Pediatric Primary Care Case Studies (68 page)

Before you see Mary again, you need to review your knowledge of type 1 and type 2 diabetes. It is not clear to you which condition she has.

Diabetes in Children

Pathophysiology of Type 2 Diabetes

Type 2 diabetes is a complex metabolic disorder having a genetic predisposition and characterized by insulin resistance and inadequate insulin secretion by the β cells of the pancreas (American Diabetes Association, 2000). Maintenance of
blood glucose levels within a physiologic range requires the orchestration of several metabolic activities: pancreatic β cells must accurately sense glucose concentration and synthesize and release insulin, and insulin must bind to its receptors and facilitate the uptake of glucose by muscle, fat, and liver (Rosenbloom & Silverstein, 2003). In an insulin-resistant state, the usual amount of insulin does not produce the desired effect; therefore, the pancreas must secrete additional insulin to maintain blood glucose levels within a physiologic range. In the early phases of insulin resistance, normal glucose tolerance is maintained by release of greater than normal levels of insulin. However, β cell function gradually declines over time, resulting in inadequate insulin secretion to meet the demands of blood glucose regulation in an insulin-resistant state.

Table 18–1 Diabetes Educational Resources for Parents, Adolescents, and School Personnel

Resources for Adolescents and Families

1. National Diabetes Education Program (NDEP)
^a
:
http://www.ndep.nih.gov/diabetes/pubs/
catalog.htm#ResChildAdol

• What Is Diabetes (NDEP-63)

• Be Active (NDEP-64)

• Stay at a Healthy Weight (NDEPP-65)

• Make Healthy Food Choices (NDEP-66)

• Dealing with the Ups and Downs of Diabetes (NDEP-87)

• Examples of treatments for hypoglycemia:
http://www.diabetesatwork.org/_files/handouts/I_B_01b_HO(1).pdf

2. American Diabetes Association
^a

• Wizdom, Type 2 Diabetes:
http://web.diabetes.org/wizdom/download/type2.asp

• Youth Zone:
http://www.diabetes.org/youthzone/youth-zone.jsp

3. Children with Diabetes Web site

• What Is Type 2 Diabetes?:
http://www.childrenwithdiabetes.com/type2/t2_whatistype2.htm

Resources for School Personnel

National Diabetes Education Program
^a

• Helping the Student with Diabetes Succeed: A Guide for School Personnel
^a

^a
Available in English and Spanish

Puberty augments the problems imposed by insulin resistance for those predisposed to type 2 diabetes. Secretion of growth hormone as part of the pubertal growth spurt further increases resistance to insulin action. Adolescents with
normally functioning pancreatic β cells secrete additional insulin to compensate for this puberty-related effect. However, when β cells do not function properly, metabolic decompensation begins and leads to a state of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) with eventual progression to type 2 diabetes (American Diabetes Association, 2000).
Table 18-2
identifies current American Diabetes Association definitions for prediabetes and diagnostic criteria for diabetes.

Epidemiology of Obesity and Type 2 Diabetes in Children

The phenomenon of type 2 diabetes in the pediatric population has emerged concurrent with the rising prevalence of overweight and obesity in U.S. youth. Data from the National Health and Nutrition Examination Survey (NHANES) indicate that approximately one third (31.9%) of U.S. children are either overweight or obese (BMI ≥ 85th percentile for age) (Ogden, Carroll, & Flegal, 2008). Among all age and gender categories, minority children have higher prevalence rates for overweight and obesity; for example, among teens, 44.5% of African American girls were overweight or obese compared to 31.7% of non-Hispanic white girls (Ogden et al., 2008).

The prevalence of type 2 diabetes has increased concurrent with the increase of pediatric overweight and obesity, with minority children disproportionately affected (Rosenbloom & Silverstein, 2003). In one large sample of Florida children cared for at pediatric diabetes centers, the percentage of children diagnosed with type 2 diabetes increased from 9.4% to 20% over a 5-year period (Macaluso
et al., 2002), although the total number of children diagnosed with diabetes remained stable during these years. Compared to children with type 1 diabetes, children with type 2 diabetes were more likely to be overweight or obese, of Hispanic ethnicity or African American race, female, and of older age.

Findings from the recent SEARCH for Diabetes in Youth Study (Liese et al., 2006), a large epidemiologic study, demonstrate that currently 154,000 children in the United States have diabetes; of these, approximately 39,000 (25%) have type 2 diabetes (Lipton, 2007). This study further suggests that the occurrence of type 2 diabetes in children less than 10 years of age is rare among U.S. children of all races and ethnicities. However, for children 10 years of age and older, race and ethnicity strongly influence the frequency of type 2 diabetes, with children of African American and Native American race most commonly affected. Therefore, it is important to consider type 2 diabetes in the differential diagnosis of older children who present with symptoms of diabetes. Although strongly linked to genetic predisposition, diet and lifestyle are also strongly implicated in the rise of type 2 diabetes in this age group. The combination of low physical activity with ingestion of high calorie, high fat foods of low nutritional quality creates an obesigenic environment leading to excess weight gain and obesity.

Obesity and Cardiovascular Disease Risk in Children

The Bogalusa Heart Study, a longitudinal epidemiologic study, was initiated in 1973 to study cardiovascular risk factors beginning in childhood. Several important relationships regarding obesity, insulin resistance, and cardiovascular risk have been identified using data from these participants. Investigators from the Bogalusa Heart Study (Svec et al., 1992) measured glucose and insulin levels in 377 children 7 to 11 years of age from a biracial community. Controlling for age, body weight, and pubertal stage, African American children had higher insulin levels compared to white children, placing African American children at higher risk for insulin resistance.

In another study (Freedman, Dietz, Srinivasan, & Berenson, 1999), researchers noted that children who were overweight were more likely to have elevations in a lipid profile component, blood pressure, and fasting insulin levels, thereby demonstrating a relationship between weight and cardio-metabolic risk. Importantly, more than half (58%) of the overweight children had at least one risk factor. Findings of this study demonstrate that, even among young children, presence of obesity is consistently related to cardiovascular risk factors. For example, among 5- to 6-year-old study participants, those who were overweight were 7.1 times more likely to have elevated triglyceride levels and 16 times more likely to have elevated systolic blood pressure compared to similar-age children of normal weight. In another study, autopsy reports of Bogalusa Heart study participants provided evidence of the presence of coronary and aortic atherosclerosis and its relationship to prior documented cardiovascular risk factors, and that severity of asymptomatic coronary artery disease increases with an increase in the number of cardiovascular risk factors (Berenson, Srinivasan, & Nicklas, 1998). Furthermore, childhood obesity results
in a relative risk of about 1.5 for all-cause mortality and 2.0 for coronary heart disease mortality (Must & Strauss, 1999).

Pathophysiology of Type 1 Diabetes in Children

Type 1 diabetes, the second most common chronic disease in childhood, affects approximately 1 in 500 children in the United States, and is the more prevalent form of diabetes among children. Metabolic manifestations of both type 1 and type 2 diabetes are similar; however, the pathophysiology of type 1 diabetes differs from that of type 2 diabetes. Type 1 diabetes is an idiopathic and immune-mediated condition resulting in permanent loss of the body’s ability to produce insulin due to progressive autoimmune destruction of the β cells of the pancreas (Asp, 2005). Approximately 75% of individuals with type 1 diabetes will test positive for the presence of autoantibodies at the time of diagnosis (Haller, Silverstein, & Rosenbloom, 2007). Prior to discovery of insulin in 1921, type 1 diabetes was a fatal disease.

Pancreatic β cell destruction occurs insidiously until the number of functioning pancreatic β cells is no longer sufficient to regulate blood glucose levels, and hyperglycemia occurs. When blood glucose concentrations exceed the kidney’s ability to conserve glucose, glucose is excreted into the urine, leading to osmotic diuresis. Symptoms of diabetes, polydipsia and polyuria, are related to hyperglycemia. Type 1 diabetes has an abrupt clinical onset and generally occurs over a 2- to 3-week period (Roche, Menon, Gill, & Hoey, 2005). If diabetes is not recognized and treated, symptoms progress to weight loss, dehydration, and ketosis resulting from breakdown of body fat, and eventually progress to diabetic ketoacidosis, an absolute state of insulin deficiency (Haller et al., 2007). Approximately 20% to 40% of new cases of type 1 diabetes present in diabetic ketoacidosis, with young children and those with poor access to health care at particular risk (Mallare et al., 2003; Roche et al., 2005; Rosenbloom, 2007).

Epidemiology of Type 1 Diabetes in Children

The etiology of type 1 diabetes is multifactorial, combining a genetic predisposition with an environmental trigger (Rennert & Francis, 1999). The incidence of type 1 diabetes varies worldwide, ranging from Finland (greater than 40 per 100,000), where incidence is highest, to China (0.1 per 100,000), where incidence is lowest. In the United States the incidence of type 1 diabetes is estimated to be 16.1 per 100,000 per year (Soltesz, Patterson, & Dahlquist, 2007). Susceptibility to type 1 diabetes can be inherited; however, approximately 85% of cases occur sporadically. Siblings of an individual with type 1 diabetes have a 40-fold higher risk of developing diabetes; similarly, a child whose parent has type 1 diabetes has a 10-fold (if mother has diabetes) to 35-fold (if father has diabetes) increased risk (Winter, 2007). Researchers have studied the relationships between a variety of environmental agents such as cow’s milk, vitamin D deficiency, and enteroviruses and development of type 1 diabetes (Eisenbarth, 2007). The TRIGR study, an international multi-site randomized controlled trial, is testing the hypothesis that compared to cow’s milk–based formula, hydrolyzed infant formula decreases risk of
developing type 1 diabetes in children with increased genetic susceptibility (TRIGR Study Group, 2007). However, to date, the factors responsible for activating autoimmune destruction of pancreatic β cells in children at risk for type 1 diabetes remain unknown.

In the 1980s, two international type 1 childhood population-based diabetes registries, Eurodiab and Diamond, were established to collect epidemiologic data (Soltesz et al., 2007) about type 1 diabetes in youth. These registries have provided important information regarding global incidence patterns, age and gender patterns, and trends over time. Incidence of type 1 diabetes increases with age, with children at highest risk during the pubertal years (10 to 14 years). Boys and girls are equally affected (Soltesz et al., 2007). The incidence of type 1 diabetes is rising globally, with the highest increase noted in children 5 years of age and younger (Dabelea et al., 2007; Gale, 2002). The SEARCH for Diabetes in Youth Study, a recent multi-center epidemiologic study of children in the United States (Dabelea et al.), demonstrates that the incidence of type 1 diabetes occurs among all racial/ethnic groups, with non-Hispanic white youth most commonly affected.