Type 1 diabetes mellitus

We are conducting a study on EVALUATION OF SUBCLINICAL NEUROPATHY IN TYPE 1 DIABETES MELLITUS in the Department of Physiology, KMC, Chennai. The purpose of this study is to diagnose subclinical involvement of central neuropathy and peripheral neuropathy in type 1 Diabetic patients. We do visual evoked potential test and sensory nerve conduction study to assess the functional integrity of visual pathway and nerve conduction for the early diagnosis of diabetic complications, which in anyway will not affect your treatment. The privacy of the patients in the research will be maintained throughout the study. In the event of publication or presentation resulting from the research, no personally identifiable information will be shared.

Comprehensive results obtained from various studies conducted upon patients with diabetes mellitus point towards a close relationship between serum levels of acute-phase reactants like uric acid and diabetes mellitus. Several studies recemia in the pathogenic process leading to endothelial dysfunction, which contribute to various local and systemic complications in long-term diabetes. Hyperuricemia has been shown to be linked to a number of conditions and disorders like gout, hypertension and diabetes mellitus. Several mechanisms have been proposed on how uric acid is elevated, reabsorption from kidney. Elevated levels of uric acid have been shown to be an independent marker in Carmine Zoccali et al., , DM, stroke, cardiovascular disease and renal disease. It remains unclear whether an increased UA level is the cause or In this background, an assessment of serum uric acid in relation to type 1 diabetes litus patients has been made. The present study was carried out on 50 type 1 diabetes mellitus cases and serum uric acid was measured spectrophotometrically. There was significant elevation in the serum uric acid levels in type 1 diabetics, lthy controls. Higher levels were observed in even though the values . Serum uric acid levels were directly related to serum glucose levels and with HbA1c. ls were directly proportional to

daily needs. Physicians faced a difficult time with the unavailability of patients’ medical records and relied on pa- tients’ memories and histories (and possibly on guesswork) to provide medical care. The added risks of phys- ical injury and emotional stress con- tributed to the woes of the patients. Relief agencies were overwhelmed by the unexpectedly large numbers of pa- tients with diabetes. The prevalence of type 1 diabetes mellitus in Texas is ⬃ 1 of every 400 to 600 children and ado- lescents. 15 Therefore, it is very impor-

• Immune-mediated diabetes. An autoimmune disorder in which the body's immune system destroys, or attempts to destroy the cells in the pancreas that produce insulin. Immune-mediated diabetes is the most common form of type 1 diabetes and is generally referred to as type 1 diabetes [5]. In pediatric type-1 diabetes mellitus (T1DM), the primary caregiver is mostly the mother. Typically, self- management education and training for the parents and their child begins with several sessions during hospitalization at the time of diagnosis, and continues over time in the context of collaborative relationship with the healthcare team [6].

Hypoglycemia is a common complication of insulin treatment in type 1 diabetes mellitus [1]. A safe blood glucose concentration varies with many factors, includ- ing rate of fall of blood glucose, duration of hypoglycemia, and age of the child [2]. Therefore, deter- mining the precise and exact blood glucose that should be considered "low" is difficult. One common bench- mark is 65-70 mg/dl (3.6-3.9 mmol/L) because this is the concentration at which counter-regulatory mechan- isms are triggered in persons without diabetes [3]. How- ever, symptoms and the clinical significance associated with specific blood glucose concentrations vary with each individual, and it is common for patients with hypoglycemia to be unaware when their glucose is low

The most severe CD-related symptoms are generally related to gastrointestinal malabsorption and include mal- nutrition, failure to thrive, diarrhea, anorexia, constipation, vomiting, abdominal distension, and pain. These features are more common in children younger than three years of age. Non-gastrointestinal symptoms of CD include short stature, pubertal delay, fatigue, vitamin deficiencies, and iron deficiency anemia and are more commonly observed in older children. The gastrointestinal presentation of CD rarely occurs in T1D patients (< 10%), but many patients with CD and T1D are either asymptomatic (silent CD) or present only mild symptoms [17,20,22]. Furthermore, the wide spectrum of CD include also subjects with positive celiac-related antibodies without diagnostic small-bowel mucosal villous atrophy. This condition is defined as potential celiac disease (pot-CD) [23-25]. Data from the majority of childhood diabetes care centers in Italy showed that prevalence of pot-CD patients in this population (higher in females than males) is 12.2%, while the preva- lence of pot-CD in the CD control population is 8.4% and only few of them present CD-related symptoms [26].

15. Rajaab HA, Baker NL, Hunt KJ, Klein R, Cleary PA, Lachin J, Virella G, Lopes- Virella MF, DCCT/EDIC Group of Investigators. The predictive role of mark- ers of inflammation and endothelial dysfunction on the course of dia- betic retinopathy in type 1 diabetes. J Diabetes Complic. 2015;29:108–14. 16. Lobo CL, Bernardes RC, Figueira JP, de Abreu JR, Cunha-Vaz JG. Three-year follow-up study of blood-retinal barrier and retinal thickness alterations in patients with Type 2 diabetes mellitus and mild nonproliferative diabetic retinopathy. Arch Ophthalmol. 2004;122:211–7.

Generally thyroid autoimmunity is more common in females than in males, this holds good for T1D also as per many cross-sectional as well as prospective studies. But there are studies which showed equal prevalence in both the gender. In our study, though the actual number of females was high, with a F: M ratio of 2:1, it was not of statistical significance. This may be due to two reasons. 1. Actual prevalence being equal; 2. Smaller study population.

Previous studies have not systematically tested metformin in patients with metabolic syndrome with T1DM. Met- formin likely reduced metabolic syndrome percentage in present study. Insulin resistance accompanied by type 1 diabetes causes the development of double diabetes and poorer glycemic control [5, 6, 9, 29]. Metformin reduces hepatic glucose production, stimulates glucose uptake in muscle, as well as improves blood flow for nutrient use. Metformin increases insulin sensitivity, reduces insulin resistance, improves insulin action, and increases peripheral glucose uptake in type 1 diabetes [18, 20, 21, 26]. Patients with C peptide-negative diabetes were included in this study in order to ignore metformin effects on beta cell function; metformin correlates with insulin resistance and beta-cell function. Hypoglycemic events [4, 20–22], lactic acidosis or vitamin B12 deficiency [26] were not observed in our metformin therapy group. However, this was a small and retrospective study, the study was not randomized or placebo-controlled and diet was not standardized prior to testing. All of which are limita- tions to our study.

There are very limited epidemiological, immunological and genetic data available for the African type 1 diabetes population, especially in southern Africa. Over the past 30 years, there have been approximately 15 publications, the majority from northern Africa, reporting on the presence of autoantibodies in the serum of African type 1 diabetic patients. The majority of papers have only addressed the presence of islet cell antibodies (ICAs).

The median direct cost for patients receiving diabetes care in the private sector was US$107. They have reported that median direct cost to the family of an individual with type 1 diabetes is US$310 (range US$45- 1936). The percentages of family income spent on diabetes care were 59%, 32%, 18% and 12% in low, middle, upper-middle and upper socio economic groups, respectively. Thus, the disease has its effects not only on the growth, development and emotional aspects of a child; it also carries the risk of long term complications with its associated morbidity and mortality with a significant effect on the economy as well.

meta-analysis should definitively end such confu- sion, but with 2 caveats. First, some of the height differences in earlier reports might conceivably be attributable to secular trends. Publication bias—the alleged tendency for journals to publish only positive results—also must be considered. Clearly, the re- ports that we analyzed primarily found positive re- sults, but for most—all but 4 papers—assessing the height at onset was a subsidiary finding, greatly reducing the likelihood of publication bias. We be- lieve that neither potential source of bias substan- tially influences the preponderance of evidence from earlier reports. At diagnosis, children with diabetes from 5 to 10 years exceed their peers in height. Younger children— or perhaps only boys—may be shorter. Small average study size prevented ade- quate assessment of the relationship of sex to stature. The observed differences between groups allow

The incidence of type 1A diabetes has increased dramati- cally in many countries during the past four decades; it is likely that some factors in the environment are changing. Several environmental factors have already been associ- ated with the development of type 1 A diabetes, such as viruses, certain constituents of diet and preservatives food. The gastrointestinal tract is likely the main system through which non-self antigens gain access. Recent data from lit- erature have emphasized the importance of the intestinal barrier, which is an entry door for viruses and proteins. In early childhood, such barrier is immature, which allows the passage of several antigens, and when these antigens are presented to T lymphocytes by the antigen presenting cells (macrophages), they will trigger an immune response which might result in a autoimmune process. Fasano A et al [20,21] have recently reported a novel pro- tein, zonulin, that modulates intestinal permeability by disassembling the intercellular tight junctions. Such pro- tein may be assessed in the plasma and studies demon- strate that its serum concentration is increased in patients with type 1 A diabetes in relation to their relatives and to controls[22], suggesting that a possible link between genetic susceptibility, increased intestinal permeability, environmental exposure to non-self antigens and devel- opment of autoimmune disease.

skin fibroblasts of patients with T1DM (T1DM-specific iPSCs, DiPSCs). These DiPSCs resembled ESCs in the global gene expression profile and were capable of differ- entiating into pancreatic cell lineages, paving the path of generating T1DM SC-β cells and making autologous stem cell-derived pancreatic progeny transplantation for T1DM possible [32]. In 2015, Millman et al. confirmed that SC-β cells derived from DiPSCs functionally resem- bled adult islet β cells both in vivo and in vitro. GSIS tests showed that under high glucose stimulation (20 mM incubation for 30 min), T1DM and nondiabetic (ND) SC-β cells secreted 2.0 ± 0.4 and 1.9 ± 0.3 mIU of human insulin per 10 3 cells, respectively, and both of these cells functioned similarly to adult primary islets in a previous study. After transplantation into ND immu- nodeficient mice, the engraft function was evaluated by serum human insulin before and 30 min after an injec- tion of glucose. At the early time point (2 weeks after transplantation), most engrafts responded to glucose and released more insulin after glucose injection, and the ra- tio of insulin secretion after glucose stimulation aver- aged 1.4 and 1.5 for T1DM and ND SC-β cells, respectively. The effects of these engrafts on insulin se- cretion were observed for several months. Of note, com- pared to the early time point, after 12–16 weeks, the human insulin content increased approximately 1.5 times after glucose stimulation [33]. It should be ac- knowledged that diversities exist among T1DM patients, and a larger number of specific stem cell lines from T1DM need to be developed for future clinical use. Al- though DiPSCs are an alternative source for cell replace- ment therapy for diabetes, some T1DM-specific stem cell lines have shown low efficiency in generating PDX1 + pancreatic progenitors [34]. Evaluated by flow cytometry, the number of IPCs derived from ND iPSCs (25–50.5%) was comparable to that of the β cells found in human primary islets, whereas the number of IPCs differentiated from T1DM iPSC lines was much lower (15.9%) [35, 36]. Upon a strict differentiation protocol, pancreatic progen- itors derived from T1DM iPSCs showed lower expres- sion of PDX1 than ND iPSCs at a specific differentiation stage. Epigenetic changes resulting from dysmetabolism in T1DM might be responsible for the poor yield of β cells from T1DM iPSCs. Transient demethylation treat- ment of DE cells rescued the expression of PDX1 by inhibiting methyl group deposition on the cytosine resi- dues of DNA and led to the differentiation of DE cells into IPCs [36]. The effect of demethylation on IPC dif- ferentiation has been shown to promote pancreatic pro- genitor induction rather than DE induction [37].

Autoimmune Markers in Young Malaysian Patients with Type I Diabetes Mellitus ORIGINAL ARTICLE Autoimmune Markers in Young Malaysian Patients With Type 1 Diabetes Mellitus W M Wan Nazaimoont, K Nor Azm[.]

Ethical approval was granted from the Research Ethics Committees at the Western Sydney Local Health District and The University of Sydney. The study population was defined as the total number of patients with Type 1 Diabetes Mellitus (Type 1 DM) and Type 2 Diabetes Mellitus (Type 2 DM) with foot ulcers at initial visit attending our outpatient Foot Wound Clinic at Westmead Hospital between January to December 2011. Diabetes Mellitus was defined according to the criteria set by the World Health Organisation (WHO). The current WHO diagnostic criteria for Diabetes Mellitus includes a fasting plasma glucose ≥ 7.0 mmol/l (126 mg/dl) or 2-hour plas- ma glucose ≥ 11.1 mmol/l (200 mg/dl) [19]. A foot ulcer was defined as a full-thickness wound located distal to the ankle (level of malleoli) [20].

We excluded patients with the following: gastrectomy, inflammatory bowel disease, chronic obstructive pulmonary disease, malignant disease (gastric, esophageal, colon, lung, pancreatic, liver, bile duct, gallbladder, breast, uterine, ovar- ian, prostate, or bladder cancer, or malignant lymphoma, leukemia, multiple myeloma), chronic kidney disease, type 1 diabetes mellitus, hypo/hyperthyroidism, a hypo/ hyperparathyroid disorder, rheumatoid arthritis (including other collagen disease), and a premenopausal status. We also excluded patients who were currently or previously treated with agents affecting BMD and causing secondary osteoporosis, including glucocorticoids, hormone replace- ment therapy, thyroid/parathyroid drugs, psychotropic drugs, anticonvulsants, selective estrogen receptor modulators, vitamin D, calcium, and bisphosphonates. This study was conducted in accordance with the tenets of the Declaration of Helsinki.

This cross-sectional study included 144 eyes of 72 preg- nant women in the third trimester divided into four groups: Group 1 consisted of 27 non-diabetic pregnant women (control group); Group 2 consisted of 15 pregnant women with GDM; Group 3 consisted of 16 pregnant women with type 2 diabetes mellitus (type 2 DM) and Group 4 consisted of 14 pregnant women with type 1 diabetes mellitus (type 1 DM). The participants were recruited between March and September 2016 at the Hospital de Clinicas de Porto Alegre (HCPA), Brazil. All participants received in person a full explanation about the study and provided written informed consent. This study was approved by the HCPA research ethics committee and was conducted in accordance with the Declaration of Helsinki guidelines.

Abstract: The objective of this study was to perform a review of the present knowledge on the epidemiology and pathogenesis of the association between celiac disease (CD) and type 1 diabetes mellitus (T1DM). Results from this review show that the estimated prevalence rate of CD in T1DM ranges from 4% to 11.5%, which seems higher in children than in adults, while there is no sex predominance in the prevalence of CD in T1DM. On the basis of the previous literature, screening for CD should be considered at diabetes diagnosis in all subjects and again within 2 and 5 years after diagnosis, even in the absence of symptoms. The anti-islet antibodies detection test, instead, is not recommended in CD, just as in the general population, except for CD patients having a relative with T1DM. Both genes and environmental factors seem to play a role in this association. HLADQ2 has been found to be the most frequent allele in the patients with both CD and T1DM, while gluten may be considered the trigger that induces the production of autoantibodies and the development, in genetically predisposed individuals, of both diseases.

To our best knowledge, this is the first cohort study to investigate the association between MPV and incident diabetes risk. Accumulating studies have demonstrated that MPV was associated with stroke [22], coronary artery disease [23] and myocardial infarction [24]. A study conducted to investigate the relationship between platelet activity and type 1 diabetes mellitus (T1DM) found that platelet activation did not precede the devel- opment of microvascular complications in T1DM [25]. Further investigation in T2DM cases [26] found that indi- viduals with T2DM accompanied by macrovascular dis- ease had higher levels of urine thromboxane metabolite.