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1.
JCO Oncol Pract ; 16(8): e660-e667, 2020 08.
Article in English | MEDLINE | ID: mdl-32119593

ABSTRACT

PURPOSE: Although studies in other clinical areas have shown that patient-clinician communication can positively influence adherence to medications, little is known about how oncologists address medication counseling during routine office visits. We describe patient-oncologist office-based discussions of oral chemotherapy treatment. METHODS: Transcripts of 24 patient-oncologist office visits were obtained from a national database. Patients were aged ≥ 19 years and prescribed capecitabine for colorectal cancer. We developed a structured coding worksheet using medication-counseling concepts previously identified as important to medication adherence and a grounded approach. Two coders reviewed transcripts for oncologists' provision of medication information, assessment of patients' adherence to medication, and the provision of self-management support for management of adverse effects. We assessed interrater reliability with Cohen κ statistics. We describe the counseling concepts present within patient-oncologist conversations and present illustrative quotes to describe how they were discussed. RESULTS: Oncologists generally provided patients who had yet to initiate therapy comprehensive medication information; those in the midst of treatment received less information. Oncologists discussed patients' continued use of the medication (or discontinuation) among all patients who had initiated therapy (N = 18). How the patient was taking the medication (ie, therapy implementation) was less commonly discussed. Medication adverse effects were also discussed in all encounters. Self-management strategies were commonly provided, albeit mostly in response to a presenting symptom and not preemptively. Patients' use of concurrent medications, financial access to therapy, and assessments of logistical arrangements were discussed more sporadically. CONCLUSION: Using audio recordings from a national sample of patient-oncologist office visits, we identified several potentially important opportunities to enhance medication counseling among patients prescribed capecitabine for the treatment of colorectal cancer.


Subject(s)
Oncologists , Physician-Patient Relations , Communication , Humans , Office Visits , Reproducibility of Results
2.
Article in English | MEDLINE | ID: mdl-27401401

ABSTRACT

Non-alcoholic steatohepatitis (NASH) is an emerging public health problem without effective therapies. Cytochrome P450 (CYP) epoxygenases metabolize arachidonic acid into bioactive epoxyeicosatrienoic acids (EETs), which have potent anti-inflammatory and protective effects. However, the functional relevance of the CYP epoxyeicosanoid metabolism pathway in the pathogenesis of NASH remains poorly understood. Our studies demonstrate that both mice with methionine-choline deficient (MCD) diet-induced NASH and humans with biopsy-confirmed NASH exhibited significantly higher free EET concentrations compared to healthy controls. Targeted disruption of Ephx2 (the gene encoding for soluble epoxide hydrolase) in mice further increased EET levels and significantly attenuated MCD diet-induced hepatic steatosis, inflammation and injury, as well as high fat diet-induced adipose tissue inflammation, systemic glucose intolerance and hepatic steatosis. Collectively, these findings suggest that dysregulation of the CYP epoxyeicosanoid pathway is a key pathological consequence of NASH in vivo, and promoting the anti-inflammatory and protective effects of EETs warrants further investigation as a novel therapeutic strategy for NASH.


Subject(s)
Cytochrome P-450 Enzyme System/metabolism , Non-alcoholic Fatty Liver Disease/enzymology , 8,11,14-Eicosatrienoic Acid/metabolism , Adult , Animals , Cytochrome P-450 CYP2J2 , Diet/adverse effects , Disease Progression , Epoxide Hydrolases/chemistry , Epoxide Hydrolases/metabolism , Female , Humans , Hydrolysis , Liver/enzymology , Male , Metabolic Syndrome/complications , Mice , Mice, Inbred C57BL , Middle Aged , Non-alcoholic Fatty Liver Disease/complications , Non-alcoholic Fatty Liver Disease/metabolism , Solubility
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