Placenta · 2015
Type 1, type 2 and gestational diabetes mellitus differentially impact placental pathologic characteristics of uteroplacental malperfusion.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Huynh Jennifer, Yamada Jessica, Beauharnais Catherine, Wenger Julia B, Thadhani Ravi I, Wexler Deborah, Roberts Drucilla J, Bentley-Lewis Rhonda
Аннотация
INTRODUCTION: During a pregnancy complicated by diabetes, the placenta undergoes a number of functional and structural pathologic changes. However, differences across studies may reflect pathophysiologic differences of diabetes types under investigation.
METHODS: We examined placental pathology from women ages 18-40 years with self-identified race/ethnicity; singleton, live births; and type 1 (T1DM; n = 36), type 2 (T2DM; n = 37), or gestational diabetes mellitus (GDM; n = 126). Clinical data were abstracted from medical records. Placental diagnoses were independently re-reviewed by a perinatal pathologist. Multivariable analyses adjusting for race, gestational weight gain, gestational age, and systolic blood pressure were conducted.
RESULTS: Women with T1DM compared with either T2DM or GDM had higher gestational weight gain (mean ± SD, T1DM vs. T2DM: 28.5 ± 12.4 vs. 20.5 ± 13.4 kg, p = 0.03; or GDM: 21.3 ± 12.7 kg, p = 0.009) and insulin use (T2DM: 100.0% vs. 85.3%, p = 0.02; or GDM: 4.0%, p < 0.001). Women with T1DM compared with either T2DM or GDM also had a similarly lower prevalence of placental infarcts in univariate analyses; however, these findings did not remain significant after multivariable adjustment. Also, placentas from women with T2DM compared to GDM had higher rates of decidual vasculopathy when excluding women with preeclampsia (10.3 vs. 1.6%, p = 0.049) and diffuse chorangiosis (62.2 vs. 32.5%, p < 0.001) but a lower rate of villous immaturity (10.8 vs. 90.5%, p = 0.007) after full adjustment.
DISCUSSION: Placental vasculopathic abnormalities differ by maternal diabetes type, potentially reflecting underlying pathophysiologic mechanisms. Further research on placental pathology and metabolic derangements is warranted.
METHODS: We examined placental pathology from women ages 18-40 years with self-identified race/ethnicity; singleton, live births; and type 1 (T1DM; n = 36), type 2 (T2DM; n = 37), or gestational diabetes mellitus (GDM; n = 126). Clinical data were abstracted from medical records. Placental diagnoses were independently re-reviewed by a perinatal pathologist. Multivariable analyses adjusting for race, gestational weight gain, gestational age, and systolic blood pressure were conducted.
RESULTS: Women with T1DM compared with either T2DM or GDM had higher gestational weight gain (mean ± SD, T1DM vs. T2DM: 28.5 ± 12.4 vs. 20.5 ± 13.4 kg, p = 0.03; or GDM: 21.3 ± 12.7 kg, p = 0.009) and insulin use (T2DM: 100.0% vs. 85.3%, p = 0.02; or GDM: 4.0%, p < 0.001). Women with T1DM compared with either T2DM or GDM also had a similarly lower prevalence of placental infarcts in univariate analyses; however, these findings did not remain significant after multivariable adjustment. Also, placentas from women with T2DM compared to GDM had higher rates of decidual vasculopathy when excluding women with preeclampsia (10.3 vs. 1.6%, p = 0.049) and diffuse chorangiosis (62.2 vs. 32.5%, p < 0.001) but a lower rate of villous immaturity (10.8 vs. 90.5%, p = 0.007) after full adjustment.
DISCUSSION: Placental vasculopathic abnormalities differ by maternal diabetes type, potentially reflecting underlying pathophysiologic mechanisms. Further research on placental pathology and metabolic derangements is warranted.