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Introduction to Drugs and Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
Adverse neonatal effects are associated with prenatal exposure to some drugs (e.g., difficulty in adaptation to life outside the womb). Drugs associated with adverse neonatal effects are not always associated with birth defects (i.e., teratogenic effects). Transient metabolic abnormalities, withdrawal, and hypoglycemia are well-documented neonatal effects of certain medications and non-medical drugs. The floppy infant syndrome and benzodiazepine use near term is an example. Patent ductus arteriosus with the use of NSAIDs (prostaglandin synthetase inhibitors such as aspirin or indomethacin) close to delivery is another well know example. The “gray baby” syndrome with high-dose chloramphenicol near term is another documented example (Table 1.1). Teratogens are frequently associated with developmental delay, but delays are also associated with fetal effects of drugs that are apparently not teratogenic.
Infections
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
An idiosyncratic, not dose-dependent reaction, causes aplastic anaemia. Chloramphenicol is also toxic to neonates particularly premature babies whose liver enzyme systems are incompletely developed. This can result in the “grey baby syndrome”. Chloramphenicol serum concentrations should be monitored in infants and children [26,27].
Diagnostic Approach to Rash and Fever in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Lee S. Engel, Charles V. Sanders, Fred A. Lopez
Prompt treatment with tetracycline decreases mortality [41,42]. Most patients’ defervesce within 2‒3 days, and these patients should receive treatment for at least 3 days after showing improvement [38,43]. Chloramphenicol, the only other antimicrobial agent recommended for the treatment of RMSF, causes gray baby syndrome and should not be used for pregnant women who are near term [43]. Gray baby syndrome occurs due to a lack of the necessary liver enzymes to metabolize chloramphenicol, resulting in drug accumulation, which leads to vomiting, ashen gray skin color, limp body tone, hypotension, cyanosis, hypothermia, cardiovascular collapse, and often death. Pregnant women who are near term may receive tetracycline because the risk of fetal damage or death is minimal. Previously, tetracycline is not recommended for pregnant women, in the first or second trimester, because of the effects on fetal bone and dental development [43]. However, doxycycline use during pregnancy probably does not pose substantial teratogenic risk [38]. Pregnant woman should be counseled about risks and benefits for treatment decision. Chloramphenicol can be administered in early pregnancy because gray baby syndrome is not a risk during the early period of fetal development [43].
Activation of Nrf2 signaling pathway by natural and synthetic chalcones: a therapeutic road map for oxidative stress
Published in Expert Review of Clinical Pharmacology, 2021
Melford Chuka Egbujor, Sarmistha Saha, Brigitta Buttari, Elisabetta Profumo, Luciano Saso
Nrf2 activation has attracted significant research interest as a therapeutic target for several chronic diseases. Its biological impact can be measured primarily by its transcriptional activities and intracellular localization [42]. Nrf2 and its principal negative regulator, the E3 ligase adaptor Kelch-like ECH-associated protein 1 (Keap1), plays a multi-faceted role in several biological processes, such as antioxidant metabolism, prevention of xenobiotic and endobiotic related oxidative damage [43], redox signaling, protection against triptolide-induced oxidative stress [44], metabolism of carbohydrates [45], lipids and iron [46], and inflammation regulation [47]. Nrf2 activation could lead to the induction of several cytoprotective genes as listed below. Nrf2-dependent NAD(P)H quinone oxidoreductase I (NQO1) catalyzes the reduction of reactive Quinones and a range of other organic compounds, responsible for redox cycling and oxidative stress [48,49]. NQO1 is responsible for reduction of free radicals and detoxification of xenobiotics and related toxicities [50].Sulfiredoxin I (Srxn1) and thioredoxin reductase I (TrxRI) act via Nrf2-dependent pathway for the reduction of ROS including hydrogen peroxide and other peroxides [51,52].Nrf2-dependent heme oxygenase-1 (HO-1) [53] is responsible for the catalytic breakdown of heme into biliverdin which is further converted into bilirubin and, thereby, plays a role in oxidative stress and inflammation in hypertension [54], sepsis [55], atherosclerosis [56] and many other diseases [57].The UDP-glucuronosyltransferase (UGT) is responsible for the catalytic conjugation of glucuronic acid moiety to various drugs, mutagens and xenobiotics in Nrf2-dependent pathway [58]. UGT plays a crucial role in drug metabolism and mediates drug resistance in several diseases, including cancer [59]. Deficiency of UGT causes a condition known as a gray baby syndrome [60].Nrf2 also regulates multidrug resistance-associated proteins (MRPs; MRP1-MRP9), which are the major transporters responsible for multidrug resistance in tumor cells [61]. MRPs are also responsible for the effluxing of compounds from organs to bile and plasma for easy excretion [62].