Role of Helicobacter pylori in refractory iron deficiency anaemia

The role of Helicobacter pylori [H. pylori] infection in the development of iron deficiency anaemia has been the focus of attention during the last decade. Confirmation of the relationship between H. pylori infections and iron deficiency anaemia has not confirmed the pathophysiologic mechanisms involved in this phenomenon was to study the levels of fasting gastric acidity [free and total] as well as the level of tumor necrosis factor alpha in refractory iron deficiency anaemic male patients seropositive for H. pylori infection versus those with seronegativity for H. pylori infection. Also, we tried to find the underlying pathophysiologic mechanism for iron deficiency anaemia observed in these patients. This study was conducted on 30 adult male patients having iron deficiency anaemia and gastroduodenitis. They were subdivided into 2 groups of matched age and haemoglobin value. Group I was seropositive for H. pylori infection and refractory to iron therapy. These patients did not receive prior treatment for eradication of H. pylori infection while group II was seronegative for H. pylori infection and was considered a control group. Patients with active bleeding or previous medical problem were excluded from the study. All patients and controls in the present study were subjected to the following at presentation: careful history taking and thorough clinical examination, complete blood picture, reticulocytes%, assessment of serum iron, total iron binding capacity, serum ferritin, IgG antihelicobacter antibody and tumor necrosis factor-alpha [TNF-alpha], stool for occult blood and measurement of gastric acidity [total and free] by chemical method. Upper endoscopy was done and multiple biopsies were taken and tested for expression of cytotoxin associated gene A [cag A] by polymerase chain reaction [PCR]. results revealed statistically significant higher values of free and total gastric acidity as well as tumor necrosis factor-alpha levels in H. pylori seropositive compared with H. pylori seronegative group. Among H. pylori seropositive group, higher value of TNF-alpha level was observed in H. pylori cagA positive [7 patients] than cagA negative patients [8 patients]. Also, haemoglobin values were inversely correlated with tumor necrosis factor-alpha levels. From this study, we can conclude that elevated serum tumor necrosis factor [TNF-alpha] in H. pylori seropositive group may be one of the underlying pathophysiologic mechanism for iron deficiency anaemia observed in these patients

Peripheral nerve affection in patients with hyperlipidemia: a clinical and electrophysiological study

Familial hypercholesterolemia is a common genetic disorder, in its heterozygous form occur in 1:500 of the general population. Peripheral neuropathy has been reported with this disorder, some related it to the use of lipid-lowering agents [statins], others related it to the disease itself. This study was conducted on 3 groups of patients: 1[st] group; 15 patients with familial hypercholesterolemia receiving statins for variable durations, 2[nd] group: 15 newly diagnosed patients with familial hypercholesterolemia not receiving statins, and a 3[rd] group: 15 healthy matching controls. None of the subjects in the 3 groups had any disease causing peripheral neuropathy e.g. diabetes mellitus, renal failure, alcohol abuse... etc. All patients and controls were subjected to nerve conduction studies in both lower limbs; sensory and motor. None of the patients or controls had symptoms or signs of peripheral neuropathy. Electrophysiohgical studies didn't show any abnormalities in 2[nd] group and controls. In patients taking statins, 3 patients had neurophysiological evidence of sensory axonal neuropathy. The results of the present study support the previous reports that statins could be a cause of sensory polyneuropathy. Further investigations are recommended to determine which patient should discontinue statin treatment and identify other treatment options