{'fraction_non_alphanumeric': 0.023851590106007067, 'fraction_numerical': 0.028268551236749116, 'mean_word_length': 5.157608695652174, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Decreased plasma glucose following indomethacin therapy in premature infants with patent ductus arteriosus.

In the course of a double-blind controlled trial of intravenous indomethacin therapy in premature infants with patent ductus arteriosus, plasma glucose was evaluated in 47 infants before and at 24, 48, and 72 hours following the medication. Twenty-two infants were assigned to the control group and 25 were in the indomethacin group. Significantly lower plasma glucose was noted at 24 (P less than 0.01) and 48 (P less than 0.05) hours in the indomethacin group as compared to the control group. There was a significant inverse correlation between the plasma glucose and the corresponding plasma indomethacin concentration (P less than 0.05) and between the plasma glucose and the corresponding plasma indomethacin concentration-time integral (P less than 0.01) at 24, 48, and 72 hours after drug administration, suggesting that the decreased plasma glucose may be related to indomethacin therapy. The results of this study indicate that endogenous prostaglandin may play a role in glucose homeostasis in premature infants.