Influence of esophageal variceal bleeding on iron status in chronic hepatitis C patients.

BACKGROUND: Disorders of serum iron balance are frequently observed in chronic hepatitis C (CHC) patients. Iron overload as well as iron deficiency anemia are common clinical findings in these patients. Variceal bleeding is also a common complication. To date, no study has discussed the influence of esophageal bleeding on iron status in anemic CHC bleeders. OBJECTIVE: Was to study reticulocyte hemoglobin content (CHr) and serum hepcidin levels in anemic CHC and to evaluate the influence of variceal bleeding on patients' iron status. METHODS: Serum hepcidin levels and CHr were assessed in 65 early phase CHC patients (20 nonanemic, 23 anemic nonbleeders, and 22 anemic bleeders), and 20 healthy controls; and were compared with the conventional indices of iron deficiency including mean corpuscular volume, mean corpuscular hemoglobin, red cell distribution width, serum iron, total iron binding capacity, transferrin saturation and ferritin. RESULTS: Hepcidin levels were comparable in patients groups, but were significantly lower in patients than in controls (P = 0.01). Child-Pugh class B patients showed significantly lower hepcidin levels than class A patients. CHr levels were comparable in all groups as well as all iron deficiency indices. Patients with ferritin values or less 100 ng/ml and CHr or less 29 pg/cell or Tfsat or less 16% are more likely to have iron deficiency [odds ratio (OR = 3.93, 95% confidence interval (CI) = 2.54-6.08; OR = 10.50, 95% CI = 1.94-56.55, respectively). CONCLUSION: Esophageal bleeding has an almost no influence on iron status in CHC patients. Serum hepcidin content is influenced by CHC disease rather than by anemia associated with or without esophageal bleeding and it could be used as a marker of early hepatic insufficiency. Assessing CHr content could add a potential utility in the detection of iron deficiency in CHC patients.

T(14;18) is not associated with mixed cryoglobulinemia or with clonal B cell expansion in egyptian patients with hepatitis C virus infection.

BACKGROUND/AIM: The mechanisms of B-cell lymphoproliferative disorders in chronic hepatitis C virus (HCV) infection are unclear. An increased prevalence of circulating monoclonal B-cells and t(14;18) has been reported. Geographic heterogeneity of prevalence of t(14;18) has been shown to exist. We investigated the prevalence of t(14;18) and B-cell clonality as possible mechanisms of lymphomagenesis in chronic HCV patients, in whom cryoglobulinemia status was previously detected. METHODS: A cohort of 111 patients was studied, including 87 patients with chronic HCV disease (18 cryoglobulinemic and 69 non- cryoglobulinemic); 24 HCV-negative, cryoglobulin negative patients with other nonimmune chronic liver diseases were enrolled as controls. The t(14;18) and IgH rearrangement (as a marker of B-cell clonality) were detected by the polymerase chain reaction. RESULTS: t(14;18) was detected in 27.6% of HCV patients and in none of the controls. Detection rates were comparable in both cryoglobulin-positive and negative groups (22.2% and 29% , respectively), p=0.769. IgH rearrangement was detected in 39.1% of HCV patients and in none of the controls. The cryoglobulin-positive group showed significantly higher prevalence of IgH rearrangement compared to the cryoglobulin-negative group (61.1% and 33.3% , respectively), p=0.03, OR=3.13 and 95% CI=1.07-9.17. t(14;18) and monoclonal IgH rearrangement detection rates were not associated with each other, p=0.467. CONCLUSIONS: t(14;18) is uncommon in HCV-mixed cryogoblulinemia Egyptian patients; it does not seem to play a role in HCV-associated MC and lymphomagenesis in our geographical area. HCV may play a role in mixed cryogoblulinemia and lymphomagenesis, probably by inducing clonal B-cell expansions.