Background: Variceal bleeding (VB), the most common lethal complication of cirrhosis, associated with high mortality. Timely prediction of esophageal varices (EV) represents a real challenge for the medical team. This study evaluated the level of plasma soluble CD 163 as a marker of the presence of EVs and to compare it with other noninvasive clinical, laboratory and ultrasonographic parameters as well as endoscopy. Methods: This prospective controlled study was conducted on 80 adults. Gp I had no oesophageal varices, gp II had small varices, gp IIIa had large varices, gp IIIb are the same patients of gp IIIa but after eradication of varices and gp IV as healthy controls. Serum samples were assayed for soluble CD 163. Results: soluble CD163 was statistically significant different between controls and all liver cirrhosis. it showed a statistically significant difference between group I and II (p = 0.009) and between group I and IIIa (p < 0.001) and between group II and IIIa (p < 0.001) but, no difference between group IIIa and IIIb (p = 0.179). Conclusion:Serum soluble CD163 is a good noninvasive predictor for the presence of EVs and it may be used for grading of EVs. Its level does not change after esophageal varices eradication.

The role of Helicobacter pylori infection in the development of iron deficiency anaemia has been the focus of attention over the past decade. However, confirmation of a relationship has not confirmed the pathophysiological mechanisms involved in the phenomenon. The aim of the present work is to study the levels of fasting gastric acidity (free and total) as well as the level of tumour necrosis factor-alpha (TNF alpha) in male refractory iron deficiency anaemia patients seropositive for H. pylori infection versus those who are seronegative. Thirty adult patients with iron deficiency anaemia and gastroduodenitis were subdivided into two groups of matched age and haemoglobin value. Group 1 was H. pylori-seropositive for infection and these patients did not receive prior treatment for eradication of H. pylori infection. Group 2 comprised patients seronegative for H. pylori infection (control group). Patients with active bleeding or previous medical problems were excluded from the study. All patients and controls were subjected to the following at presentation: history taking and thorough clinical examination, complete blood picture, reticulocytes (%), assessment of serum iron, total iron binding capacity, serum ferritin, IgG anti-Helicobacter antibody and TNF alpha, stool for occult blood and measurement of gastric acidity (total and free). Upper endoscopy was performed and multiple biopsies were taken and tested for expression of cytotoxin-associated gene A (cagA) by the polymerase chain reaction (PCR). Results showed significantly higher values of free and total gastric acidity as well as TNF alpha levels in Group 1 compared to controls (Group 2). Among those in Group 1, higher TNF alpha levels were seen in seven H. pylori cagA-positive patients than in eight cagA-negative patients. Haemoglobin values were inversely correlated with TNF alpha levels. Thus, elevated serum TNF alpha in the H. pylori-seropositive group may be one of the underlying pathophysiological mechanism for iron deficiency anaemia observed in these patients.

Human leukocyte antigen (HLA) alloimmunisation was only 14% in the children with β thalassemia major we studied. Surprisingly FNHTRs were not more common in those with HLA antibodies. Splenectomy plays a role in reducing the frequency of transfusion and HLA alloimmunisation. Washed and filtered RBCs are comparable in reducing FNHTRs and in inducing haemoglobin rise.