Patients who develop hepatic decompensation with ascites have a poor prognosis and often experience other complications including spontaneous bacterial peritonitis, hepatic encephalopathy and variceal bleeding. We hypothesised that smartphone (SP)-enabled remote monitoring of patients with ascites may enable early detection of infection and acute decompensation, facilitate timely intervention and improve patient outcomes. Aim: We aimed to design, develop and implement a remote monitoring system (RMS) for outpatients with cirrhotic ascites. Method: We undertook surveys with patients and hepatologists to quantify the demand for a RMS and identify issues regarding implementation. A smartphone and a web-based application were developed as a RMS. Patients used the RMS in a 6-week prospective non-randomised trial. Results: We surveyed 27 patients (mean age 56 years, 18 (67%) were male, 16 (59%) had Childs Pugh B cirrhosis, and 20 (74%) had a history of alcoholic liver disease) and 5 hepatologists. There were 19 patients (70%) who reported that they would use a RMS. The RMS was used by 10 patients for a mean 53.8days (11-70), who entered 20.6 (0-71) updates. A total of 18 automated alerts occurred. 22% of automated alerts resulted in clinically significant changes to management, such as inpatient admission n=1 (6%), early outpatient appointment n=1 (6%) and reinforced adherence n=2 (11%). Conclusion: We have successfully designed an internet-enabled RMS for outpatients with cirrhotic ascites that could be used as an adjunct to existing outpatient services. Future studies will optimise the alert thresholds, assess long-term patient adoption and quantify clinical impact.
The biliary output of carcinoembryonic antigen (CEA) in bile fistula rats following treatment with the microtubule poisons vinblastine and colchicine increased 3-fold over a 4-hr period. Cytochalasin B and the inactive colchicine derivative lumicolchicine had no effect. These treatments did not effect the rate of CEA clearance from the circulation. Biliary output of low molecular weight fragments from CEA degradation was decreased in the presence of colchicine and vinblastine. Mechanical obstruction of the bile duct for 3 days followed by relief of obstruction resulted in a 3-fold increased output of CEA into the bile. These results are consistent with a paracellular mechanism for CEA transport from blood to bile. Biliary duct obstruction and vinblastine and colchicine probably affect the permeability of junctional complexes between hepatocytes allowing CEA to penetrate more easily.
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