Oxycodone is a semisynthetic μ- and κ-opioid receptor with agonist with a broad scope of use including postoperative analgesia as well as control of neuropathic and cancer pain. Advantages over other opioids include prolonged duration of action, greater potency than morphine and lack of histamine release or ceiling effect. Individual responses to oxycodone can vary due to genetic differences. This review article aims to summarize the oxycodone literature and provide context on its pharmacogenomics and pharmacokinetics. The evidence for clinical effect of genetic polymorphisms on oxycodone is conflicting. There is stronger evidence linking polymorphic genetic enzymes CYP2D6 and CYP3A with therapeutic outcomes. Further, research is needed to discern all of oxycodone\'s metabolites and their contribution to the overall analgesic effect.

As a kind of haemoglobin, cytochrome P450 enzymes (CYP450) participate in the metabolism of many substances, including endogenous substances, exogenous substances and drugs. It is estimated that 60% of common prescription drugs require bioconversion through CYP450. The influence of macrolides on CYP450 contributes to the metabolism and drug-drug interactions (DDIs) of macrolides. At present, most studies on the effects of macrolides on CYP450 are focused on CYP3A, but a few exist on other enzymes and drug combinations, such as telithromycin, which can decrease the activity of hepatic CYP1A2 and CYP3A2. This article summarizes some published applications of the influence of macrolides on CYP450 and the DDIs of macrolides caused by CYP450. And the article may subsequently guide the rational use of drugs in clinical trials. To a certain extent, poisoning caused by adverse drug interactions can be avoided. Unreasonable use of macrolide antibiotics may enable the presence of residue of macrolide antibiotics in animal-origin food. It is unhealthy for people to eat food with macrolide antibiotic residues. So it is of great significance to guarantee food safety and protect the health of consumers by the rational use of macrolides. This review gives a detailed description of the influence of macrolides on CYP450 and the DDIs of macrolides caused by CYP450. Moreover, it offers a perspective for researchers to further explore in this area.

BACKGROUND: Steroid-induced osteonecrosis of the femoral head (ONFH) in young adults is a challenging disorder that can impairs the quality of life of a patient. The disease also leads to frequent occurrences of collapse of the femoral head and resultant dysfunction of the hip joint. In recent years, some scholars have studied steroid-induced lipid metabolism disorder and achieved the effect of steroid-induced ONFH treatment. This study aims to review the investigations on the hepatic CYP3A (cytochrome P4503A enzyme) genetic polymorphisms in steroid-induced ONFH patients. We then further explore its activity correlation with the development of steroid-induced ONFH in a rabbit model.
METHODS: A systematic literature search of articles was conducted in PubMed, Web of Science, Google Scholar, Springerlink, and the Chinese National Knowledge Infrastructure database up to February 2017. Twelve relevant articles were retrieved. The odds ratios, standard mean difference, and 95% confidence intervals were calculated to assess the effect of hepatic CYP3A activity on the rabbit model with steroid-induced ONFH. Fixed-effects and random-effects models were used to analyze the heterogeneity. Begg\'s funnel plot was used to assess publication bias.
RESULTS: High hepatic CYP3A activity significantly decreased the risk for steroid-induced ONFH in the rabbit model (p <. 05). The CYP3A gene may be potentially associated with increased risk of steroid-induced ONFH in the human allele model.
CONCLUSIONS: The study suggests that high hepatic CYP3A activity decreases the risk of steroid-induced ONFH.

Bedaquiline has recently been approved for the treatment of pulmonary multidrug-resistant tuberculosis (TB) as part of combination therapy in adults. It is metabolized primarily by the cytochrome P450 isoenzyme 3A4 (CYP3A4) to a less-active N-monodesmethyl metabolite. Phase I and Phase II studies in healthy subjects and patients with drug-susceptible or multidrug-resistant TB have assessed the pharmacokinetics and drug-drug interaction profile of bedaquiline. Potential interactions have been assessed between bedaquiline and first- and second-line anti-TB drugs (rifampicin, rifapentine, isoniazid, pyrazinamide, ethambutol, kanamycin, ofloxacin and cycloserine), commonly used antiretroviral agents (lopinavir/ritonavir, nevirapine and efavirenz) and a potent CYP3A inhibitor (ketoconazole). This review summarizes the pharmacokinetic profile of bedaquiline as well as the results of the drug-drug interaction studies.