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Background Tranexamic acid reduces surgical bleeding and reduces death due to bleeding in patients with trauma. Meta-analyses of small trials show that tranexamic acid might decrease deaths from gastrointestinal bleeding. We aimed to assess the effects of tranexamic acid in patients with gastrointestinal bleeding. Methods We did an international, multicentre, randomised, placebo-controlled trial in 164 hospitals in 15 countries. Patients were enrolled if the responsible clinician was uncertain whether to use tranexamic acid, were aged above the minimum age considered an adult in their country (either aged 16 years and older or aged 18 years and older), and had significant (defined as at risk of bleeding to death) upper or lower gastrointestinal bleeding. Patients were randomly assigned by selection of a numbered treatment pack from a box containing eight packs that were identical apart from the pack number. Patients received either a loading dose of 1 g tranexamic acid, which was added to 100 mL infusion bag of 0•9% sodium chloride and infused by slow intravenous injection over 10 min, followed by a maintenance dose of 3 g tranexamic acid added to 1 L of any isotonic intravenous solution and infused at 125 mg/h for 24 h, or placebo (sodium chloride 0•9%). Patients, caregivers, and those assessing outcomes were masked to allocation. The primary outcome was death due to bleeding within 5 days of randomisation; analysis excluded patients who received neither dose of the allocated treatment and those for whom outcome data on death were unavailable. This trial was registered with Current Controlled Trials, ISRCTN11225767, and ClinicalTrials.gov, NCT01658124.

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Th e kidney, which is an integral part of the drug excretion system, was reported as one of the targets of cadmium toxicity. Early events of cadmium toxicity in the cell include a decrease in cell membrane fl uidity, breakdown of its integrity, and impairment of its repair mechanisms. Phosphatidylcholine and vitamin E have a marked fl uidizing eff ect on cellular membranes. We hypothesized that Livolin forte® (LIV) could attenuate kidney damage induced by cadmium in rats. Twenty-fi ve adult male Wistar rats were divided into fi ve groups of fi ve rats each: group I (control group) received 0.3 ml/kg/day of propylene glycol for six weeks; group II was given 5 mg/kg/day of cadmium (Cd) i.p for 5 consecutive days; group III rats were treated in a similar way as group II but were allowed a recovery period of 4 weeks; group IV was treated with LIV (5.2 mg/kg/day) for a period of 4 weeks after inducing renal injury with Cd similarly to group II; and group V was allowed a recovery period of 2 weeks after a 4-week LIV treatment (5.2 mg/kg/day) following Cd administration. A significant increase in plasma creatinine, urea, uric acid, and TBARS were observed in groups II and III compared to the control rats. Signifi cant reductions in total protein, glucose, and GSH activity were also recorded. Th e urine concentrations of creatinine, urea, and uric acid in groups II and III were signifi cantly lower than the control group. Th is fi nding was accompanied by a signifi cant decrease in creatinine and urea clearance. Post-treatment with LIV caused signifi cant decreases in plasma creatinine, urea, uric acid, and TBARS. Signifi cant increases in total protein, glucose, and GSH activity of groups IV and V were observed compared to group II. A signifi cant increase in urine concentrations of creatinine, urea, and uric acid and signifi cant decreases in total protein, glucose, and GSH activity were observed in groups IV and V compared to group II. Photomicrographs of the rat kidneys in groups IV and V showed an improvement in the histology of their renal tissue when compared to group II, with features similar to the control rats. Additionally, group III showed an improvement in the histoarchitecture of the kidney compared with group II, although occasional atrophy of some glomeruli and shrinking of renal corpuscles was observed.

Objective: Livolin forte ® (LIV) is a hepatoprotective drug that is being used in hospitals worldwide in the treatment and management of liver diseases. However, as it appear through the available published literature, the physiological effects of the drug on the liver using a rat model of hepatotoxicity is not yet well established. This study assessed the curative and prophylactic effects of LIV on carbon tetrachloride (CCl4) induced liver damage in rats. Methods: Twenty-four adult Wistar rats were randomly divided into four groups: group I (normal control) received 0.3 ml/kg/day of propylene glycol for one month; group II (toxicant control) was given 0.7 ml/kg/day of CCl4 dissolved in olive oil (1:1, v/v) orally for 7 days; group III received 5.2 mg/kg/day of LIV for one month followed by CCl4 for one week; group IV received CCl4 for one week and subsequently LIV (5.2 mg/kg/day) was administered for one month. Half of the rats were sacrificed one day after the last treatment, the other half after a 2-week recovery period. Results: The toxicant control group had significantly higher AST and ALT activities, total bilirubin and lower total protein and GSH levels compared to the normal control rats. Similarly, significant increase in serum activities of AST and ALT were observed in group III compared to the normal control rats a day after the last treatment with CCl4, whereas after the recovery period no significant differences were observed in nearly all the parameters. Moreover, group IV showed no significant differences in the parameters mentioned above compared to the normal control rats a day after the last treatment with LIV and after the recovery period. Conclusion: The results of this study indicated that LIV was better as a curative agent rather than a prophylactic agent in rats.