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Placental Transport of Erythromycin and Its Effect on Placental Inflammatory Factors

Overview
Journal Pak J Med Sci
Specialty General Medicine
Date 2023 Jan 25
PMID 36694753
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Abstract

Objective: Erythromycin is used for prevention and control of infectious perinatal morbidity. It has been hypothesised that erythromycin crosses the placenta and has an effect on the production of placental inflammatory factors. We evaluated the transport of erythromycin in an ex-vivo closed perfusion system of the placenta and determined its effect on the production of placenta inflammatory markers.

Methods: In 2013, a prospective basic science study was conducted at the placental laboratory of College of Medicine and Health Sciences, United Arab Emirates. Six term placentas from uncomplicated pregnancies were studied using the ex-vivo dual closed-loop human placental cotyledon perfusion technique. Erythromycin was added to the perfusate in the maternal compartment. Samples were obtained from the maternal and fetal up to 240 minutes.

Results: The reference antipyrine was detected in the fetal circulation in the first 15 minutes after addition of the drug. At this point the mean antipyrine was 49.90±2.10μg/ml in the maternal perfusate and 7.1±1.56μg/ml in fetal perfusate. The fetal and maternal concentration became similar at 120 minutes. The transfer of antipyrine from maternal to fetal compartment was 98.66%. The differences between perfusion groups were non-significant that indicates the perfusion of placentas was comparable. After media exchange in both sides, erythromycin was added to the maternal perfusate. The experimental period of four hours was continued with medium circulation on both maternal and fetal circulation. The concentration of erythromycin decreased in the maternal circuit by 36.4% and increased in the fetal circuit by 65%. The concentration of IL-6 in the maternal circuit was normal.

Conclusion: Erythromycin crossed the placenta and did not inhibit the production of IL-6. Future studies are needed concerning neonatal adverse effects and the development of antibiotic resistance.

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