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Type 1 diabetes is a chronic illness characterized by the bodya€™s inability to produce insulin due to the autoimmune destruction of the beta cells in the pancreas. Blood glucose tests using capillary blood samples, reagent sticks, and blood glucose meters are the usual methods for monitoring day-to-day diabetes control.
Measurement of HbA1c levels is the best method for medium-term to long-term diabetic control monitoring.
The aim of dietary management is to balance the child's food intake with insulin dose and activity and to keep blood glucose concentrations as close as possible to reference ranges, avoiding extremes of hyperglycemia and hypoglycemia.
Most pediatric patients with diabetes have type 1 diabetes mellitus (T1DM) and a lifetime dependence on exogenous insulin.
Type 2 diabetes mellitus (nona€“insulin-dependent diabetes mellitus [NIDDM]) is a heterogeneous disorder.
Hypoglycemia is probably the most disliked and feared complication of diabetes, from the point of view of the child and the family. Manage mild hypoglycemia by giving rapidly absorbed oral carbohydrate or glucose; for a comatose patient, administer an intramuscular injection of the hormone glucagon, which stimulates the release of liver glycogen and releases glucose into the circulation. Occasionally, a child with hypoglycemic coma may not recover within 10 minutes, despite appropriate therapy.
Hypoglycemia was a particular concern in children younger than 4 years because the condition was thought to lead to possible intellectual impairment later in life. Diabetic ketoacidosis (DKA) is much less common than hypoglycemia but is potentially far more serious, creating a life-threatening medical emergency.
If children persistently inject their insulin into the same area, subcutaneous tissue swelling may develop, causing unsightly lumps and adversely affecting insulin absorption. The most common cause of acquired blindness in many developed nations, diabetic retinopathy is rare in the prepubertal child or within 5 years of onset of diabetes.
In a patient with nephropathy, the albumin excretion rate (AER) increases until frank proteinuria develops, and this may progress to renal failure. Progression may be delayed or halted by improved diabetes control, administration of angiotensin-converting enzyme inhibitors (ACE inhibitors), and aggressive blood pressure control. A child younger than 15 years with persistent proteinuria may have a nondiabetic cause and should be referred to a pediatric nephrologist for further assessment.
Autonomic changes involving cardiovascular control (eg, heart rate, postural responses) have been described in as many as 40% of children with diabetes.
Gastroparesis is another complication, and it which may be caused by autonomic dysfunction. Although this complication is not seen in pediatric patients, it is a significant cause of morbidity and premature mortality in adults with diabetes. The combination of peripheral vascular disease and peripheral neuropathy can cause serious foot pathology. Although Addison disease is uncommon, affecting less than 1% of children with diabetes, it is a life-threatening condition that is easily missed.
Originally described in approximately 30% of patients with type 1 diabetes mellitus, limited joint mobility occurs in 50% of patients older than age 10 years who have had diabetes for longer than 5 years. Limited joint mobility is associated with increased risks for diabetic retinopathy and nephropathy. The glucose level at which symptoms develop varies greatly from individual to individual (and from time to time in the same individual), depending in part on the duration of diabetes, the frequency of hypoglycemic episodes, the rate of fall of glycemia, and overall control. Most cases (95%) of type 1 diabetes mellitus are the result of environmental factors interacting with a genetically susceptible person. The frequency of diabetes development in children with a mother who has diabetes is 2-3%; this figure increases to 5-6% for children with a father who has type 1 diabetes mellitus. Human leukocyte antigen (HLA) class II molecules DR3 and DR4 are associated strongly with type 1 diabetes mellitus. Patients expressing DR3 are also at risk for developing other autoimmune endocrinopathies and celiac disease. Patients expressing DR4 are usually younger at diagnosis and more likely to have positive insulin antibodies, yet they are unlikely to have other autoimmune endocrinopathies. Environmental factors are important, because even identical twins have only a 30-60% concordance for type 1 diabetes mellitus and because incidence rates vary in genetically similar populations under different living conditions.[19] No single factor has been identified, but infections and diet are considered the 2 most likely environmental candidates.
Viral infections may be the most important environmental factor in the development of type 1 diabetes mellitus,[20] probably by initiating or modifying an autoimmune process. Nitrosamines, chemicals found in smoked foods and some water supplies, are known to cause type 1 diabetes mellitus in animal models; however, no definite link has been made with humans.
The known association of increasing incidence of type 1 diabetes mellitus with distance from the equator may now have an explanation. Streptozotocin and RH-787, a rat poison, selectively damages islet cells and can cause type 1 diabetes mellitus. The overall annual incidence of diabetes mellitus is about 24.3 cases per 100,000 person-years. A population-based, nationwide cohort study in Finland examined the short -and long-term time trends in mortality among patients with early-onset and late-onset type 1 diabetes.
Different environmental effects on type 1 diabetes mellitus development complicate the influence of race, but racial differences are evident. Type 1 diabetes mellitus can occur at any age, but incidence rates generally increase with age until midpuberty and then decline.[26] Onset in the first year of life, although unusual, can occur, so type 1 diabetes mellitus must be considered in any infant or toddler, because these children have the greatest risk for mortality if diagnosis is delayed. Apart from severe DKA or hypoglycemia, type 1 diabetes mellitus has little immediate morbidity. Information on mortality rates for type 1 diabetes mellitus is difficult to ascertain without complete national registers of childhood diabetes, although age-specific mortality is probably double that of the general population.[29, 30] Children aged 1-4 years are particularly at risk and may die due to DKA at the time of diagnosis. The complications of type 1 diabetes mellitus can be divided into 3 major categories: acute complications, long-term complications, and complications caused by associated autoimmune diseases.
Acute complications, which include hypoglycemia, hyperglycemia, and DKA, reflect the difficulties of maintaining a balance between insulin therapy, dietary intake, and exercise.
Long-term complications arise from the damaging effects of prolonged hyperglycemia and other metabolic consequences of insulin deficiency on various tissues. Associated autoimmune diseases are common in type 1 diabetes mellitus, particularly in children who have HLA-DR3. Medscape's clinical reference is the most authoritative and accessible point-of-care medical reference for physicians and healthcare professionals, available online and via all major mobile devices. The clinical information represents the expertise and practical knowledge of top physicians and pharmacists from leading academic medical centers in the United States and worldwide. More than 6000 evidence-based and physician-reviewed disease and condition articles are organized to rapidly and comprehensively answer clinical questions and to provide in-depth information in support of diagnosis, treatment, and other clinical decision-making.
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Medscape is the leading online destination for healthcare professionals seeking clinical information. Most pediatric patients with diabetes have type 1 and a lifetime dependence on exogenous insulin. Most require 2 or more injections of insulin daily, with doses adjusted on the basis of self-monitoring of blood glucose levels. Diabetes mellitus (DM) is a chronic metabolic disorder caused by an absolute or relative deficiency of insulin, an anabolic hormone. Most patients with type 2 diabetes mellitus have insulin resistance, and their beta cells lack the ability to overcome this resistance.[5] Although this form of diabetes was previously uncommon in children, in some countries, 20% or more of new patients with diabetes in childhood and adolescence have type 2 diabetes mellitus, a change associated with increased rates of obesity. Children hate the symptoms of a hypoglycemic episode and the loss of personal control it may cause. Where appropriate, an alternative therapy is intravenous glucose (preferably no more than a 10% glucose solution). Under no circumstances should further treatment be given, especially intravenous glucose, until the blood glucose level is checked and still found to be subnormal.
In a child with diabetes, blood sugar levels rise if insulin is insufficient for a given glucose load. Users of insulin pumps, by virtue of absent reservoirs of subcutaneous insulin, may present with ketosis and more normal blood glucose levels.
The prevalence and severity of retinopathy increase with age and are greatest in patients whose diabetic control is poor. Blood pressure rises with increased AER, and hypertension accelerates the progression to renal failure. Regular urine screening for microalbuminuria provides opportunities for early identification and treatment to prevent renal failure.
Hyperglycemic effects on axons and microvascular changes in endoneural capillaries are amongst the proposed mechanisms. Cardiovascular control changes become more likely with increasing duration and worsening control.[14] In adults, peripheral neuropathy usually occurs as a distal sensory loss.
Gastric emptying is significantly delayed, leading to problems of bloating and unpredictable excursions of blood glucose levels. People with type 1 diabetes mellitus have twice the risk of fatal myocardial infarction (MI) and stroke that people unaffected with diabetes do; in women, the MI risk is 4 times greater. Smoking, hypertension, hyperlipidemia, and poor diabetic control greatly increase the risk of vascular disease. Addison disease may reduce the insulin requirement and increase the frequency of hypoglycemia. The condition restricts joint extension, making it difficult to press the hands flat against each other. Improved diabetes control over the past several years appears to have reduced the frequency of these additional complications by a factor of approximately 4. Insulin reduces blood glucose levels by allowing glucose to enter muscle cells and by stimulating the conversion of glucose to glycogen (glycogenesis) as a carbohydrate store. The kidneys cannot reabsorb the excess glucose load, causing glycosuria, osmotic diuresis, thirst, and dehydration.
This interaction leads to the development of autoimmune disease directed at the insulin-producing cells of the pancreatic islets of Langerhans. Monozygotic twins have a 60% lifetime concordance for developing type 1 diabetes mellitus, although only 30% do so within 10 years after the first twin is diagnosed. More than 90% of whites with type 1 diabetes mellitus express 1 or both of these molecules, compared with 50-60% of the general population. These patients are more likely to develop diabetes at a later age, to have positive islet cell antibodies, and to appear to have a longer period of residual islet cell function. The expression of both DR3 and DR4 carries the greatest risk of type 1 diabetes mellitus; these patients have characteristics of both the DR3 and DR4 groups. Breastfed infants have a lower risk for type 1 diabetes, and a direct relationship is observed between per capita cow's milk consumption and the incidence of diabetes.
Substantial variations are observed between nearby countries with differing lifestyles, such as Estonia and Finland, and between genetically similar populations, such as those in Iceland and Norway.
The results suggest that in those with early-onset type 1 diabetes (age 0-14 y), survival has improved over time.
These variations strongly support the importance of environmental factors in the development of type 1 diabetes mellitus. Males are at greater risk in regions of high incidence, particularly older males, whose incidence rates often show seasonal variation. Frequency and timing of severe hypoglycemia affects spatial memory in children with type 1 diabetes. A 3-19-year follow-up study on diabetic retinopathy in patients diagnosed in childhood and treated with conventional therapy. Development and progression of microalbuminuria in a clinic sample of patients with insulin dependent diabetes mellitus.
The effect of subclinical hypothyroidism on metabolic control in children andadolescents with Type 1 diabetes mellitus. Occurrence of celiac disease after onset of type 1 diabetes: a 6-year prospectivelongitudinal study. Changes in frequency and severity of limited joint mobility in children withtype 1 diabetes mellitus between 1976-78 and 1998. Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes.
Epidemiology of childhood IDDM in Northern Ireland 1989-1994: low incidence in areas with highest population density and most household crowding.
A prospective study of the role of coxsackie B and other enterovirus infections in the pathogenesis of IDDM.
The association between ultraviolet B irradiance, vitamin D status and incidence rates of type 1 diabetes in 51 regions worldwide. Time trends in mortality in patients with type 1 diabetes: nationwide population based cohort study. Genetic interaction among three genomic regions creates distinct contributions to early- and late-onset type 1 diabetes mellitus.


The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus.
Microvascular and macrovascular complications associated with diabetes in children and adolescents. Global standardization of glycated hemoglobin measurement: the position of the IFCC Working Group.
Clinic-integrated behavioral intervention for families of youth with type 1 diabetes: randomized clinical trial.
Routine hospital admission versus out-patient or home care in children at diagnosisof type 1 diabetes mellitus. Probiotic use in infancy and islet autoimmunity in The Environmental Determinants of Diabetes in the Young (TEDDY) study [abstract 170].
Association between diabetes control and visits to a multidisciplinary pediatric diabetes clinic.
Care of children and adolescents with type 1 diabetes: a statement of the AmericanDiabetes Association.
The delivery of ambulatory diabetes care: structures, processes, and outcomes of ambulatory diabetes care.
Short acting insulin analogues versus regular human insulin in patients withdiabetes mellitus. Comparison of metabolic control in a cross-sectional study of 2,873 children and adolescents with IDDM from 18 countries. Persistent differences among centers over 3 years in glycemic control and hypoglycemiain a study of 3,805 children and adolescents with type 1 diabetes from the HvidA?A?re Study Group. Cyclosporin increases the rate and length of remissions in insulin-dependent diabetes of recent onset. Immunotherapy for the prevention and treatment of type 1 diabetes: human trials and a look into the future.
Disturbed Eating Behavior and Omission of Insulin in Adolescents Receiving Intensified Insulin Treatment: A nationwide population-based study. Thyroid function and autoimmunity in children and adolescents with Type 1 Diabetes Mellitus.
Interventions for Diabetic Retinopathy in Type 1 Diabetes: Systematic Review and Meta-analysis.
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Plus, more than 600 drug monographs in our drug reference include integrated dosing calculators. Insulin replacement is accomplished by giving a basal insulin and a preprandial (premeal) insulin. Insulin is produced by the beta cells of the islets of Langerhans located in the pancreas, and the absence, destruction, or other loss of these cells results in type 1 diabetes (insulin-dependent diabetes mellitus [IDDM]). Other patients may have inherited disorders of insulin release, leading to maturity onset diabetes of the young (MODY) or congenital diabetes.[6, 7, 8] This topic addresses only type 1 diabetes mellitus.
In the absence of insulin, however, severe hyperglycemia, dehydration, and ketone production contribute to the development of DKA. They are more likely to present with nausea, vomiting, and abdominal pain, symptoms similar to food poisoning. Necrobiosis lipoidica affects 1-2% of children and may be more common in children with poor diabetic control. Insulin also inhibits the release of stored glucose from liver glycogen (glycogenolysis) and slows the breakdown of fat to triglycerides, free fatty acids, and ketones.
If insulin is injected into a treated child with diabetes who has not eaten adequate amounts of carbohydrates, blood glucose levels progressively fall. These cells are progressively destroyed, with insulin deficiency usually developing after the destruction of 90% of islet cells. In contrast, dizygotic twins have only an 8% risk of concordance, which is similar to the risk among other siblings. One survey suggests enteroviral infection during pregnancy carries an increased risk of type 1 diabetes mellitus in the offspring.
Some cow's milk proteins (eg, bovine serum albumin) have antigenic similarities to an islet cell antigen. Survival of those with late-onset type 1 diabetes (15-29 y) has deteriorated since the 1980s, and the ratio of deaths caused by acute complications has increased in this group.
Type 1 diabetes mellitus is 1.5 times more likely to develop in American whites than in American blacks or Hispanics. Most deaths result from delayed diagnosis or neglected treatment and subsequent cerebral edema during treatment for DKA, although untreated hypoglycemia also causes some deaths. Debbie Matthews, Colleagues at the Royal Victoria Infirmary, Newcastle upon Tyne, for reading through the manuscript and for years of support.
Customize your Medscape account with the health plans you accept, so that the information you need is saved and ready every time you look up a drug on our site or in the Medscape app. The basal insulin is either long-acting (glargine or detemir) or intermediate-acting (NPH). The most serious complication of DKA is the development of cerebral edema, which increases the risk of death and long-term morbidity.
Without insulin, a child with type 1 diabetes mellitus wastes away and eventually dies due to DKA. Paradoxically, type 1 diabetes mellitus incidence is higher in areas where the overall burden of infectious disease is lower. Current evidence suggests that when immigrants from an area with low incidence move to an area with higher incidence, their rates of type 1 diabetes mellitus tend to increase toward the higher level. Easily compare tier status for drugs in the same class when considering an alternative drug for your patient. The preprandial insulin is either rapid-acting (lispro, aspart, or glulisine) or short-acting (regular). Very young children at the time of first diagnosis are most likely to develop cerebral edema. Additionally, insulin inhibits the breakdown of protein and fat for glucose production (gluconeogenesis) in the liver and kidneys.



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