Imatinib (Gleevec, Novartis), an inhibitor of BCR-ABL, platelet-derived growth factor, and KIT receptor tyrosine kinases, is widely used in the treatment of chronic myelogenous leukemia and gastrointestinal stromal tumors. We describe a case of activation of chronic hepatitis B infection associated with imatinib therapy.

Objective: To determine whether acid-induced injury to the esophagus is decreased by early dilutional therapy with water or milk.Methods: A controlled in-vitro animal model for acid injury to the esophagus was carried out using esophagi harvested from 70 SpragueDawley rats of both sexes and weighing 250-350 g. One control and six experimental groups each containing ten esophagi were instilled with 1 mL of 0.5 normal solution of hydrogen chloride (N HCI). Dilution with water or milk was performed at 0, 5. or 30 minutes postinjury in the experimental groups. No dilution was performed with the control group. Specimens were maintained in an oxygenated saline bath for a @-minute experimental period and then fixed in 10% formalin for histologic evaluation. Injury severity was rated by blinded histopathologic examination using scores of 0 (no injury), 1 (minor), 2 (moderate), and 3 (severe) for the histopathologic categories: cornified epithelial cells (CEs), granular cells (GCs), granular cell nuclei (GNs), and basal cells (BCs). Red blood cells were scored as positive or negative for lysis. Results:The controls showed the most severe outcomes. Significant differences in injury occurred for all time periods and histopathologic categories, except for the GN/water and BCimilk histopathologic categoryltreatment groups. However, a linear trend analysis was significant for all histopathologic categories except BC. These analyses support decreased injury in the earlier treated groups. Injury severity was highest in the most superficial cell layer (CE).Conclusions: Emergency therapy with water or milk reduces acute acid injury to the esophagus. Earlier treatment is associated with decreased injury severity. This research supports the use of dilutional therapy with water or milk for acute acid injury to the esophagus.

Objective: I ) To evaluate whether neutralization therapy with weak acid is effective in reducing observed histopathologic esophageal tissue injury secondary to liquid alkali. 2 ) to quantify the temperature change of the neutralizing agent. and 3 ) to determine the effect of interval t o therapy on injury severity.Methods: Harvested Sprague-Dawley rat esophagi were catheterized and placed in an oxygenated saline bath (37°C) for 60 minutes and then fixed in 10% formalin. Nine groups ( t i = 10) were perfused with 50% sodium hydroxide (NaOH). Six of the groups were treated hy neutralization with cooled orange juice (OJ) or cola that was maintained between 2'C and 4°C. This was performed at 0, 5. or 30 minutes after injury. In addition, two positive control groups were exposed to OJ or cola at time 0 and were not exposed to strong alkali. A third control group was exposed to strong alkali hut was not administered any subsequent treatment. The temperature of the neutralizing agent was recorded prior to instillation and after exiting the esophagus. Blinded pathologic scoring of 0 (no injury) to 3 (severe) was performed for six histopathologic categories: epithelial cell viability, cornified epithelial cell differentiation, granular cell differentiation. epithelial cell nuclei, muscle cells, and muscle cell nuclei. Comparisons were made among treatment times using the Kruskal-Wallis test and linear trend analysis. Results:For each histopathologic category and each treatment mode, the Kruskal-Wallis test showed significant differences between the groups (p < 0.003) over time. Trend analyses showed more severe injury with delayed ncutralization therapy ( p < 0.05) for each treatment mode and histopathologic category. Conclusion:Early neutralization therapy with OJ or cola reduces acute esophageal alkali injury. Additional in-vivo study is needed before neutralization therapy is adopted for clinical use.