Background: The contribution of HSCs to liver regeneration in different forms of liver injury remains debatable. Accordingly, many studies were carried out to verify whether various liver lesions (as liver resection, transplantation and acute and chronic forms of liver failure) can activate bone marrow by mobilizing peripheral blood hematopoietic stem cells (HSCs) (CD34/ CD133+ cells) putatively able to induce liver repopulation. Many conflicting data were reported. Aim of the work: It is intended in this current study to determine the degree of mobilization of BM-derived HSCs into the peripheral blood of patients with chronic hepatic affection and correlating it with various grades of liver damage. Subjects and Methods: this study was conducted on 30 patients with Child A, B and C grades of chronic liver disease (10 patients for each stage). 10 healthy subjects were enrolled as controls. The percent of circulating HSCs was determined by flowcytometric phenotypic analysis and compared among the different groups of patients. Also, isolation of such cells was done by magnetic cell sorting technique using the Mini-MACS separator for further ultrastructural assessment by Transmission Electron Microscopy (TEM). Results: The chronic liver disease group, compared to the healthy control group, exhibited no significant difference in the percentage of circulating CD133+cells (0.419 % ± 0.194, 0.419% ± 0.252 and 0.277% ± 0.160 in Child A, B and C respectively versus 0.456 % ± 0.119 in control ). Regarding the level of CD34+ cells, a statistically significant increase was found between child A chronic liver disease group and control group (mean ± SD; 1.183% ± 0.785 in child A versus 0.519% ± 0.201 in control group ) (p<0.05). However no statistical significant difference could be found between Child B and C chronic liver disease patients and control group or between each other (0.532% ± 0.370 and 0.768% ± 0.332 in Child B and C respectively vs. 0.519% ± 0.201 in healthy controls). It was even found that in Child C, circulating HSC levels were decreased, though not significantly, as compared to the healthy subjects as well as to the milder Child A and B liver patients. Ultrastructural characteristics of isolated cells were compared in healthy and hepatic patients. The cells described in both groups were generally similar in appearance with no evidence of structural changes.TEM analysis revealed typical features of an immature phenotype. Conclusion: Our data showed that chronic lesions of any degree of severity did not evoke bone marrow (BM) to mobilize HSCs into the circulation This could be due to: i) Defective hemopoiesis usually encountered in chronic liver diseases or ii) The toxic mileu of the chronic-damage liver interfering with extrahepatic stem cell-mediated liver repair.The recovery process seems to be mainly dependent on proliferating endogenous liver progenitors. Hence defining the underlying mechanisms interfering with BM activation and HSC mobilization is warranted.