Development of Hepatic Steatosis After Chemotherapy for Non-Hodgkin Lymphoma.

Nonalcoholic fatty liver disease is the most common liver disorder in the developed world. Although typically reflecting caloric overload, it can also be secondary to drug toxicity. We aimed to describe the incidence and risk factors for de novo steatosis during chemotherapy for non-Hodgkin lymphoma (NHL). In this retrospective case-control study, adult patients with NHL were treated with rituximab, cyclophosphamide, doxorubicin, prednisone, and vincristine (R-CHOP) or R-CHOP + etoposide (EPOCH-R). Patients with liver disease or steatosis were excluded. Abdominal computed tomography was performed pretreatment and at 3- to 6-month intervals and reviewed for steatosis. Patients with de novo steatosis were matched 1:1 to controls by age, sex, and ethnicity. Of 251 treated patients (median follow-up 53 months), 25 (10%) developed de novo steatosis, with the vast majority (23 of 25; 92%) developing it after chemotherapy. Of those, 14 (61%) developed steatosis within the first 18 months posttreatment and 20 (87%) within 36 months. Cases had higher baseline body mass index (BMI; mean ± SD, 29.0 ± 6.5 versus 26.0 ± 5.2 kg/m2; P = 0.014) and hyperlipidemia (12% versus 2%; P = 0.035). Although their weights did not change during chemotherapy, BMI in cases increased by 2.4 ± 2 kg/m2 (mean ± SD) from end of treatment to steatosis compared to 0.68 ± 1.4 in controls (P = 0.003). Etoposide-containing regimens were associated with a shorter time to steatosis (median 34 weeks versus 154 weeks; P < 0.001) despite similar baseline risk factors. Conclusion: The recovery period from NHL chemotherapy appears to be a "hot spot" for development of fatty liver, driven by early posttreatment weight gain, especially in subjects with baseline risk factors.

CIED malfunction in patients receiving radiation is a rare event that could be detected by remote monitoring.

INTRODUCTION: An increasing number of patients with cardiac devices require radiation therapy for treatment of a variety of cancers. This study aimed to identify the incidence and predictors of cardiac implantable electronic devices (CIED) malfunction in a real-world population that has received radiation therapy. METHODS: This retrospective cohort study included 109 adult patients who received radiation therapy at the University of Rochester Medical Center, Radiation Oncology Department, between 2000 and 2015. Sixty patients had pacemakers and 49 had automatic implantable cardioverter defibrillators. Subjects received either high energy (16 MV) and/or low energy (6 MV) photon beams with or without electron beams (6-16 MeV). We included interrogations done from first day of radiation and up to 3 months' postradiation therapy. Outcomes analyzed were device-related malfunctions and device-related clinical events. Fisher's exact, Wilcoxon, and Kruskall-Wallis tests were used for bivariate analysis. Logistic regression with robust adjustment was used for multivariate analysis. RESULTS: We identified six device-related malfunctions. All events were minor and included partial settings reset leading to loss of historical data, pacing thresholds changes, lead impedance changes, and LV output increase. Two patients had device-related clinical events, including dyspnea and diaphragmatic-stimulation. In bivariate analysis, CIED malfunction was associated with CIED duration in situ. In multivariate analysis, there was no significant statistical association between adverse events and beam energy type, CIED location, or dose of radiation delivered to the target. CONCLUSIONS: CIED malfunctions are uncommon in real-world patients and associated with minor clinical events. In our cohort, remote CIED monitoring would have identified all events.