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Grubb RL Franks ME Toro J Middelton L Choyke L Fowler S Torres-Cabala C Glenn GM Choyke P Merino MJ Zbar B Pinto PA Srinivasan R Coleman JA Linehan WM 《The Journal of urology》2007,177(6):2074-2080
PURPOSE: Hereditary leiomyomatosis and renal cell cancer is a recently described hereditary cancer syndrome in which affected individuals are at risk for cutaneous and uterine leiomyomas, and kidney cancer. Our initial experience revealed the aggressive behavior of these renal tumors, often with early metastasis, despite small primary tumor size. We report the clinical characteristics and urological treatment of patients with hereditary leiomyomatosis and renal cell cancer associated renal tumors. MATERIALS AND METHODS: A total of 19 patients with hereditary leiomyomatosis and renal cell cancer associated renal tumors were evaluated. The 11 women and 8 men had a median age at diagnosis of 39 years (range 22 to 67), and a median clinical and radiological followup of 34 months (range 6 to 141). Hereditary leiomyomatosis and renal cell cancer manifestations in patients with renal tumors included cutaneous leiomyomas in 11 of 17 evaluable patients (65%) and uterine leiomyomas in 7 of 7 evaluable females (100%). RESULTS: Median pathological tumor size was 7.8 cm (range 1.5 to 20). Histological subtypes were consistent with hereditary leiomyomatosis and renal cell cancer renal carcinoma. Four of 7 patients with 2.0 to 6.7 cm T1 tumors had spread to regional lymph nodes or metastases at nephrectomy. Overall 9 of 19 patients (47%) presented with nodal or distant metastases. CONCLUSIONS: Renal tumors in patients with hereditary leiomyomatosis and renal cell cancer syndrome are significantly more aggressive than those in patients with other hereditary renal tumor syndromes. In contrast to other familial renal cancer syndromes, the observation of 3 cm or less renal tumors associated with hereditary leiomyomatosis and renal cell cancer is not recommended. Careful followup of affected and at risk individuals in families is necessary. 相似文献
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目的 采用高效液相色谱-串联质谱法(HPLC-MS/MS)测定SD大鼠血浆中N-[(3-烯丙基-2-羟基)苯亚甲基]-2-(4-苄基-高哌嗪-1-基)乙酰肼富马酸盐(SM-1),并计算大鼠重复ig给药的药动学参数,评价SM-1的药动学特征。方法 将60只健康SPF级SD大鼠随机分为阴性对照组、溶媒对照组和SM-1低、中、高剂量组,每组16只动物(阴性对照组和溶媒对照组为6只动物),雌雄各半。每天ig给药1次,各组分别给予水、溶媒或SM-1 50、100、200 mg·kg-1,给药体积10 mL·kg-1,连续给药4周,于首次给药和末次给药阶段进行药动学采血测定。采用经验证的HPLC-MS/MS法测定SD大鼠血浆中SM-1浓度。使用Phoenix WinNonlin 7.0软件进行血药浓度-时间数据分析与药动学参数计算。结果 SD大鼠ig给予SM-1后,在50~200 mg·kg-1剂量,SD大鼠体内的平均峰浓度(Cmax)及药时曲线下面积(AUC0~t)随剂量的增加而增加,各剂量组动物平均Cmax及AUC0~t比值与剂量比相近。连续给药后,低、中、高剂量组均未出现明显的蓄积。雌性大鼠SM-1的暴露高于雄性大鼠。结论 连续给药28 d后,SM-1在大鼠体内未出现明显的蓄积,雌性大鼠SM-1的暴露高于雄性大鼠。 相似文献
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Harnessing the hypoxia-inducible factor in cancer and ischemic disease 总被引:10,自引:0,他引:10
87.
HPLC法测定富马酸卢帕他定的含量 总被引:1,自引:0,他引:1
目的 建立HPLC法测定富马酸卢帕他定的含量。方法采用高效液相色谱法,以Diamonsil(钻石)C18柱(4.6×250mm,5μm)为色谱柱,pH-4.0磷酸盐缓冲液-甲醇(35:65)为流动相,流速1.0ml/min,检测波长244nm。结果富马酸卢帕他定在1.0012-100.12μg/ml范围内线性关系良好(r=0.9999),平均回收率为99.91%(RSD=0.58%)。结论所建立的方法准确、简便、快速,适用于富马酸卢帕他定的质量控制。 相似文献
88.
细粒棘球蚴囊壁的延胡索酸酶(FH)活力为911—14333,磷酸烯醇式丙酮酸羧激酶(PEPCK)与丙酮酸激酶(PK)的活力之比为2.2—2.7,表明囊壁的糖代谢以酵解途径为主,感染小鼠用甲苯达唑、阿苯达唑或吡喹酮ig治疗,剂量各为25—50,300和500mg·kg~(-1)·d~(-1),连给7—14d,未见对FH有明显的影响,而PK和PEPCK则可明显被前二种药物所抑制。 相似文献
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Long‐term entecavir or tenofovir disoproxil fumarate therapy in treatment‐naïve chronic hepatitis B patients in the real‐world setting 下载免费PDF全文
R. Idilman F. Gunsar M. Koruk O. Keskin C. E. Meral M. Gulsen A. H. Elhan U. S. Akarca C. Yurdaydin 《Journal of viral hepatitis》2015,22(5):504-510
The aim of this study was to determine the long‐term efficacy of entecavir (ETV) and tenofovir disoproxil fumarate (TDF) on the natural course of disease in chronic hepatitis B patients (CHB) with/without cirrhosis in clinical practice. A total of 355 treatment‐naïve CHB patients were enrolled into the study. The primary outcome measure was viral suppression as defined by serum HBV DNA level <20 IU/mL. A secondary outcome measure was to determine the development of Hepatocellular carcinoma (HCC). Virological and biochemical responses were similar between the two treatment groups over time. The presence of cirrhosis and hepatitis B e antigen (HBeAg) positivity did not appear to impact viral suppression. The cumulative probability of HBeAg loss was 41% at 4 years of therapy. Hepatitis B surface antigen (HBsAg) loss occurred in four patients. Model for End‐Stage Liver Disease score was significantly improved from baseline to week 48 and 96 under antiviral therapy (P = 0.013, P = 0.01). HCC was diagnosed in 17 patients (4.8%). The cumulative probability of the development of HCC was 3.3% at 1 year and 7.3% at 4 years of therapy. The development of HCC was independently associated with older age (P = 0.031) and the presence of cirrhosis (P = 0.004). Serum creatinine levels and creatinine clearance remained stable over time. ETV and TDF effectively maintained virological and biochemical responses in long‐term follow‐up of CHB patients with/without cirrhosis. HCC may still develop, although at a lower rate, and is more likely to develop in patients with cirrhosis, especially in older patients. 相似文献