OBJECTIVES: To examine whether high insulin resistance versus high inflammation identifies subtypes of preeclampsia. METHODS: A cytokine panel, glucose and insulin were measured in 37 preeclampsia plasma samples. Wilcoxon rank sum assessed median concentration of HOMA(IR) by pro-inflammatory:anti-inflammatory ratio. Regression stratifying by BMI and preterm birth was conducted. RESULTS: There was no difference in median HOMA(IR) by the pro-inflammatory:anti-inflammatory ratio (p = 0.16). No subsets scatterplot clusters emerged. A positive correlation between HOMAlog and the ratio was significant (p = 0.04). CONCLUSIONS: No dichotomous subsets of preeclampsia by inflammation versus insulin resistance were detected. Contrary to our hypothesis, insulin resistance was higher as inflammation increased in preeclampsia.
OBJECTIVES: To examine whether high insulin resistance versus high inflammation identifies subtypes of preeclampsia. METHODS: A cytokine panel, glucose and insulin were measured in 37 preeclampsia plasma samples. Wilcoxon rank sum assessed median concentration of HOMA(IR) by pro-inflammatory:anti-inflammatory ratio. Regression stratifying by BMI and preterm birth was conducted. RESULTS: There was no difference in median HOMA(IR) by the pro-inflammatory:anti-inflammatory ratio (p = 0.16). No subsets scatterplot clusters emerged. A positive correlation between HOMAlog and the ratio was significant (p = 0.04). CONCLUSIONS: No dichotomous subsets of preeclampsia by inflammation versus insulin resistance were detected. Contrary to our hypothesis, insulin resistance was higher as inflammation increased in preeclampsia.
Authors: Risto Kaaja; Hannele Laivuori; Pekka Pulkki; Matti J Tikkanen; Vilho Hiilesmaa; Olavi Ylikorkala Journal: Metabolism Date: 2004-11 Impact factor: 8.694