Differentiating type 1 type 2 diabetes mellitus quizlet,january transfer window update fifa 14,january 4 1981 chinese zodiac years - PDF Books

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Double Diabetes: The Search for a Treatment Paradigm in Children and AdolescentsBenjamin U. Pozzilli P, Guglielmi C, Caprio S, Buzzetti R: Obesity, autoimmunity, and double diabetes in youth. Hedley AA, Ogden CL, Johnson CL, Carroll MD, Curtin LR, Flegal KM: Prevalence of overweight and obesity among US children, adolescents, and adults, 1999-2002.
Flegal KM, Wei R, Ogden C: Weight-for-stature compared with body mass index-for-age growth charts for the United States from the Centers for Disease Control and Prevention.
Ogden CL, Flegal KM, Carroll MD, Johnson CL: Prevalence and trends in overweight among US children and adolescents, 1999-2000. Ogden CL, Carroll MD, Curtin LR, McDowell MA, Tabak CJ, Flegal KM: Prevalence of overweight and obesity in the United States, 1999-2004. Troiano RP, Flegal KM, Kuczmarski RJ, Campbell SM, Johnson CL: Overweight prevalence and trends for children and adolescents. Williams J, Wake M, Hesketh K, Maher E, Waters E: Health-related quality of life of overweight and obese children. Schwimmer JB, Burwinkle TM, Varni JW: Health-related quality of life of severely obese children and adolescents. Reinehr T, Schober E, Wiegand S, Thon A, Holl R: Beta-cell autoantibodies in children with type 2 diabetes mellitus: subgroup or misclassification? Libman IM, Becker DJ: Coexistence of type 1 and type 2 diabetes mellitus: "double" diabetes? CDC: Epidemiology of Type 1 and Type 2 Diabetes Mellitus Among North American Children and Adolescents. Hathout EH, Thomas W, El-Shahawy M, Nahab F, Mace JW: Diabetic autoimmune markers in children and adolescents with type 2 diabetes.
Dabelea D, Pettitt DJ, Jones KL, Arslanian SA: Type 2 diabetes mellitus in minority children and adolescents. Laine AP, Nejentsev S, Veijola R, Korpinen E, Sjoroos M, Simell O, Knip M, Akerblom HK, Ilonen J: A linkage study of 12 IDDM susceptibility loci in the Finnish population.
Cho YS, Chen CH, Hu C, Long J, Ong RT, Sim X, Takeuchi F, Wu Y, Go MJ, Yamauchi T, Chang YC, Kwak SH, Ma RC, Yamamoto K, Adair LS, Aung T, Cai Q, Chang LC, Chen YT, Gao Y, Hu FB, Kim HL, Kim S, Kim YJ, Lee JJ, Lee NR, Li Y, Liu JJ, Lu W, Nakamura J, Nakashima E, Ng DP, Tay WT, Tsai FJ, Wong TY, Yokota M, Zheng W, Zhang R, Wang C, So WY, Ohnaka K, Ikegami H, Hara K, Cho YM, Cho NH, Chang TJ, Bao Y, Hedman AK, Morris AP, McCarthy MI, Takayanagi R, Park KS, Jia W, Chuang LM, Chan JC, Maeda S, Kadowaki T, Lee JY, Wu JY, Teo YY, Tai ES, Shu XO, Mohlke KL, Kato N, Han BG, Seielstad M: Meta-analysis of genome-wide association studies identifies eight new loci for type 2 diabetes in east Asians.
Pozzilli P, Guglielmi C, Pronina E, Petraikina E: Double or hybrid diabetes associated with an increase in type 1 and type 2 diabetes in children and youths.
Sesti G, Federici M, Hribal ML, Lauro D, Sbraccia P, Lauro R: Defects of the insulin receptor substrate (IRS) system in human metabolic disorders. Foti D, Chiefari E, Fedele M, Iuliano R, Brunetti L, Paonessa F, Manfioletti G, Barbetti F, Brunetti A, Croce CM, Fusco A, Brunetti A: Lack of the architectural factor HMGA1 causes insulin resistance and diabetes in humans and mice.
Mortensen HB, Robertson KJ, Aanstoot HJ, Danne T, Holl RW, Hougaard P, Atchison JA, Chiarelli F, Daneman D, Dinesen B, Dorchy H, Garandeau P, Greene S, Hoey H, Kaprio EA, Kocova M, Martul P, Matsuura N, Schoenle EJ, Sovik O, Swift PG, Tsou RM, Vanelli M, Aman J: Insulin management and metabolic control of type 1 diabetes mellitus in childhood and adolescence in 18 countries. Frayling TM, Timpson NJ, Weedon MN, Zeggini E, Freathy RM, Lindgren CM, Perry JR, Elliott KS, Lango H, Rayner NW, Shields B, Harries LW, Barrett JC, Ellard S, Groves CJ, Knight B, Patch AM, Ness AR, Ebrahim S, Lawlor DA, Ring SM, Ben-Shlomo Y, Jarvelin MR, Sovio U, Bennett AJ, Melzer D, Ferrucci L, Loos RJ, Barroso I, Wareham NJ, Karpe F, Owen KR, Cardon LR, Walker M, Hitman GA, Palmer CN, Doney AS, Morris AD, Smith GD, Hattersley AT, McCarthy MI: A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Hypponen E, Virtanen SM, Kenward MG, Knip M, Akerblom HK: Obesity, increased linear growth, and risk of type 1 diabetes in children. Back rashes can be caused by allergies, irritants, dry skin, or some sort of skin condition.
A back rash can cause a lot of pain and discomfort, so it is important to treat it as soon as you can.
Irritants that can cause a back rash include soaps, detergents and plants such as poison oak and poison ivy.
Your back rash also might be caused by a skin condition such as psoriasis, eczema or a sunburn. When I had a red rash on my back and needed some relief, I soaked in a warm oatmeal bath for about 15 minutes. One of the most frustrating things about having an itchy rash on your back is how hard it is to treat it yourself. I live alone, and when I needed to treat a rash on my back, my arms wouldn't stretch around far enough to reach all the places I needed to.
I have never really had sensitive skin, but when I tried out a new laundry detergent, I noticed a rash on my back that spread to my stomach and shoulders. This was an itchy rash on my back which drove me crazy. The Expert Committee on Clinical Guidelines for Overweight in Adolescent Preventive Services. Rashes can be caused by a variety of ailments, some of which are medical skin conditions, and some of which are caused by irritants that touch the skin.
In the case of a back rash caused by detergent or soap, it might simply be necessary to remove the item of clothing, wash your back with water and a gentle soap, and put on clothing that has been washed with a chemical and fragrance-free detergent. Gentle creams, including aloe vera gel or a hydrocortisone cream, can help relieve some irritation and itching.
An oatmeal bath has been known to stop itching and irritation caused by certain skin conditions, and ice packs can be placed on the back to cool the area.
In some cases, it might be necessary to see a doctor or dermatologist, particularly if the rash is causing you a lot of pain and does not go away quickly. For irritants that cause greater problems, such as blisters and bumps, it might be necessary to wash the area and place a cold compress on it to reduce swelling.
In all cases, it is best to have your back exposed to air as much as possible to heal the affected area, but bandages should be used to cover any blisters in order to reduce the risk of infection. You should not expose your back to direct sunlight while you experiencing these symptoms, because the sun's rays can make them worse.
There are store-bought and homemade remedies that can be used to treat the swelling, bumps and redness that tend to be the main symptoms of a rash. An antihistamine can be taken orally to help reduce itching and redness, but this can cause drowsiness and should be used only according to the instructions on the package. A healthcare professional should be called if the symptoms do not go away after a few days, if you appear to have an infection or if a fever develops. Type 1 diabetes (T1D) is caused by autoimmune destruction of the insulin-producing beta cells of the pancreas. Type 2 diabetes (T2D) results from a combination of insulin resistance and beta cell insulin secretory defect. The rising prevalence of childhood obesity has made it more difficult to differentiate between these types of diabetes in children.
There is a new expression of diabetes in children known as double diabetes, or hybrid diabetes.
This is a clinical state where both T1D and T2D co-exist in the same individual as shown in Figure 1 below.Childhood obesity is one of the most serious public health challenges of the 21st century [1].
There has also been a parallel increase in the prevalence of many obesity-related co-morbid conditions [9] such as T2D, dyslipidemia, hypertension, obstructive sleep apnea, poor quality of life and mortality in adulthood [10-13]. Although obesity is associated primarily with T2D due to insulin resistance, [14], it may also impact T1D morbidity. T1D is caused by autoimmune destruction of the beta cells of the pancreas leading to insulinopenia.

In type 1A, individuals have one or more of the anti-islet cell (including glutamic acid decarboxylase, and insulinoma antigen-2) or anti-insulin antibodies. In type 1B these antibodies are absent, but the clinical and biochemical features are similar to 1A. T2D is characterized by insulin resistance and absence of diabetes-associated antibodies in serum.A new subset of diabetes, called double diabetes is becoming increasingly prevalent as a result of the epidemic of childhood obesity [16-18].
In this condition, individuals with T1D have insensitivity to insulin that is most often associated with obesity; and individuals with T2D have antibodies against the pancreatic beta cells [14] (Figure 1).
The reported rate of new cases among youth was 19 per 100,000 each year for T1D, and 5.3 per 100,000 for T2D [20].
However, reports show that about 25% of children with T1D are either overweight or obese [21]. Other reports show that about 35% of children and adolescents with T2D have at least one diabetes-associated antibody [22]. Some authors estimate that about one in three children and adolescents with newly diagnosed diabetes has double diabetes. The major difficulty with establishing a prevalence rate for double diabetes is that there are no precise definitions for the different types of diabetes presenting in youth [1]. For example, obesity and ketoacidosis can be found in both T1D and T2D [23], and the age of diagnosis is now a poorly differentiating factor [24].
In other cases, the clinical features of double diabetes are not apparent at diagnosis but evolve over time [18].3. One of such genes resulting from a genetic variance in insulin receptor substrate 1 (IRS-1) plays an important role in insulin resistance, a key component of T2D, and also in ? cell apoptosis which is associated with T1D [33]. High mobility group A1 (HMGA1) protein, a product of the Hmga1 gene has been identified as a crucial effector in the control of glucose homeostasis, such that impaired HMGA1 function may contribute to the development of specific forms of diabetes [34]. HMGA1-deficient indiviuduals have reduced insulin receptor expression, reduced insulin signaling and decreased insulin secretion similar to the phenotype of T2D [34]. Obese or overweight children have been reported to develop T1D at younger ages than children of normal weight [35]. The SEARCH for Diabetes in Youth Study [36] reported an obesity prevalence rate of 12.6% in US youth with T1D. The study also reported a higher prevalence of overweight status (BMI 85th – 95th percentile) among youth with T1D than in those without diabetes (22.1% vs. Many of the major genetic factors involved in the etiopathogenesis of T2D appear to promote the development of the disease through their influence on obesity and feeding behavior [38]. There is evidence that rapid growth and obesity in early childhood might increase the risk of T1D [35,39]. The strong environmental basis for this obesity pandemic and influence on feeding behavior was recently outlined in a World Health Organization Technical Report [40] which states that ‘Changes in the world food economy have contributed to shifting dietary patterns, for example, increased consumption of energy-dense diets high in fat, particularly saturated fat, and low in unrefined carbohydrates. These patterns are combined with a decline in energy expenditure that is associated with sedentary lifestyle, motorized transport, labor-saving devices at home, the phasing out of physically-demanding manual tasks in the workplace, and leisure time that is preponderantly devoted to physically undemanding pastimes’. However, despite the established association between obesity and the increasing prevalence of T1D, it is unclear how these environmental processes lead to ? cell destruction. Some reports have linked high titers of glutamic acid decarboxylase autoantibody to an increase in body mass index (BMI) [41] which suggests that increased BMI might favor the development of an autoimmune response towards ? cells.
This is in line with other reports indicating that a combination of obesity and insulin resistance speeds up the process of beta cell destruction [35,42]. Other proposed mechanisms for beta cell destruction include the the role of upregulation of autoimmune response by obesity-associated inflammatory cytokines, and hyperleptinemia-associated T-cell activation [43,44]. In additon to the above mechanistic models, several hypotheses have been advanced to explain the association between obesity and rising prevlaence of T1D.
The most prominent of these hypotheses is the accelerator hypothesis which states that T1D and T2D are the same disease state set in different genetic backgrounds [46]. It originally proposed three major factors as the basis for the development of diabetes: genetic predisposition, insulin resistance and intrinsic rate of beta cell loss. The accelerators have now been reduced to two without altering the premise of the hypothesis [46].
The first is insulin resistance which is believed to accelerate ?-cell apoptosis while rendering them more immunogenic. It posits that insulin resistance is the primary driver for the development of diabetes in a susceptible individual and argues that insulin resistance increases through weight gain as does the rate of onset of diabetes [47]. The second accelerator is the hierachy of responsive genes whose reactivity modulates the gradient of ?-cell declining function [46]. The central premise of the accelerator hypothesis is based on studies reporting rising incidence of obesity [6,48] and T1D in children [49,50]. These findings were strengthened by reports of an association between weight gain and an increased risk to develop diabetes mellitus [51-53], as well as several reports from Europe indicating that an increasing number of children are being diagnosed with T1D at an earlier age [54-58]. This hypothesis proposes a direct cause and effect relationship between obesity and the development of both T1D and T2D, and states that as the population becomes heavier (fatter), diabetes appears earlier, thus suggestive of a true acceleration rather than an incidental risk association [59]. The accelerator hypothesis is controversial because studies designed to prove its validity have reached various conclusions [35,60-65].
Reports from the United Kingdom indicated a relationship between younger age at diagnosis of T1D and higher body mass index (BMI) in Middlesbrough [35], and Plymouth [64],but not in Birmingham [61]. Other European studies of large cohorts of German and Austrian children with T1D supported the hypothesis [62,63], although studies from Spain and Australia [66,67] did not. Dabelea et al [65] tested the hypothesis in six centers in the US (Cincinnati, Colorado, Hawaii, Seattle, South Carolina, Southern California) and found a significant relationship between BMI standard deviation score (SDS) and age at diagnosis only among patients with low C-peptide values at diagnosis. Evertsen et al [50] reported a significant inverse relationship between age at diagnosis and BMI SDS in their Wisconsin cohort. Thus, there is no consensus on the validity of the hypothesis among children and adolescents with T1D in the United States.4.
On the other hand, patients with T1D are usually thought to be thin, may present with ketosis, and have diabetes associated autoantibodies.
The rate of the development of these features of increased metabolic load depends on the individual’s genetic makeup and his or her degree of weight gain. These patients are usually overweight or obese and require a high dose of insulin to maintain euglycemia because of obesity-related insulin resistance [31,69]. DiagnosisThere is the need to formulate universal diagnostic criteria to facilitate the recognition of double diabetes either at the time of onset of hyperglycemia or in the course of the disease process. Pozzilli et al [16,31] recently introduced the concept of ‘metabolic load’ to describe the features of T2D and ‘autoimmune load’ to describe the features of T1D. They stated that in an obese child or adolescent with hyperglycemia, an increased ‘metabolic load’ and a reduced ‘autoimmune load’ are features of double diabetes (Figure 1). Based on this principle, they advanced the following clinical and biochemical guidelines to facilitate the diagnosis of double diabetes: The presence of clinical features of T2D, hypertension, dyslipidemia, increased body mass index with increased cardiovascular risk, compared with children with classical T1D. However, because insulin resistance is central to the pathophysiological mechanism of double diabetes, optimal management of this condition necessitates the addition of insulin sensitizers to the patient’s therapeutic regimen under appropriate clinical circumstances [18]. Intensification of lifestyle modification strategies should be encouraged to maintain normal weight and attenuate insulin resistance.

The burden of poor glycemic control in children and adolescentsThe availability of insulin analogs and diabetes monitoring devices has improved diabetes care around the world. However, according to recent studies, the prevalence of poorly-controlled diabetes in youth is still high [70]. This poor glycemic control predisposes the youth to acute and chronic complications of diabetes. Thus only a minority of children and adolescents meet the recommended glycemic targets.The physiological factors that contribute to poor glycemic control in youth are in part related to the hormonal changes in puberty.
Puberty is associated with relative insulin resistance, reflected in a two- to threefold increase in the peak insulin response to oral or intravenous glucose [71]; insulin-mediated glucose disposal is approximately 30% lower in adolescents than in prepubertal children or young adults [72]. This physiologic insulin resistance of puberty is of minimal consequence in the presence of adequate beta-cell function [73].
The cause of this physiologic resistance is likely the transitory increased activity of the growth hormone-insulin growth factor axis, as well as sex steroids, which coincides with the physiologic insulin resistance of adolescence [74] and act as counter-regulatory hormones. As a result of these physiological changes, insulin dosages are often increased to overcome the resistance to insulin, but metabolic control still frequently worsens during the later stages of pubertal development [37].
Alternative therapeutic strategiesThe increasing insulin resistance and deterioration of glycemic control in adolescents create a great need for alternative therapeutic strategies in adolescents with T1D.
One such strategy is the addition of a drug that improves insulin sensitivity such as metformin, a biguanide that acts principally by increasing insulin sensitivity in the liver by inhibiting hepatic gluconeogenesis and thereby reducing hepatic glucose production [75].
Other minor mechanisms include decreasing fatty acid oxidation and intestinal glucose absorption [76], and increasing peripheral insulin sensitivity by enhancing glucose uptake in the muscles [77]. Metformin has mainly been used in adult patients with T2D and several studies have shown beneficial effects on body weight, blood lipid levels and metabolic control [78-80]. Randomized controlled trials with metformin in adolescents with T2D reported an improvement in fasting plasma glucose level [81]. However, there have been conflicting reports from studies in adolescents with T1D [75-77,82,83].
The main drawback of these studies was the small sample size and lack of reporting on long term benefit and safety of adjunctive therapy in many of them [84].Evidence for the coexistence of insulin resistance and insulin deficiency in childhood-onset T1D adults has been demonstrated by the insulin-glucose clamp technique [85,86].
Furthermore, two randomized, placebo-controlled trials have investigated the role of adjunctive metformin therapy in adolescents with T1D. Both studies reported no difference in mean body mass index and serum lipids in the metformin versus placebo group after 3 months of therapy. Hamilton et al [75] reported no significant changes in mean insulin sensitivity, measured by frequently sampled glucose after intravenous glucose tolerance test, after 3 months of metformin therapy in the metformin versus placebo group.
Hamilton et al [75] reported a significant change in the mean daily insulin dose in the metformin group in comparison to the placebo group after 3 months of metformin therapy of -0.14 vs.
However, Sarnblad [77] did not find a significant difference in the daily insulin dosage between the metformin and placebo groups after 3 months of therapy (1.1 vs.
This is important because this sub-set of diabetic youth is known to be insulin resistant and may require a careful titration of insulin doses. Adjunctive metformin therapy to achieve glycemic control may also be more effective in this subset of diabetes patients. Furthermore, even though these randomized controlled trials were designed to investigate the effectiveness of adjunctive metformin therapy compared to insulin therapy alone, they were not designed to compare metformin adjunctive therapy to protocol-driven, optimized insulin therapy. Neither study demonstrated a strong head-to-head comparison of adjunctive metformin to patient-directed, treat to target insulin regimen to ensure optimal insulin delivery during the study. Such a comparison is critical because poor glycemic control contributes to insulin resistance [87] as there is an inverse relationship between glycemic control (as determined by HbA1c) and insulin sensitivity (estimated by glucose infusion rate during euglycemic-hyperinsulinemic clamp) [88]. The need for an insulin titration regimen for double diabetesIn general, patients with double diabetes are overweight or obese and the resultant insulin resistance increases their insulin requirement [1].
However, in addition to requiring a high insulin dose, evidence suggests that many patients often do not have insulin doses titrated sufficiently to achieve target levels of glucose control [89,90]. These patients remain on suboptimal doses of insulin and fail to reach treatment targets [91]. In a recent study Blonde et al [91] demonstrated the efficacy of algorithm-guided, patient titration of once daily long acting insulin in normalizing HbA1c in adult patients with T2D.
In that study, fasting plasma glucose level decreased throughout the first 8 weeks of the study and then generally remained flat for each treatment group. Mean weight changes from baseline to the end of the study were small and did not differ significantly between groups. Our group is conducting a randomized control trial to explore the role of protocol-driven treat-to-target regimen in children and adolescents with double diabetes. Given the rising prevalence of obesity in the general population we speculate that many children with T1D will eventually develop double diabetes.
Thus, it is timely to devise an appropriate management protocol to treat this burgeoning sub-population.
Our aim is to primarily study this group of patients to determine the role of protocol-driven, treat-to-target regimen alone or in combination with metformin therapy in their care.
Given the conflicting reports on the efficacy of adjunctive metformin therapy in adolescents with T1D, this double blind, randomized, placebo controlled trial will demonstrate the effect of meformin on HbA1c reduction under optimized insulin titration regimen. Secondly, we will investigate whether a titrated insulin regimen alone would have a superior-, or similar effect to combined metformin and titrated insulin regimen in children and adolescents with double diabetes and how this modality of treatment compares to standard insulin therapy.Blonde et al [91] demonstrated that self-titration regimens facilitate empowerment of patients, allowing them to become more involved in their treatment, which can result in improved glycemic control. Patient-directed insulin titration is increasingly important as health care practitioners often do not have the resources to advise patients with the frequency needed to effectively titrate their insulin doses to maintain euglycemia. Optimal patient empowerment through self-titration regimens is critical for the motivation to reach treatment targets.7. Therefore, it is possible that these individuals are at higher risk for the microvascular and metabolic complications of T1D and the macrovascular complications of T2D [18]. This is supported by investigations by Orchard et al [85,92], in the Epidemiology of Diabetes Complications Study, who reported that patients with T1D who have a positive family history of T2D were at greater risk for cardiovascular disease than those who did not. Furthermore, data from the Diabetes Control and Complications Trial (DCCT) show that weight gain and central obesity are associated with insulin resistance, hypertension, and dyslipidemia in T1D [93], and data from Epidemiology of Diabetes Interventions and Complications (EDIC) Study show that central obesity is an independent risk factor for incident microalbuminuria in individuals with T1D [94].
However, both DCCT and EDIC follow up studies show that intensive diabetes therapy results in a uniform, major reduction in (and significant protection from) microvascular disease [95], even in overweight or obese T1D patients [92].
Thus, there is the need to devise a consensus treatment regimen that would ensure the best glycemic and metabolic outcome for patients with double diabetes.8. ConclusionsThe global pandemic of obesity in children and adolescents has resulted in a new expression of diabetes mellitus known as double diabetes.
There is no consensus on the best therapeutic modality for this new expression of diabetes mellitus. However, optimal therapeutic options must address the coexistence of both metabolic and autoimmune components of diabetes mellitus in the patient.

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