Investigation of a possible association between refractory iron deficiency anaemia to an underlying remote helicobacter pylori infection

Helicobacter pylon is a bacterial infection accounts as the prevalent gastric pathogen. Helicobacter has been associated with many extradigestive disorders, as refractory iron deficiency anaemia [Sideropenic]. The aim of this case control study was to investigate the role of remote Helicobacter pylon infection in refractory iron deficiency anaemia [RIDA]; together with comparing two different methods for diagnosis of Helicobacter pylon infection. The study was conducted on thirty patients proved refractory IDA by therapeutic trial. Thirty normal non anaemic subjects were included as controls. Helicobacter pylon testing included stool antigen and Helicobacter pylon PCR. The Helicobacter pylon stool antigen test revealed 12 positive cases out of 30 IDA cases. Five of them were stool PCR cagA positive and four were stool PCR ureC positive. There was 100% agreement between PCR cagA and the stool antigen test in the detection of Helicobacter pylon infection [p=0.003]. Stool PCR cagA had a diagnostic accuracy of 76.67 and likelihood ratio of 3.57. There was 100% agreement between PCR ureC and the stool antigen test in the detection of Helicobacter pylon infection [p=0.009]. Stool FCR ureC had a diagnostic accuracy of 73.33 and likelihood ratio of 3.25. There was a very highly significant difference between the mean 3 of serum ferritin, serum iron, TIBC and transferrin saturation of Helicobacter pylon stool antigen positive and negative subjects [p<0.001]. Conclusion: There was a very highly significant association between Helicobacter pylon infection and refractory iron deficiency anaemia. Serum ferritin levels were significantly lower in Helicobacter pylon stool antigen positive cases than in negative cases [p< 0.001]. Helicobacter pylon positive cases were 2.7 times more likely to develop anaemia than negative cases. The Heticobacterpyioni stool antigen testing by ELISA proved to be more reliable compared to the stool PCR which is tedious and time consuming

Eotaxin and other immunological markers, metabolic and anthropometric factors in relation to circulating adiponectin level in type 2 diabetic patients and individuals with impaired glucose metabolism

Hypoadiponectinemia is associated with insulin resistance and predicts the incidence of type 2 diabetes and coronary artery disease. Chronic subclinical inflammation and activation of innate immunity are involved in the pathogenesis of type 2 diabetes. Since obesity is associated with hypoadiponectinemia and with increased circulating levels of various immunological markers, which are both major risk factors for the development of type 2 diabetes, so the aim of this study was to investigate the association of hypoadiponectinemia and low grade systemic inflammation in type 2 diabetic patients as well as subjects with impaired glucose tolerance. Sixty male age matched subjects were included in the study. They were divided into 3 groups each of twenty as follows: newly diagnosed patients with type 2 diabetes mellitus [group I], patients with impaired glucose tolerance [group II] and healthy subjects with normal glucose tolerance [group Ill] as a control group. Patients and controls were subjected to full history taking, clinical examination stressing on blood pressure, BMI and WHR; laboratory investigations including FPG, PPG, HbA1C, fasting insulin and HOMA-IR index, lipid profile [TG, total cholesterol, HDL-C, LDL-C], serum uric acid, serum adiponectin and some immunological markers including WBC, acute phase reactants [CRP], TN F-alpha and eotaxin. In type 2 diabetic patients, plasma adiponectin levels were strongly negatively correlated with CRP, fasting TG, fasting insulin, HOMA-IR and fasting glucose [P < 0.001] and strongly positively correlated with HDL-cholesterol [P < 0.001]. Inverse correlations were found between adiponectin levels and WHR, postprandial glucose, and TNF-alpha [P < 0.05]. No significant correlation was found between adiponectin level and eotaxin [P > 0.05]. In subjects with IGT, an inverse relation was found between adiponectin and fasting glucose [P < 0.05]. The mean values of immunological markers [eotaxin, TNF-alpha, CRP and WBC] were significantly higher in type 2 diabetics versus control group. Subjects with IGT showed significant lower levels of eotaxin and TNF-alpha than diabetic patients, while they showed significant higher levels of eotaxin, TN F-alpha and CRP than controls [P < 0.05]. The mean value of adiponectin was significantly lower in type 2 diabetic patients than in subjects with IGT and the control group [P < 0.05]. The studied clinical and anthropometric parameters, lipid profile, parameters of glycemic control, fasting insulin and HOMA-IR were significantly higher in group I versus group II and the control group [P < 0.05]. Our results support the hypothesis that hypoadiponectinemia may be associated with low grade inflammation, metabolic abnormalities and dyslipidemia. Therefore, adiponectin may be an important link between inflammation and type 2 diabetes as it was negatively correlated with markers of inflammation in such patients

Study of plasma visfatin level in women with gestational diabetes mellitus during and after pregnancy and its relation to insulin sensitivity

The insulin-mimetic adipocytokine visfatin is highly expressed in visceral fat and whose blood levels correlate with obesity. It lowers blood glucose, improves insulin sensitivity, and recently found to act as an insulin analogue on the insulin receptors. It has been associated with insulin resistance in some studies and regulated by glucose. To evaluate the role of visfatin in GDM, typically associated with increased insulin resistance, we determined visfatin levels in women with GDM and in healthy pregnant controls. Furthermore, visfatin concentrations were investigated after delivery in a subgroup of women with GDM. 30 women with GDM [group I] and 15 age-matched healthy pregnant controls [group II] at 24-28 weeks of gestation were included in the study. All women were subjected to full history taking, complete physical examination and anthropometric measures including BMI and WHR. Venous blood samples for lipid profile, glucose, insulin and visfatin concentrations were taken 1 hour before a standard 75g OGTT and was carried out after overnight fast. Venous blood samples were repeated for glucose, insulin and visfatin 30, 60, 120 minutes after an oral glucose load. Insulin sensitivity was estimated using ISI derived from OGTT. A subgroup of 15 women with GDM [group III] was investigated for all these parameters 2 weeks after delivery. Fasting plasma visfatin concentrations were significantly higher in the gestational diabetes mellitus group during the course of pregnancy [69.04 +/- 18.41 ng/ml] than in healthy pregnant control group [31.22 +/- 24.74 ng/ml] [P<0.05]. The fasting plasma levels of visfatin showed significant drop in GDM women 2 weeks after labour [45.86 +/- 6.89 ng/ml] than during the course of pregnancy [69.04 +/- 18.41 ng/dl] [P<0.05]. The glucose-induced changes in visfatin and insulin calculated by AUC were significantly higher in GDM group during pregnancy than in healthy normal controls. The mean values of the area under the curve for glucose, insulin and visfatin curves showed significant reduction in GDM women 2 weeks after labour [P<0.05]. Significant positive correlations were detected between fasting visfatin and WHR, fasting glucose, as well as fasting insulin in GOM women during pregnancy and 2 weeks after labour. Fasting visfatin levels were negatively and significantly correlated with peripheral insulin sensitivity index in the three studied groups [P<0.05]. The precise significance of our findings indicates that adipocytokine visfatin may play a role in the pathogenesis of gestational diabetes mellitus. However, the study of the regulation of visfatin in GDM merits further considerations and further experiments are needed to clarify its role in such disease