Vinorelbine plus cisplatin
Was equipped with a range of skills that are highly relevant to writing my thesis and useful transferable skills. Now that I have started to write up my thesis, it's made life much easier knowing how to go about setting up paragraphs, indexes, tables of contents, headers and footers etc, ' she says. `Not only would I recommend that PhD students enrol on as many of these courses as possible, I would also strongly suggest that their supervisors play an active role in encouraging them to do so. After all, it's in their interests to have a more confident, efficient and competent student working for them!' See kcl.ac igrad.
Antineoplastics, alkylating agents, cisplatin cddp.
Levels Hb below which transfusion should be given ; . However, in cancer treatmentassociated anaemia most people would be transfused if Hb 8 100 ml, and few people if Hb 12 100 ml. However, at an individual level, decisions would be influenced by factors such as symptomology, when the Hb level was measured in relation to treatment ; and whether patients had previously benefited from transfusion. For information on the number of units required per transfusion, and related statistics, see page 28 of the Assessment Report ; . There are two main problems associated with blood transfusion. The first is the risk of infection see Table 1.
Hydrocortisone 100mg should be given with bleomycin on D9 and D16 to prevent rigors. For patients on Cycle 1 whose EDTA is not yet available, Cockcroft and Gault may be used to predict GFR. Cisplatin dose should be adjusted if necessary once EDTA available. EDTA should only be repeated if the result is border-line at the start of treatment or if there is 30% change in serum creatinine. Ensure careful review so that side effects such as peripheral neuropathy, hearing loss and pulmonary toxicity are detected early. Check electrolytes additional potassium, calcium or magnesium may be required. Weight should be recorded prior to and at the end of cisplatin treatment, and a strict fluid balance chart should be maintained. An average urine output of at least 100ml hr must be maintained throughout treatment, and cisplatin infusion should not be commenced unless this urine output is achieved. If the urine output is inadequate, the patient should be assessed and urine output increased by administering 500ml Sodium Chloride 0.9% IV + furosemide 20 40mg. Furosemide 20 40mg po may also be given if there is a positive fluid balance of 1.5.
72, no 3, 2005 - original paper overexpression of protein kinase c enhances cisplatin-induced cytotoxicity correlated with p53 in gastric cancer cell line yoshihiko iioka a , kenji mishima b , nakanobu azuma c , akihiko tsuchida a , yu takagi a , tatsuya aoki a , ichiro saito b a third department of surgery, tokyo medical university, tokyo, b department of pathology, tsurumi university school of dental medicine, yokohama, and c tokatsu clinic hospital, chiba, japan address of corresponding author pathobiology 2005; 2-159 doi: 1 1159 000084119 ; key words protein kinase c p53 gastric cancer cisplatin signaling molecules abstract objective: an important issue in cancer therapy is to investigate the mechanism for cellular sensitivity to anticancer agents such as cisplatin.
Cisplatin prices
Long Term Analysis of Survival in the European Randomized Trial Comparing Vinorelbine Cisplatin to Vindesine Cisplatin and Vinorelbine Alone in Advanced Non-Small Cell Lung Cancer T. Le Chevalier, D. Brisgand, J.C. Soria, J.Y. Douillard, J.L. Pujol, P. Ruffie, V. Aberola and S. Cigolari Oncologist 2001; 6; 8-11 DOI: 10.1634 theoncologist.6-suppl 1-8 and cladribine!
Dunton by which carboplatin is cleared from the body. Carboplatin causes dose-limiting and cumulative myelosuppression, characterized by thrombocytopenia, granulocytopenia, and anemia. Thrombocytopenia following carboplatin therapy is frequent and severe [18, 19]. Treatment with growth factors G-CSF [Neupogen; Amgen Inc.; Thousand Oaks, CA] in conjunction with epoetin alfa ; can mitigate leukopenia and anemia, but abrogation of thrombocytopenia without transfusions remains a challenge [20, 21]. Although cumulative myelosuppression is the main toxicity associated with carboplatin, there is also a significant risk of neurotoxicity and hypersensitivity reactions. A recent study at the Cleveland Clinic Cancer Center [22] reported that hypersensitivity to carboplatin developed in 12% of carboplatin-treated patients. Because of the possibility of fatal cross-hypersensitivity, the use of cisplatin in patients who have developed hypersensitivity to carboplatin is not recommended [23]. Although carboplatin and cisplatin are the current standards of care for first-line therapy of ovarian cancer, their long-term toxicities present challenges in the treatment of patients with relapsed ovarian cancer. Paclitaxel Paclitaxel Taxol; Bristol-Myers Squibb ; is a nonplatinum-based cytotoxic agent approved for the first-line treatment of advanced ovarian cancer. Paclitaxel exhibits high antitumor activity when used in combination with carboplatin [24]. However, the use of paclitaxel may be limited by cumulative peripheral neurotoxicity, and a rapid-onset sensory neuropathy can occur, especially with high-dose regimens [25]. The peripheral neuropathy is due to axonopathy, and motor and autonomic nerves appear to be unaffected by paclitaxel [26]. The resultant painful myalgias and arthralgias can severely impact the patient's quality of life [27]. The acute dose-limiting toxicity of paclitaxel is granulocytopenia; however, other common acute adverse events include alopecia, nausea, vomiting, diarrhea, mucositis, and hypersensitivity [28]. To decrease the incidence and severity of hypersensitivity reactions, patients should receive pretreatment with steroids. Concomitant steroid therapy allows paclitaxel to be administered over a 3-hour infusion period, which is less myelosuppressive than the 24-hour infusion protocol used previously [29]. A limited phase I evaluation of escalatingdose paclitaxel administered weekly as a 1-hour infusion demonstrated a lack of cumulative myelosuppression, mucositis, or grade III neuropathy with this regimen, though the efficacy of this regimen remains to be determined [30]. These results underscore the relationship between toxicity and method of administration, as well as the importance of considering the mode of delivery when.
Gemcitabine and cisplatin for bladder cancer
The pivotal toxicology and toxicokinetic studies, as well as the safety pharmacology studies were performed in accordance with Good Laboratory Practice GLP ; regulations. Other pharmacodynamic and pharmacokinetic studies do not fall under these regulations. Applicable International Conference on Harmonization ICH ; and EMEA guidance documents were referred to during the development of the compound. Pharmacology Primary pharmacodynamics in vitro in vivo ; The activity of pemetrexed against a broad range of human tumours was evaluated in two separate colony-forming assays. In the first, dose-dependent responses were observed, including in tumour types generally considered to be chemoresistant. The activity of pemetrexed was similar to that of other agents evaluated concurrently cisplatin, 5-fluorouracil, irinotecan, and paclitaxel ; and was not completely cross-resistant with that of the other agents tested [31]. The applicant presented the results of a second test using a panel of 71 specimens of slightly different tumour spectrum from the first test. At 10 g ml, responding tumour types included colon cancer at 21% 3 14 ; , NSCLC at 57% 8 14 ; , breast cancer at 47% 7 15 ; , and ovarian cancer at 18% 3 17 ; . Cisplatin and paclitaxel-resistant mesothelioma and NSCLC were sensitive to pemetrexed. The activity of pemetrexed against a diverse group of tumour cell lines was tested in 72-hour growth inhibition studies using media that typically contained 1 to 3 folic acid. The IC50 values were found to range from 4 to 220 nM [32-38]. Similar results were reported using a panel of unselected colorectal carcinoma cell lines [39]. According to a study conducted by the applicant, tumour growth inhibition was demonstrated against breast, pancreas, lung, and colon tumour xenografts in mice following 10 daily treatments by pemetrexed at 300 mg kg, the MTD for this dosing schedule in these animals. Intraperitoneal treatment of a colorectal carcinoma xenograft in CD1 nude mice resulted in 70% tumour growth inhibition measured 5 days after the end of treatment and about 17 days tumour growth delay, compared to vehicle-treated control mice [34]. Against established tumours, the activity of pemetrexed was minimal at doses below 200 mg kg, especially when given less frequently than ten daily injections. No antitumour effect was observed when three daily intraperitoneal injections of pemetrexed at 100 mg kg were administered to mice bearing HT-29 colorectal carcinoma xenograft of about 300 mg size [40]. In contrast, antitumor activity could be demonstrated when mice were only given two biweekly intraperitoneal injections of pemetrexed at 500 mg kg when tumours became palpable ~19 mm3 ; [41]. The high circulatory levels of folate and thymidine in murine plasma, which are about 10 and 5 times, respectively, greater than those found in human plasma, can adversely affect the activity of antifolate compounds [34, 35, 42]. Mice fed a low folate diet were also much more sensitive to the toxic effects of pemetrexed, with the MTD being 60- to 250-fold depending on mouse strain ; less than that in mice maintained on a normal high-folate ; diet [35, 42]. In mice on a low-folate diet, the authors found that dietary folic acid protected mice from toxicity without negative influence on the efficacy of pemetrexed [35]. Pharmacodynamic mechanisms Pemetrexed is a structural analogue of folic acid and uses the same biochemical machinery as natural folates for membrane transport and intracellular polyglutamation. Similar to the natural folates, polyglutamated forms of pemetrexed are better retained in the cell and have higher affinity than parent compound for certain folate-dependent enzymes. Inhibition of several of these enzymes by pemetrexed and its polyglutamates causes depletion of nucleotide pools that is associated with growth inhibition and possibly cell death and clofarabine.
Breast cancer cisplatin
Mg123 m2 and 20 mg m2, respectively, with these drugs administered i.v. on days 1, 8, 15, and 22 of a 42-day cycle 4 weeks on 2 weeks off ; . Cisplatin was administered first, followed immediately by irinotecan as a 90-min infusion. All patients received i.v. fluid before the cisplatin infusion, consisting of 500 ml of normal saline containing 2 g of magnesium sulfate and 12.5 mg of mannitol. Etoposide was administered i.v. over 1 h, 2 days after each infusion of irinotecan cisplatin days 3, 10, 17, ; , with the etoposide dose escalated in cohorts of three patients. The initial dose of etoposide was 50 mg m2, with dose escalation occurring in 25 mg m2 increments. In the second and subsequent cohorts, the treatment schedule was modified to a 21-day, 2-weeks-on 1-week-off cycle, with irinotecan cisplatin given on days 1 and 8 and etoposide on days 3 and 10. Furthermore, the protocol was amended to allow administration of etoposide p.o. as two doses 12 h apart. The initial oral etoposide dose was 50 mg m2 every 12 h, based on a maximum-tolerated dose of 75 mg m2 for i.v. etoposide and an expected bioavailability of about 50% 13 ; . Calculated oral etoposide doses were rounded to the nearest 50 mg. A neutrophil count 1000 ml was required for initiation of each cycle of therapy and for each weekly treatment. a ; DLT was defined as any of the following toxicities occurring during the first cycle of therapy: absolute neutrophil count 500 ml or platelet count 20, 000 ml for 7 days; b ; irreversible grade 2 and any grade 35 nonhematologic toxicity except nausea vomiting in the absence of aggressive antiemetic therapy; c ; two or more consecutive week dose holds. If one patient in a cohort experienced a DLT, three additional patients would be enrolled at the same dose level. If none of the subsequent three patients experienced a DLT, then the dose of etoposide was escalated. Maximum-tolerated dose MTD ; was defined as the dose level that preceded a dose level at which two or more patients experienced a DLT. Clinical Evaluation. Pretreatment evaluation included physical examination, complete blood count CBC ; , serum chemistries, electrocardiogram, urinalysis, and chest X-ray. All measurable disease was documented by physical examination and or any appropriate imaging studies before the initiation of protocol therapy. Additionally, any relevant biochemical tumor markers were obtained before therapy. After treatment, a history and physical examination, CBC, serum chemistries, and urinalysis were performed weekly. CBCs were performed twice weekly for the first two weeks. ; Urine dipsticks were obtained before each cycle of therapy and weekly for the first 3 weeks of therapy. A urinalysis was performed if the urine dipstick was abnormal. Disease measurable by physical examination or on plain radiographs was evaluated after each cycle of therapy. Other imaging procedures required for response determination were obtained after every two cycles of treatment. Toxicity was assessed weekly using NCI Common Toxicity Criteria, version 2.0. Responses were evaluated either by physical examination or by appropriate imaging studies according to WHO criteria 14 ; . Pharmacokinetics. Heparinized blood samples were obtained immediately before starting the irinotecan infusion on day 1 at 30 min after start of the infusion and at 0, 5, 15, and 30 min and 1, 2, 3, and 24 h after the end of the infusion. Total lactone carboxylate ; concentrations of irinotecan and SN-38 were measured by HPLC with fluorescence detection as de.
Cisplatin patient assistance programs
6. Luo, L., Salunga, R. C., Guo, H., Bittner, A., Joy, K. C., Galindo, J. E., Xiao, H., Rogers, K. E., Wan, J. S., Jackson, M. R., and Erlander, M. G. Gene expression profiles of laser-captured adjacent neuronal subtypes. Nat. Med., 5: 117122, 1999. Van Gelder, R. N., von Zastrow, M. E., Yool, A., Dement, W. C., Barchas, J. D., and Eberwine, J. H. Amplified RNA synthesized from limited quantities of heterogeneous cDNA. Proc. Natl. Acad. Sci. USA, 87: 16631667, 1990. Naasani, I., Seimiya, H., Yamori, T., and Tsuruo, T. FJ5002: a potent telomerase inhibitor identified by exploiting the disease-oriented screening program with COMPARE analysis. Cancer Res., 59: 4004 4011, Ross, D. T., Scherf, U., Eisen, M. B., Perou, C. M., Rees, C., Spellman, P., Iyer, V., Jeffrey, S. S., Van de Rijn, M., Waltham, M., Pergamenschikov, A., Lee, J. C., Lashkari, D., Shalon, D., Myers, T. G., Weinstein, J. N., Botstein, D., and Brown, P. O. Systematic variation in gene expression patterns in human cancer cell lines. Nat. Genet., 24: 227235, 2000. Scherf, U., Ross, D. T., Waltham, M., Smith, L. H., Lee, J. K., Tanabe, L., Kohn, K. W., Reinhold, W. C., Myers, T. G., Andrews, D. T., Scudiero, D. A., Eisen, M. B., Sausville, E. A., Pommier, Y., Botstein, D., Brown, P. O., and Weinstein, J. N. A gene expression database for the molecular pharmacology of cancer. Nat. Genet., 24: 236 244, Bohren, K. M., Bullock, B., Wermuth, B., and Gabbay, K. H. The aldo-keto reductase superfamily. cDNAs and deduced amino acid sequences of human aldehyde and aldose reductases. J. Biol. Chem., 264: 95479551, 1989. Tang, J. Y., Hwang, B. J., Ford, J. M., Hanawalt, P. C., and Chu, G. Xeroderma pigmentosum p48 gene enhances global genomic repair and suppresses UV-induced mutagenesis. Mol. Cell, 5: 737744, 2000. Maekawa, M., Ishizaki, T., Boku, S., Watanabe, N., Fujita, A., Iwamatsu, A., Obinata, T., Ohashi, K., Mizuno, K., and Narumiya, S. Signaling from Rho to the actin cytoskeleton through protein kinases ROCK and LIM-kinase. Science Wash. DC ; , 285: 895 898, Pinkel, D. Cancer cells, chemotherapy and gene clusters. Nat. Genet., 24: 208 209, Ambrosini, G., Adida, C., and Altieri, D. C. A novel anti-apoptosis gene, survivin, expressed in cancer and lymphoma. Nat. Med., 3: 917921, 1997. Green, D. R. Apoptotic pathways: paper wraps stone blunts scissors. Cell, 102: 1 4, Staunton, J. E., Slonim, D. K., Coller, H. A., Tamayo, P., Angelo, M. J., Park, J., Scherf, U., Lee, J. K., Reinhold, W. O., Weinstein, J. N., Mesirov, J. P., Lander, E. S., and Golub, T. R. Chemosensitivity prediction by transcriptional profiling. Proc. Natl. Acad. Sci. USA, 98: 1078718792, 2001. Dan, S., and Yamori, T. Repression of cyclin B1 expression after treatment with adriamycin, but not cisplatin in human lung cancer A549 cells. Biochem. Biophys. Res. Commun., 280: 861 867 and clofibrate.
Cisplatin used with
The strong diuretic action of sodium thiosulfate also increases elimination of both compounds, thus minimizing the time the remaining cisplatin is in the kidneys.
Alimta cisplatin lung cancer
1998 ; cancer chemother pharmacol a randomized study of doxorubicin versus doxorubicin plus cisplatin in endocrine-unrespons 1985 ; cancer reduction of systemic drug exposure after hepatic arterial infusion of doxorubicin with co 1993 ; surgery enhancement of doxorubicin-induced cytotoxicity by hyperthermia in ehrlich ascites cells and clorazepate.
Metastatic disease, effective systemic treatment will become even more important for prolonging survival. Until now, chemotherapy has not been proven effective in patients with pancreatic cancer. The actual response rate to chemotherapy with 5fluorouracil 5-FU ; in many studies is below 10% [2]. Many efforts to improve the efficacy of 5-FU by either biochemical modulation with leucovorin or interferon, or combination with mitomycin C, doxorubicin and streptozotocin, have failed [3]. The protracted infusion of 5-FU in combination with cisplatin has been proven to be slightly more effective, at the expense of increased toxicity [4, 5]. Gemcitabine difluorodeoxycytidine; dFdC ; is a nucleoside analog with activity in a broad spectrum of solid tumors [6]. In two phase II trials, the objective response rate of
| Gemzar cisplatin hodgkin'sB28 FIRST LINE POLICHEMOTHERAPY PCT ; WITH CARBOPLATIN CBDCA ; PLUS VINORELBINE VNB ; IN PATIENTS PTS ; WITH ADVANCED NON SMALL CELL LUNG CANCER NSCLC ; : A PHASE II TRIAL Gianluca Cotroneo, Giovanbattista Rod, Maribel Duluc, Riccardo Ratti, Isabella Ricci, Giuseppe Nastasi U.O. Oncologia MedicaA.O., Italy Background: PCT combination with Cisplatin CDDP ; and VNB is largely used in advanced NSCLC, being considered one of the most effective schedules with a response rate RR ; ranging between 32 and 49%. CBDCA discloses a better toxicity profile than CDDP and the combination with VNB has been tested in a previous phase I study. Aims: To evaluate the feasibility and tolerability of PCT with CBDCA 300 mg mq 1 plus VNB 25 mg mq 1, 8 day q 21 in NSCLC stage IIIB IV. Patients and methods: From 10 1998 and 10 2002 we treated 23 pts. stage IIIB: 5, IV: 18 ; , 21M 2F, median age 63.3 years 4276 ; , PS 0 1 with 110 total cycles, median cycle pts 4.6. Palliative radiotherapy RT ; was performed for symptomatic metastases of the brain 4 ; , bone 3 ; , and mediastinal nodes 1 ; . The most frequent sites of metastases were: CNS 7, bone 5, liver 4, nodes 21, lung 9, suprarenal glands 3, pleural effusion 9, pericardial effusion 4. Results: 23 pts were evaluable for response WHO criteria ; : RR 7 30.4% ; , with CR 8.7% ; , SD 8 23 34.8% ; , PD 8 23 34.8% CB RR + SD ; 73.9% ; and for grade III IV toxicity OMS criteria ; : 9 23 neutropenia 39.1% ; , 4 23 thrombocytopenia 17.3% ; , 8 23 anemia 34.8% 39 110 cycles were delayed due to hematological toxicities and G-CSF was delivered 6 times and a 20% reduction of dosage was necessary in 2 cases for a total of 4 cycles after relapsing grade IV neutropenia. MST was 7.1 + , MDR 7.7 + and median duration of stabilization was 3.6 months. Conclusions: This schedule is feasible and safe, particulary regarding neuropathy and renal failure, with frequent delivery of CDDP maintaining efficacy similar to that of the CDDP + VNB regimen. The CB obtained is especially remarkable and clove.
Cisplatin gemzar regimen
Exercisecautiontopreventinadvertentcisplatinoverdosage. m2per especiallySGOT, aswell withthefollowingstatement: CALL DR. IF DOSE asbilirubin, 100 MG M2 CYCLE. a STABILITY afurthercourseof Other Events CisplatinInjectionisasterile, multidosevialwithout preservatives. abnormalities, hiccups, elevatedserumamylase, andrash. Alopecia, malaise, asthenia, anddehydrationhavebeen Store at 1525C 5977F ; . Do not refrigerate. Protect unopened container from light. Store in carton until reports, contents are used. leukemogenicagents. extravasationofcisplatin verityofthelocaltissuetoxicity Gastrointestinal fluorescentroomlight. greaterthan0.5mg mLmayresultintissuecellulitis, fibrosis, treatedwithcisplatin, andareoccasionallysoseverethat Procedures for proper handling and disposalofanticancer andnecrosis. drugsshouldbeconsidered veralguidelinesonthissubject OVERDOSAGE hours.Variousdegreesofvomiting, nauseaand oranorexia Caution should be exercised to prevent inadvertent necessaryorappropriate. overdosage with cisplatin. Acuteoverdosagewiththisdrug Delayednauseaandvomiting beginsorpersists24hoursor mayresultinkidneyfailure, liverfailure, deafness, ocular alwayswear moreafterchemotherapy ; hasoccurredinpatientsattaining toxicity includingdetachmentoftheretina ; , significant myelosuppression, intractablenauseaandvomitingand or neuritis.Inaddition, deathcanoccurfollowingoverdosage. settings, pharmacies, storerooms, andhomehealthcare Diarrheahasalsobeenreported. settings, transport OTHER TOXICITIES withinafacility, overdosage.Hemodialysis, evenwheninitiatedfourhours aftertheoverdosage, HOW SUPPLIED CisplatinInjection, 1mg mL, isavailableasfollows: cerebrovascular NDC Numbers Contents Size accident, thromboticmicroangiopathy HUS ; , orcerebral 0703-5747-11 50mg 50mLmultipledosevial DOSAGE AND ADMINISTRATION 0703-5748-11 100mg 100mLmultipledosevial Note: Needles or intravenous sets containing aluminum REFERENCES combinationofbleomycin, parts that may come in contact with cisplatin should not be used for preparation or administration. Aluminum reacts 1. ONSClinicalPracticeCommittee ncerChemotherapy although with cisplatin, causing precipitate formation and a loss of PA: OncologyNursingSociety; 1999: 32-41. notessential, itis potency. 2. Metastatic Testicular Tumors thesecasesisthedisease, underlyingvascularcompromise, antineoplasticdrugs.Washington, DC: DivisionofSafety, bleomycin, vinblastine, hypomagnesemia, oracombinationof anyofthesefactors. Services, NationalInstitutesofHealth; 1992 Dept is20mg m2IVdailyfora5daycycle. ofHealthandHumanServices, PublicHealthService Serum Electrolyte Disturbances PublicationNIH92-2621. Hypomagnesemia, hypocalcemia, hyponatremia, hypokalemia, Metastatic Ovarian Tumors 3. 253: 1590-1592. m IVpercycleonceeveryfourweeks DAY1 ; . 4. Generally, AvailablefromLouisP.Jeffrey, ScD, Chairman, National 2 cisplatinis600mg m IVonceevery4weeks DAY1 ; . cisplatin. 179 LongwoodAvenue, Boston, MA02115. reported. Incombinationtherapy, cisplatinandcyclophosphamideare 5. administeredsequentially. Hyperuricemia agents.Med J Aust.1983; 1: 426-428. Asasingleagent, 2 of100mg m IVpercycleonceeveryfourweeks. 6. JonesRB, FrankR, MassT.Safehandlingof chemotherapeuticagents: areportfromTheMountSinai creatinine. Advanced Bladder Cancer MedicalCenter Cancer J Clin.1983; 33: 258-263. 2 m , and 7. doseof5070mg m2IVpercycleonceevery3to4weeks drugs.Am J Hosp Pharm.1990; 47: 1033-1049. reducesuricacidlevels. and 2 initialdoseof50mg m percyclerepeatedevery4weeksis 8. Neurotoxicity SeeWARNINGSsection ; recommended. OSHAWork-PracticeGuidelines. ; J Health-Syst Neurotoxicity, Pharm.1996; 53: 1669-1685. prolongedtherapy 4to7months however, neurologic Issued: August2007 developduringtreatment, symptomsofneuropathymaybegin althoughthis Manufacturedby: TevaParenteralMedicines, Inc. however, may Irvine, CA92618 peripheralneuropathy. SeePRECAUTIONS: Geriatric Use. ; Lhermitte'ssign, dorsalcolumnmyelopathy, andautonomic neuropathyhavealsobeenreported.
Reduce or reducing cisplatin toxicity
The objective of this study was to evaluate the comparative effects of antihypertensive agents in patients with diabetes and normoalbuminuria. Randomized, controlled trials that compared any antihypertensive agent with placebo or another agent in hypertensive or normotensive patients with diabetes and normoalbuminuria albumin excretion rate 30 mg d ; were identified on Medline, in Embase, on the Cochrane Controlled Trials Register, in conference proceedings, and by contacting investigators. Two authors independently extracted data on renal outcomes and other patient-relevant outcomes e.g., mortality, serious cardiovascular events ; and assessed quality of trials. Analysis was by a random-effects model, and results were expressed as relative risk RR ; and 95% confidence intervals CI ; . Sixteen trials 7603 patients ; were identified, six of angiotensin-converting enzyme inhibitors ACEi ; versus placebo, six of ACEi versus calcium antagonists, one of ACEi versus calcium antagonists or combined ACEi and calcium antagonist, and three of ACEi versus other agents. Compared with placebo, ACEi significantly reduced the development of microalbuminuria six trials, 3840 patients; RR 0.60; 95% CI 0.43 to 0.84 ; but not doubling of creatinine three trials, 2683 patients; RR 0.81; 95% CI 0.24 to 2.71 ; or all-cause mortality four trials, 3284 patients; RR 0.81; 95% CI 0.64 to 1.03 ; . Compared with calcium antagonists, ACEi significantly reduced progression to microalbuminuria four trials, 1210 patients; RR 0.58; 95% CI 0.40 to 0.84 ; . A significant reduction in the risk for developing microalbuminuria in normoalbuminuric patients with diabetes has been demonstrated for ACEi only. It seems that the effect of ACEi is independent of baseline BP, renal function, and type of diabetes, but data are too sparse to be confident that these are not important effect modifiers, and an individual patient data meta-analysis is required. J Soc Nephrol 16: 30813091, 2005. doi: 10.1681 ASN.2004080634 and codeine.
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JS. Normal anal sphincter anatomy and ageand sex-related variations at high-spatialresolution endoanal MR imaging. Radiology 2000; 217: 395 Briel JW, Zimmerman DD, Schouten WR. Factors predictive of outcome after surgery for faecal incontinence. Br J Surg 2001; 88: 729 Madoff RD, Parker SC, Varma MG, Lowry AC. Faecal incontinence in adults. Lancet 2004; 364: 621 Baig MK, Wexner SD. Factors predictive of outcome after surgery for faecal incontinence. Br J Surg 2000; 87: 1316 Wexner SD, Marchetti F, Jagelman DG. The and cisplatin.
In order to maintain the pre-hydration and permit the administration of pemetrexed, the pemetrexed should be administered as follows: Provided urine output is satisfactory see below ; , approx. 30 minutes before cisplatin is due, stop the sodium chloride 0.9% pre-hydration Administer the pemetrexed Restart the remainder of the sodium chloride 0.9% pre-hydration Urine output should be maintained at 100 ml hour before for at least 2 hours ; , during and after chemotherapy. Accurate fluid balance sheet must be kept. Mannitol 10% infusion is the preferred diuretic. If urine output remains 100ml hr, a further dose of 100ml may be given by intravenous infusion over 10 minutes. Urine output should increase within 30 minutes of commencing the infusion. If urine output remains 100ml hr after 30 minutes, a 10 mg stat IV bolus of Furosemide may be given to increase urine output. If 30 minutes after the furosemide dose urine output has still not improved, the Consultant should be contacted for advice. Ensure Cisplatin is commenced by 15.00 hours at the latest so an adequate renal output can be maintained. Patients must be advised to drink 2 litres of fluid over next 24 hours. Dose Modifications Dose adjustments at the start of a subsequent cycle should be based on nadir haematologic counts or maximum non-haematologic toxicity from the preceding cycle of therapy. Treatment may be delayed to allow sufficient time for recovery. Upon recovery, patients should be retreated using the guidelines below and cogentin.
Cisplatin and etoposide
Cisplatin side effects infection
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The mechanism of action of cisplatin
Cisplatin prices, gemcitabine and cisplatin for bladder cancer, breast cancer cisplatin, cisplatin patient assistance programs and cisplatin used with. Alimta cisplatin lung cancer, gemzar cisplatin hodgkin's, cisplatin gemzar regimen and reduce or reducing cisplatin toxicity or cisplatin and etoposide.
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