Diabetes, pre-diabetes and insulin resistance screening in Native American children and youth.

OBJECTIVES: Early identification of pre-diabetes and insulin resistance (IR) provides an important window of opportunity for diabetes prevention. Little is known about the prevalence of pre-diabetes and IR in Native American (NA) youth. We designed a cross-sectional, community-based study of NA children to estimate the prevalence of diabetes, pre-diabetes and IR and their association with other diabetes risk factors. STUDY DESIGN: NA children (5-18 years) were screened with body mass index (BMI), blood pressure, oral glucose tolerance test (OGTT), lipids, insulin and highly sensitive C-reactive protein (hsCRP), and calculated homeostatic model assessment of IR (HOMA-IR). RESULTS: Mean age of the cohort (n=201) was 10.8 ± 3.8 years (± s.d.; 94/107 M/F). BMI percentile for age and sex (BMI%) was elevated (≥ 85 th percentile) in 58.6% of 5-11 years and 51.1% of 12-18 years, and positively correlated with HOMA-IR, blood pressure, triglycerides and hsCRP (P<0.05). The prevalence rate for pre-diabetes and diabetes were 6.5% (3.5-10.8%) and 1.0% (0.1-3.6%), respectively. Mean HOMA-IR was greater in the older than younger age group while prevalence of pre-diabetes was the same. Those with pre-diabetes and diabetes had a greater HOMA-IR, abdominal circumference and BMI% than normal youth. CONCLUSION: In the first prospective, community-based screening for pre-diabetes, IR and diabetes in United States NA youth using OGTT, while the number of diabetes cases was low, pre-diabetes was found in a significant number of youth, particularly in those with BMI ≥ 95 th%. As proportions of pre-diabetes were similar in 5-11 and 12-18 year olds, diabetes risk begins early in NA youth.

Epstein-Barr virus burden in adolescents with systemic lupus erythematosus.

OBJECTIVE: We sought to determine whether patients with systemic lupus erythematosus (SLE) and a presumed primary or reactivated Epstein-Barr virus (EBV) serologic response had evidence of an active EBV infection. BACKGROUND: Patients with SLE often have what appears to be a primary or reactivated EBV serologic response. If these patients then present with fever, fatigue, adenopathy or leukopenia, it is not clear whether these symptoms are caused by worsening SLE or EBV infection. Establishing the correct diagnosis is crucial for management. METHODS: We examined the EBV burden in 13 adolescents with SLE and a presumed primary or reactivated EBV serologic response. All were taking prednisone; 2 each were also on azathioprine or intravenous pulse cyclophosphamide. EBV serologies were performed for all, and EBV burdens were assessed via immortalization assays and EBV DNA amplification of blood and saliva at least once. RESULTS: Seven patients had serologic patterns indicative of a primary EBV infection, while six had serologies indicative of a reactivated (secondary) EBV infection. Two of the latter were the only ones in whom a small amount of biologically active EBV was detected. CONCLUSION: In our series active EBV infection was not seen in most patients, despite serologic data that could be interpreted as a primary or reactivated infection. Thus the serologic profiles were more likely a consequence of immune dysregulation secondary to SLE or its therapy rather than rampant infection with EBV.