No abstract

Background/Aims: Data about the effects of inflammatory bowel disease (IBD) on various functions of the nervous and cardiovascular systems are limited. In this study, the visual neuronal and cardiovascular functions of patients with IBD were evaluated by measuring visual evoked potentials (VEP) and pulse wave velocity (PWV), respectively. Materials and Methods: There were three study groups: the Crohn's disease (CD) group (n=25), the ulcerative colitis (UC) group (n=30), and a healthy control (C) group (n=25). The exclusion criteria were as follows: patients with IBD were in remission, had no extra-intestinal manifestations of the disease, had no additional chronic disease(s), and had been receiving medical treatment for their IBD without any previous surgical intervention. VEP amplitudes (mV) and the N2 and P2 latencies (ms) were recorded for visual-neuronal analysis of all study groups. For cardiovascular assessment in all study groups, PWV was measured noninvasively as follows: the carotid-femoral PWV with the Complior Colson device (The authors have no conflict of interest.) and the PWV along the aorta with two ultrasound strain-gauge pressure-sensitive transducers (TY-306 Fukuda pressure-sensitive transducers -Fukuda Denshi Co, Tokyo, Japan) fixed transcutaneously over the course of a pair of arteries separated by a known distance. The right femoral and right common carotid arteries were the ones used. Results: The PWV levels of the CD and UC groups were significantly higher than those in the C group (p<0.001). In the bilateral recording of the VEP, the N2 latencies of the CD (p<0.05) and UC (p<0.01) groups were significantly longer than those in the C group. Conclusion: In this study, we showed vascular and visual neuronal impairments at a subclinical stage in patients with both types of IBD.

Clinoptilolite administration reduces oxidant activity and supports antioxidant response after partial hepatectomy.

This study was designed to investigate the effects of iron supplementation on the parameters of oxidative stress in the skeletal muscle tissue of hyperthyroidism induced rats. Hyperthyroidism was found to cause an increase in thiobarbituric acid-reactive substances (TBARS) and copper zinc superoxide dismutase (Cu, Zn SOD) activity, but decreases in the glutathione-peroxidase (GSH Px) activity and glutathione (GSH). Iron supplementation caused an increase in TBARS and a decrease in GSH. Iron supplementation in hyperthyroid rats attenuated the hyperthyroid state, but lowered the plasma ferritin level, which is considered an indicator of thyroid hormone action. Iron supplementation caused no additional increase in the TBARS in hyperthyroid rats, ameliorated the decrease in GSH content and abolished the induction of Cu, Zn SOD. Our findings suggested no increase, but a decrease, in the risk of oxidative stress in iron supplemented hyperthyroid rats. Whether supplementation of iron would have similar effects in humans should be further investigated in clinical studies.