Serum zonulin levels in patients with liver cirrhosis:Prognostic implications

BACKGROUND Increased gut permeability and bacterial translocation play an important role in liver cirrhosis.Zonulin is a recently recognized protein involved in the disintegration of the intestinal barrier.AIM To investigate possible differences in serum zonulin levels among patients with different cirrhosis stages and their potential prognostic implications.METHODS Consecutive cirrhotic patients who attended our liver clinic were included in the study.Serum zonulin levels,clinical,radiological and biochemical data were collected at baseline.Patients who accepted participation in a regular surveillance program were followed-up for at least 12 mo.RESULTS We enrolled 116 cirrhotics[mean Child-Turcotte-Pugh(CTP)score:6.2±1.6;model for end-stage liver disease score:11±3.9].The causes of cirrhosis were viral hepatitis(39%),alcohol(30%),non-alcoholic fatty liver disease(17%),and other(14%).At baseline,53% had decompensated cirrhosis,48% had ascites,and 32% had history of hepatic encephalopathy.Mean zonulin levels were significantly higher in patients with CTP-B class than CTP-A class(4.2±2.4 ng/dL vs 3.5±0.9 ng/dL,P=0.038),with than without ascites(P=0.006),and with than without history of encephalopathy(P=0.011).Baseline serum zonulin levels were independently associated with the probability of decompensation at 1 year(P=0.039),with an area under the receiving operating characteristic of 0.723 for predicting hepatic decompensation.Higher CTP score(P=0.021)and portal vein diameter(P=0.022)were independent predictors of mortality.CONCLUSION Serum zonulin levels are higher in patients with more advanced chronic liver disease and have significant prognostic value in identifying patients who will develop decompensation.

Esophageal manifestation in patients with scleroderma

The esophagus is the most commonly affected part of the gastrointestinal system in patients with systemic sclerosis(SSc).Esophageal involvement may lead to a significant reduction in patient quality of life.The exact pathophysiology is complex and not yet fully elucidated.Ultimately,esophageal smooth muscle becomes atrophied and replaced by fibrous tissue leading to severe motility disturbance of the distal esophagus.Symptoms are mainly attributed to gastroesophageal reflux disease and to esophageal dysmotility.Compelling evidence has correlated esophageal involvement to the severity of pulmonary disease.No formed guidelines exist about the diagnostic modalities used to assess esophageal disease in patients with SSc,though upper gastrointestinal endoscopy is the first and most important modality used as it can reveal alterations commonly observed in patients with SSc.Further exploration can be made by high resolution manometry and pH-impedance study.Proton pump inhibitors remain the mainstay of treatment,while prokinetic agents are commonly used as add-on therapy in patients with symptoms attributed to gastroesophageal reflux disease not responding to standard therapy as well as to motility disturbances.Gastroesophageal reflux disease symptoms in patients with SSc are frequently difficult to manage,and new therapeutic modalities are emerging.The role of surgical treatment is restricted and should only be preserved for resistant cases.