Lorraine E Levitt Katz

The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States

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Publications (30)119.08 Total impact

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    ABSTRACT: Insulin-like growth factor (IGF)-I and IGF binding protein (IGFBP)-1 have been linked to cardiovascular disease (CVD) risk and pathophysiology in adults, but there are limited data in youth. The aim of the study was to examine the relationship between IGF and IGFBP-1 with traditional and non-traditional CVD risk factors including inflammatory markers and body composition in an obese pediatric cohort. A cross-sectional study. The study was carried out at a university children's hospital. Sixty-one obese non-diabetic adolescents. Fasting IGF-I, IGFBP-1, lipoprotein profiles, high-sensitivity C-reactive protein (hsCRP), and total adiponectin as well as insulin sensitivity measures, blood pressure (BP), and anthropometrics. IGFBP-1 was negatively associated with insulin sensitivity measures, body mass index (BMI), and diastolic BP in males. IGF-I was negatively associated with hsCRP (r = -0.479, p < 0.0005), and IGFBP-1 was positively associated with adiponectin (r = 0.545, p < 0.0005). The IGF-I/CRP and IGFBP-1/adiponectin associations remained significant when controlling for both BMI and insulin sensitivity index (SI ). Both IGF-I and IGFBP-1 were negatively associated with waist circumference (r = -0.327 and r = -0.275, respectively) and sagittal abdominal diameter (r = -0.333 and r = -0.371, respectively), while IGFBP-1 was negatively associated with fat mass (r = -0.347, p = 0.01) as well as neck circumference and fat-free mass in males. Controlling for BMI z-score and SI , IGFBP-1 remained negatively associated with diastolic blood pressure (r = 0.706, p = 0.001 and neck circumference (r = -0.548, p = 0.15) in males. IGF-I and IGFBP-1 associate with CVD risk markers and may add to clinical assessments of cardiometabolic dysfunction in youth. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
    Pediatric Diabetes 12/2014; · 2.08 Impact Factor
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    ABSTRACT: Sagittal abdominal diameter (SAD) was obtained in 65 adolescents referred for assessment of cardiometabolic risk. We found that SAD was associated with cardiometabolic risk factors independent of BMI in males, but that SAD was not superior to BMI or other measures of abdominal adiposity for the detection of metabolic syndrome.
    Diabetes research and clinical practice 01/2014; · 2.74 Impact Factor
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    ABSTRACT: Although the American Academy of Sleep Medicine (AASM) mandates that periodic limb movements during sleep (PLMS) be scored on every polysomnogram, and considers a periodic limb movement index (PLMI) > 5/h abnormal in children, there is a lack of community-derived data regarding the prevalence of PLMS in children, and no data to support this cutoff value. Therefore, the aim of this study was to determine the prevalence of PLMS in a sample of normal children.
    Sleep 01/2014; 37(8):1349-52. · 5.10 Impact Factor
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    ABSTRACT: OBJECTIVES: To assess the association of weight loss and insulin sensitivity, glucose tolerance, and metabolic syndrome (MS) in obese adolescents following weight loss treatment, and to determine the threshold amount of weight loss required to observe improvements in these measures. STUDY DESIGN: A randomized, controlled behavioral weight loss trial was conducted with 113 obese adolescents. Changes in fasting insulin, homeostasis model assessment of insulin resistance, whole body insulin sensitivity index (WBISI), body mass index (BMI), and MS criteria were assessed at baseline and at month 4. RESULTS: There was significant improvement in all measures of insulin sensitivity at month 4. Mean fasting insulin dropped from 22.3 to 16.6 μU/mL (P < .0001). Homeostasis model assessment of insulin resistance decreased significantly from 4.9 to 3.7 (P = .001) and WBISI increased significantly from 2.87 to 3.98 (P < .0001). An 8% reduction in BMI led to a significant improvement in WBISI (P = .03) and was the optimal threshold. Fewer individuals met criteria for MS after weight loss (P = .0038), although there were no significant changes in the individual features of the syndrome. CONCLUSIONS: In this trial, weight loss at month 4 was associated with improved insulin sensitivity in obese adolescents. An approximate decrease in BMI of 8% was the threshold level at which insulin sensitivity improved. As more weight loss programs are designed for obese adolescents, it will be important to have reasonable weight loss goals that will yield improvements in metabolic and cardiovascular disease risk factors.
    The Journal of pediatrics 05/2013; · 4.02 Impact Factor
  • Terri Lipman, Sarah Ratcliffe, Rhona Cooper, Lorraine E Levitt Katz
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    ABSTRACT: BACKGROUND: Population-based (PB) registries of type 1 diabetes (T1D) in children have been essential in determining the geographic, racial and temporal patterns of the disease. There is a paucity of PB data on the prevalence of type 1 and type 2 diabetes (T2D) in youth. METHODS: Prevalence of diabetes in children was determined using a PB survey of the 628 schools in Philadelphia. Data obtained included type of diabetes, DOB, race, gender, date of diagnosis, diabetes treatment, and most recent height and weight. RESULTS: The survey was completed by nurses at 510 schools (81% of schools) representing 252,896 children (70% of children in Philadelphia). Prevalence (per 1000) was computed assuming data were missing at random. The survey identified 492 school children with diabetes (355 T1D, 88 T2D, 49 type unknown). Overall prevalence of T1D was 1.58 (0.73 W, 0.56 AA, 0.50 H) and T2D was 0.35 (0.03 W, 0.28 AA, 0.05 H). Mean age of diagnosis was T1D= 8.6 yr, T2D= 11.9 yr. T1D was greater in males, T2D in females. Of children with T2D, 25% were treated with insulin. BMI was >95th % in 20% of children weighed; 10% of T1D, 57% of T2D. CONCLUSIONS: Although the Philadelphia Pediatric Diabetes Registry is the longest ongoing US incidence registry of its kind, these are the first PB prevalence data of children with diabetes in Philadelphia, PB studies in schools are able to capture children with diabetes who are diagnosed and treated in a variety of settings. THE SIGNIFICANT FINDING (S) OF THE STUDY: The Philadelphia data demonstrate that T1DM is 4.5 times more prevalent than T2DM in children. Although there has been a marked increase of T2DM, it is critical to recognize that T1DM continues to be a much greater risk for children. THIS STUDY ADDS: Few studies have examined the prevalence of diabetes in youth because of inherent difficulties in case ascertainment. These data are among the few derived from a population based prevalence study of type 1 and type 2 diabetes in youth.
    Journal of Diabetes 03/2013; · 2.94 Impact Factor
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    ABSTRACT: Background. Insulin resistance increases type 2 diabetes risk in obese adolescents. Thus, quantitative tools measuring insulin sensitivity and secretion are important for risk assessment. Methods. Forty-four obese pubertal adolescents underwent oral glucose tolerance test (OGTT) and frequently sampled intravenous glucose tolerance test (FSIGT). We correlated OGTT-derived whole body sensitivity index (WBISI) with FSIGT-derived insulin sensitivity index (Si). Insulinogenic index (IGI) from OGTT was compared with acute insulin response to glucose (AIRg) from FSIGT. Results. Fasting insulin (r = -.64, P < .0005) and glucose (r = -.39 P ≤ .0005) predicted Si. The OGTT-derived index WBISI correlated with the FSIGT-derived Si (r = .608, P < .0005). IGI correlated with AIRg from FSIGT (r = .704, P < .0005). Conclusions. OGTT-based measures correlated with FSIGT-derived measures of insulin sensitivity and secretion. In particular, we demonstrated that WBISI can be a reliable alternative to FSIGT-derived Si in clinical settings where OGTT is a more feasible option.
    Clinical Pediatrics 03/2013; 52(3):247-53. · 1.27 Impact Factor
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    ABSTRACT: OBJECTIVE The purpose of this study was to describe the incidence of type 1 diabetes in children in Philadelphia from 2000-2004, compare the epidemiology to the previous three cohorts in the Philadelphia Pediatric Diabetes Registry, and, for the first time, describe the incidence of type 2 diabetes.RESEARCH DESIGN AND METHODS Diabetes cases were obtained through a retrospective population-based registry. Hospital inpatient and outpatient records were reviewed for cases of type 1 and type 2 diabetes diagnosed from 1 January 2000 to 31 December 2004. The secondary source of validation was the School District of Philadelphia. Time series analysis was used to evaluate the changing pattern of incidence over the 20-year period.RESULTSThe overall age-adjusted incidence rate in 2000-2004 of 17.0 per 100,000 per year was significantly higher than that of previous cohorts, with an average yearly increase of 1.5% and an average 5-year cohort increase of 7.8% (P = 0.025). The incidence in white children (19.2 per 100,000 per year) was 48% higher than in the previous cohort. Children aged 0-4 years had a 70% higher incidence (12.2 per 100,000 per year) than the original cohort; this increase was most marked in young black children. The overall age-adjusted incidence of type 2 diabetes was 5.8 per 100,000 per year and was significantly higher in black children.CONCLUSIONS The incidence of type 1 diabetes is rising among children in Philadelphia. The incidence rate has increased by 29% since the 1985-1989 cohort. The most marked increases were among white children ages 10-14 years and black children ages 0-4 years. The incidence of type 1 diabetes is 18 times higher than that of type 2 in white children but only 1.6 times higher in black children.
    Diabetes care 01/2013; · 7.74 Impact Factor
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    ABSTRACT: To compare lipoprotein profiles of prediabetic to normoglycemic obese adolescents. Cross-sectional study of 95 obese, pubertal adolescents (12-17 years), who underwent oral glucose tolerance test, lipid panel, and lipoprotein subclass particle analysis (nuclear magnetic resonance spectroscopy). Univariate and linear regression analyses compared prediabetic and normoglycemic groups. Of 95 obese adolescents enrolled in the study, 22.1% (n = 21) had prediabetes. They were similar to normoglycemic adolescents (n = 74) in age, race, body mass index, standard lipids, total low-density lipoprotein particles (LDL-P), and total high-density lipoprotein particles (HDL-P). However, prediabetics had higher concentrations of small LDL-P (714.0 ± 288.0 vs 537.7 ± 266.5 nmol/L, P = .01) and smaller LDL-P size (20.73 ± 0.41 vs 21.18 ± 0.65 nm, P = .003), than normoglycemic youth. Prediabetics had higher small HDL-P (18.5 ± 3.8 vs 16.6 ± 3.9 umol/L, P = .046), lower large HDL-P (4.49 ± 2.0 vs 6.32 ± 2.6 umol/L, P = .004), and smaller HDL-P size (8.73 ± 0.31 vs 9.01 ± 0.39 nm, P = .003). After adjusting for demographics, Tanner stage, and body mass index using multiple linear regression, all differences remained significant except for small HDL-P. After additional adjustment for Homeostasis Model Assessment-Insulin Resistance Index, only LDL-P size difference remained significant. Obese prediabetic adolescents have a significantly more atherogenic lipoprotein profile compared with obese normoglycemic peers. Prediabetic adolescents may benefit from more aggressive interventions to decrease future cardiovascular risk.
    The Journal of pediatrics 05/2012; 161(5):881-6. · 4.02 Impact Factor
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    ABSTRACT: Sleep deprivation is associated with increased risk of adult type 2 diabetes mellitus (T2DM). It is uncertain whether sleep deprivation and/or altered sleep architecture affects glycemic regulation or insulin sensitivity or secretion. We hypothesized that in obese adolescents, sleep disturbances would associate with altered glucose and insulin homeostasis. This cross-sectional observational study of 62 obese adolescents took place at the Clinical and Translational Research Center and Sleep Laboratory in a tertiary care children's hospital. Subjects underwent oral glucose tolerance test (OGTT), anthropometric measurements, overnight polysomnography, and frequently sampled intravenous glucose tolerance test (FSIGT). Hemoglobin A(1c) (HbA(1c)) and serial insulin and glucose levels were obtained, indices of insulin sensitivity and secretion were calculated, and sleep architecture was assessed. Correlation and regression analyses were performed to assess the association of total sleep and sleep stages with measures of insulin and glucose homeostasis, adjusted for confounding variables. We found significant U-shaped (quadratic) associations between sleep duration and both HbA(1c) and serial glucose levels on OGTT and positive associations between slow-wave sleep (N3) duration and insulin secretory measures, independent of degree of obesity, pubertal stage, sex, and obstructive sleep apnea measures. Insufficient and excessive sleep was associated with short-term and long-term hyperglycemia in our obese adolescents. Decreased N3 was associated with decreased insulin secretion. These effects may be related, with reduced insulin secretory capacity leading to hyperglycemia. We speculate that optimizing sleep may stave off the development of T2DM in obese adolescents.
    Diabetes care 09/2011; 34(11):2442-7. · 7.74 Impact Factor
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    ABSTRACT: The study objective was to examine the prevalence of depressive symptoms and relationships to quality of life and demographics in the Treatment Options for Type 2 Diabetes in Adolescents and Youth (TODAY) study's large, ethnically diverse youth with type 2 diabetes. A total of 704 youth with type 2 diabetes <2 years' duration, aged 10-17 years, and BMI ≥85th percentile completed depressive symptoms and quality of life measures. Some 14.8% reported clinically significant depressive symptoms, and older girls had significantly higher rates than older boys. Rates of significant depressive symptoms were similar to those of healthy adolescents and lower than those of teens with type 1 diabetes. Elevated depressive symptoms, particularly in older girls, suggest clinicians assess vulnerability.
    Diabetes care 08/2011; 34(10):2205-7. · 7.74 Impact Factor
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    ABSTRACT: Children with obesity and insulin resistance (IR) have decreased adiponectin and have increased cardiovascular risk. Adiponectin has antiatherogenic effects, but its mechanism is unclear. Our objectives were 1) to compare lipoprotein subclass particles among obese and lean adolescents and delineate their relationships with IR and 2) to measure relationships between adiponectin and lipoproteins and their dependence on body mass index (BMI) and/or IR. DESIGN, SETTING, PATIENTS, AND MAIN OUTCOME MEASURES: This was a cross-sectional study of 57 obese and 38 lean pubertal adolescents, measuring lipoprotein subclass particles (nuclear magnetic resonance spectroscopy), lipids, adiponectin, and homeostasis model assessment of IR (HOMA-IR). Obese had higher low-density lipoprotein (LDL) cholesterol (P = 0.018), higher small LDL particles (LDL-P) (P < 0.0005), smaller LDL-P size (P < 0.0005), smaller high-density lipoprotein particle (HDL-P) size (P < 0.0005), lower HDL cholesterol (HDL-C) (P < 0.0005), and higher small HDL-P (P = 0.009) compared with lean. HOMA-IR was higher in obese than lean (P < 0.0005) and positively associated with triglycerides, large very LDL-P, and small HDL-P and negatively with HDL-P size in obese. Adiponectin was lower in obese than lean (P < 0.0005) and was positively associated with LDL-P size, HDL-P size, and HDL-C and negatively with triglycerides, small LDL-P, large very LDL-P, and small HDL-P in obese. Using linear regression adjusting for demographics, Tanner stage, BMI, and HOMA-IR in all adolescents, adiponectin was positively associated with LDL-P size (P = 0.028), HDL-P size (P < 0.0005), and HDL-C (P = 0.042) and negatively with small LDL-P (P = 0.009) and small HDL-P (P = 0.004). Obese adolescents have lower adiponectin levels than lean, and a more atherogenic lipoprotein profile, associated with increased IR. Adiponectin was inversely associated with atherogenic lipoproteins in adolescents, even after adjusting for obesity and IR. This is the first such report in children, and suggests a relationship between adiponectin and lipoproteins in adolescents independent of BMI and IR.
    The Journal of Clinical Endocrinology and Metabolism 03/2011; 96(5):1549-54. · 6.31 Impact Factor
  • Pamela Abrams, Lorraine E Levitt Katz
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    ABSTRACT: Childhood obesity is rising to epidemic proportions throughout the world, and much emphasis has been placed on the long-term consequences that can result later, in adulthood. This article reviews the metabolic consequences of obesity that can manifest as disease during the childhood years. Obese children suffer from many disease processes once thought to affect only adults. They can have type 2 diabetes mellitus, and potentially early β cell failure with rapid progression to an insulin requirement. There is a high prevalence of fatty liver disease in obese children, and complications such as steatohepatitis and even cirrhosis can develop during childhood. Visceral fat has been shown to have many different properties than subcutaneous fat, and children with central adiposity can develop the metabolic syndrome with insulin resistance, hypertension, and dyslipidemia. Hyperandrogenism, sleep disturbances, and many types of orthopedic complications can also develop in young children. Physicians should not only warn obese children and their families about the long-term consequences of obesity for which they are at risk in adulthood, they should also screen for the many diseases that may already be present.
    Current opinion in endocrinology, diabetes, and obesity 02/2011; 18(1):23-7. · 3.77 Impact Factor
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    ABSTRACT: To determine the course of glycemic decline in a pediatric cohort with type 2 diabetes mellitus (T2DM) by defining longitudinal changes in hemoglobin A1c (HbA1c) and insulin requirement. We also followed markers of insulin reserve (fasting C-peptide and IGFBP-1) over time. Participants included two groups: (1) T2DM Nonacidotic (NA) (n = 46); and (2) T2DM diabetic ketoacidosis (n = 13). HbA1c, insulin dose, and fasting C-peptide and IGFBP-1 were obtained at baseline and every 6 months for 4 years. At baseline, Mann Whitney tests demonstrated that the diabetic ketoacidosis group had higher HbA1c (P = .002), required more insulin (P = .036), and had lower C-peptide (P = .003) than the NA group. Baseline insulin dose (Spearman r = -0.424, P = .009) and baseline IGFBP-1 (Spearman r = -0.349, P = .046) correlated negatively with C-peptide. Over time, HbA1c, insulin dose, and C-peptide changed significantly in a complex manner, with group differences. HbA1c reached a nadir at 6 to 12 months and began to rise after 1.5 years. Insulin requirements reached a nadir at 1 year and began to rise after 2 years. Unlike adults, children with T2DM require increasing insulin doses over a 4-year period, and diabetic ketoacidosis at diagnosis predicts greater β-cell decline over time.
    The Journal of pediatrics 01/2011; 158(1):106-11. · 4.02 Impact Factor
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    ABSTRACT: Use of meal replacements (MRs) in lifestyle modification programs (LMPs) for obese adults significantly increases weight loss, compared with prescription of an isocaloric conventional diet (CD). This 12-month randomized trial examined 113 obese adolescents (mean ± s.d. age of 15.0 ± 1.3 years and BMI of 37.1 ± 5.1 kg/m2) who were assigned to a LMP, combined with meal plans of 1300-1500 kcal/day of CD (self-selected foods) or MR (three SlimFast shakes, one prepackaged meal, five vegetable/fruit servings). After month 4 (phase 1), participants originally treated with MR were unmasked to their phase 2 (months 5-12) random assignment: continued use of MR (i.e., MR+MR) or transitioned to CD (i.e., MR+CD). Participants initially treated with CD in phase 1, continued with CD (i.e., CD). All three groups were treated for an additional 8 months (phase 2). Regression models were used to evaluate percentage change in BMI from baseline to month 4 (phase 1), months 5-12 (phase 2), and baseline to month 12. At month 4, participants assigned to MR (N = 65) achieved a mean (±s.e.) 6.3 ± 0.6% reduction in BMI, compared to a significantly (P = 0.01) smaller 3.8 ± 0.8% for CD participants (N = 37). In phase 2, BMI increased significantly (P < 0.001) in all three conditions, resulting in no significant (P = 0.39) differences between groups in percentage change in BMI at month 12. Across groups, mean reduction in BMI from baseline to month 12 was 3.4 ± 0.7% (P < 0.01). Use of MR significantly improved short-term weight loss, compared with CD, but its continued use did not improve maintenance of lost weight.
    Obesity 12/2010; 19(6):1193-9. · 3.92 Impact Factor
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    Sheela N Magge, Nicolas Stettler, Abbas F Jawad, Lorraine E Levitt Katz
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    ABSTRACT: To test the hypothesis that overweight siblings of children with type 2 diabetes mellitus (T2DM) have a higher prevalence of abnormal glucose tolerance (AGT) compared with other overweight children. This was a cross-sectional study of overweight (body mass index [BMI] >or= 95(th) percentile) subjects, age 8 to 17 years, with at least 1 sibling age >or= 12 years. The primary outcome was AGT, as assessed by the oral glucose tolerance test (2-hour glucose >or= 140 mg/dL). The secondary outcome was insulin resistance by homeostasis model assessment (HOMA). The sibling (n=20) and control (n=42) groups were similar in terms of age, sex, racial distribution (largely African American), pubertal status, and BMI. The prevalence of AGT in the sibling group was 40.0% (n=8), compared with 14.3% (n=6) in controls (P= .048, Fisher exact test; unadjusted odds ratio=4.0; 95% confidence interval=1.2 to 13.5). Univariate analysis did not identify confounders for either outcome. There were no significant differences in HOMA or hemoglobin A1c between the 2 groups. Overweight siblings of children with T2DM had 4 times greater odds of having AGT compared with other overweight children. This group may represent a particularly high-risk population to target for screening and pediatric T2DM prevention.
    The Journal of pediatrics 12/2008; 154(4):562-566.e1. · 4.02 Impact Factor
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    ABSTRACT: Postprandial hypoglycemia (PPH) is a frequent complication of Nissen fundoplication in children. The mechanism responsible for the PPH is poorly understood, but involves an exaggerated insulin response to a meal and subsequent hypoglycemia. We hypothesize that increased glucagon-like peptide-1 (GLP-1) secretion contributes to the exaggerated insulin surge and plays a role in the pathophysiology of this disorder. The aim of the study was to characterize glucose, insulin, and GLP-1 response to an oral glucose load in children with symptoms of PPH after Nissen fundoplication. Ten patients with suspected PPH and a history of Nissen fundoplication and eight control subjects underwent a standard oral glucose tolerance test at The Children's Hospital of Philadelphia. Blood glucose (BG), insulin, and intact GLP-1 levels were obtained at various time points. Children ages 4 months to 13 years old were studied. Change scores for glucose, insulin, and intact GLP-1 were recorded after an oral glucose tolerance test. All cases had hypoglycemia after the glucose load. Mean BG at nadir (+/- sd) was 46.7 +/- 11 mg/dl for cases (vs. 85.9 +/- 21.3 mg/dl; P < 0.0005). Mean change in BG from baseline to peak (+/- sd) was 179.3 +/- 87.4 mg/dl for cases (vs. 57.8 +/- 39.5 mg/dl; P = 0.003). Mean change in BG (+/- sd) from peak to nadir was 214.4 +/- 85.9 mg/dl for cases (vs. 55.9 +/- 41.1 mg/dl, P < 0.0005). Mean change in insulin (+/- sd) from baseline to peak was 224.3 +/- 313.7 microIU/ml for cases (vs. 35.5 +/- 22.2 microIU/ml; P = 0.012). Mean change in GLP-1 (+/- sd) from baseline to peak was 31.2 +/- 24 pm (vs. 6.2 +/- 9.5 pm; P = 0.014). Children with PPH after Nissen fundoplication have abnormally exaggerated secretion of GLP-1, which may contribute to the exaggerated insulin surge and resultant hypoglycemia.
    Journal of Clinical Endocrinology &amp Metabolism 10/2008; 94(1):39-44. · 6.43 Impact Factor
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    ABSTRACT: We hypothesized that most patients with 22q11.2 deletion and a history of hypocalcemia have inadequate parathyroid function, manifested by intact parathyroid hormone levels below normal. We aimed to evaluate intact parathyroid hormone levels both during normocalcemia and at hypocalcemia, in this population. Retrospective chart review of 103 patients with 22q11.2 deletion born since 1997 and cared for at the Children's Hospital of Philadelphia. Calcium and intact parathyroid hormone drawn simultaneously were recorded, along with clinical presentation at hypocalcemia. Forty-seven simultaneous Ca/intact parathyroid hormone values were available. Seventy-nine percent of calcium levels and 81% of parathyroid hormone levels were within normal range. There were 19 patients with a history of symptomatic hypocalcemia, for whom any available simultaneous Ca/parathyroid hormone levels, before, during, or after hypocalcemia were analyzed. In this subgroup, 59% of calcium and 76% of parathyroid hormone levels were normal. None had an intact parathyroid hormone of >39.2 pg/mL at hypocalcemia. Seventy-three percent of hypocalcemic events had a precipitating stressor. Hypoparathyroidism in 22q11.2 deletion is mild, manifesting as a phenomenon of decreased parathyroid hormone reserve. Subjects are normocalcemic most of the time, but are unable to mount elevated intact parathyroid hormone levels, and therefore unable to correct hypocalcemia, in response to stressors.
    Genetics in medicine: official journal of the American College of Medical Genetics 04/2008; 10(3):224-8. · 3.92 Impact Factor
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    ABSTRACT: Children with new onset diabetes (n = 175) were evaluated over 12-months. Patients were presumptively diagnosed with type 2 diabetes mellitus (T2DM) (n = 26) based on obesity, a relative with T2DM, the ability to wean from insulin, and absence of glutamic acid decarboxylase-65 (GAD-65) antibodies. We hypothesized that markers of insulinization at diagnosis, including fasting C-peptide and insulin-like growth factor-binding protein (IGFBP)-1, in addition to initial CO(2) levels and urine ketones, would help in distinguishing type 1 diabetes mellitus (T1DM) from T2DM. Children with T1DM (84 male, 65 female) had a mean age of 8.7 +/- 4.3 yr and a racial background of 78% white, 19% black, and 3% other. In contrast, children with T2DM (13 female, 13 male) had a mean age of 14.2 +/- 3.1 yr with a racial background of 58% black, 27% white, and 15% other. Fasting C-peptide level was 0.38 +/- 0.37 ng/mL in T1DM vs. 2.66 +/- 2.14 ng/mL in T2DM; a C-peptide of 0.85 ng/mL had 83% sensitivity in distinguishing T1DM from T2DM. Fasting IGFBP-1 level was 38.1 +/- 39.1 ng/mL (T1DM) vs. 3.6 +/- 4.5 ng/mL (T2DM); a value of 3.6 ng/dL could distinguish the two types of diabetes with 93% sensitivity. Urinary ketones were found in 79% of children with T1DM compared with 56% of those with T2DM, and the magnitude was associated with type of diabetes. Initial CO(2) level for T1DM was 17.9 +/- 6.9 mmol/L vs. 22.7 +/- 5.7 mmol/L for T2DM; a value of 21.5 mmol/L could distinguish the two types of diabetes with 83% sensitivity. In addition to obesity, family history of T2DM, and absence of GAD-65 antibodies, children with new-onset T2DM may be distinguished from those with T1DM by a combination of biochemical parameters (C-peptide, IGFBP-1, CO(2), and urine ketones).
    Pediatric Diabetes 05/2007; 8(2):53-9. · 2.08 Impact Factor
  • Lorraine E Levitt Katz, Máire Abraham, Line Johansen, Abbas F Jawad
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    ABSTRACT: To evaluate the effects of fasting on serum leptin levels in lean children. Seventeen children, age 7.7 +/- 4.3 years with mean body mass index (BMI) of 16.7 +/- 2.7 kg/m(2), underwent standard diagnostic fasts for suspected hypoglycemia. Blood was sampled at 6-hour intervals for glucose, insulin, C-peptide, leptin, free and total insulin-like growth factor-1, insulin-like growth factor-binding protein-1, growth hormone, cortisol, ketones, and free fatty acids. Subjects fasted 15 to 40 hours, and initial leptin levels were related to BMI and age. Leptin declined by 0.5 ng/mL per each fasting hour (P = .008), using a longitudinal mixed effects model. Leptin dropped significantly from an initial mean +/- SEM during the first 6 hours of 15.9 +/- 5.5 ng/mL to 3.5 +/- 0.9 ng/mL at the end of fasting. Mixed longitudinal effects models demonstrated that leptin was significantly related to insulin over time (P < .0001) as well as C-peptide (P < .0001). Significant relations were also seen with total insulin-like growth factor-1 over time, beta-hydroxybutyrate and insulin, and insulin-like growth factor-binding protein-1 and insulin. After 6 hours, leptin levels steadily decline during prolonged fasting in lean children. The decline probably is related to the suppression of insulin secretion. Although baseline leptin levels were related to BMI and age, in the final fasting sample, leptin levels showed minimal variation in this pediatric cohort encompassing a wide age range.
    Journal of Pediatrics 12/2006; 149(6):798-802. · 4.04 Impact Factor
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    ABSTRACT: To determine the epidemiology of type 1 diabetes in children in Philadelphia, Pennsylvania, from 1995 through 1999 and compare these data with previous cohorts. This is a report of a retrospective population-based registry maintained since 1985. Hospital records meeting the following criteria were reviewed: newly diagnosed type 1 diabetes, age 0-14 years, residing in Philadelphia at the time of diagnosis, and diagnosed from 1 January 1995 to 31 December 1999. The secondary source of validation was the School District of Philadelphia. Incidence rates by race and age were compared with 1985-1989 and 1990-1994 cohorts. A total of 234 case subjects were identified, and the registry was determined to be 96% complete. The overall age-adjusted incidence rate in Philadelphia was 14.8 per 100,000/year. Incidence rates in Hispanic children (15.5 per 100,000/year) and white children (12.8 per 100,000/year) have been relatively stable over 15 years. The incidence in black children (15.2 per 100,000/year), however, has increased dramatically, rising 64% in children 5-9 years of age (14.9 per 100,000/year) and 37% in the 10- to 14-year age-group (26.9 per 100,000/year). The overall incidence of type 1 diabetes in Philadelphia is increasing and is similar to other U.S. registries. These are the first data reporting a higher incidence in black children in a registry of children 0-14 years of age. The etiology of the marked increase in incidence in the black population is unknown and underscores the need to establish type 1 diabetes as a reportable disease, so that environmental risk factors may be thoroughly investigated.
    Diabetes Care 12/2006; 29(11):2391-5. · 7.74 Impact Factor

Publication Stats

305 Citations
119.08 Total Impact Points

Institutions

  • 2002–2014
    • The Children's Hospital of Philadelphia
      • • Division of Endocrinology and Diabetes
      • • Department of Pediatrics
      Philadelphia, Pennsylvania, United States
  • 2004–2006
    • University of Pennsylvania
      • Department of Pediatrics
      Philadelphia, Pennsylvania, United States
  • 2005
    • Texas Tech University Health Sciences Center
      • Department of Pediatrics
      Lubbock, TX, United States