Serum adipokines and low density lipoprotein subfraction profile in hypopituitary patients with growth hormone deficiency

The aim was to evaluate the concentrations of lipid subfractions in relation to adipokines and metabolic parameters in adult growth hormone (GH)-deficient hypopituitary patients on conventional replacement therapy. The study included 21 GH deficient-hypopituitary patients (age: 36.0 ± 15.1 years, male/female: 7/14) on conventional replacement therapy other than GH and 20 comparable controls (age: 37.3 ± 14.0 years, male/female: 6/14). Lipid subfractions (Lipoprint system), serum adipokine (leptin, adiponectin, resistin) concentrations, body composition, a surrogate marker for insulin resistance (HOMA) and conventional lipid profile were evaluated. No statistically significant difference was found with respect to HOMA, adipokine concentrations and anthropometric parameters between patients and controls except for significantly increased waist-to-hip ratio in hypopituitary group. Total and LDL cholesterol concentrations were significantly higher in the patients. LDL particle size (268.88 ± 3.16 vs. 271.31 ± 3.11 ?, P = 0.151) and small-dense LDL subfraction did not differ significantly. According to logistic regression analysis, triglyceride concentrations ≥1.69 mmol/L was the sole parameter significantly and independently predicted small (<268 ?) LDL particle size (P = 0.019) in the whole group. Increased triglyceride concentrations affect LDL particle size in GH-deficient hypopituitary patients. Small dense LDL seems not directly contribute to atherogenic potential in hypopituitarism.     

Silent brain infarcts: A cause of depression in the elderly?

The present study included 1047 elderly participants. At baseline, brain magnetic resonance imaging (MRI) was performed to detect infarcts and white matter lesions; further, depressive disorders were assessed. Participants were followed up during 3.6 years to determine incident and recurrent depression. We found an increased risk of recurrent depression associated with silent brain infarcts.     

Effects of Glycoprotein IIb/IIIa Inhibition on QT Dispersion in Patients with Unstable Angina and Non-Q-Wave Myocardial Infarction

Acute coronary ischemia augments inhomogeneity in ventricular repolarization, which significantly correlates with ventricular fibrillation. The effects of glycoprotein IIb/IIIa receptor inhibition on QT interval dispersion (QTd), and the effects of QTd changes on in-hospital, 30 day, and long-term cardiac events in patients with unstable angina (UA) and non-Q-wave myocardial infarction (MI) have not been investigated previously. Eighty-three patients presenting with Braunwald class IIIB UA or non-Q-wave MI were randomized to standard therapy (aspirin and unfractionated heparin, 42 patients) or tirofiban therapy: addition to standard therapy (41 patients). QT interval dispersion (QTd) and corrected QTd (QTcd) were measured prior to therapy, and 6, 24, 48, 72, and 96 hours after the initiation of the treatment. In both groups QTd and QTcd were higher than normal limits during the admission, prior to therapy. The first QTd and QTcd were not different between two groups; the remaining values were significantly lower in tirofiban group except the first and last QTd (p values for QTd at 6, 24, 48, 72, and 96 hours are 0.057, 0.045, 0.0006, 0.04, and NS, respectively, and for QTcd, they are 0.017, 0.046, 0.0004, 0.012, and 0.01, respectively). When the first QTd and QTcd compared to the following measurements in each group, the first significant decrease occurred at 6th hour (p = 0.004 for QTd, and 0.004 for QTcd) in tirofiban group, whereas in standard therapy group it was occurred at 48th hour (p = 0.02) for QTd, and 72nd hour (p = 0.019) for QTcd. While the incidence of in-hospital acute MI, recurrent refractory angina, and total major cardiac events were significantly lower in the tirofiban group (p = 0.03, 0.04, and 0.01, respectively) that early QTd recovery observed, the 30 day and long-term incidence of major cardiac events were not different between the two groups. GP IIb/IIIa receptor inhibition in addition to heparin treatment causes a faster recovery of increased QT dispersion, and the early recovery of QTd is associated with a reduction in in-hospital major cardiac events.     

The role of angiotensin converting enzyme genotype in coronary artery ectasia

Coronary artery ectasia (CAE) is characterised by irregular, diffuse, saccular, or fusiform dilatation of the coronary arteries. Although the underlying mechanisms are not fully understood, CAE is considered to be an original form of vascular remodelling in response to atherosclerosis. However, it is not clear why some patients develop CAE while most do not. Experimental data suggest that activation of the renin angiotensin system may lead to an increased inflammatory response in the vessel wall or to an activation of matrix metalloproteinases. In addition, an insertion/deletion (ID) polymorphism of angiotensin converting enzyme (ACE) has been associated with coronary vascular tone and the development of aneurysms. Accordingly, we hypothesised that the gene polymorphism of ACE may be a potential factor influencing the genesis of CAE. We retrospectively evaluated 112 patients who underwent coronary angiography. ACE ID genotype was determined in two groups of patients. Group 1 consisted of 56 patients who were found to have CAE. Group 2 consisted of 56 patients with significant coronary artery disease (CAD) (> 50% stenosis in any of the major epicardial coronary arteries or their branches) but without any evidence of coronary ectasia. Polymerase Chain Reaction (PCR) was used to detect ACE genotype. The ratio of DD genotype was found to be greater in group 1 than group in 2 (39% versus 18%, respectively, P < 0.05). When assessed according to the presence of the I allele, it was greater was greater in group 2 than in group 1 (82.1% versus 60.7%, respectively, P < 0.05). The results indicate that an ACE DD genotype may be a risk factor for CAE.     

The beneficial effects of 18β-glycyrrhetinic acid following oxidative and neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion in a C57BL/J6 mouse model

This study investigated the effects of 18β-glycyrrhetinic acid (GA) on neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. All subjects (n = 40) were equally divided into four groups: (1) sham-operated (SH), (2) I/R, (3) GA, and (4) GA+I/R. The SH group was used as a control. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and the mice were treated with the vehicle for 10 days. In the GA group, mice were given GA (100 mg/kg) for 10 days following a median incision without carotid occlusion. In the GA+I/R group, the I/R model was applied to the mice exactly as in the I/R group, and they were then treated with the same dose of GA for 10 days. Cerebral I/R significantly induced oxidative stress via an increase in lipid peroxidaitons and a decrease in elements of the antioxidant defense systems. However, GA treatment was protective against the oxidative effects of I/R by inducing significant increases in antioxidant defense systems and a significant decrease of lipid peroxidations. Additionally, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue, but these neurodegenerative effects were eliminated by GA treatment. Therefore, the current study demonstrated that GA treatment effectively prevents oxidative and histological damage in the brain caused by global I/R. In this context, GA may be useful for the attenuation of the negative effects of global cerebral I/R and, in the future, it may be a viable and safe alternative treatment for ischemic stroke in humans.     

Mycobacterial infection of intraparenchymal bronchogenic cysts

Bronchogenic cysts (BCs) may rarely cause some interesting and unusual complications. Although infection is a common complication of BCs, there are only two patients with BC infected with mycobacterium in English literature. Two intraparenchymal BCs infected with mycobacterium are presented here as unusual complications. Cystectomy was performed for the cysts. They were given antituberculosis treatment. No complication or recurrences were detected in follow up period.     

Inact?ve hepatitis B surface antigen carriers and intrafamilial tramsmission: results of a 10-year study

Background/Aims

The aims of the present study were to determine the outcomes of inactive hepatitis B virus (HBV) surface antigen (HBsAg) carriers over a 10-year study period and to elucidate the HBV serological profile of their family members.

Methods

We retrospectively analyzed the medical files of inactive HBsAg carriers followed up at the Department of Infectious Diseases of Kocatepe University Medical Faculty Hospital between March 2001 and January 2011.

Results

In total, 438 inactive HBsAg carriers were enrolled in this trial. The follow-up period was 33.7±22.5 months (mean±SD). Anti-hepatitis-B surface antibody seroconversion occurred in 0.7% of cases, while chronic hepatitis B was found in 0.5%. The anti-hepatitis-D virus (HDV) status was evaluated in 400 patients and anti-hepatitis C virus (HCV) in 430. It was found that 1% and 0.2% were positive for anti-HDV and anti-HCV, respectively. HBV serology was investigated in at least 1 family member of 334/438 (76.3%) patients. The HBsAg positivity rate was 34.6% in 625 family members of 334 patients. A comparison of the HBsAg positivity rates in terms of HBV DNA levels in index cases revealed that HBsAg seropositivity rates were higher in family members of HBV DNA-negative patients than in family members of HBV DNA-positive cases (P=0.0001).

Conclusions

The HBsAg positivity rate was higher in family members of inactive HBsAg carriers than in the general population; these family members therefore have a higher risk of HBV transmission. Furthermore, despite negative HBV DNA levels, transmission risk was not reduced in these patients, and horizontal transmission seems to be independent of the HBV DNA value.