The purpose of this article was to examine metabolic risk factors for type 2 diabetes in children and adolescents as a function of maternal versus paternal family history of type 2 diabetes and to examine whether differences in these risk factors emerge during adolescent growth.A total of 247 overweight Latino children (baseline age = 11.1 +/- 1.7 years) with a parental history of type 2 diabetes were followed annually for 5 years (2.2 +/- 1.2 observations/child) with measures of insulin sensitivity, acute insulin response to glucose, and disposition index. Longitudinal linear mixed-effects modeling was used to evaluate the influence of maternal versus paternal family history of type 2 diabetes on changes in diabetes risk factors over age.Insulin sensitivity and the disposition index decreased over age (beta = -0.052 and beta = -0.033, P < 0 0.01). Acute insulin response to glucose and fasting and 2-h glucose increased (beta = 0.019, beta = 0.002, and beta = 0.003, P < 0.01). Declines in insulin sensitivity were significantly greater in participants whose maternal grandmothers had a history of type 2 diabetes (beta = -0.03, P = 0.03). Declines in the disposition index (beta = -0.02, P = 0.04) and increases in fasting glucose were significantly influenced by a maternal history of type 2 diabetes (beta = 0.60, P < 0.05).Maternal but not paternal family history for diabetes may have a significant impact on insulin dynamics, becoming more pronounced during growth in overweight Latino adolescents. Further research is clearly warranted.
For phase III RCTs, sample heterogeneity is useful for both generalizability of findings and providing insight into treatment effects for specific subgroups. Prior studies in stroke rehabilitation have rarely explored differences in intervention effects between racial and ethnic subgroups across participating sites. We examined participant characteristics across centers, with the hypothesis that strategic use of a multi-center structure across 3 distinct urban geographical areas (Atlanta, GA, Los Angeles, CA and Washington, DC) would generate a sample diverse enough to explore differences in treatment effects by racial and ethnic subgroups Methods: The ICARE Stroke Initiative is a randomized multi-center clinical trial designed to compare the effectiveness of the Accelerated Skill Acquisition Program (ASAP) to an equivalent dose of usual and customary outpatient occupational therapy (DEUCC) and a monitoring only usual therapy group (UCC). Demographics, stroke characteristics and cognitive outcomes collected at baseline for randomized participants (N = 361) were compared across the 3 centers using ANOVA or χ2 tests for continuous and categorical outcomes, respectively. Results: We found significant differences in race and ethnicity (p<0.001); the highest proportion of African-Americans came from the Atlanta and DC centers, and the highest proportion of Hispanic/Latinos came from the Los Angeles center. Additional unanticipated differences between centers in baseline characteristics include: age, referral source, stroke location, stroke severity as measured by the NIH Stroke Scale, Short Blessed Memory Test, DKEF’s verbal fluency sub-score of category switching, and pre-randomization hours of outpatient occupational therapy (p<0.05). Conclusions: ICARE’s strategic center selection resulted in a diverse and robust dataset, allowing for post hoc exploration of treatment effect differences by subgroup and for the intention-to-treat analysis, determination of generalizability of treatment effects across a racially and ethnically diverse population.
Introduction: The diagnosis of acute pancreatitis is defined by fulfillment of 2 out of 3 criterion: serum lipase greater than three times the upper limit of normal (>3x ULN); abdominal pain consistent with acute pancreatitis; imaging consistent with acute pancreatitis. The origin and clinical significance of hyperlipasemia (3xULN) without abdominal pain or imaging abnormalities consistent with pancreatitis is unclear. Methods: We prospectively studied patients who had a serum lipase level > 3x ULN after being admitted to LA County Hospital from January 2014 to April 2015. They were identified by a daily laboratory query used to support an ongoing RCT of goal directed therapy for acute pancreatitis (NCT 01761539). Nonpancreatic hyperlipasemia was defined as patients with a serum lipase > 3x ULN but did not meet the other criterion for pancreatitis. Primary outcome was the etiology of the hyperlipasemia in this group. Secondary outcomes included comparisons between length of hospitalization, time to tolerance of enteral feeding, ICU admission and mortality between patients with pancreatitis and nonpancreatic hyperlipasemia. Baseline differences in demographic and biochemical parameters were also compared. Results: 221 patients presented with lipase > 3x ULN: 170 met criterion for acute pancreatitis and 51 did not. The leading etiologies for non-pancreatitis hyperlipasemia were decompensated cirrhosis and renal failure (Table 1). Patients with non-pancreatitis hyperlipasemia required less fluid (p < 0.001) and tolerated an oral diet after a shorter interval (p < 0.001) than those with acute pancreatitis. There was no difference in length of hospitalization, ICU admission, or mortality between the two groups. Non-pancreatitis hyperlipasemia patients were also significantly older and had more comorbidities (Charlson Index) (Table 2). In addition they presented with lower serum lipase levels (360 ± 36 vs 1453 ±135 IU/L, p < 0.001) but a higher BUN level (33.0 ± 5.5 vs 15.9 ± 1.0, p < 0.001) and creatinine (2.3 ± 0.7 vs 1.4 ± 0.4, p < 0.001).Table 1: Etiologies of Non-Pancreatitic HyperlipasemiaTable 2: Baseline Characteristics and Clinical Course of Pancreatitis versus Non-Pancreatitic HyperlipasemiaConclusion: Elevated serum lipase level has many non-pancreatic origins with liver and renal failure being most frequent. Patients with nonpancreatic hyperlipasemia generally have lower serum lipase levels and are usually older with more comorbidities than those with pancreatitis. These clinical features can help clinicians expeditiously distinguish between the two entities.Figure 1
