Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. Use of tamsulosin in patients with urinary calculi to increase spontaneous stone passage.

A short cut review was carried out to establish whether tamsulosin enhances the chances of spontaneous stone expulsion in renal colic. Thirty-five papers were found using the reported searches, of which two (a meta-analysis and one further randomised controlled trial) presented the best evidence to answer the clinical question. The author, date and country of publication, patient group studied, study type, relevant outcomes, results and study weaknesses of these papers are presented in table 3. It is concluded tamsulosin may be useful during periods of watchful waiting to enhance ureteric stone expulsion.

Anticoagulants prevent monocrotaline-induced hepatic parenchymal cell injury but not endothelial cell injury in the rat.

Monocrotaline (MCT) is a pyrrolizidine alkaloid plant toxin that produces hepatotoxicity in humans and animals. Human exposure to MCT occurs through consumption of contaminated grains and herbal medicines. Administration of MCT to rats stimulates activation of the coagulation system and fibrin deposition in the liver. Fibrin deposition occurs simultaneously with endothelial cell damage and prior to hepatic parenchymal cell injury. Accordingly, the hypothesis that activation of the coagulation system is required for MCT-induced liver injury was tested. Treatment of rats with either heparin or warfarin significantly reduced MCT-induced activation of the coagulation system and the increase in alanine aminotransferase activity in the plasma, a biomarker of hepatic parenchymal cell injury. Histopathological examination of liver sections revealed that heparin decreased parenchymal cell necrosis but did not affect central venular endothelial cell damage, congestion and dilation of the sinusoids, or hemorrhage in the liver. Morphometric analysis revealed that 28% of the area of livers from MCT-treated rats contained regions of coagulative necrosis, whereas less than 5% of the area of livers from rats treated with MCT and heparin contained these regions. By contrast, neither heparin nor warfarin prevented MCT-induced damage to endothelial cells in the liver as estimated by increased plasma hyaluronic acid concentration. These results suggest that activation of the coagulation system is required for MCT-induced parenchymal cell injury but not endothelial cell injury in the liver.