to DM1 A, DM1 B includes patients with the same or similar characteristics, without auto-immunity or predisposing HLA haplotypes data. As it has only been described recently as entity, little is known of its aetiology, development and prognosis An SR of observational studies 17 analyzed the clinical usefulness of the determination of some immunological markers, such as the antiglutamate decarboxylase 65 (GADA) antibodies, the islet cell antibodies (ICA), the insulin antibodies (IAA), the anti-tyrosine ph Continue reading >>

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