The combination of B + E in patients who had advanced HCC showed significant, clinically meaningful antitumor activity. B + E warrant additional evaluation in randomized controlled trials.

BACKGROUND. Growth factor overexpression, including epidermal growth factor receptor (EGFR) expression, is common in hepatocellular cancers. Erlotinib is a receptor tyrosine kinase inhibitor with specificity for EGFR. The primary objective of this study was to determine the proportion of hepatocellular carcinoma (HCC) patients treated with erlotinib who were alive and progression‐free (PFS) at 16 weeks of continuous treatment. METHODS. Patients with unresectable HCC, no prior systemic therapy, performance status (PS) of 0, 1, or 2, and Childs‐Pugh (CP) cirrhosis A or B received oral erlotinib 150 mg daily for 28‐day cycles. Tumor response was assessed every 2 cycles by using Response Evaluation Criteria in Solid Tumors (RECIST; National Cancer Institute Cancer Therapy Evaluation Program, Bethesda, Md) criteria. Patients accrued to either “low” or “high” EGFR expression cohorts; each cohort had stopping rules applied when there was a lack of efficacy. RESULTS. Forty HCC patients were enrolled. Median age was 64 years (range, 33–83 years), sex distribution was 32 males and 8 females, performance scores were 40% PS 0, 55% PS 1, Childs‐Pugh distribution was 75% A and 20% B. There were no complete or partial responses; however, 17 of 40 patients achieved stable disease at 16 weeks of continuous therapy. The PFS at 16 weeks was 43%, and the median overall survival (OS) was 43 weeks (10.75 months). No patients required dose reductions of erlotinib. No correlation between EGFR expression and outcome was found. CONCLUSIONS. Results of this study indicated that single‐agent erlotinib is well tolerated and has modest disease‐control benefit in HCC, manifested as modestly prolonged PFS and OS when compared with historical controls. Cancer 2007. Published 2007 by the American Cancer Society.

Adverse reactions to commonly prescribed medications and to substances of abuse may result in severe toxicity associated with increased morbidity and mortality. According to the Center for Disease Control, in 2013, at least 2113 human fatalities attributed to poisonings occurred in the United States of America. In this article, we review the data regarding the impact of systemic sodium bicarbonate administration in the management of certain poisonings including sodium channel blocker toxicities, salicylate overdose, and ingestion of some toxic alcohols and in various pharmacological toxicities. Based on the available literature and empiric experience, the administration of sodium bicarbonate appears to be beneficial in the management of a patient with the above-mentioned toxidromes. However, most of the available evidence originates from case reports, case series, and expert consensus recommendations. The potential mechanisms of sodium bicarbonate include high sodium load and the development of metabolic alkalosis with resultant decreased tissue penetration of the toxic substance with subsequent increased urinary excretion. While receiving sodium bicarbonate, patients must be monitored for the development of associated side effects including electrolyte abnormalities, the progression of metabolic alkalosis, volume overload, worsening respiratory status, and/or worsening metabolic acidosis. Patients with oliguric/anuric renal failure and advanced decompensated heart failure should not receive sodium bicarbonate.

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In this large retrospective case series, a high success rate of DBC was achieved by using dye-free guidewire techniques. This technique has associated lower rates of complications in comparison to those reported earlier.