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Evidence of Placental Hypoxia in Maternal Sleep Disordered Breathing
Sanjita Ravishankar1,2, Ghada Bourjeily3,4, Geralyn Lambert-Messerlian1,2
11 Department of Pathology, Women and Infants Hospital, Providence, RI 02905, USA.
Sleep disordered breathing (SDB) represents a spectrum of disorders, including habitual snoring and obstructive sleep apnea (OSA). Sleep disordered breathing is characterized by chronic intermittent hypoxia, airflow limitation, and recurrent arousals, which may lead to tissue hypoperfusion, hypoxia, and inflammation. In this study, we aimed to examine whether SDB during pregnancy was associated with histopathologic evidence of chronic placental hypoxia and/or uteroplacental underperfusion. The placentas of women with OSA (n = 23) and habitual snoring (n = 78) as well as nonsnorer controls (n = 47) were assessed for histopathologic and immunohistochemical markers of chronic hypoxia and uteroplacental underperfusion. Fetal normoblastemia was significantly more prevalent in SDB placentas than in those of nonsnorer controls (34.6% and 56.5% in snorers and OSA, respectively, versus 6.4% in controls). Expression of the tissue hypoxia marker carbonic anhydrase IX (CAIX) was more common in OSA placentas than controls (81.5% and 91.3% in snorers and OSA, respectively, versus 57.5% in controls). Adjusting for confounders such as body mass index, diabetes mellitus, or chronic hypertension did not alter the results. The uteroplacental underperfusion scores were similar among the 3 groups. Our findings suggest that SDB during pregnancy is associated with fetoplacental hypoxia, as manifested by fetal normoblastemia and increased placental carbonic anhydrase IX immunoreactivity. The clinical implications and underlying mechanisms remain to be determined.
Sleep disordered breathing (SDB) represents a spectrum of disorders, including habitual snoring and obstructive sleep apnea (OSA). Sleep disordered breathing is characterized by chronic intermittent hypoxia, airflow limitation, and recurrent arousals, which may lead to tissue hypoperfusion, hypoxia, and inflammation. In this study, we aimed to examine whether SDB during pregnancy was associated with histopathologic evidence of chronic placental hypoxia and/or uteroplacental underperfusion. The placentas of women with OSA (n = 23) and habitual snoring (n = 78) as well as nonsnorer controls (n = 47) were assessed for histopathologic and immunohistochemical markers of chronic hypoxia and uteroplacental underperfusion. Fetal normoblastemia was significantly more prevalent in SDB placentas than in those of nonsnorer controls (34.6% and 56.5% in snorers and OSA, respectively, versus 6.4% in controls). Expression of the tissue hypoxia marker carbonic anhydrase IX (CAIX) was more common in OSA placentas than controls (81.5% and 91.3% in snorers and OSA, respectively, versus 57.5% in controls). Adjusting for confounders such as body mass index, diabetes mellitus, or chronic hypertension did not alter the results. The uteroplacental underperfusion scores were similar among the 3 groups. Our findings suggest that SDB during pregnancy is associated with fetoplacental hypoxia, as manifested by fetal normoblastemia and increased placental carbonic anhydrase IX immunoreactivity. The clinical implications and underlying mechanisms remain to be determined.
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