Incidence of local complications and risk factors associated with peripheral intravenous catheter in neonates

Abstract OBJECTIVE To evaluate the incidence of complications related to the use of peripheral intravenous catheter in neonates and identify the associated risk factors. METHOD Prospective cohort study conducted in a Neonatal Intensive Care Unit. Participants were the hospitalized neonates undergoing peripheral intravenous puncture in the period from February to June 2013. RESULTS The incidence of complications was 63.15%, being infiltration/extravasation (69.89%), phlebitis (17.84%) and obstruction (12.27%). The risk factors were the presence of infection (p = 0.0192) and weight at the puncture day (p = 0.0093), type of intermittent infusion associated with continuous infusion (p <0.0001), endotracheal intubation (p = 0.0008), infusion of basic plan (p = 0.0027), total parenteral nutrition (P = 0.0002), blood transfusion associated with other infusions (p = 0.0003) and other drugs (p = 0.0004). Higher risk of developing complications in the first 48 hours after puncture. CONCLUSION A high rate of complications related to the use of peripheral intravenous catheter, and risk factors associated with infection, weight, drugs and infused solutions, and type of infusion.

A genome-wide approach accounting for body mass index identifies genetic variants influencing fasting glycemic traits and insulin resistance.

Recent genome-wide association studies have described many loci implicated in type 2 diabetes (T2D) pathophysiology and β-cell dysfunction but have contributed little to the understanding of the genetic basis of insulin resistance. We hypothesized that genes implicated in insulin resistance pathways might be uncovered by accounting for differences in body mass index (BMI) and potential interactions between BMI and genetic variants. We applied a joint meta-analysis approach to test associations with fasting insulin and glucose on a genome-wide scale. We present six previously unknown loci associated with fasting insulin at P < 5 × 10(-8) in combined discovery and follow-up analyses of 52 studies comprising up to 96,496 non-diabetic individuals. Risk variants were associated with higher triglyceride and lower high-density lipoprotein (HDL) cholesterol levels, suggesting a role for these loci in insulin resistance pathways. The discovery of these loci will aid further characterization of the role of insulin resistance in T2D pathophysiology.

Sähköiset julkaisut ja standardit : seminaari tutkijoille ja tietohuollon ammattilaisille Suomessa

Anna Leena Lind

Causal relationship between obesity and vitamin D status: bi-directional Mendelian randomization analysis of multiple cohorts.

BACKGROUND: Obesity is associated with vitamin D deficiency, and both are areas of active public health concern. We explored the causality and direction of the relationship between body mass index (BMI) and 25-hydroxyvitamin D [25(OH)D] using genetic markers as instrumental variables (IVs) in bi-directional Mendelian randomization (MR) analysis. METHODS AND FINDINGS: We used information from 21 adult cohorts (up to 42,024 participants) with 12 BMI-related SNPs (combined in an allelic score) to produce an instrument for BMI and four SNPs associated with 25(OH)D (combined in two allelic scores, separately for genes encoding its synthesis or metabolism) as an instrument for vitamin D. Regression estimates for the IVs (allele scores) were generated within-study and pooled by meta-analysis to generate summary effects. Associations between vitamin D scores and BMI were confirmed in the Genetic Investigation of Anthropometric Traits (GIANT) consortium (n = 123,864). Each 1 kg/m(2) higher BMI was associated with 1.15% lower 25(OH)D (p = 6.52×10⁻²⁷). The BMI allele score was associated both with BMI (p = 6.30×10⁻⁶²) and 25(OH)D (-0.06% [95% CI -0.10 to -0.02], p = 0.004) in the cohorts that underwent meta-analysis. The two vitamin D allele scores were strongly associated with 25(OH)D (p≤8.07×10⁻⁵⁷ for both scores) but not with BMI (synthesis score, p = 0.88; metabolism score, p = 0.08) in the meta-analysis. A 10% higher genetically instrumented BMI was associated with 4.2% lower 25(OH)D concentrations (IV ratio: -4.2 [95% CI -7.1 to -1.3], p = 0.005). No association was seen for genetically instrumented 25(OH)D with BMI, a finding that was confirmed using data from the GIANT consortium (p≥0.57 for both vitamin D scores). CONCLUSIONS: On the basis of a bi-directional genetic approach that limits confounding, our study suggests that a higher BMI leads to lower 25(OH)D, while any effects of lower 25(OH)D increasing BMI are likely to be small. Population level interventions to reduce BMI are expected to decrease the prevalence of vitamin D deficiency.

Sukulaisuus sukupolvia yhdistämässä

Kirjoitus perustuu Sukupolvet ja valta -seminaarissa 18.4.1997 pidettyyn esitelmään