Esophageal ulcers are a rare cause of upper gastrointestinal bleeding. This report describes the etiology, treatment, complications, and outcome of esophageal ulcers. An esophageal ulcer is defined as a discrete break in the esophageal mucosa with a clearly circumscribed margin; esophageal ulcers were seen in 88 patients from a total of 7,564 esophagogastroduodenoscopies done by one surgeon at an urban hospital from 1991 to 2001. All hospital reports were reviewed. The etiology of esophageal ulcers included the following: gastrointestinal reflux disease (GERD) (n=58, 65.9%), drug induced (n=20, 22.7%), candidal (n=3, 3.4%), caustic injury (n=2, 2.3%), and herpes simplex virus (HSV), human immunodeficiency virus (HIV), marginal ulcer, foreign body, and unknown etiology (n=1 of each, 1.1%). The mean size of GERD-induced esophageal ulcers and drug-induced esophageal ulcers was 2.78 and 2.92 cm, respectively; 80.3% of GERD-induced esophageal ulcers and 13.8% of drug-induced esophageal ulcers were located in the lower thoracic esophagus. Morbidity (n=44, 50%) included hemorrhage (n=30, 34%), esophageal stricture (n=11, 12.5%), and esophageal perforation (n=3, 3.4%). Nonoperative therapy sufficed in 81 patients (92%). Three patients (3.4%) had a recurrence of esophageal ulcers. Fifteen patients (17.0%) required endoscopic intervention including esophageal dilatation for stricture in 11 patients and endoscopic hemostasis for esophageal bleeding in four patients. Surgery (n=7, 8.0%) was reserved for esophageal stricture and perforation. Two patients (2.3%) died from complications of esophageal ulcers: hemorrhage in one and perforation in one. Three patients died of their primary disease. GERD and drug ingestion are common causes of esophageal ulcers. Midesophageal ulcers have a greater tendency to hemorrhage compared with ulcers at the gastroesophageal junction; this may reflect the etiology. Strictures complicate GERD-induced esophageal ulcers but not drug-induced esophageal ulcers. Esophageal dilatation is an effective treatment for most strictures associated with esophageal ulcers. Esophageal ulcers rarely cause death.

.-We investigated the effect of muscle metaboreflex activation on left circumflex coronary blood flow (CBF) and vascular conductance (CVC) in conscious, chronically instrumented dogs during treadmill exercise ranging from mild to severe workloads. Metaboreflex responses were also observed during mild exercise with constant heart rate (HR) of 225 beats/min and ␤ 1-adrenergic receptor blockade to attenuate the substantial reflex increases in cardiac work. The muscle metaboreflex was activated via graded partial occlusion of hindlimb blood flow. During mild exercise, with muscle metaboreflex activation, hindlimb ischemia elicited significant reflex increases in mean arterial pressure (MAP), HR, and cardiac output (CO) (ϩ39.0 Ϯ 5.2 mmHg, ϩ29.9 Ϯ 7.7 beats/min, and ϩ2.0 Ϯ 0.4 l/min, respectively; all changes, P Ͻ 0.05). CBF increased from 51.9 Ϯ 4.3 to 88.5 Ϯ 6.6 ml/min, (P Ͻ 0.05), whereas no significant change in CVC occurred (0.56 Ϯ 0.06 vs. 0.59 Ϯ 0.05 ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ; P Ͼ 0.05). Similar responses were observed during moderate exercise. In contrast, with metaboreflex activation during severe exercise, no further increases in CO or HR occurred, the increases in MAP and CBF were attenuated, and a significant reduction in CVC was observed (1.00 Ϯ 0.12 vs. 0.90 Ϯ 0.13 ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ; P Ͻ 0.05). Similarly, when the metaboreflex was activated during mild exercise with the rise in cardiac work lessened (via constant HR and ␤ 1-blockade), no increase in CO occurred, the MAP and CBF responses were attenuated (ϩ15.6 Ϯ 4.5 mmHg, ϩ8.3 Ϯ 2 ml/min), and CVC significantly decreased from 0.63 Ϯ 0.11 to 0.53 Ϯ 0.10 ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 . We conclude that the muscle metaboreflex induced increases in sympathetic nerve activity to the heart functionally vasoconstricts the coronary vasculature.exercise; ischemia; skeletal muscle; vascular conductance WHEN EXERCISING skeletal muscle does not receive sufficient blood flow to meet metabolic demands, metabolites (e.g., lactic acid, H ϩ , and diprotonated phosphate) accumulate and stimulate afferent neurons, which evoke a reflex increase in sympathetic nerve activity (SNA) and mean arterial pressure (MAP), known as the muscle metaboreflex (1, 2, 8, 13, 18-21, 23, 27). The capability of the metaboreflex to correct a blood flow deficit lies in its ability to increase perfusion pressure, which is achieved via increases in cardiac output (CO) and vasoconstriction within nonischemic vascular beds (15,16,21,22). Both the increase in CO and its redistribution during metaboreflex activation is aimed at eliminating any existing mismatch between O 2 delivery and O 2 demand in the exercising skeletal muscle.Previous studies (2, 28) in normal dogs have shown that during mild-to-moderate workloads, the major mechanism utilized by the muscle metaboreflex to improve blood flow to the ischemic muscle is to raise CO. This increase in CO is achieved via increases in heart rate (HR), ventricular performance, and central blood volume mobilization (18,19,22,24). In contrast, when increases in ...

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Spontaneous perforation of the extrahepatic biliary tree is rare in adults. Although perforation of the hepatic, common hepatic, common bile, and cystic ducts has been reported, review of the English literature reveals only four cases of cystic duct perforation, each attributed to calculi. We herein report the first known case of spontaneous perforation of the cystic duct in the absence of biliary calculi.

4444 Background: In patients with chronic unexplained neutrophilic leukocytoses (UNL), underlying Chronic Myeloid Leukemia (CML) is a concern. In these patients, peripheral blood BCR-ABL mutation analyses using fluorescent in situ hybridization (FISH) is often performed to investigate for CML. Diagnostic yield of this test, in patients presenting UNL and especially in those with mild leukocytoses is uncertain. Objective: To establish the overall incidence BCR-ABL mutation in patients with UNL using peripheral blood FISH analyses. To determine the incidence within subgroups based on severity of leukocytoses. To explore the association between a positive test and the presenting clinical and laboratory features. Patients and Methods: We performed a retrospective chart review (2000–2010) of adult patients referred to the hematology service at the Dallas Veterans Administration Medical Center for evaluation of UNL. All patients had undergone, peripheral blood BCR-ABL mutation analyses by FISH. Neutrophilic leukocytoses were defined as a white blood count (WBC) above 11 × 109/L along with an absolute neutrophil count (ANC) greater than 7 × 109/L. It was considered unexplained, if it persisted on repeat testing and the referring physician deemed its etiology as uncertain. The primary end point was incidence of BCR-ABL positivity in patients with UNL. Incidence of BCR-ABL positivity within subgroups based on degree of WBC elevation defined as mild (11–20 × 109/L), moderate (>20–50 × 109) or severe (>50 × 109) was also calculated. Univariate and multivariate regression analyses of various laboratory and clinical features was performed to identify any confounding variables. Results: The median time from discovery of leukocytoses to the performing the test was 1545 days (n=285). 26 (9.1%) patients were found to be positive for BCR-ABL (n= 286). Majority had mild leukocytoses (n=202). The incidence increased with the severity of leukocytoses. Mild = 4/202 (2%), moderate = 9/62 (14.5%), severe = 13/22 (59.1%). On univariate analyses, a positive test was associated with presence of an elevated LDH (OR=107 CI 14.17–809.99), myeloid left shift (OR=107 CI 14.17–809.99) and hepatosplenomegaly (OR 3.87 CI 1.57–9.54). On multivariate regression, the presence of a myeloid left shift was strongly associated with a positive test (OR=67.20 CI 8.36–540.36). Myeloid left shift was seen in 3/4 (75%) of patients with a mild leukocytoses and positive test for BCR-ABL, Conclusion: In patients with UNL, peripheral blood FISH for BCR-ABL mutation should be restricted to those with moderate to severe leukocytoses. Incidence of BCR-ABL is especially low (2%) in patients with mild leukocytoses (<20 × 109/L). In these patients BCR-ABL testing should be limited to those with an unexplained myeloid left shift. Disclosures: No relevant conflicts of interest to declare.

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