Is Mid-trimester Insulin Resistance Predictive of Subsequent Puerperal Infection? A Secondary Analysis of Randomized Trial Data.
Objective The objective of this study was to examine whether there is an association between insulin resistance and subsequent development of puerperal infection by measuring insulin resistance in the mid-trimester using the homeostasis model assessment (HOMA:IR). Methods Secondary analysis of low-risk nulliparas enrolled in a multicenter preeclampsia prevention trial. HOMA:IR was measured on fasting plasma glucose and insulin concentrations among low-risk nulliparas between 22 and 26 weeks' gestation. Median HOMA:IR was compared between women who did and did not develop puerperal infection using Wilcoxon rank sum test. Logistic regression was used to control for potential confounders. Results Of 1,180 women with fasting glucose and insulin available, 121 (10.3%) had a puerperal infection. Median HOMA:IR was higher among those with subsequent puerperal infection (4.3 [interquartile, IQR: 2.2-20.5] vs. 2.6 [IQR: 1.5-6.7], p < 0.0001). After controlling for potentially confounding variables HOMA:IR was only marginally associated with an increased risk of development of puerperal infection, adjusted odds ratio: 1.01 (95% confidence interval: 1.00-1.02; p = 0.04) per unit increase. Elevated HOMA:IR performed poorly as a predictor of puerperal infection, with a positive predictive value of 15% and a negative predictive value of 92%. Conclusion Though associated with an increased risk of puerperal infection, insulin resistance, measured by HOMA:IR, is not a clinically useful predictor of puerperal infection.
Department of Obstetrics and Gynecology, Women & Infants Hospital, Brown University, Providence, Rhode Island.
Brenna L
BL
Hughes
The George Washington University Biostatistics Center, Washington, District of Columbia.
Rebecca G
RG
Clifton
Department of Obstetrics and Gynecology, University of Alabama at Birmingham, Birmingham, Alabama.
John C
JC
Hauth
Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas, Texas.
Kenneth J
KJ
Leveno
Department of Obstetrics and Gynecology, University of Cincinnati, Cincinnati, Ohio.
Leslie
L
Myatt
The Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, Maryland.
Uma M
UM
Reddy
Department of Obstetrics and Gynecology, University of Utah, Salt Lake City, Utah.
Michael W
MW
Varner
Department of Obstetrics and Gynecology, Columbia University, New York, New York.
Ronald J
RJ
Wapner
Department of Obstetrics and Gynecology, MetroHealth Medical Center, Case Western Reserve University, Cleveland, Ohio.
Brian M
BM
Mercer
Department of Obstetrics and Gynecology, Northwestern University, Chicago, Illinois.
Alan M
AM
Peaceman
Department of Obstetrics and Gynecology, Children's Memorial Hermann Hospital, University of Texas Health Science Center at Houston, Houston, Texas.
Susan M
SM
Ramin
Department of Obstetrics and Gynecology, Oregon Health & Science University, Portland, Oregon.
Jorge E
JE
Tolosa
Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, Texas.
George
G
Saade
Department of Obstetrics and Gynecology, Wayne State University, Detroit, Michigan.
Yoram
Y
Sorokin
D000328:Adult; D015992:Body Mass Index; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance; D016015:Logistic Models; D011225:Pre-Eclampsia / Q000517:prevention & control; D011247:Pregnancy; D011264:Pregnancy Trimesters; D011379:Prognosis; D011645:Puerperal Infection / Q000097:blood* / Q000453:epidemiology*; D014481:United States / Q000453:epidemiology; D055815:Young Adult
D007328:Insulin