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Drug-eluting bead transarterial chemoembolization (DEB-TACE) is a well-established, minimally invasive interventional treatment for nonresectable hepatocellular carcinoma (HCC). Generally, TACE is regarded as safe and effective with a low complication rate. However, remote gastrointestinal ischemia due to the carryover of embolic material into visceral arteries is a rare but serious complication of TACE. In this report, we present a case of duodenal ulceration with contained perforation and severe necrotizing pancreatitis after TACE in a patient with nonresectable HCC and underlying hepatitis C virus associated with Child-Pugh stage B liver cirrhosis. This patient showed, for the first time, complete endoscopic and clinical recovery within 2 months of conservative treatment. Considering the high mortality rate from surgical intervention in all previously reported patients, the significant recovery potential demonstrated by our case suggests conservative treatment with antibiotics and parenteral nutrition combined with close clinical, radiological, and endoscopic monitoring should be considered in all clinically stable patients without signs of peritonism or septic sequelae.

Context: Proton pump inhibitor (PPI) increases the risk of decrease in bone mineral density (BMD). However, whether calcitrol improves this situation is unknown. Objective: The current study investigates the effects of calcitriol on BMD in patients with esomeprazole therapy. Materials and methods: Three hundred and eighty-six participants with gastrointestinal ulcerations were enrolled and randomly assigned into controlled and supplemented groups. Participants in the controlled group were prescribed esomeprazole (20 mg/qd), while the supplemented group was prescribed esomeprazole (20 mg/qd) and calcitriol (2.5 μg/qd). BMD, serum levels of calcium, carboxy-terminal collagen crosslinks (CTX), and alkaline-phosphatase (ALP) were assessed. Results: (1) No significant between-group difference of age, gender, smoking, previous glucocorticoid use and hemoglobin level was found; (2) after 10.6 ± 0.8 d of PPI therapy, BMD T score in the controlled group was slightly increased compared with initial (−1.25 ± 0.08 versus −1.28 ± 0.06, p = 0.084), while there was no change in the supplemented group (−1.25 ± 0.05 versus −1.26 ± 0.03, p = 0.308); (3) during study termination, calcium level in the supplemented group was slightly higher than the controlled group (2.05 ± 0.03 mmol/L versus 2.01 ± 0.05 mmol/L, p = 0.073), while no significant differences of CTX (366.57 ± 43.71 pg/mL versus 373.15 ± 50.23 pg/mL, p = 0.036) and ALP were found among these two groups (50.47 ± 9.32 U/L versus 52.23 ± 10.45 U/L, p = 0.075). Conclusion: Patients with gastrointestinal ulcerations with esomeprazole therapy, calcitriol supplement showed no efficacy on BMD changes. [ABSTRACT FROM AUTHOR]

Stress is a major etiologic factor in the pathogenesis of gastric and duodenal ulceration, as first described in rats by Hans Selye. In patients with “peptic ulcers” duodenal ulcers are more frequent than gastric ulcers (except in Japan). Thus, our research during the last three decades focused on the molecular mechanisms of duodenal ulcer in rodent models of chemically induced duodenal ulceration, and here we review our three recent findings: Endothelins (ET-1), the immediate early gene egr-1 and imbalance of angiogenic/antiangiogenic molecules. Namely, we found an enhanced expression and release of ET-1 within 15–30 min after the administration of duodenal ulcerogen cysteamine, resulting in local ischemia that triggers the expression of hypoxia-inducible factors (HIF-1α). Our gene expression studies also revealed an early (0.5–2 h) increase in the expression of egr-1 that is followed (12–24 h) by upregulation of angiogenic growth factors (e.g., VEGF, bFGF, PDGF). Surprisingly, this event is also associated with an enhanced production of angiostatin and endostatin that probably counteract the beneficial effect of angiogenic molecules. Thus, the initial injury to endothelial and epithelial cells in duodenal ulceration seems to be aggravated (and not initiated) by HCl and proteolytic enzymes. The resulting mucosal necrosis does not rapidly heal because of the imbalance of VEGF and angiostatin/endostatin, hence duodenal ulcers develop. The experimental ulcers Selye described morphologically are now characterized at the molecular and genome level, involving unexpected mediators like ET-1, egr-1 and angiogenesis-related molecules. [ABSTRACT FROM AUTHOR]

The pharmacokinetic behaviour of a single oral 150 mg ranitidine dose was studied in six patients with severe chronic renal failure (CRF) (creatinine clearance 2-18 ml/min) and compared to that in ten patients with duodenal ulceration but normal renal function (N) (creatinine clearance 69-125 ml/min). Although the maximum concentrations (C) were significantly higher in CRF group when compared to N group ( p<0.025) there was no difference in the time taken to reach C ( t). The area under the curve (AUC) was also significantly larger in the CRF group ( p<0.001) than in the N group. Within the CRF group there was a large variation in C (CV = 38%) and AUC (46%) which may reflect variable bioavailability of ranitidine. The terminal elimination rate constant ( β) was significantly smaller ( p<0.001) in CRF group when compared with N group resulting in a median t for the CRF group of 7.3 h, 2.4 times that of N group. The recovery of unchanged ranitidine in the urine was significantly less in CRF group ( p<0.001) despite a great interindividual variation in both groups. A significant linear relationship between β and creatinine clearance was shown ( r=0.81 p<0.001). The results indicate that ranitidine elimination is appreciably reduced in renal failure. It is tentatively suggested that the standard 150 mg dose should be halved while keeping the dose interval unchanged at twelve hours in patients with severe renal failure (creatinine clearance less than 30 ml/min). [ABSTRACT FROM AUTHOR]

The pharmacokinetics of orally administered ranitidine were studied in 17 male patients with chronic duodenal ulceration. The patients were divided into 2 groups, 10 responders and 7 nonresponders, on the basis of their endoscopic response to ranitidine treatment. The 10 responders were studied both after a single 150 mg dose (SD) and after multiple dosing (MD) with ranitidine 150 mg twice daily for 4 weeks. The area under the curve (AUC) and maximum concentration (C) were significantly higher ( p<0.01 and p<0.05, respectively) after MD than after SD, but the half-life (t) and minimum concentration (C) 12 h postdosing did not differ. The non-responders were studied after MD only and their pharmacokinetic characteristics were compared with those of responders. No differences between the 2 groups were found. However, 2 non-responders had particularly low plasma ranitidine levels and high acid output. Such patients may need larger doses of ranitidine for adequate suppression of gastric acid. Five patients (4 responders and 1 non-responder) received ranitidine 20 mg i.v. The drug followed a two-compartment model, with mean values for t, volume of distribution steady-state and total plasma clearance of 80 min, 701 and 680 ml/min, respectively. The oral bioavailability of ranitidine in these 5 patients showed wide variation (27-76%; mean 51%). [ABSTRACT FROM AUTHOR]

Summary: A surgical clip in the cystic pedicle migrating to the duodenum is a rare complication of laparoscopic cholecystectomy (LC). Usually patients present with bleeding ulcer. We report a case of postcholecystectomy pain due to clip migration into the duodenum. This was a case of postcholecystectomy pain 4 months after LC was performed. Ultrasonography and liver function tests were normal. Endoscopy showed two clips at the base of a small duodenal ulcer. Removal of the clips treated the complication. This rare complication can be a cause of postcholecystectomy pain. A good surgical technique using the utmost care can reduce the incidence of such a complication. [Copyright &y& Elsevier]