Role of Helicobacter pylori in refractory iron deficiency anaemia

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.