Association of glucocorticoid and type 1 corticotropin-releasing hormone receptors gene variants and risk for depression during pregnancy and post-partum.

Women with postnatal depression (PND) appear to have abnormal hypothalamic pituitary adrenal (HPA) axis responses to stress, which might involve a genetic variability component. We investigated association of genetic variants in the glucocorticoid receptor (GR, NR3C1) and corticotropin releasing hormone receptor 1 (CRHR1) genes with increased risk for PND. Two hundred pregnant women were recruited prospectively and PND risk was assessed by the Edinburgh Postnatal Depression Scale (EPDS) during pregnancy and again 2-8 weeks post-natally (CW-GAPND study). The BclI and ER22/23EK single nucleotide polymorphisms (SNPs) of the GR and the haplotype-tagged rs1876828, rs242939 and rs242941 SNPs of the CRHR1 associated with genetic risk to depressive disorders were genotyped. A cut-off score of 10 was used to detect increased risk of PND. Association analysis was carried out in 140 patients that completed the study protocol. The BclI and rs242939 SNPs were over-represented in women with postnatal EPDS score ≥10 with significant allele association (p = 0.011 and <0.001, respectively) and risk ratios of 2.9 (95% CI: 1.2-6.9) for BclI, 4.9 (2-12) for rs242939 and 5.48 (2.13-14.10) for both. The rs242939 SNP was also associated with increased EPDS values during pregnancy. Moreover, the G-G-T haplotype of the CRHR1 was significantly over-represented in patients with high EPDS scores, with risk ratio of 3.22 (95% CI: 1.91-5.42). This is the first evidence that specific SNPs of genes involved in 'stress' responses might contribute in the genetics of high-risk for depression during pregnancy and postpartum.

Multi-centre observational study of spurious hyperkalaemia due to EDTA contamination.

BACKGROUND: A multi-centre observational study investigating the prevalence of spurious hyperkalaemia due to potassium ethylenediaminetetraacetic acid (kEDTA) contamination. METHODS: Serum EDTA was measured in anonymised serum samples with a serum potassium > 6.0 mmol/L collected over a one month period in five different hospital laboratories. Two of the participating laboratories routinely screen all hyperkalaemic samples for EDTA contamination. RESULTS: EDTA contamination was present in 4.1% (range 1.2%-6.7%) of hyperkalaemic samples. In three laboratories, without routine EDTA screening, 50% "EDTA contaminated" were identified by laboratory staff, the remaining 50% samples were undetected and reported as genuine hyperkalaemia. In these laboratories, EDTA was not measurable in 2 samples reported as "EDTA contaminated". CONCLUSIONS: Spurious hyperkalaemia due to kEDTA contamination is relatively common. Education regarding correct blood collection technique offers the best strategy in preventing EDTA sample contamination. Gross kEDTA contamination is easily identified by laboratory staff in samples with marked unexpected hyperkalaemia and hypocalcaemia. Spurious hyperkalaemia due to modest kEDTA contamination may only be confidently detected by measurement of serum EDTA.