Saccharomyces boulardii CNCM I-745 reduces the duration of diarrhoea, length of emergency care and hospital stay in children with acute diarrhoea.

Evidence from the literature has shown that Saccharomyces boulardii provides a clinically significant benefit in the treatment of acute infectious diarrhoea in children. In this multicentre, randomised, prospective, controlled, single blind clinical trial performed in children with acute watery diarrhoea, we aimed to evaluate the impact of S. boulardii CNCM I-745 in hospitalised children, in children requiring emergency care unit (ECU) stay and in outpatient settings. The primary endpoint was the duration of diarrhoea (in hours). Secondary outcome measures were duration of hospitalisation and diarrhoea at the 3(rd) day of intervention. In the whole study group (363 children), the duration of diarrhoea was approximately 24 h shorter in the S. boulardii group (75.4±33.1 vs 99.8±32.5 h, P<0.001). The effect of S. boulardii (diarrhoea-free children) was observed starting at 48 h. After 72 h, only 27.3% of the children receiving probiotic still had watery diarrhoea, in contrast to 48.5% in the control group (P<0.001). The duration of diarrhoea was significantly reduced in the probiotic group in hospital, ECU and outpatient settings (P<0.001, P<0.01 and P<0.001, respectively). The percentage of diarrhoea-free children was significantly larger after 48 and 72 h in all settings. The mean length of hospital stay was shorter with more than 36 h difference in the S. boulardii group (4.60±1.72 vs 6.12±1.71 days, P<0.001). The mean length of ECU stay was shorter with more than 19 h difference in the probiotic group (1.20±0.4 vs 2.0±0.3 days, P<0.001). No adverse effects related to the probiotic were noted. Because treatment can shorten the duration of diarrhoea and reduce the length of ECU and hospital stay, there is likely a social and economic benefit of S. boulardii CNCM I-745 in adjunction to oral rehydration solution in acute infectious gastroenteritis in children.

The evaluation of cord blood interleukin-1ß levels in normal and caesarean deliveries.

OBJECTIVE: The aim of this prospective study was to establish the cord blood interleukin 1ß (IL-1ß) levels and asphyxia enzymes in term newborns and their relationship between delivery modes. We investigated whether cord blood level of IL-1ß could be used as a reliable marker for detecting hypoxic stress and to determine the optimal cut-off level for IL-1ß. METHODS: The study was designed prospectively. Cord blood samples were obtained at the time of delivery from 75 noninfected full-term neonates for the purpose of measuring cord blood levels of IL-1ß. Women were classified into three groups according to the mode of delivery (20 vaginal delivery, 29 urgent caesarean section (with foetal distress) and 26 elective caesarean section). All cases were followed-up by hospitalization. Umbilical cord sampling was carried out for IL-1ß, umbilical artery gas parameters and other asphyxia enzymes at the time of delivery. Cord blood IL-1ß was measured by enzyme-linked immunosorbent assay. The perinatal outcomes of the cases were recorded after birth. Demographic characteristics, neonatal outcomes and laboratory findings were compared in all the three groups. RESULTS: IL-1ß levels showed statistically significant difference between groups (p < 0.01). The relationship was found between IL-1ß cord blood levels and the mode of delivery. IL-1ß levels of urgent caesarean section group were significantly higher than elective caesarean section and normal delivery group (p:0.001 and p:0.001, respectively). Normal delivery levels were significantly higher than the elective caesarean group (p:0.001). CONCLUSION: Urgent section (foetal distress) and vaginal delivery (labour) were each associated with elevated IL-1ß cord blood levels in noninfected full-term neonates, while only elective caesarean section was associated with decreased IL-1ß levels. For the evaluation of newborns at high risk for perinatal hypoxic stress, cord blood IL-1ß levels may lead the way. On the other hand, the mode of delivery may be associated with the effects on the immune system. Further investigations with larger patient groups are required to confirm our results.

N-acetylcysteine prevents doxorubucine-induced cardiotoxicity in rats.

This study is designed to observe the effects of N-acetylcysteine (NAC) on doxorubucine-induced cardiac toxicity in rats both histologically and biochemically. Totally 32 rats divided equally into four groups were studied. The first group received only 200 mg/kg NAC intraperitoneal (i.p.) once every 24 h for 5 days (group 1); the second group received 20 mg/kg doxorubucine (DOX) i.p. single dose plus NAC 200 mg/kg i.p. once every 24 h for 5 days (group 2); the third group received DOX 20 mg/kg DOX i.p. single dose (group 3) and the fourth group, which is also the control group, received saline (group 4). Following 24 h of the final dose, blood samples were drawn from a portal vein and heart tissue were obtained. Tissue thiobarbituric acid reactive substance (TBARS) and nitric oxide (NO) levels were highest in the DOX group. In the DOX-treated rats, serum TBARS, NO, aspartate transaminase, lactate dehydrogenase and creatine kinase levels were highest when compared with other groups. Except for serum superoxide dismutase levels, all other parameters differed significantly between the DOX plus NAC group and the DOX group. In the DOX plus NAC group, general architecture was preserved better than the DOX group and myofibril loss was minimal compared with the DOX group. NAC demonstrated, both biochemically and histologically, to be effective in the prevention of DOX-induced cardiotoxicity in rat models. Evaluation of NAC's effect on DOX toxicity warrants further clinical trials on cancer patients.

The scintigraphic evaluation and genetic correlation of joint involvements in pediatric patients with familial Mediterranean fever.

PURPOSE: We aimed to evaluate the articular involvements in pediatric patients with familial Mediterranean fever (FMF) with joint symptoms by bone scintigraphy and to correlate the involved joints with the gene mutations. MATERIALS AND METHODS: A total of 41 newly diagnosed patients in pediatric age group (28 girls and 13 boys; mean age 9.14 ± 2.91 years) with joint involvement symptoms were included in this study. Scintigraphic images were obtained at 5th min (blood pool or early phase) and starting at 3 h (late phase) after (after tracer injection) intravenous administration of technetium-99m (99mTc)-methylendiphosphonate (MDP). Genomic DNA was isolated from leukocytes using standard salting out procedure. The sequencing data were analyzed. RESULTS: Of the 41 patients, arthritis was found in 21 (51.2%) patients. Of the 21 patients, there was single joint involvement in 15 (71.4%) patients and multiple joint involvement in six (28.6%) patients. The mean age of patients with joint involvement (8 ± 2.3 years) were considerably lower than the patients without joint involvement (10.35 ± 3.04 years), and this was statistically significant (p = 0.008). The most commonly involved joints were ankles and knees. Multiple joint involvements were most frequently observed in the M694V and M694I gene mutations (16.7%). CONCLUSIONS: We use and recommend the bone scintigraphy in patients with FMF to determine the presence and distribution of arthritis, since bone scintigraphy is inexpensive, noninvasive, easy-to-use, and also is more sensitive in the diagnosis and distribution of arthritis than conventional radiological methods and clinical examination.

Protective effects of thymoquinone on vancomycin-induced nephrotoxicity in rats.

AIM: Oxidative stress has been implicated as a potential responsible mechanism in the pathogenesis of vancomycin (VCM)-induced renal toxicity. Therefore, we aimed to investigate the protective effect of thymoquinone (TQ) against VCM-induced nephrotoxicity by tissue oxidant/antioxidant parameters and histological changes in rats. MATERIALS AND METHODS: Wistar albino rats were randomly separated into four groups consisting of seven rats per group. The groups had normal saline (control group), VCM, VCM and TQ and TQ, respectively. VCM was injected intraperitoneally at a dose of 200 mg/kg and continued at 12-h intervals for 7 days. TQ was injected intraperitoneally at a dose of 10 mg/kg and continued at 24 h intervals for 8 days. Animals were killed and blood samples were analyzed for the levels of serum blood urea nitrogen (BUN) and creatinine (Cr). Kidney specimens were analyzed for levels of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as well as for histopathological changes. RESULTS: We found that the levels of serum BUN, Cr and kidney tissue MDA were increased in the VCM group. Activities of SOD and GSH-Px in kidney tissue were decreased. TQ administration ameliorated significantly these changes. CONCLUSION: These results indicate that the TQ produces a protective mechanism against VCM-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.

Effects of erdosteine on hemostasis: an experimental study.

AIM: In this study, the effects of erdosteine (ED) on the platelet function and coagulation were investigated in adult rats. MATERIALS AND METHOD: Twenty-eight male Wistar albino rats were divided into four groups. The control rats in group I (n = 7) were given only 0.5 cc of normal saline daily through oral gavage. Group II (n = 7) rats were administered 3 mg/kg ED through oral gavage for 3 days; while group III (n = 7) rats were given 10 mg/kg ED through oral gavage for 3 days; and group IV (n = 7) rats were administered 30 mg/kg ED through oral gavage for 3 days. Prothrombin time (PT), activated prothromboplastin time (aPTT), international normalized ratio (INR), coagulation factors and complete blood counts were measured from the blood drawn. RESULTS: There were a lot of differences between ED groups and control group, and among ED groups. The found differences were level of PT, aPTT, INR, coagulation factors, and number of platelets. DISCUSSION: We consider that ED which is used as a mucolytic agent in child clinics may affect hemostasis and coagulation in a dose-dependent manner. ED should be used carefully by the patients with coagulation disorders, since there is no information available in the package insert and literature screening regarding the effect of ED.

Effects of erdosteine on cyclosporin-A-induced nephrotoxicity.

AIM: In cyclosporin-A (CsA)-induced toxicity, oxidative stress has been implicated as a potential responsible mechanism. Therefore, we aimed to investigate the protective role of erdosteine against CsA-induced nephrotoxicity in terms of tissue oxidant/antioxidant parameters and light microscopy in rats. MATERIALS AND METHODS: Wistar albino rats were randomly separated into four groups. Group 1 rats treated with sodium chloride served as the control, group 2 rats were treated with CsA, group 3 with CsA plus erdosteine, and group 4 with erdosteine alone. Animals were killed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), uric acid (UA), total protein (TP), and albumin (ALB) levels. Kidney sections were analyzed for malondialdehyde (MDA) and nitric oxide (NO) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as for histopathological changes. RESULTS: In the CsA group, MDA, GSH-Px, BUN, and Cr levels were increased. The TP and ALB levels were decreased. These changes had been improved by erdosteine administration. Other biochemical parameters did not show any significant change. CONCLUSION: These results indicate that erdosteine produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.