Fasting adiponectin in relation to the metabolic syndrome in patients with coronary artery disease

Metabolic syndrome and coronary artery disease [CAD] are increasing worldwide. The relationship between metabolic syndrome and fasting serum adiponectin concentration in CAD patients is not well elucidated. The aim of present study is to explore the relationship between serum adiponectin concentrations and the presence of metabolic syndrome [MetS] among patients with CAD. Sixty five patients with CAD; defined as more than 50% stenosis in any segment by coronary angiography, and twenty five matched controls, were enrolled in this study. The study was carried out in Cardiology Department Assuit University hospital between October 2009 and July 2010. Metabolic syndrome was defined according to International Diabetes Federation criteris. The blood samples including complete blood count, fasting blood glucose, liver function tests, creatinine, urea, adiponectin, high sensitive-C reactive protein [hs-CRP], insulin and lipids profile were obtained after overnight fasting. The homeostatic model assessment of insulin resistance [HOMA-IR] was calculated as: HOMA-IR = fasting blood glucose [mmol/l] x fasting serum insulin [micro U/ml]/22.5. Patients with CAD had significantly lower plasma adiponectin concentrations than those without CAD [P<0.013] and higher hs-CRP [P<0.009] and HOMA-IR [P<0.03]. Metabolic syndrome was present in 41 patients [63%] among CAD group. Fasting adiponectin values for these patients tended to decrease significantly in comparison to patients without metabolic syndrome [P value= 0.037]. Negative correlations were found between adiponectin and body mass index [BMI] [r=-0.205, P<0.05], waist circumference [WC] [r= -0.306, P<0.003], triglycerides [r= -0.222, P < 0.036] and hs-CRP [r= -0.223, P< 0.035] whereas a positive correlation was found between adiponectin and HDL [r= 0.273, P<0.003]. Also, adiponectin was significantly lower in patients with multi-vessel disease compared to other [P<0.05] whereas hs-CRP and HOMA-IR were significantly higher in patients with multi-vessel disease with [P<0.01 and 0.03] respectively. Serum adiponectin concentration is inversely correlated with metabolic syndrome among patients with CAD. Lower adiponectin concentration, and higher HOMA-IR and hs-CRP are associated with Cad and metabolic syndrome, and may be useful for risk stratification of CAD patients. The measurement of plasma adiponectin, HOMA-IR and hs-CRP levels may be useful for prediction of severity of coronary artery disease

Can serum fibrosis markers predict medium/large oesophageal varices in patients with liver cirrhosis?

Non-invasive predictors of medium/large oesophageal varices [LOVs] could reduce the number of screening endoscopies. As portal hypertension is a consequence of liver fibrosis, serum fibrosis markers were evaluated together with other variables as possible non-invasive predictors of medium OV/LOV. A total of 154 cirrhotic patients with splenomegaly and 30 healthy control subjects were recruited in a prospective study in two gastroenterology centres in Upper Egypt. Clinical parameters assessed included Child-Pugh class, liver size and ascites. Laboratory parameters included complete blood count, liver function tests, and aspartate aminotransferase [AST]/platelet ratio. Transforming growth factor-p! [TGF-beta [1]], alpha2 macro globulin [A[2]M] and hyaluronic acid [HA] were assayed. Ultraso-nographic examination was done for assessment of liver span, portal vein diameter and detection of minimal ascites. Oesophageal varices were diagnosed and graded by oesophagogastroduodenoscopy. Fifty-four patients [35%] had no or small varices and 100 [65%] patients had medium OV/LOV by endoscopy. On multivariate analysis, the independent predictors of medium OV/LOV were the presence of ascites [beta = 0.258, p = 0.047] and serum HA [beta = 0.449, p = 0.009]. The receiver operating characteristic curve for HA showed the area under the curve to be 0.916. The sensitivity, specificity, positive and negative predictive values and diagnostic accuracy of HA at a cut-off value of 207 micro g T[1] were 94%, 77.8%, 88.7%, 87.5% and 88.3%, respectively. The presence of ascites and serum HA level higher than 207 micro g T[1] can predict the presence of medium OV/LOV in cirrhotic patients. This would help physicians to identify patients who would most likely benefit from screening endoscopy and thus, reduce costs and discomfort from unnecessary endoscopic procedures

Interferon-gamma, immunoglobulin-E and vascular endothelial growth factor in children with papular urticaria

Papular urticaria [PU] is a common childhood disorder. It is a chronic allergic disease caused by insect bites. Both immediate and delayed type hypersensitivity reactions could be involved in the pathogenesis of PU. The immediate reaction is responsible for the immunoglobulin-E [IgE] response supported by T-helper 2 [Th2] cells while the delayed reaction is mediated by Thl cytokines particularly interferon-gamma [IFN-alpha]. Mast cells which are effector cells of IgE-mediated immune responses, can release vascular endothelial growth factor [VEGF] after IgE-dependant activation. VEGF was reported to play a role in the pathogenesis of many allergic conditions. This study included 28 children with papular urticaria and 15 age and sex-matched healthy controls. The age of the patients ranged from 2 to 7 years [mean, 3.5 years]. The duration of PU ranged from 3 months to 4 years. IFN-alpha, IgE and VEGF levels were quantitatively determined in serum of patients and controls by Enzyme Linked Immuno-Sorbent Assays [ELISA]. Children with papular urticaria showed significantly elevated serum levels of IFN-alpha, IgE and VEGF compared to healthy controls [p<0.05, p<0.001 and p<0.001 respectively]. A significant positive correlation was demonstrated between serum levels of IFN-y and IgE in children with papular urticaria [r-= 0.941, p<0.01]. Papular urticaria could be mediated by a complex immune response involving more than one mechanism, with evidence for both Thl response [increased production of IFN-alpha] and Th2 response [increased production of IgE] with a possible role for VEGF

Significance of antikeratin antibodies in discrimination between rheumatoid arthritis and polyarthritis associated with hepatitis C infection

Hepatitis C virus [HCV] injection is often associated with extrahepatic manifestations among which arthropathy is common. HCV-related arthritis commonly present as rheumatoid-like arthritis, with positive rheumatoid factor [RF]. In this study, we try to distinguish between rheumatoid arthritis [RA] and polyarthritis associated with HCV infection using a marker more specific to RA than the rheumatoid factor [RF] namely anitkeratin antibody [AKA]. Serum AKAs were evaluated [by indirect immunofluorescence technique] in two groups of patients ,all were RF seropositive. Group I. 25 patients with HCV associated polyarthralgia or arthritis. Group II: 25 patients with RA fulfilling the American college of Rheumatology [ACR] revised criteria. In addition 15 healthy individuals served as controls. All patients of group II as well as healthy controls were HCV seronegative. Other investigations were done for all groups such as erythrocyte sedimentation rate [ESR], C reactive protein [CRP] and antinuclear antibody [ANA]. Plain X ray of both hands were done for all patients to exclude the patients with bone erosion. The study revealed that anitkeratin antibodies were detected in 15/25 [60%] patients with true RA and only 3/25[12%] patients with HCV-related arthritis. AKA were not found in the sera of the healthy controls. The specificity and sensitivity of AKA in RA group were 88% and 60% respectively. Anitkeratin antibody is highly specific for RA and its estimation may increase the diagnostic performance of RA. AKA is a useful marker in discrimination between patients with true RA and those with HCV-associated arthritis

Leptin in obesity and type II diabetes mellitus: the merit of molecular methods in understanding pathogenesis

Leptin, the obese [OB] gene product, is a cytokine-like hormone that plays an important role in energy homeostasis. Mutation of OB in mice results in profound obesity and type II diabetes as part of a syndrome that resembles morbid obesity in humans. This work was done to evaluate the importance of leptin in the pathogenesis of obesity, to study the relationship between serum leptin level and type II diabetes mellitus, and to compare molecular methods versus conventional serum leptin measurements in this respect. The study was done on 34 obese non diabetic patients, 61 non-insulin dependent diabetic patients [NIDDM], and 15 healthy volunteers as controls. Special investigations included serum leptin, insulin, C-peptide, cortisol, and growth hormone. Expression of leptin and leptin receptor were examined by RT-PCR in fat tissues of lipectomy samples from obese subjects. The results of this study revealed that there was significant elevation in leptin level in both obese and diabetic groups compared to controls. There was significant reduction in insulin levels in obese group compared to control group and a significant elevation in C-peptide level in diabetic non-obese group compared to control group. Serum leptin levels showed different patterns in cases of obesity ranging from low or normal to high leptin levels, which cannot by itself explain the cause of obesity. Leptin mRNA was expressed in 66.2% of cases and undetectable in 33.8% of cases. One sample showed longer than expected leptin amplicon. On the other hand, leptin receptor mRNA was detectable in 29.3% and undetectable in 70.7% of samples. This work shows that both NIDDM and obesity are two linked clinical situations in the sense that either of them seems to predispose to the other. Obese have significantly higher mean levels of serum glucose and lower levels of serum insulin and have tendency for developing diabetes. On the other hand, diabetics have higher BMI and have tendency for developing obesity. Serum leptin alone is not enough to explain the pathogenesis of obesity, but molecular methods for measuring both leptin and leptin receptor expressions might be important to explain the pathogenesis of obesity in some cases with hyperleptinemia