腹腔化疗联合腹部透热全身热疗治疗恶性腹水

目的 探讨腹部透热全身热疗系统在复治性恶性腹水腹腔化疗治疗中的辅助及增效治疗作用价值及意义.方法 实验组为抽放恶性腹水后腹腔内灌注DDP+5-Fu为主药物后即刻行高功率微波腹部透热全身热疗,恒温期温度41-42 ℃,维持60分钟以上.对照组为仅行腹腔灌注化疗,用药方法同实验组.结果 50例复治恶性腹水总缓解率64%,其中实验组77.3%,对照组46.4%,前者有效率明显高于后者,(P＜0.05),实验组及对照组患者中位生存时间分别为32周及28周,二组不同治疗方法的毒副反应发生率及程度无统计意义上差异.结论 以腹腔灌注化疗联合经腹透热全身热疗治疗晚期肿瘤恶性腹水较常规单纯腹腔化疗疗效好,且毒副反应少,并有一定程序延长患者生存期作用,有临床实际应用价值.     

化疗联合腹部高频热疗治疗晚期卵巢癌伴腹水的临床研究

目的:观察用多西他赛全身化疗和卡铂腹腔灌注化疗联合腹部高频热疗治疗晚期卵巢癌腹水患者的临床疗效及毒副反应。方法:34例晚期卵巢癌腹水患者,18例采用多西他赛全身化疗+卡铂腹腔灌注化疗,16例用多西他赛全身化疗+卡铂腹腔灌注化疗联合腹部高频热疗。多西他赛75 mg/m2,静脉滴注第1天,卡铂AUC=5,腹腔灌注给药第1天,高频热疗在腹腔灌注卡铂后2小时进行,以后隔日1次,21天为1周期,4周期后评价疗效。结果:常规化疗组的有效率为55.6%,高频热疗组的有效率为87.5%,两组差异有统计学意义(P<0.05);KPS评分,常规化疗组的改善率为61.1%,高频热疗组的改善率为93.8%,两组差异有统计学意义(P<0.05);化疗过程中的主要毒副反应是胃肠道反应、白细胞减少、血小板减少和脱发,差异无统计学意义(P>0.05);从第二周期化疗开始,高频热疗组腹水消退的患者明显较常规化疗组增多,两组间差异有统计学意义(P<0.05)。结论:用多西他赛全身化疗和卡铂腹腔灌注化疗联合腹部高频热疗可显著提高晚期卵巢癌腹水患者的治疗效果、改善患者的生活质量和控制腹水的生长,而不增加毒副作用。     

腹部射频热疗联合化疗治疗Ⅳ期胃癌的近期疗效观察

目的:观察腹部射频热疗联合FOLFOX6方案腹腔化疗治疗Ⅳ期胃癌的近期疗效和毒副反应.方法:96例入选者随机分为研究组和对照组.两组均给予FOLFOX6方案化疗.腹膜转移和腹水患者给予腹腔灌注化疗.研究组50例,每周期第1、3、5天给予腹部射频热疗60 min.对照组46例,不进行热疗.每14 d重复,完成4个周期1个月后评价近期疗效、腹部疼痛治疗有效率和毒副反应.结果:研究组近期疗效为72.0%,对照组为39.1%,两组差异有统计学意义,P<0.05.研究组腹部疼痛患者42例,疼痛治疗有效率95.2%,对照组腹部疼痛患者40例,疼痛治疗有效率62.5%,两组差异有统计学意义,P<0.05.两组毒副反应差异无统计学意义,P>0.05.结论:腹部射频热疗可以提高静脉化疗和腹腔化疗的近期疗效,提高腹部疼痛治疗有效率,不增加毒副反应.     

射频热疗加腹腔热灌注化疗联合静脉双途径化疗治疗恶性腹水疗效分析

目的：探讨射频热疗加腹腔热灌注化疗和静脉双途径化疗治疗恶性腹水的疗效和毒副反应。方法：20例恶性腹水患者采用常规腹腔穿刺，放置中心静脉导管，尽量引流腹水彻底后，将43℃无菌生理盐水1500～2000ml加5-FU0．5～1．0g经导管快速滴入腹腔，第1、4、8、11天，然后沿导管放置传感器进行腹腔温度的测定，随后行腹部SR-1000型射频透热治疗70分钟，并同时进行全身静脉化疗，奥沙利铂100mg第1、8天或顺铂40～60mg第1、8天，21天为一周期。结果：全组患者最高治疗温度为43．5cc，最低治疗温度为40．5℃，平均治疗温度41．5℃。腹水有效率为90％(18／20)，盆、腹腔肿瘤有效率为58．8％(10／17)，全组患者中位生存期10个月，一年生存率75％。脂肪硬结发生率20％，腹痛发生率为25％，其他毒副反应较轻，能耐受。结论：射频热疗加腹腔热灌注化疗和静脉双途径化疗治疗恶性腹水疗效高，毒副反应轻，且对腹、盆腔肿瘤病灶也有较好的疗效，值得进一步的推广应用。     

腹腔灌注化疗加热疗治疗恶性腹水疗效观察

目的：观察腹腔灌注化疗加局部热疗治疗恶性腹水的疗效.方法：将70例恶性腹腔积液患者随机分为治疗组（35例）和对照组（35例）.腹腔置管引流腹水后,给予顺铂50mg腹腔灌注化疗,治疗组行腹腔灌注化疗后即刻行腹部局部热疗,对照组仅行腹腔灌注化疗,每周1次,4次后评价疗效.结果：治疗组总有效率（CR＋ PR）为77.14％,对照组总有效率（CR＋PR）为45.71％,两组比较差异有统计学意义（P＜0.05）.结论：腹腔灌注化疗加腹部局部热疗治疗恶性腹水较单纯腹腔灌注化疗疗效好,值得临床推广.     

腹腔热灌注配合双途径化疗治疗消化道恶性肿瘤的临床观察

目的 观察腹腔热灌注配合全身双途径化疗治疗消化道恶性肿瘤的近期 有效率、腹水控制情况、毒副反应。方法 58例被随机分为实验组和对照组，对照组单纯应用全身化疗，实验组采用双途径化疗。结果 实验组近期有效率56．67％，腹水有效率为72．73％，对照组近期有效率为32．29％，腹水有效率为30％，差异有显著性（P＜0．05）。副反应两组对比，差异无显著性（P＞0．05）。结论 腹腔热灌注配合全身双途径化疗是治疗消化道恶性肿瘤－有效、毒副反应较轻的方法。     

腹腔热化疗治疗卵巢癌合并腹水临床疗效观察

目的探讨腹腔热化疗治疗卵巢癌合并腹水的疗效及毒副反应。方法将入选病例随机分为两组,治疗组采用腹腔热疗联合腹腔灌注化疗;对照组则仅行腹腔灌注化疗,剂量与治疗组相同,未进行腹腔热疗。结果治疗组卵巢肿瘤治疗总有效率60.5%（23/38）,对照组为28.6%（10/35）,两组比较差异有显著性（P〈0.05）;治疗组腹水治疗总有效率84.2%（32/38）,对照组为57.1%（20/35）,两组比较差异有显著性（P〈0.05）。而两组患者治疗前后T淋巴细胞亚群结果比较,差异有显著性（P〈0.05）。毒副反应主要为胃肠道反应、骨髓抑制及腹痛,两组毒副反应比较,差异无显著性（P〉0.05）。结论热疗联合化疗药物腹腔灌注治疗卵巢癌合并腹水具有协同效应,增强抗癌效果、提高免疫力并抑制肿瘤细胞活性,治疗毒副反应可耐受。     

肿瘤患者腹腔热灌注化疗及局部热疗的护理

腹腔转移是晚期恶性肿瘤常见的并发症,也是临床治疗中比较棘手的问题[1]。外周静脉化疗腹腔药物浓度低,不仅效果差,且全身毒副反应严重。近年来,热化疗引起了人们的关注,热疗联合腹腔灌注化疗被认为是治疗这类肿瘤的有效手段之一[2]。为此我科利用腹腔热灌注化疗及局部热疗治疗腹腔肿瘤及腹     

低渗热灌注腹腔化疗治疗胃肠肿瘤恶性腹水的临床研究

目的　探讨低渗热灌注腹腔化疗治疗胃肠肿瘤恶性腹水的临床价值。方法　实验组 32例胃肠肿瘤恶性腹水患者应用大量加热的生理盐水灌洗腹腔结合低渗热灌注顺铂腹腔化疗 ,对照组 40例患者接受单纯顺铂腹腔化疗。结果　实验组腹水控制缓解率 ,1年、2年生存率 ,一般状况改善率均有提高 ,与对照组相比均存在显著差异 (P <0 .0 5) ;两组毒副反应无显著性差异。结论　低渗热灌注腹腔化疗治疗胃肠肿瘤恶性腹水是一种高效、安全、简便的新疗法 ,值得进一步研究和临床推广     

腹腔化疗联合腹部透热全身热疗治疗恶性腹水

50例分为A组22例，放尽腹水后腹腔内灌注DDP40～60mg＋5Fu0．5～0．75g等药物，即刻用大功率微波全身治疗仪行腹部透热全身热疗，恒温期温度41～42℃，维持〉60min。B组28例仅行腹腔灌注化疗，方法同A组。两组均予2次／周，2～3w后评价。结果：治疗后腹水总缓解率A组77．3％，明显高于B组46．4％；中位生存时间A组32w，稍高于B组28w。认为A组疗法治疗该腹水疗效较好，且毒副反应少，对延长生存期有积极意义。     

Nitrosation by alkyl nitrites. Catalysis by inorganic salts

Isobutyl nitrite is an effective nitrosating agent at acidic, neutral and basic pH in the presence of species arising from phosphate ion. The reaction is first-order in isobutyl nitrite and amine. In the reaction of isobutyl nitrite with sulfanilamide, the pH dependence reflects the change in concentration of the various protonated forms of phosphate, with H3PO4 and H2PO4- most strongly affecting the rate. In the reaction of isobutyl nitrite with dipropylamine, the pH dependence also reflects the change in the concentration of unprotonated amine.     

Chemoprevention by S-adenosyl-L-methionine of rat liver carcinogenesis initiated by 1,2-dimethylhydrazine and promoted by orotic acid

Chemoprevention of liver carcinogenesis by S-adenosyl-Lmethionine(SAM) was studied in F344 male rats. The rats were given 1,2-dimethylhydrazine(1,ZDMH) 2 HCl (100 mg/kg, i.p.) 18 h after two-thirds hepatectomy.One week later they were fed a semisynthetic basal diet containing1% orotic acid (OA) for 29 weeks. At this time the rats weretransferred to the basal semisynthetic diet and were killed3 weeks later. SAM treatment (384 µmol/kg/ day, im.),was started 1 week after 1,2-DMH and was continued up to theend of the experiment. Controls received solvent alone. SAMexerted an inhibitory effect on the induction of preneoplasticand neoplastic lesions. For example, nodules with diametersof 1-2 and 2-6 mm exhibited a decrease in both incidence andnumber per liver, while no such inhibitory effect was seen inthe category of larger nodules. Furthermore, hepatocellularcarcinoma (HCC) also exhibited a decrease in the SAM-treatedgroup. The numberniver and incidence were 0.04 and 4.8% respectivelyin the SAM-treated group, compared to 0.38 and 37.8% in thecontrol group. Microscopic examination showed the presence ofwell-differentiated carcinomas and atypical nodules in controlrats, while only one small, well-differentiated tumor and onenodule with patterns of initial transformation were seen inSAM-treated rats. No patchy staining of glutathione-S-transferase,indicative of remodeling, was observed in nodules of both SAM-treatedand control rats. Nodules and HCCs developing in SAM-treatedrats exhibited a relatively high number of apoptotic bodies.Apoptotic bodies count showed 2.8-and 1.8-fold increases innodules and HCCs of SAM-treated rats with respect to controls.These results indicate that SAM exerts a chemopreventive effecton hepatocarcinogenesis induced by the OA model. SAM seems tobe more effective in inhibiting nodule to HCC progression thanon the growth of nodule per se. The inhibitory effect is associatedwith an increase in cell loss by apoptosis in nodules and HCC.     

Post-treatment skin reactions reported by cancer patients differ by race, not by treatment or expectations

Cancer patients may experience skin problems while undergoing chemotherapy and radiation therapy. Frequency of skin reactions may be influenced by skin pigmentation and psychological factors. A Symptom Inventory completed by 656 cancer patients nationwide before and after chemotherapy, radiation therapy, or chemotherapy plus radiation therapy was analysed to determine if treatment type, race (Black vs White), and pretreatment expectations influenced post-treatment skin reactions. Subsequent analysis of a local Symptom Inventory completed weekly for 5 weeks by 308 patients receiving radiation therapy examined severity of reported skin reactions. Significantly more patients receiving radiation therapy had stronger expectations of skin problems (62%) than patients receiving chemotherapy (40%, P=0.001) or chemotherapy plus radiation therapy (45%, P=0.003). Overall, expectations did not correlate with patient reported post-treatment skin problems in white (r=0.014, P=0.781) or black (r=0.021, P=0.936) patients. Although no significant difference was found between black and white patients in their pretreatment expectations of skin problems (P=0.32), black patients (10 out of 18, 56%) reported more skin problems than white patients (90 out of 393, 23%, P=0.001). Similarly, the local study showed that significantly more black patients (1 out of 5, 20%) reported severe skin reactions at the treatment site than white patients (12 out of 161, 8%). A direct correlation was observed between severity of skin problems and pain at the treatment site (r=0.541, P<0.001). Total radiation exposure did not significantly correlate with the report of skin problems at the treatment site for white or black patients. Overall, black patients reported more severe post-treatment skin problems than white patients. Our results suggest that symptom management for post-treatment skin reactions in cancer patients receiving radiation treatment could differ depending on their racial background.     

Fibromatosis: benign by name but not necessarily by nature

Aggressive fibromatoses, also known as desmoid tumours, are rare fibrous tissue proliferations with a tendency for slow, local infiltrative growth. There is an association with Gardner's syndrome and familial adenomatous polyposis. Histologically they are fairly bland with no abnormal mitoses or necrosis. They do not metastasize, but can cause significant morbidity through their locally destructive effects. Magnetic resonance imaging is the method of choice for diagnosis, pre-treatment planning and post-treatment follow-up. Surgical excision with a wide margin is the treatment of choice. However, there is a tendency for local recurrence and repeated excision may result in a poor functional or cosmetic outcome. Radiotherapy is used to reduce local recurrence rates after excision and is also used to treat inoperable tumours. Long-lasting remissions can be obtained. Treatment is now planned using modern three-dimensional conformal techniques, similar to those used in soft tissue sarcoma management. There is no definite dose-response relationship, but doses of 50-60 Gy in 1.8-2 Gy fractions are recommended. Systemic therapy has been used for lesions not controlled by surgery or radiotherapy, or less commonly, as a primary treatment. Tamoxifen and non-steroidal anti-inflammatory agents are used most often as they are relatively non-toxic, but there is limited experience with cytotoxic chemotherapy and biological agents. There are no randomised trials to help guide the management of this locally aggressive 'benign' tumour and treatment decisions are best made by the local soft tissue sarcoma multidisciplinary team.     

Stimulation of glycolysis by placental polypeptides and inhibition by duramycin

Placental polypeptides present in crude preparations of transforming growth factors stimulate glycolysis when added to quiescent 3T3 cells, normal rat kidney, and chick embryo fibroblasts. The stimulation was apparent over a time period of at least 90 min and was seen at glucose concentrations ranging from 1 to 30 mM. Duramycin, an antibiotic isolated from Streptomyces cinnamomeus, inhibits the polypeptide-stimulated and nonstimulated glycolysis of intact cells, since it permeabilizes cells to Pi and nucleotides. However, duramycin also inhibits the Na+-K+-ATPase as well as the ouabain-insensitive Mg2+-ATPase of plasma membranes. Duramycin has no effect on glycolysis catalyzed by cell-free extracts of Ehrlich ascites tumor cells in the presence of mitochondrial ATPase but partially inhibits glycolysis when ADP and Pi are generated by ATPases of plasma membrane preparations.     

Enhancement by methionine enkephalin of colon carcinogenesis induced by azoxymethane

The effect of the opioid receptor agonist methionine enkephalin (Met-enkephalin) and the opioid receptor antagonist naloxone on colonic carcinogenesis induced by azoxymethane was investigated in Wistar rats. Rats received ten weekly injections of 7.4 mg/kg of body weight of azoxymethane and injections of Met-enkephalin (50 micrograms/kg of body weight), naloxone (2 mg/kg of body weight), or Met-enkephalin (50 micrograms/kg of body weight) plus naloxone (2 mg/kg of body weight) once every 2 days. In wk 40, the group treated with Met-enkephalin had a significantly increased incidence of colonic tumors. A combination of Met-enkephalin and naloxone attenuated the enhancing effect by Met-enkephalin on the development of colonic tumors. Administration of naloxone alone had no influence on colonic tumorigenesis. During and after administration of the carcinogen, the bromodeoxyuridine-labeling indices of the colon mucosa and/or cancers were significantly increased in rats treated with Met-enkephalin. However, a combination of Met-enkephalin and naloxone significantly decreased the labeling indices of the colon mucosa and/or cancers. These findings indicate that Met-enkephalin enhanced colon carcinogenesis and that naloxone attenuated this enhancement. Because naloxone is an opioid receptor antagonist, these findings also indicate that the enhancing effect of Met-enkephalin on colon carcinogenesis may be mediated through opioid receptors.     

Production of plasminogen activator by cells transformed by herpesviruses.

Plasminogen activator is produced by hamster cells transformed by human herpesviruses. These cell lines have previously been shown to be oncogenic when injected s.c. into newborn syngeneic hamsters. Lysis of fibrin overlays by these cell lines was plasminogen dependent. Normal hamster embryo fibroblasts and a hamster cell line transformed by PARA-7 (an adenovirus-SV 40 hybrid) failed to produced lysis. In separate experiments fibrin overlay of lytically infected secondary rabbit kidney cells did not show induction of this activity during the normal course of productive infection. The human cell line TE-85 clone F-5, a clonal cell line from a human osteogenic sarcoma, failed to produce plasminogen activator, but two separate clones of these cells that were morphologically transformed after exposure to UV-inactivated herpes simplex virus type 2 produced rapid lysis of the fibrin overlay. Clonal variation was observed in herpes simplex virus types 1 and 2-transformed hamster lines and is under investigation. It is suggested that plasminogen activator detection may serve as a convenient assay system for transformation of normal cells by herpesviruses.     

Enhancement by ethyl alcohol of experimental hepatocarcinogenesis induced by N-nitrosomorpholine

The effects of ethyl alcohol (EtOH) during or after treatment with N-nitrosomorpholine (NNM) on hepatocarcinogenesis, ornithine decarboxylase (ODC) activity and the labeling index of the liver were investigated in male Sprague-Dawley rats. Rats were given drinking water containing NNM for 8 weeks and received i.p. injections of 1 g EtOH/kg body weight every other day during or after treatment with NNM. Pre-neoplastic and neoplastic lesions staining positively for glutathione-S-transferase, placental type (GST-P), were examined immunohistochemically. At the end of experiment at week 16, administration of EtOH after NNM treatment had no significant effect on the number and size of GST-P-positive hepatic lesions, whereas administration of EtOH during NNM treatment significantly increased the number and percentage area but not the mean area of GST-P-positive hepatic lesions. EtOH caused significant increases in the ODC activity of the liver and in the labeling indices of enzyme-altered lesions and the adjacent hepatocytes after the cessation of EtOH administration but not during EtOH treatment. Our findings indicate that EtOH enhances hepatocarcinogenesis and suggest that this effect may be closely related to the increases in ODC activity and cell proliferation in enzyme-altered lesions and the adjacent liver after EtOH treatment. Int. J. Cancer 71: 1045-1048, 1997. © 1997 Wiley-Liss Inc.