Persistent serpentine supravenous hyperpigmented eruption associated with docetaxel

Various mucocutaneous reactions have been reported with the use of systemic docetaxel. We describe a 47-year-old man who developed a persistent serpentine supravenous hyperpigmented eruption (PSSHE), beginning at the site of docetaxel injection and spreading along the superficial venous network in the anterior aspect of the right forearm and distal arm. The eruption occurred after the first infusion of docetaxel following insufficient venous washing. A second infusion was administered through a vein in the other forearm, but this time, abundant venous washing was performed and a similar eruption did not occur. To our knowledge, this is the second report of docetaxel-induced supravenous discoloration and we discussed the terminology and mechanism of this unique reaction.     

优秀女子赛艇运动员比赛前后血乳酸、血尿素及血清肌酸激酶跟踪测试

目的:跟踪测试优秀女子赛艇运动员比赛前后血乳酸、血尿素及血清肌酸激酶的变化,探讨女子赛艇运动员机体能量物质代谢和赛后疲劳恢复的特点。方法:选取2005-07/09湖北省水上运动中心优秀女子运动员14名,其中国家健将级运动员7名,国家一级运动员7名;平均年龄(22±4)岁,训练年限(4.1±1.4)年,身高(174.2±3.1)cm,体质量(68.6±4.7)kg。14名运动员分别于2000m划艇比赛当日晨空腹、赛前15min、赛后5min,1h及24h抽取指尖血60μL,进行血乳酸、血尿素、血清肌酸激酶检测。结果:14名运动员全部进入结果分析。①比赛前后运动员血乳酸水平的变化:运动员空腹血乳酸水平为(1.22±0.45)mmol/L,赛前15min为(2.89±0.49)mmol/L。赛后5min血乳酸浓度高达(11.51±1.72)mmol/L,与空腹水平比较差异有显著性意义(t=3.077,P<0.01)。赛后24h血乳酸浓度显著下降至(1.76±0.24)mmol/L,与空腹水平基本接近(t=0.027,P>0.05)。②比赛前后运动员血尿素水平的变化:与空腹血尿素水平比较,运动员赛后5min血尿素浓度明显升高[(5.45±0.47),(6.13±1.00)mmol/L;t=2.416,P<0.05]。赛后24h血尿素浓度下降至(5.94±0.85)mmol/L,仍高于空腹水平(t=2.682,P<0.05)。③比赛前后运动员血清肌酸激酶活性的变化:与赛前比较,运动员赛后5min血清肌酸激酶活性明显升高[(3.38±1.58),(6.13±3.25)nkat/L;t=4.968,P<0.01]。赛后1h血清肌酸激酶活性开始下降,至赛后24h与赛前基本相似(t=1.537,P>0.05)。结论:①赛后5min血乳酸、血尿素、血清肌酸激酶活性显著高于赛前,赛后1h血乳酸消除迅速,但仍未恢复到正常水平。提示赛艇是一种以糖酵解系统为主、无氧 有氧代谢混合型供能的运动项目。②赛艇比赛使酸性产物生成增多,血乳酸、血尿素、血清肌酸激酶可作为运动强度和机能恢复的指标。③赛艇比赛后至少24h内,机体处于蛋白质降解增强状态,建议恢复期增加饮食糖和蛋白质摄入量,以促进合成代谢,加快功能恢复过程。     

Severe hyperlipidemia in apolipoprotein E2 homozygotes due to a combined effect of hyperinsulinemia and an SstI polymorphism

More than 90% of patients with type III hyperlipoproteinemia are homozygous carriers of the apolipoprotein (apo) E*2 allele. The great majority of these apoE2(Arg158-->Cys) homozygotes in the general population, however, are normolipidemic. Apparently, expression of the hyperlipidemic state requires additional genetic and/or environmental factors, suggesting a multifactorial etiology. To elucidate these additional risk factors, we analyzed normolipidemic and hyperlipidemic apoE2 homozygotes. Hyperinsulinemia was observed in 27 of 49 apoE2 homozygotes and associated with elevated lipid levels: hyperinsulinemic apoE2 homozygotes had type III hyperlipoproteinemia 6 times more often than apoE2 homozygotes with normal insulin levels (odds ratio 6.2, P=0.02). We screened the normolipidemic and hyperlipidemic apoE2 homozygotes for common variants in candidate genes involved in lipolysis-the APOA1-C3-A4 gene cluster, lipoprotein lipase, and hepatic lipase-and analyzed for associations with the expression of hyperlipidemia. In the hyperinsulinemic group, the 7 carriers of the SstI polymorphism (S2) in the APOC3 gene displayed severely elevated VLDL cholesterol (P(insulin by SstI)<0.001) and VLDL triglyceride (P(insulin by SstI)<0.01) and low levels of HDL (P(insulin by SstI)<0.02). In the normoinsulinemic group, no such relation of the SstI polymorphism with hyperlipidemia was observed. These data provide the first evidence for a combined effect of hyperinsulinemia and the SstI polymorphism on the expression of hyperlipidemia in apoE2 homozygotes.     

Acceptance of preventive treatment in migraine patients: Results of a survey

Abstract Background: The number of migraine patients eligible for preventive treatment is considerably higher than the number of patients actually using it. This study explores reasons for this discrepancy. Methods: An explorative survey among patients and their general practitioners (GPs) participating in a trial on preventive medication. Migraine patients who were eligible for preventive treatment (n =?75) attended an evaluation consultation with their GP to optimize migraine treatment. GPs and patients who did not start preventive treatment were asked if they had discussed the possibility of preventive treatment and, if so, why they decided not to start it. Results: Of the 32 GPs, 8 (25%) did not discuss the possibility of preventive treatment with their patients; in 4 because of perceived lack of effectiveness. Patients who did not start preventive treatment (n =?43) used less triptans and had less psychological distress compared to those who did start (n =?32). Main reasons for patients not starting were negative attitudes towards medication in general, fear of medication side-effects, previous unsuccessful attempts, attacks not being severe enough, and impact of migraine on daily life acceptable. Conclusion: The decision of the individual patient and their GP to start preventive treatment is not only determined by attack frequency, but also depends on the impact of the headache attacks on their daily life and their negative attitude towards medication.