黄芪总黄酮对扑热息痛所致肝损伤的防护机理探讨

目的 :研究黄芪总黄酮对扑热息痛所致肝损伤的防护机理。方法 :用高压液相测定扑热息痛及代谢产物和苯巴比妥诱导睡眠模型研究黄芪总黄酮 (TFA)对扑热息痛的代谢及TFA抗扑热息痛所致损伤的机理。结果 :TFA可明显降低尿中硫醚胺酸的浓度 ,其变化与TFA浓度成反比 ;但对其它代谢产物的影响无明显统计学差异。苯巴比妥诱导小鼠睡眠实验结果显示 ,TFA (10 0mg·kg^-1)本身对苯巴比妥代谢无明显影响 (P>0 .05) ,扑热息痛 (400mg·kg^-1)可显著延长小鼠的睡眠时间 (P<0.001) ;但TFA (100mg·kg^-1)明显缩短扑热息痛所延长的苯巴比妥诱导的睡眠时间 (P<0.005)。结论 :TFA抗扑热息痛损伤的作用机理可能与TFA抑制扑热息痛某些代谢过程以及降低扑热息痛代谢过程中产生毒性代谢产物有关。     

Transport of diclofenac by breast cancer resistance protein (ABCG2) and stimulation of multidrug resistance protein 2 (ABCC2)-mediated drug transport by diclofenac and benzbromarone

Diclofenac is an important analgesic and anti-inflammatory drug, widely used for treatment of postoperative pain, rheumatoid arthritis, and chronic pain associated with cancer. Consequently, diclofenac is often used in combination regimens and undesirable drug-drug interactions may occur. Because many drug-drug interactions may occur at the level of drug transporting proteins, we studied interactions of diclofenac with apical ATP-binding cassette (ABC) multidrug efflux transporters. Using Madin-Darby canine kidney (MDCK)-II cells transfected with human P-glycoprotein (P-gp; MDR1/ABCB1), multidrug resistance protein 2 (MRP2/ABCC2), and breast cancer resistance protein (BCRP/ABCG2) and murine Bcrp1, we found that diclofenac was efficiently transported by murine Bcrp1 and moderately by human BCRP but not by P-gp or MRP2. Furthermore, in Sf9-BCRP membrane vesicles diclofenac inhibited transport of methotrexate in a concentration-dependent manner. We next used MDCK-II-MRP2 cells to study interactions of diclofenac with MRP2-mediated drug transport. Diclofenac stimulated paclitaxel, docetaxel, and saquinavir transport at only 50 microM. We further found that the uricosuric drug benzbromarone stimulated MRP2 at an even lower concentration, having maximal stimulatory activity at only 2 microM. Diclofenac and benzbromarone stimulated MRP2-mediated transport of amphipathic lipophilic drugs at 10- and 250-fold lower concentrations, respectively, than reported for other MRP2 stimulators. Because these concentrations are readily achieved in patients, adverse drug-drug interactions may occur, for example, during cancer therapy, in which drug concentrations are often critical and stimulation of elimination via MRP2 may result in suboptimal chemotherapeutic drug concentrations. Moreover, stimulation of MRP2 activity in tumors may lead to increased efflux of chemotherapeutic drugs and thereby drug resistance.     

Appendectomy due to lead poisoning: a case-report

Background

Lead poisoning is a common occupational health hazard in developing countries and many misdiagnoses and malpractices may occur due to unawareness of lead poisoning symptoms.

Case presentation

We report a case of occupational lead poisoning in an adult battery worker with abdominal colic who initially underwent appendectomy with removal of normal appendix. Later on he was diagnosed with lead poisoning and was treated appropriately with lead chelator (CaNa₂EDTA).

Conclusion

Lead poisoning is frequently overlooked as the differential diagnosis of acute abdomen which may result in unnecessary surgery. Appropriate occupational history taking is helpful in making a correct diagnosis. Occupational lead poisoning is a preventable disorder and a serious challenge for the health and labor authorities in developing countries.     

氟伐他汀对高脂血症患者的降脂及改善血液流变学疗效

目的：研究氟伐他汀对高血脂患者的降脂及改善血液流变学临床疗效。方法：选择是血患者４６例,给予氟伐他汀口服４０ｍｇ,每晚一次,一周后改为２０ｍｇ、疗程４－８周,分别观测治疗前、后的血脂及血液流变学指标。结果：治疗后的ＴＣ、ＴＧ及ＬＤＬ均明显降低,而ＨＤＬ升高不明显。全血比粘度、血浆比粘度及红细胞压积均明显降低,结论：氟伐他汀不但能降低ＴＣ、ＴＧ及ＬＤＬ水平,而且能改善流变学指标。