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Introduction and aim Neuropsychiatric complications that develop after living donor liver transplantation (LT) are frequently encountered, though not adequately estimated among Egyptian recipients. We aimed to estimate the frequency of neuropsychiatric manifestations and neurocognitive functional changes after living donor LT. Patients and methods A prospective observational cohort study was conducted to evaluate 30 adult patients with end-stage liver disease preoperatively in a single Egyptian Transplant Center from November 2012 till January 2014. Relevant preoperative, intraoperative, and postoperative data were recorded and recollected and at 3 and 6 months of follow-up. The assessment included neurologic evaluation, Child–Turcotte–Pugh score, model of end-stage liver disease score, clinical hepatic encephalopathy staging scale, West Haven criteria, and International Society for Hepatic Encephalopathy and Nitrogen Metabolism score for semiquantitative assessment of encephalopathy. Results Hepatitis C virus was the main etiology for liver disease in 27 (90%) patients. Overt hepatic encephalopathy was seen in 26.6%, whereas covert hepatic encephalopathy occurred in 43.3%. Postoperatively, 76.7% of the patients demonstrated neuropsychiatric manifestations, with 50% of them showing mainly early major events, namely, encephalopathy. Late minor manifestation rates were 50%. Early cyclosporine administration and cold ischemia time longer than 40 min were significant predictors of occurrence of early neurologic events postoperatively (P=0.031 and 0.025, respectively). Both risk factors were associated with earlier and higher rates of neurologic complications. Conclusion Patients of living donor LT are at increased risk of developing early postoperative major neurologic sequelae, which become of less clinical significance later on. The patients’ cognitive functions improve with time after transplant.

Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide. It was reported to account for about 4.7 % of chronic liver disease in Egyptian patients. The present study aimed at studying the different factors that may be implicated in the relationship of schistosomiasis mansoni with HCC in Egypt. A total of 75 Egyptian patients with primary liver tumours (HCC) were enrolled in this study. They were subjected to full history taking and indirect hemagglutination assay (IHA) for the diagnosis of schistosomiasis. According to the results, the patients were categorized into two groups: Group I: 29 patients with negative IHA for schistosomiasis and hepatitis C virus (HCV) positive with no history or laboratory evidence of previous or current Schistosoma mansoni infection. Group II: 46 patients with positive IHA for schistosomiasis and HCV positive. The significant higher proportion of HCC patients in the present study had concomitant HCV and schistosomiasis (61.3 %) compared to HCC patients with HCV alone (38.7 %) suggesting that the co-infection had increased the incidence of HCC among these patients. Analysis of the age distribution among HCC patients revealed that patients in Group II were younger in age at time of diagnosis of HCC with mean age 57.1 years, as compared to patients in Group I with mean age 64.3 years with a highly significant statistical difference between the 2 groups. HCC in Group II was more common in rural residents while it was more common in urban areas in Group I with a significant statistical difference between the 2 groups. Analysis of the sex distribution among the studied groups showed that HCC was more common in males than females in both groups. As regards the aggression of HCC, it was more commonly multifocal and larger in size in patients with concomitant infection than in patients with HCV alone.

The burden of hepatocellular carcinoma (HCC) in Egypt has been increasing with a doubling in the incidence rate in the past 10 years, which necessitates the investigation of the possible risk factors to its development. The present study aimed at investigating the role of Schistosoma mansoni infection as a risk factor for development of HCC. Five hundred parasite free mice were categorized into four groups: Group I (induction of carcinoma by diethylnitrosamine (DEN)), Group II (DEN+Infection), Group III (Infection) and Group IV (Control). Groups I and II were further subdivided into 4 subgroups according to the dose of DEN given. Serum samples from each group were examined for levels of tumor markers alpha fetoprotein (AFP) and ferritin by ELISA, then mice were sacrificed and subjected to histopathological examination of their livers. These were repeated every week till the end of the experiment. The results of the histopathological examination clarified the role of S. mansoni in enhancing and aggravating the carcinogenic effect of DEN; dysplastic changes appeared earlier, with a higher grade and with a smaller dose of DEN in Group II compared to Group I. Serum levels of tumor markers showed earlier statistically significant differences in Group II than in Group I when compared to Group IV. We conclude that S. mansoni accelerates hepatic dysplastic changes in the presence of other risk factors making cancer appear early and with a more aggressive nature, compared to the same risk in absence of schistosomiasis.