Increased CD14(+) monocytes with loss of HLA expression were seen in patients with higher stage disease, more aggressive pathology, and in relapse or refractoriness to treatment. Identifying therapeutic strategies to overcome the suppressive properties of these monocytes could be of value.
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.
Background: P53 polymorphism involves the substitution of an arginine for a proline at codon position 72. Many studies have investigated a genetic link between this variation and response to treatment in cancer. This study aimed to study p53 codon72 polymorphism in relation to cytogenetic response to imatinib treatment in patients with chronic myeloid leukemia (CML). Methods: This study was conducted on 54 CML patients presented to Clinical Oncology Department, Menoufia University during the period from June 2013 and April 2015. They were classified according to their cytogenetic response to imatinib therapy into 40 CML patients cytogenetic responder to imatinib and 14 CML patients cytogenetic non responder to imatinib. Patients were genotyped for P53codon72 polymorphism using Polymerase Chain Reaction (PCR). Follow up of the patients should be done after 3, 6, 9, 12 and 18 months after diagnosis. And was done by CBC, conventional cytogenetic and FISH. Results: Age, gender, hematologic and cytogenetic response to imatinib in CML patients did not differ significantly among P53 codon72 genotypes (arg /arg, arg /pro and pro /pro) (P ¼ 0.44, p ¼ 0.45 and p ¼ 0.11 respectively). P53 codon72 polymorphism did not significantly alter the risk to imatinib cytogenetic unresponsiveness (P ¼ 0.9221). Conclusions: It could be concluded that P53 codon72 polymorphism is not associated with imatinib unresponsiveness in CML.
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