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Novo Nordisk A/S Servier these companies did not take part in any aspect of the development of the guideline. Unfortunately such optimal management is not reaching many, perhaps the majority, of the people who could benefit. Reasons include the size and complexity of the evidence-base, and the complexity of diabetes care itself. Many guidelines have appeared internationally, nationally, and more locally in recent years, but most of these have not used the rigorous new guideline methodologies for identification and analysis of the evidence. Many countries around the world do not have the resources, either in expertise or financially, that are needed to develop diabetes guidelines. Published national guidelines come from relatively resource-rich countries, and may be of limited practical use in less well resourced countries. This presented a unique challenge as we tried to develop a guideline that is sensitive to resource and cost-effectiveness issues. Many national guidelines address one group of people with diabetes in the context of one health-care system, with one level of national and health-care resources. This is not true in the global context where, although every health-care system seems to be short of resources, the funding and expertise available for health-care vary widely between countries and even between localities. This guideline represents an update of the first guideline and extends the evidence base by including new studies and treatments which have emerged since the original guideline was produced in 2005. Levels of care All people with diabetes should have access to the broad range of diabetes services and therapies and no person should be denied any element of effective diabetes care. It is recognised that in many parts of the developing world the implementation of particular standards of care is limited by lack of resources. This guideline provides a practical approach to promote the implementation of cost-effective evidence-based care in settings between which resources vary widely. The approach adopted has been to advise on three levels of care: Recommended care is evidence-based care which is cost-effective in most nations with a well developed service base, and with health-care funding systems consuming a significant part of national wealth. Recommended care should be available to all people with diabetes and the aim of any health-care system should be to achieve this level of care. However, in recognition of the considerable variations in resources throughout the world, other levels of care are described which acknowledge low and high resource situations. Global Guideline for Type 2 Diabetes Limited care is the lowest level of care that anyone with diabetes should receive. It acknowledges that standard medical resources and fully-trained health professionals are often unavailable in poorly funded health-care systems. Nevertheless this level of care aims to achieve with limited and costeffective resources a high proportion of what can be achieved by Recommended care. Only low cost or high cost-effectiveness interventions are included at this level. Comprehensive care includes the most up-to-date and complete range of health technologies that can be offered to people with diabetes, with the aim of achieving best possible outcomes. However the evidence-base supporting the use of some of these expensive or new technologies is relatively weak. Limited care: Care that seeks to achieve the major objectives of diabetes management, but is provided in health-care settings with very limited resources ­ drugs, personnel, technologies and procedures. Comprehensive care: Care with some evidence-base that is provided in health-care settings with considerable resources. Each comment received was reviewed and changes were made where the evidence-base confirmed these to be appropriate. Individuals who prepared the original sections were invited to review and update their section taking into consideration new evidence and new treatments. The updated guideline was sent out for wide consultation and was modified, where appropriate, according to comments received. Detection programmes are usually based on a two-step approach: · Step1-Identifyhigh-riskindividualsusinga risk assessment questionnaire. Use of HbA1c as a diagnostic test for diabetes requires that stringent quality assurance tests are in place and assays are standardised to criteria aligned to the international reference values, and there are no conditions present which preclude its accurate measurement. The principles for screening are as for Recommended care Diagnosis should be based on fasting laboratory plasma glucose (preferred) or capillary plasma glucose if only point-of-care testing is available.

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Foot ulceration and lower limb amputation in type 2 diabetic patients in Dutch primary health care. Diabetics with foot lesions and amputations in the region of Horny Zitmy Ostrov 1993­1995. The team approach It should be clear that the spectrum of diabetic foot problems requires the involvement of individuals from many specialties. The diabetic foot cannot be regarded as the sole responsibility of the diabetologist, and a number of reports over the last decade have promoted the benefits of a multidisciplinary approach to diabetic foot care [96]. This started in the early 1990s when the concept of the "annual review" was adopted by most national diabetes societies. This requires that all patients with diabetes be screened on an annual basis for evidence of long-term complications [97]. There is increasing evidence from a number of longterm studies that the adoption of this approach not only in hospital but in community care, has been associated with a reduced incidence of foot problems [98­101]. The improved management of diabetic foot care in the district of Leverkusen, Germany, ultimately resulted in a 37% reduction in non-traumatic amputations in patients with diabetes; however, this took more than 10 years after the establishment of specialist foot care [98]. Finally, a sustained reduction in major amputations has been reported from Sweden over the last 20 years suggesting that a substantial decrease in diabetes-related amputations can not only be achieved, but maintained over a long period of time [101]. The prevalence of foot ulceration and its correlates in type 2 diabetic patients: a population-based study. The prevalence and incidence of lower extremity amputation in a diabetic population. Lower extremity amputation in diabetic and non-diabetic patients: a population-based study from Eastern Finland. Temporal association between the incidence of foot ulceration and the start of dialysis in diabetes mellitus. The relationship between callus formation, high foot pressures and neuropathy in diabetic foot ulceration. Diabetic foot syndrome: evaluating the prevalence and incidence of foot pathology in Mexican Americans and non-Hispanic whites from a diabetes disease management cohort. Ethnic differences in plantar pressures in diabetic patients with peripheral neuropathy. Causal pathways for incident lower-extremity ulcers in patients with diabetes from two settings. Multicentre study of the incidence and predictive factors for diabetic foot ulceration. Education for secondary prevention of foot ulcers in people with diabetes: a randomised controlled trial. Evaluation of the self-administered indicator plaster neuropad for the diagnosis of neuropathy in diabetes. A comparative study of the Podotrack, a simple semi-quantitative plantar pressure measuring device, and the optical paedobarograph in the assessment of pressures under the diabetic foot. Use of experimental padded hosiery to reduce abnormal foot pressures in diabetic neuropathy. Efficacy of multilayered hosiery in reducing in-shoe plantar foot pressure in high-risk patients with diabetes. Preventing diabetic foot ulcer recurrence in high-risk patients: use of temperature monitoring as a selfassessment tool. Skin temperature monitoring reduces the risk for diabetic foot ulceration in high-risk patients. Efficacy of injected liquid silicone in the diabetic foot to reduce risk factors for ulceration: a randomized double-blind placebocontrolled trial. The effect of silicone injections in the diabetic foot on peak plantar pressure and plantar tissue thickness: a 2-year follow-up. The description and classification of diabetic foot lesions: systems for clinical care, research and audit. Transforming growth factor-beta 1,2,3 and receptor type 1 and 2 in diabetic foot ulcers. Activity patterns of patients with diabetic foot ulceration: patients with active ulcers may not adhere to a standard pressure offloading regimen. A randomised trial of two irremovable offloading devices in the management of plantar neuropathic diabetic foot ulcers. Semi-quantitative analysis of the histopathological features of the neuropathic foot ulcers: effects of pressure relief.

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Embryogenesis and malformations Maternal hyperglycemia is a major cause of fetal malformation. Clinical and animal studies implicate a combination of metabolic, maternal and fetal factors in the etiologies of diabeticrelated malformations [91]. Improved identification and classification of monogenetic and mitochondrial forms of diabetes have shown that some of these rarer forms of diabetes are associated with fetal structural abnormalities, and distinct phenotypes that are independent of maternal glycemic control have been identified (see Chapter 15). It is not only associated with early-onset diabetes and renal cysts, but also with a variety of other urogenital and pancreatic anomalies in the offspring [92]. There are well-documented genetic susceptibilities to glucose-mediated malformations in rodents which are likely to occur in human pregnancies [93]. Following improvements in obstetric and neonatal care, congenital malformations now represent the major cause of diabetesrelated perinatal morbidity and mortality. Over the last 40 years, diabetes-related congenital malformations rates have been 4­10%. This high rate is especially poignant as good metabolic control around the time of organogenesis lessens this risk [86,94­106]. Multiple anomalies are more common in diabetic pregnancies than in non-diabetic pregnancies. This suggests the teratogenic insult occurs early in embryologic development [107,108]. A greater than threefold excess of severe cardiac anomalies including transposition of the great arteries, truncus arteriosus and tricuspid atresia occurs in diabetic pregnancies [110]. Anomalies of the circulatory system and neural tube were threefold higher than expected among the diabetic pregnancies. Congenital malformations ­ lessons from animal studies Rodent studies show diabetes-associated fetal malformations that are broadly similar to those of humans, although the susceptibility to particular different diabetes-related malformations depends on the maternal species and strain [93,111]. Apoptosis in the mammalian pre-implantation blastocyst is a natural process that eliminates abnormal cells. Hyperglycemia modifies the expression of key apoptotic regulatory genes and normalizing hyperglycemia in mice during the periconception period normalizes the expression of these genes [112]. In rodents, maternal hyperglycemia reduces the number of blastocysts formed and the total cell mass of those that survive. In a hyperglycemic environment, blastocyst cell mass is reduced predominately from the inner cell layer and insulin treatment of hyperglycemic female dams, starting at the time of conception protects the blastocyst from these changes [113]. Insulin may act as a growth factor during early mammalian embryogenesis, influencing mitosis, apoptosis and differentiation through insulin receptors expressed on blastocysts [114]. Animal studies, predominantly in the rodent, implicate glucose as the major teratogen in diabetic pregnancies. Many of the cellular processes induce oxygen-derived free radical production and increased oxidative stress which provide a plausible unifying mechanism by which supraphysiologic concentrations of metabolic substrates, including glucose, pyruvate and hydroxybutyrate, could be teratogenic [91,116­118]. Hyperglycemia at the time of embryogenesis exposes the fetal mitochondria to a high influx of glucose-generated pyruvate that, by overwhelming the immature mitochondrial electron transport chain, may result in an excess of reactive oxygen species (mainly superoxide) being 892 Diabetes in Pregnancy Chapter 53 generated. Myoinositol has an important role as a precursor for a number of secondary messengers and may contribute to diabetic teratogenesis. Cultured rodent embryos in high glucose concentrations have decreased inositol uptake and become inositol deficient [121­125]. Inositol supplementation to embryos cultured in high glucose media or dietary addition to diabetic pregnant rodents protects against glucose-mediated malformation [126,127]. By contrast, the addition of an inositol uptake inhibitor to the culture medium of rodent embryos causes inositol deficiency and embryonic dysmorphogenesis, which is reversible if inositol is added to the culture [128]. Antioxidants diminish both embryonic dysmorphogenesis induced by hyperglycemia and inositol uptake inhibitors, suggesting a possible link between malformations and oxidative stress [129]. Human studies have not shown any evidence for abnormal folate metabolism in pregnant women with diabetes [135]. In rodent studies, folic acid supplementation protects against diabetes-induced malformations [120]. Diabetic control and malformations There is a clear association between congenital abnormalities and maternal glucose control in early pregnancy as assessed by HbA1c [2,85,89,95,101,102,136­141]. Despite the evidence that diabetic fetal malformation rates approach those of the general antenatal population when glycemic control from conception through to the end of organogenesis is tightly controlled [142­ 144], the incidence of serious birth defects has changed little over the last few decades [103,140,145].

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If blood glucose increases >30 mg/dL overnight, an increase in basal may be needed, while a decrease of >30 mg/dL would indicate that basal should be lowered. Insulin Pump Basal Rate the insulin pump actually uses rapid-acting insulin to create basal insulin, delivering tiny pulses of insulin every few minutes 24 h a day. Many people start off with a single basal rate, given as insulin units/hour, and then they fine-tune their basal rates to change throughout the day as their insulin needs vary. Unless you go through long periods of not eating during the day, the majority of the variability in blood glucose levels will be due to the bolus insulin, not the basal rate. The 50:50 Principle of Insulin Management Children: In children, basal insulin accounts for 25­50% of their total daily insulin. As kids get older and approach puberty, their percent as basal insulin increases and approaches the need of adults, which is ~50% of the total daily insulin dose. Adults: Generally this ratio is 50:50, but it varies depending on the person and their circumstances. Occasionally, however, someone will have a high basal rate-totaling 80­90% of their daily insulin requirement. These individuals have to eat at regular intervals so as not to be driven too low by their basal insulin dose. If this works for an individual, then there may be no reason to change; however, many will end up gaining weight because they are eating for the insulin. Small increments, with changes in both basal and bolus patterns, will bring the values into a better balance. And remember, if something is working correctly for you, you may not need to change it. Rapid-acting insulin, taken before meals and snacks, is the preferred choice, but short-acting regular insulin will do if rapid-acting insulin is not an option or if you/your child eats high-fat foods frequently. High-fat meals are absorbed more slowly and may Insulin and Delivery Devices 55 best be covered by short-acting regular insulin, which has a longer duration of action than rapid-acting insulin. The premeal insulin amount is based on a carbohydrate dose plus a correction dose. Working with a dietitian and your diabetes provider is the best way to figure out the doses. Some people need the same amount of insulin for the carbs at different times of the day, and some people need more or less at the different meal times. For example, teenagers and adults typically need more insulin for the carbs at breakfast than later in the day, whereas school-aged children often need less insulin for lunch compared with the rest of the day. For children, the insulin for carbs and correction depends on how much the child weighs and where they are in puberty. Some people start with fixed doses that assume a fairly standard amount of carbohydrate with each meal. There are various formulas for determining these doses and they are different in children (where they are more specific) and in adults (where they tend to be more generic; also known as ballpark estimating). One good rule of thumb is that if your premeal glucose is in the 100s, take insulin 10 min before eating; if it is in the 200s, take insulin 20 min before eating; and if it is in the 300s, take insulin 30 min before eating. The bolus component of the insulin regimen covers the rise in blood glucose that results from eating meals and snacks. The basic bolus equation looks something like this: Bolus dose = (carbohydrate dose + correction dose - active insulin) Ч physical activity adjustment Each person has unique insulin needs, so the I:C is personal. The insulin-to-carb ratio is typically between 1:5 and 1:20 for adolescents and adults and between 1:10 and 1:40 for children. A good starting carb ratio for a relatively lean adult is 1:15 (1 unit of insulin for every 15 g of carbs eaten). So sometimes you need to use different types of bolus doses, such as combination boluses (some up front, some later) or extended boluses (giving the bolus over time instead of all at once). Insulin pumps calculate active insulin automatically and subtract it from the bolus dose. This helps prevent something called "stacking," in which people give too much insulin too soon after the last dose, causing a low blood glucose reaction to occur. This value estimates how much your blood glucose drops for every unit of bolus insulin you take.

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Obesity, especially visceral adiposity, and abnormalities of glucagon secretion commonly contribute to the disease process, while cellular disturbances of nutrient metabolism participate both as causes and consequences of glucotoxicity and lipotoxicity [9­11]. An ideal approach to therapy might therefore address the basic endocrine defects, but any other safe means of ameliorating the hyperglycemia and attendant biochemical disruptions should provide clinical benefits. Note that insulin was introduced earlier than is usual in clinical practice, and insulin was also used as necessary when oral agents were deemed inadequate. Although glycemic control (illustrated by the HbA1c level) deteriorated 453 Part 6 Treatment of Diabetes Table 29. An epidemiologic analysis showed that benefits of intensive therapy continued to accrue until glucose levels were returned to the normal range [13]. Moreover, the benefits of earlier "intensive" control were continued during an unrandomized post-trial follow-up (median 8. This illustrates the glycemic "legacy" effect in which early intensive glycemic control confers an extended reduction in complications, even when control deteriorates at later stages in the disease process. Other large randomized trials [15­17] have confirmed fewer microvascular complications amongst those receiving more intensive glycemic management (Table 29. This may be ascribed to unique features of the trial design outside of normal practice in an aging population at high cardiovascular risk with a long previous duration of inadequately controlled diabetes given extensive medications and experiencing high rates of hypoglycemia. Indeed, an acceptable HbA1c value does not preclude excessive daily fluctuations in glycemia with hyperglycemic excursions and hypoglycemic troughs, the latter often unrecognized nocturnally (see Chapter 33). Survival of a myocardial event appears to be reduced by hypoglycemia as well as hyperglycemia [18]. Guidelines and algorithms Factors to consider when selecting a glycemic target for a particular patient are deliberated in detail in Chapter 20, but it is pertinent to reiterate here that the general principle is to safely return glycemia as close to normal as practicable, avoiding hypoglycemia, minimizing potential drug interactions, and observing other necessary cautions and contraindications. Current treatment algorithms [19­25] provide a framework for initiating and intensifying therapy, but clinical judgment should be applied to harmonize this with patient circumstances. Thus, a younger, newly diagnosed individual without co-morbidity who is responsive to therapy might be expected to meet a more rigorous target, while an elderly infirm individual with co-morbidity and a long history of problems with diabetes control may require more flexiblity. Management of hyperglycemia should always be part of a comprehensive management program to address coexistent disease and modifiable cardiovascuar risk factors. It is emphasized that diet, exercise and other lifestyle measures should be introduced at diagnosis and reinforced at every appropriate opportunity thereafter. These measures can provide valuable blood glucose lowering efficacy and may initially enable the desired glycemic target to be achieved (see Chapters 22 and 23); however, even when lifestyle advice is successfully implemented, the progressive natural history of the disease dictates that the majority of patients will later require pharmacologic therapy, and this should be introduced promply if the glycemic target is not met or not maintained. The main tissues through which they exert their glucose-lowering effects are illustrated in Figure 29. Although there are several different classes from which to choose, many dilemmas continue to impinge on both strategy and individualization of treatment. It is also pertinent to note the link between postprandial hyperglycemic excursions and cardiovascular risk, which mandates the need to also address this component of the hyperglycemic day profile [27]. Additionally, consideration should be given to the improvements in glycemic control that can be achieved through the treatment of obesity (see Chapter 14) [28]. By the time of diagnosis, insulin resistance is usually well established and does not usually progress with extended duration of the disease [8]. Nevertheless, the association between insulin resistance and cardiovascular risk warrants the amelioration of insulin resistance as a valued therapeutic strategy. The ongoing deterioration in glycemic control after diagnosis is largely attributed to a further progressive decline in -cell function [8]. Thus, preserving -cell function and mass are important considerations in maintaining long-term glycemic control. If -cell function deteriorates beyond the capacity of oral agents to provide adequate glycemic control, then the introduction of insulin should not be delayed. Incorporating some or all of the above into the treatment process is inevitably a challenge, and the need to Table 29. Treatment with these agents at the time of conception and during the first trimester has not been shown to have any adverse effects on mother or fetus, and judicious use of metformin has been shown to reduce miscarriage and gestational diabetes. Insulin remains the preferred antidiabetic medication in pregnancy, however, having a substantial evidence base for safety and flexibility.

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The opinions and perspectives of the Testimonial Authors whose content is featured in this work are entirely their own and do not represent the policies or positions of the American Diabetes Association. To purchase more than 50 copies of this book at a discount, or for custom editions of this book with your logo, contact the American Diabetes Association at the address below or at booksales@diabetes. Title: the type 1 diabetes self-care manual: a complete guide to type 1 diabetes across the lifespan for people with diabetes, parents, and caregivers / Jamie Wood and Anne Peters. To the parents of children living with type 1 diabetes, who are strong and work so hard to keep their children healthy, and to the children and adolescents living with type 1 diabetes, who are the bravest and coolest kids out there. Contents Dedication Acknowledgments Chapter 1: the Basics of Type 1 Diabetes Chapter 2: Autoantibodies: How Type 1 Diabetes Begins Chapter 3: Your Blood Glucose Goals Chapter 4: the Diabetes Team Chapter 5: Insulin and Delivery Devices Chapter 6: Nutrition Chapter 7: Highs and Lows Chapter 8: Physical Activity Chapter 9: Mental Health Chapter 10: Heart and Head Chapter 11: Eyes, Kidneys, and Nerves Chapter 12: Sexual Health for Him and Her, and Reproduction Chapter 13: Preteens, Teens, and Young Adults Chapter 14: the Golden Years Chapter 15: Toward a Cure Appendix Index iii vii 1 11 23 35 45 65 77 93 105 117 131 149 161 171 179 189 193 v Acknowledgments this book was funded by a generous grant from the Leona M. Lori Laffel, Jane Chiang, and David Kendall, who were essential to the creation of that book. We are indebted to the contributions of various writers who helped draft versions of this manuscript and patient stories: Erika Gebel Berg, Mary Ziotas Zacharatos, Marie McCarren, and Lindsey Wahowiak. We thank the members of the diabetes community, our patients, our friends, and most of all our families, who (mostly) forgive us our long working hours and provide an abundance of joy. Type 1 diabetes has unique features and, contrary to popular belief, is not a disease only of children; it occurs at any age and in people of every race, shape, and size. This book was written to discuss type 1 diabetes in everyone, from infants to the elderly, from those who are newly diagnosed to those who have had it for many years. Type 1 diabetes can be diagnosed at any age and in people of every race, shape, and size. It is often frustrating for people with type 1 diabetes to be misperceived as someone with type 2 diabetes. Although there are many similarities between type 1 and type 2 diabetes, the cause of each is very different. However, we are discovering more "overlap" between the types, especially for adults who are newly diagnosed, and this can be confusing. Glucose is found inside cells, where it is changed into energy as needed, as well as in the bloodstream, where it is carried around to all of our organs. Our bodies have a wonderful and complicated system for making sure that blood glucose levels are normal day in and day out. Before eating, normal blood glucose levels are 70­100 mg/dL, while after eating the blood glucose levels never go above 140 mg/dL (Table 1. If our glucose levels were to fall too low, we would lose the ability to think and function normally. If they were to go too high, it could cause damage to the body that happens over the course of many years. Patients are diagnosed as having diabetes if their blood glucose is 126 mg/ dL when fasting, their blood glucose is 200 mg/dL and they have symptoms of diabetes, and/or their A1C result is 6. An oral glucose tolerance test is rarely used to diagnose people with diabetes, and if the blood glucose level is 200 mg/dL 2 h after drinking a sugary sweet drink, the diagnosis of diabetes may be made. In most cases, except in those who are very sick, any test should be repeated to confirm the diagnosis. In the absence of unequivocal hyperglycemia, results should be confirmed by repeat testing. The Basics of Type 1 Diabetes 3 Normal blood glucose level is usually around 100 mg/dL. People with diabetes check their blood glucose levels by poking their fingertips or using continuous glucose monitoring (see p. In addition to checking the blood glucose level directly, there is a way to track blood glucose levels over time known as the A1C. It does not replace daily blood glucose monitoring, but in combination with daily readings, an A1C can determine how well the current diabetes treatment plan is working (Table 1. A person who is elderly and troubled by hypoglycemia may have a goal of an A1C <8%.

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Glucose accumulation in the blood causes hyperglycemia that in turn leads to several complications associated with diabetes. Hexosamine and polyol pathways, activation of protein kinase C etc) have been proposed to explain the mechanism by which hyperglycemia leads to vascular and other complications in patients. Apart from some classical explanations, many unconventional theories have been recently proposed suggesting a major involvement of oxidative stress in diabetes. This report summarizes the classical approach to explain diabetic complications and analyzes the role of oxidative stress and free radicals in the pathogenesis of the disease. Introduction Free Radicals in Diabetes 3 Diabetes is a metabolic disorder responsible for numerous deaths each year around the world [1]. It has been reported recently that the risk for most cardiovascular diseases in the United States has decreased over the past 40 years, except, diabetes. Health care costs for diabetes are estimated to be nearly $100 billion per year in the United States [2]. Diabetes is associated with improper generation or utilization of the hormone insulin. The pancreatic cells (beta cells) produce insulin, which helps the cell to take up glucose produced by metabolism of food. Since, diabetes is associated with defects in insulin production, cells of Figure 1: Insulin helps in assimilation of glucose produced by metabolism of food. During lack of insulin, Glucose cannot be taken up by the cell and accumulates in the blood [5]. This leads to excessive glucose in blood, a condition called hyperglycemia [3] (Figure1). Other common symptoms associated are excessive urination, extreme hunger, weight loss, irritable temper, fatigue, inefficient wound healing, dry skin and vision impairment [3]. It accounts for about 10% of all diagnosed cases and is found in infants at birth. It is an autoimmune disease whereby the immune system of the body goes haywire and destroys its own pancreatic cells. This is usually found in adults and accounts for about 90-95% of diabetes cases [4]. Most of these complications can be avoided by dietary restrictions and proper exercise. It has been shown that physical activity of about 30 min/day significantly reduces the risk of cardiovascular diseases in diabetic patients [5]. It usually does not cause any birth defects, but increases the chances of these women developing diabetes at an older age [5]. Diabetic complications In general, four pathways have been suggested to be involved in diabetic complications. Increased hexosamine pathway flux the common theme in most of these pathways is the induction of oxidative stress during hyperglycemia by a certain mechanism, which eventually leads to diabetic complications. Thus, irrespective of which pathway predominates, oxidative stress appears to be the underlying cause of majority of the diabetic complications. These reducing sugars can cause glycation of proteins leading to their inactivation (Figure 2). Figure 2: Formation of advanced glycation endproducts can lead to inactivation of certain important proteins. Glycation derived free radicals can cause fragmentation of protein, oxidation of nucleic acids and initiation of lipid peroxidation [7,8] 2. During hyperglycemina, flux through this pathway is increased as oppsed to glycolysis. This modified sugar can cause oxidative stress, leading to diabetic complications [7]. This makes the intracellular environment more oxidized, leading to oxidative stress, which in turn causes diabetic complications [11] (Figure 5). Most diabetic complications such as retinopathy and neovascularization are results of improper vascular functions.

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Talk to your doctor, nurse, dietitian, and pharmacist to learn how to manage your diabetes. Hable con su mйdico, enfermera, nutricionista y farmacйutico para aprender a controlar la diabetes. The medical information found on this website should not be used in place of a consultation with your doctor or other health care provider. You should always seek the advice of your doctor or otherqualifiedhealthcareproviderbeforeyoustartorstopanytreatmentorwithanyquestionsyoumayhaveaboutamedicalcondition. Walker In type 1 diabetes, your body does not produce insulin, which is the hormone necessary for processing glucose. It stays in the blood, and when you have too much glucose in your blood, it can damage your organs and other parts of your body. Therefore, people with type 1 diabetes must take insulin in order to manage their blood glucose levels and make sure their bodies get the energy they need. Type 1 diabetes used to be called juvenile diabetes or insulin-dependent diabetes, and you may still hear those names used. Type 1 Diabetes Causes Type 1 diabetes is an autoimmune disorder, which means that the immune system turns against your body. Instead of protecting the body, the immune system in people with type 1 diabetes starts to destroy beta cells-and those are the cells that are in charge of making insulin. Some thoughts are: a genetic susceptibility to developing type 1 diabetes certain viruses (for example, German measles or mumps) environmental factors Regardless of what triggers the immune system to turn against the beta cells, the end result is the same in type 1 diabetes: gradually, all beta cells are destroyed and the body is no longer able to produce insulin. Type 1 Diabetes Symptoms Type 1 diabetes develops gradually, but the symptoms come on suddenly. Type 1 Diabetes Diagnosis To diagnose type 1 diabetes, doctors use several blood tests: Glycated hemoglobin (A1c) test: In 2010, the American Diabetes Association said that the A1c test can be used to help diagnosis type 1 diabetes. The A1c test shows your average blood glucose (blood sugar) level over the past 2 to 3 months. Random blood glucose test: As the name implies, this is a random test of your blood glucose level-no preparation or warning on your part. If your random blood glucose level is 200 mg/dL or higher, then you may have diabetes. If the fasting blood glucose level is 126 mg/dL or higher on 2 separate occasions, then you may have diabetes. In fully diagnosing type 1 diabetes, the doctor will also ask about your symptoms, and he or she may also test for the presence of ketones in your urine. Ketones are created when fat is broken down, and if your body can longer process glucose, it will turn to breaking down fat for energy. High levels of ketones are dangerous, and some people with type 1 diabetes have high levels when they are first diagnosed. What Happens After a Type 1 Diabetes Diagnosis Once you-or your child-is diagnosed with type 1 diabetes, treatment can begin to help regulate blood glucose levels. You will have a diabetes treatment team that will help you make the transition to this new world of type 1 diabetes. Many patients are prescribed very complicated regime of diet, exercise, and medication including several pills a day. Such complexity of treatment and factors like age, duration of diseases, depression, disabilities, psychosocial issues and life style changes directly or indirectly influences diseases self management. Adherence to treatment regimen is the key link between treatment and outcome in medical care. Low medication adherence has assumed importance as it seriously undermines the benefits of current medical care and imposes a significant financial burden on individual patients and the health care system as a whole. Poor adherence to the prescribed medication regimen is a critical health care concern for the health care providers all over the world. The problem of making sure the patient follow prescriptions is as old as medicine itself. Medication adherence richly deserves attention and much impetus is needed to develop new ideas and theories to improve it.


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