Afro-Egypt J Infect  Endem  Dis  2015 March ; 5(1):33-39  

 

Risk of Hepatic Encephalopathy in Diabetic Decompensated Liver Diseased Patients with Post- HCV Liver cirrhosis                                   Salem GA, Jouda AA

Tropical Medicine Department, Faculty of Medicine, Zagazig University, Egypt

ghadasalem69@gmail.com

 

ABSTRACT

Background and study aim: Hepatic encephalopathy (HE) is a complex and variable neuropsychiatric syndrome that is seen in patients with acute and chronic  liver diseases. Diabetes mellitus (DM) is more prevalent in patients with post HCV cirrhosis. Because diabetes mellitus may be associated with delayed gastrointestinal transit and promoting constipation, increasing intestinal bacterial overgrowth and increasing glutaminase activity, we speculated that its presence in patients  with HCV related cirrhosis would  predispose to and exacerbate hepatic encephalopathy.

 

Patients and Methods: This study included 264 patients with severely decompensated post-HCV cirrhosis, 132 diabetic cirrhotic patients and 132 non-diabetic cirrhotic patients as control group. History is taken for all patients regarding the number of attacks of encephalopathy he experienced in the past three months, the duration of diabetes and the anti-diabetic medication he uses. All patients in the study performed liver function tests, abdominal ultrasound, complete blood count and HBA1c level for diabetic patients as well as psychometric  tests for hepatic coma.

Results: Diabetic patients had higher frequency of all grades of hepatic encephalopathy mean number of attacks for each patient in the past three months is 1.9±0.3 vs 0.8±0.1 in non-diabetics with unclear precipitating factor in 43% of diabetic patients versus 23% in non-diabetic patients. Patients on oral hypoglycemic drugs represented 14.3% of diabetic patients. Patients with HBA1c >11% were 43% among patients on oral hypoglycemic drugs vs 23% with insulin. Patients on oral hypoglycemic drugs had higher frequency of hepatic coma. The mean number of attacks experienced by each patient rises with increased concentration of HBA1c from 0.8±0.2 at level <7% to 6.4±3for level >11%. The mean number of attacks increased with the duration of diabetes from 1±0.4 for <5 years to 6.4±3.1for >15 years.

Conclusion: The frequency of HE was higher in diabetic patients without other obvious precipitating factor. Patients with uncontrolled diabetes and patients on oral hypoglycemic drugs, and those with longer duration of diabetes seem to have higher risk of developing HE.