Our results suggest that reduced PON1 activity may be related to increased oxidant and decreased antioxidant levels. These data indicated that oxidant/antioxidant imbalance may play a role in the etiopathogenesis of AA.

Deficiency of vitamin B12 should be considered in the differential diagnosis of infants who present with skin and mucosal lesions.

Background. Several reports have demonstrated an association between psoriasis and cardiovascular diseases. P wave dispersion (PWD) is the most important electrocardiographic (ECG) markers used to evaluate the risk of atrial arrhythmias. QT dispersion (QTD) can be used to assess homogeneity of cardiac repolarization and may be a risk for ventricular arrhythmias. Aim. To search PWD and QTD in patients with psoriasis. Methods. Ninety-four outpatient psoriasis patients and 51 healthy people were evaluated by physical examination, 12-lead ECG, and transthoracic echocardiography. Severity of the psoriasis was evaluated by psoriasis area and severity index (PASI). Results. Mean disease duration was 129.4 ± 83.9 (range, 3–360) months and PASI ranged from 0 to 34.0 (mean ± SD; 7.6 ± 6.7). Compared to control group, psoriatic patients had significantly shorter Pmax and Pmin durations, longer QTcmax, and greater PWD and QTcD. Transmitral deceleration time (DT) and isovolumetric relaxation time (IVRT) were significantly longer among psoriasis patients. QTcD and PWD were significantly correlated with disease duration (r = 0.693, P < 0.001, and r = 0.368, P = 0.003, resp.). Conclusions. In this study, we found that both PWD and QTcD are increased in psoriasis patients compared to healthy subjects. In addition, they had longer DT and IVRT.

Our results indicate that RAS is associated with decreased PON1 activity and increased oxidative stress that plays a crucial role in the pathogenesis of RAS. Further studies on a larger number of patients are needed to verify these results.

The aim of this study was to determine possible protective influences of selenium (Se), N-acetylcysteine (NAC), and vitamin E (Vit E) against acute ethanol (EtOH) intoxication. Thirty-six rats were divided into six groups: I (control), II (EtOH), III (EtOH + Se), IV (EtOH + Vit E), V (EtOH + NAC), and VI (EtOH + mix). Except group I, EtOH was given the other pretreated (groups III, IV, V, and VI) and untreated groups (group II). Compared with the EtOH group, serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, creatine kinase, and creatine kinase-MB levels were significantly decreased in all pretreated groups, whereas slightly diminished amylase and lipase were observed. Compared with the control group, a remarkably lower total antioxidant status (TAS), but higher total oxidant status (TOS), and oxidative stress index (OSI) were seen in brain, liver, and kidney tissues. The values of these parameters were less affected from EtOH-exposed brain tissue of EtOH + NAC and liver of EtOH + mix groups. Both significant decrease of catalase activity and marked increases of adenosine deaminase and myeloperoxidase were determined only in liver tissue of the EtOH group. Activities of these enzymes were restored in almost all pretreated groups. Moreover, an increase of xanthine oxidase activity was prevented in brain tissue of pretreated groups. In histopathological examination of the liver, hydropic degeneration, sinusoidal dilatation, mononuclear cell infiltration, and marked congestion, which were seen in the EtOH group, were prevented in all pretreated groups. Relative protection against acute EtOH toxicity, in both single and combined pretreatments of Se, NAC, and Vit E supplementation, was probably through antioxidant and free radical-neutralizing effects of foregoing materials.