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Materials. Dexrazoxane was from either Chiron Corporation Amsterdam, the Netherlands ; or Pfizer Kalamazoo, MI ; . Etoposide and doxorubicin were from Pfizer A S Copenhagen, Denmark ; and daunorubicin was from Rhone-Poulenc Rohrer Holte, Denmark ; . Fentanyl-fluanisone hypnorm was from Janssen-Cilag Bierkeroed, Denmark ; and midazolam dormicum ; was from Roche Hvidovre, Denmark ; . All drugs were commercially obtained. Cell culture. Methocult contained 1% methylcellulose in Iscove's modified Dulbecco's medium, 1% bovine serum albumin, 100 nmol L.
See arrows in Fig. 5A ; in the same secretory granules that also contain OT-NP-ir seen as small, 10 nm gold ; . Also shown is a non-OT nerve terminal presumably containing VP ; that contains neither label arrowhead in Fig. 5A ; , and an OTterminal but with no EGFP asterisk in Fig. 5B ; . These data indicate that the EGFP is packaged into OT-NP containing secretory granules for axonal transport to the pituitary in these subcellular organelles. Because the secretory granules are also the vehicles for regulated, calcium-dependent ; secretion of OT and OT-NP from nerve terminals in the pituitary, we then examined whether the EGFP fluorescence could be secreted in a calcium-dependent manner.
Groundwater and or surface water contaminant levels exceeding levels specified in 18 aac 70 water quality standards ; except those parameters documented as having natural background levels already exceeding these limits; sudden, abrupt, or significant increases in any one or more pollutants which are attributable to site operation regardless of the listed mcls; or statistically significant change over background levels.
Purpose: To determine whether agents that target topoisomerase I and II could be administered sequentially. Design: A Phase I study was conducted to evaluate sequential treatment with bolus IV doxorubicin followed 48 h later by topotecan given as a 30-min i.v. infusion on 3 consecutive days, with additional cycles of therapy repeated every 3 weeks. Characteristics of the 22 patients entered into the study were: 13 male and 9 female; median age, 49.5 range 33 66 ; years; Eastern Cooperative Oncology Group performance status, 0 1; and normal cardiac, hematological, hepatic, and renal function. All patients had received prior therapy median 2 prior regimens ; . Results: The maximum tolerated dose of the combination was 25 mg m2 doxorubicin and 5.25 mg m2 topotecan 1.75 mg m2 day 3 ; . Neutropenia was the dose-limiting toxicity. Attempts to further escalate the dose using 5 g kg granulocyte colony-stimulating factor proved unsuccessful because of thrombocytopenia. Among the 17 patients who were evaluable for response, 6 had a partial response, and 4 showed evidence of disease stabilization. The partial responses occurred in patients with small cell lung cancer 3 of 7 ; , non-small cell lung cancer 1 of 6 ; , esophageal adenocarcinoma 1 of 2 ; , and ovarian carcinoma 1 of 1 ; , and it lasted for 3 6 months. Administration of doxorubicin 2 days before topotecan did not alter topotecan pharmacokinetics.
Doxorubicin dexrazoxane
Outpatient and ambulatory health services. AIDS Drug Assistance Program treatments under section 2616. AIDS pharmaceutical assistance. Oral health care. Early intervention services described in subsection e ; - Part C. Health insurance premium and cost sharing assistance for lowincome individuals in accordance with section 2615. Home health care. Medical nutrition therapy. Hospice services. Home and community-based health services as defined under section 2614 c ; - Part B Mental health services. Substance abuse outpatient care. Medical case management, including treatment adherence services.
This table will be updated as the toxicity profile of the agent is revised. Updates will be distributed to all Principal Investigators at the time of revision. The current version can be obtained by contacting ADEERSMD tech-res . Your name, the name of the investigator, the protocol and the agent should be included in the e-mail. Also reported on STI571 trials but with the relationship to STI571 still undetermined: autoimmune reaction; cardiac ischemia infarction; cardiopulmonary arrest; left ventricular systolic dysfunction; DIC; insomnia; dry skin; duodenal perforation; esophageal fistula; gastritis; GI ulcer; ileus; respiratory tract hemorrhage; urinary hemorrhage; febrile neutropenia; hypercalcemia; hypomagnesemia; lipase; seizure; blurred vision; ocular surface disease; voice changes; kidney stones; Guillain-Barre syndrome and dronabinol.
HILDEN ET AL Table 1. Results of Cytogenetics, Southern Analysis of the MLL Gene, and RT-PCR for the MLL AF4 Fusion Transcript in Infant ALL.
Out 7 months after the first operation. No gross tumour was found during the second surgery, and frozen sections of suspicious areas were negative for tumour. Likewise, paraffinembedded biopsy samples from several parts of the peritoneum were found to contain only well-differentiated glia and villi. There was no evidence of disease. In addition, left ovarian specimens revealed a corpus luteal cyst, and the patient's menstrual cycle continued throughout the treatment. Seven months after the SLO, however, the patient showed peritoneal fluid retention that was highly dependent on the stage of her menstrual cycle. The patient was 27 years old when first seen in our infertility section, with irregular ovulatory cycles. Her serum hormone levels at day 3 of the cycle were as follows: FSH, 13.53 mIU ml follicular phase normal range: 5.214.4 mIU ml LH, 4.36 mIU ml follicular phase normal range: 1.87.6 mIU ml prolactin, 12.45 ng ml normal range: 3.2026.2 ng ml and estradiol, 38.03 pg ml follicular phase normal range: 19255 pg ml ; . All tumour markers, including Ca125, CA19-9, CEA, fetoprotein and -hCG, were within the normal range. The patient underwent hysterosalpingography, and left tubal passage was confirmed. Her partner's sperm was normal. We first thought that the patient might be able to become pregnant as a matter of natural course, without the use of assisted reproduction technology ART ; . However, the adnexa in this patient were floating in a substantial amount of peritoneal fluid, which we surmised was making it difficult for the fimbria to retrieve the oocyte. In an effort to achieve pregnancy, the patient underwent a short regimen of GnRH agonist. Initially, 300 IU of human menopausal gonadotrophin Nikken Chemicals, Tokyo, Japan ; was administered from day 3 to day 8 of her menstrual cycle. The number of developed follicles was four. She then received hCG on day 9, and four oocytes were retrieved 34 h later, after the retained peritoneal fluid 300 ml ; was removed by vaginal puncture. After the specimen was cytocentrifuged, an air-dried smear was stained with Giemsa stain and alcohol-fixed smears were stained with Papanicolaou stain and periodic acid Schiff PAS ; alcian blue stain. We analysed cancer cells and found no evidence for cancer. All of the oocytes were successfully fertilized and reached the 3- to 5-cell stage on day 2 after fertilization. The patient elected to have three embryos transferred on that day. The remaining embryo was cryopreserved. The patient conceived and gestated dichorionic twins but suffered from abdominal tenderness due to accumulation of peritoneal fluid as a result of the embryo transfer. On five occasions during the period extending from day 10 after embryo transfer to the 11th week of gestation, this fluid 3.5 l in total ; was removed from the Douglas pouch by puncture. No peritoneal fluid was obtained with the last puncture. After 29 weeks of gestation, the patient presented with preterm labour and was administered a tocolytic agent, ritodrine. The tocolysis was successful, and a healthy female infant weighing 2380 g and a male infant weighing 2198 g were delivered by selective Caesarean section after 36 weeks of gestation. At that time, there was no evidence of residual tumour, but a filmy adhesion between the peritoneum and uterus was observed, suggesting the earlier peritoneal fluid retention was due to a pseudocyst. 2 and dss.
Doxorubicin drug action
This document is the country report on the Notified Bodies in Spain. It describes the actual status of Notified Bodies in Spain at 01st June 2002.
Acute ear infection: If ear pain or discharge persists. Refer Urgently to hospital. Chronic ear infection: Check that the mother is wicking the ear correctly. Encourage her to continue. If no ear pain or discharge, praise the mother for her careful treatment. If she has not yet finished the 10 days of antibiotic, tell her to use all of it before stopping. FEEDING PROBLEM and dulcolax.
The cytochrome P450 P4501 ; group of enzymes are the predominant catalysts of phase I xenobiotic metabolism in humans and other mammals, catalyzing a variety of monooxygenation reactions including, among others, aliphatic and aromatic hydroxylation, epoxidation, N- and O-dealkylation, and N-and S-oxidation. In humans, approximately 15 enzymes from the CYP13 families are responsible for the metabolic clearance of most lipophilic chemicals. Among this group, forms from the same subfamily show discrete but often overlapping substrate specificities. CYP2C9, one of the most important forms in overall drug metabolism, is distinguished from other human CYP2C forms by a preference for substrates bearing a negative charge at physiological pH Smith and Jones, 1992; Mancy et al., 1995 however, neutral or positively charged substrates may also be substrates. Various models have been developed to explain the preference for anionic substrates.
T. W. Kensler. Environmental Health Sciences, Johns Hopkins University, Baltimore, MD. The development of Nrf2 knockout mice provided the first key insights into the toxicological importance of this transcription factor signaling pathway. As examples, Nrf2 knockout mice are more sensitive to the hepatotoxicity of acetamino and duragesic.
Ries F, see Piccart MJ Riethmuller G, see Braun S Rifon J, see Sureda A Rigas JR, see Khuri FR Riggins GJ, see Polyak K Riggins J, see Smith TJ Riley R, see Burchill SA Rilli M, see Guermazi A Rimer BK, see Demark-Wahnefried W Ringborg U, see Mrtenson ED Ringden O, see Saarinen-Pihkala UM Riofrio M, see Delaloge S --see Taamma A Ripamonti C, see Cherny N --see Mercadante S Ris MD, Packer R, Goldwein J, Jones-Wallace D, Boyett JM. Intellectual Outcome After Reduced-Dose Radiation Therapy Plus Adjuvant Chemotherapy for Medulloblastoma: A Children's Cancer Group Study, 3470 Rischin D, see Albanell J Rischin D, Peters L, Hicks R, Hughes P, Fisher R, Hart R, Sexton M, D'Costa I, von Roemeling R. Phase I Trial of Concurrent Tirapazamine, Cisplatin, and Radiotherapy in Patients With Advanced Head and Neck Cancer, 535 Risques RA, see Esteller M Risse EKJ, see Herder GJM Ritchey K, see Evans WE Ritchey ML, see Green DM Ritter G, see Scott Ritter J, see Creutzig U Rittweger K, see Motzer RJ Ritvanen A, see Moller TR Ritz J, see Soiffer RJ Riva A, see Khayat D --see Nabholtz JM Rivera E, see Seidman AD Rivera E, Valero V, Syrewicz L, Rahman Z, Esteva FL, Theriault RL, Rosales MM, Booser D, Murray JL, Bast RC Jr, Hortobagyi GN. Phase I Study of Stealth Liposomal Doxorubicin in Combination With Gemcitabine in the Treatment of Patients With Metastatic Breast Cancer, 1716 Riviere A, see von Pawel J `.
Ifosfamide doxorubicin
The anthracycline doxorubicin has been in clinical use for several decades, and is still among the most widely used chemotherapeutic agents for treatment of a variety of neoplasms Weiss, 1992; Zagotto et al., 2001; Lothstein et al., 2001 ; . Despite many years of research in developing new and better anthracyclines, little or no change in the molecular structure of doxorubicin made it to the clinic. However, with the development of liposomal formulations, its delivery to at least certain types of tumors underwent a major improvement Tardi et al., 1996; Gabizon, 2001 ; . Compared to systemic application of free doxorubicin, liposomal doxorubicin exhibits significant advantages, such as reduced normal tissue toxicities Orditura et al., 2004 ; . Improved loading procedures, resulting in high doxorubicin encapsulation efficiencies, further increased the therapeutic index of entrapped doxorubicin Papahadjopoulos et al., 1991; Horowitz et al., 1992; Haran et al., 1993 ; . Another major step forward was the development of polyethyleneglycol PEG ; -coated liposomes. This coating prevents opsonization and reduces the uptake by macrophages from the reticulo-endothelial system, in turn resulting in prolonged circulation times, as compared to free doxorubicin or to non-coated liposomes Papahadjopoulos et al., 1991; Vaage et al., 1992; Robert and Gianni, 1993; Gabizon et al., 1996; Uster et al., 1996 ; . PEG-liposome-encapsulated doxorubicin commercially available as Caelyx and Doxil ; is now in clinical use for the treatment of various types of neoplasms, and innovations such as covalent attachment of tumor-specific antibodies or ligands will further enhance drug targeting and therapeutic value Park et al., 2002; Pan et al., 2003 ; . The endothelial lining of healthy blood vessels effectively prevents escape of liposomes from the circulation. In contrast, angiogenesis-associated vascular abnormalities of many solid tumors do allow extravasation of long-circulating PEG-liposomes into the tumor stroma Yuan et al., 1994 ; . Despite the resulting accumulation in tumor tissue, the liposomes are not taken up by the tumor cells. Instead, their doxorubicin load is gradually released into the interstitial space Horowitz et al., 1992; Harasym et al., 1997 ; . Given the intracellular localization of its molecular targets, sufficient cellular uptake of doxorubicin is required for its action Speth et al., 1988; Lothstein et al., 2001 ; . However, doxorubicin does not possess the optimal degree of lipophilicity and echinacea.
RESPIRATORY VIRAL INFECTIONS are an important cause of asthma attacks 13 ; . Viral infections account for 80 85% of asthma exacerbations in children 17 ; and 50 55% in adults 4 ; . Virus-induced hyperresponsiveness in animals and humans is blocked by atropine, indicating a role for the parasympathetic nerves 3, 6, 8 ; . In the lungs, acetylcholine released from parasympathetic nerves onto postjunctional M3 muscarinic receptors causes smooth muscle contraction and bronchoconstriction. Acetylcholine also binds to inhibitory prejunctional M2 muscarinic receptors on parasympathetic nerves, suppressing acetylcholine release and.
Doxorubicin fluorescence spectra
Overview: Faulk Pharmaceuticals, Inc. FPI ; has a platform of targeted therapeutics with areas of application in cancer and infectious diseases. These are protected by issued and pending patents. The lead compound is a new chemical entity consisting of a conjugate of transferrin a plasma protein ; with doxorubicin an FDA approved cancer drug, Adriamycin ; that targets transferrin receptors found on a wide array of cancer cells. The conjugate has been shown to be highly potent in numerous cell lines by the National Cancer Institute NCI ; as well as in cancer cells known to be resistant to doxorubicin. These transferrin-doxorubicin TRF-DOX ; conjugates have been studied in human patients in England and in the USA. Large market opportunities await targeted anti-cancer drugs that have maximum effectiveness with minimal toxicity while providing a therapeutic option for numerous drug resistant cancers. FPI is seeking M for a ; preclinical studies to file an IND for TRF-DOX with the FDA, b ; production of TRF-DOX, and c ; Phase I and Phase II Clinical studies. Technology: Transferrin is a normal blood protein that transports iron to cells through transferrin receptors. The vast majority of normal, resting, adult cells have low iron needs and express few if any transferrin receptors on their surfaces. In contrast, cancer cells have high metabolic requirements and express ~100 K transferrin receptors per cell. This disparity underpins the drug-targeting specificity of TRF-DOX for cancer cells. Drug targeting requires less drug and the use of less drug causes less drug toxicity. In addition, drug resistance is a major cause of treatment failure, particularly in reoccurring cancers. Drug resistance often is the result of efflux pumps that remove drugs from cells. Thus, other targeting approaches often do not overcome drug resistance because when the targeting agent releases its drug into cells, the free drug simply is pumped out. In contrast, the mechanism of TRF-DOX is that it kills by binding to and disrupting necessary enzymes on the surface of cells, thus avoiding the efflux pumps of resistance. In vitro studies; The lead transferrin-targeted drug TRF-DOX ; has been shown by collaborators at the NCI-Developmental Therapeutics Program to be highly active in 60-cell line panels for 8 different types of human cancers. Note in the following Table that TRF-DOX has lower LD50 values than DOX, vinblastin accept ovary ; , cisplatin and paclitaxel Taxol ; , all of which are first-line drugs in the treatment of cancer. Numbers in the Table are microMolar drug concentrations: Cancer Melanoma Leukemia Lung Colon Ovary Renal Prostate Breast TRF-DOX Doxorubicin 0.5 3.2 0.6 Vinblastin 31.6 40 Cisplatin Paclitaxel 63.1 100 80 and efalizumab.
We thank Prof. Y.-S. Ho Wayne State University, Detroit, MI ; for providing the cDNA of manganese superoxide dismutase Mn SOD ; and Prof. J. D. Crapo National Jewish Medical and Research Center, Denver, CO ; for providing the antibody to Mn SOD. The skillful technical assistance of Raija Sirvio is acknowledged. This study was supported in part by the Universities of Oulu and Helsinki, the Finnish Antituberculosis Association Foundation, and the Sigrid Juselius Foundation. Address for reprint requests and other correspondence: V. Kinnula, Univ. of Oulu, Dept. of Internal Medicine, Kajaanintie 50A, 90220 Oulu, Finland E-mail: vuokko.kinnula oulu.fi ; . Received 27 May 1999; accepted in final form 22 December 1999. REFERENCES 1. Akashi M, Takagi S, and Hachiya M. Anti-cancer agent OK432 induces manganese superoxide dismutase in human granulocytes. Int J Cancer 68: 384390, 1996. Al-Kabban M, Stewart MJ, Watson ID, and Reglinski J. The effect of doxorubicin on the glutathione content and viability of cultured human lung cancer cell lines A549 and GLC4210. Clin Chim Acta 24: 121129, 1990. Babiak RM, Campello AP, Carnieri EG, and Oliveira MB. Methotrexate: pentose cycle and oxidative stress. Cell Biochem Funct 16: 283293, 1998. Beutler E. Glutathione peroxidase. In: Red Cell Metabolism: A Manual of Biochemical Methods. New York: Grune & Stratton, 1975, p. 7173. 5. Bradford M. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principal of protein-dye binding. Anal Biochem 72: 248254, 1976. Chomczynski P and Sacchi N. Single-step method of RNA isolation by acid guanidium thiocyanate-phenol-chloroform extraction. Anal Biochem 162: 156159, 1987. Cobbs CS, Levi DS, Aldape K, and Israel MA. Manganese superoxide dismutase expression in human central nervous system tumors. Cancer Res 56: 31923195, 1996. Crapo JD and Tierney DF. Superoxide dismutase and pulmonary oxygen toxicity. J Physiol 226: 14011407, 1974. Das KC, Guo XI, and White CW. Protein kinase deltadependent induction of manganese superoxide dismutase gene expression by microtubule-active anticancer drugs. J Biol Chem 18: 3463934645, 1998. Das KC, Lewis-Molock Y, and White CW. Activation of NF- B and elevation of MnSOD gene expression by thiol reducing agents in lung adenocarcinoma A549 ; cells. J Physiol Lung Cell Mol Physiol 269: L588L602, 1995. 11. Das KC and White CW. Activation of NF-kappaB by antineoplastic agents. Role of protein kinase C. J Biol Chem 272: 14914 14920, De Haan JB, Cristiano F, Iannello R, Bladier C, Kelner MJ, and Kola I. Elevation in the ratio of Cu Zn-superoxide dismutase to glutathione peroxidase activity induces features of cellular senescence and this effect is mediated by hydrogen peroxide. Hum Mol Genet 5: 283292, 1996. Habig W and Jakoby W. Assays for differentiation of glutathione S-transferase. Methods Enzymol 77: 398405, 1981. Hatcher EL, Alexander JM, and Kang YJ. Decreased sensitivity to adriamycin in cadmium-resistant human lung adenocarcinoma A549 cells. Biochem Pharmacol 53: 747754, 1997. Ho Y-S. Transgenic models for the study of lung biology and disease. J Physiol Lung Cell Mol Physiol 266: L319L353, 1994. 16. Ho Y-S, Vincent R, Dey MS, Slot JW, and Crapo JD. Transgenic models for the study of lung antioxidant defense: enhanced manganese-containing superoxide dismutase activity gives partial protection to B6C3 hybrid mice exposed to hyperoxia. J Respir Cell Mol Biol 18: 538547, 1998. Hohmeier H-E, Thigpen A, Tran VV, Davis R, and Newgard CB. Stable expression of manganese superoxide dismutase MnSOD ; in insulinoma cells prevents IL-1B-induced cytotoxicity and doxorubicin.
Doxorubicin p53 u2os
Send reprint requests to: Robin Fuchs-Young, UT M.D. Anderson Cancer Center, Department of Carcinogenesis, Park Rd. 1C, Smithville, TX 78957. E-mail: rofy sprd1.mdacc.tmc and eletriptan.
| Doxorubicin cardiac side effects15. Graham MV, Emami B. Cancers of the lung and mediastinum. In: Khan FM, Potish RA, editors. Treatment Planning in Radiation Oncology. Baltimore: Williams and Wilkins 1998; 56786. 16. Valley JF, Mirimanoff RO. Comparison of treatment techniques for lung cancer. Radiother Oncol 1993; 28: 16873. Senan S, von Sornsen de KJ, Samson M, Tankink H, Jansen P, Nowak PJ, et al. Evaluation of a target contouring protocol for 3D conformal radiotherapy in non-small cell lung cancer. Radiother Oncol 1999; 53: 24755. Baird JA. The pathways of lymphatic spread of carcinoma of the lung. Br J Surg 1965; 52: 86875. Oyzizu T, Sagawa M, Sato M, Sakurada A, Matsumura Y, Ono S, et al. The pattern of mediastinal nodal involvement in lung cancer according to tumor-located lobe abstract ; . Kyobu Geka 1999; 52: 8904. Schinkel C, Mueller C, Reinmiedl J, Hoomann H, Zimmer S, Dienemann H, et al. Mediastinal lymph node infiltration in non-small cell lung cancer and its role in curative surgery. Scand Cardiovasc J 1999; 33: 2868. Emami B, Kaiser L, Simpson J, Shapiro S, Roper C, Lockett MA. Postoperative radiation therapy in non-small cell lung cancer. J Clin Oncol 1997; 20: 4418. Armstrong J, Ginbey CM. The impact of three-dimensional radiation on the treatment of non-small cell lung cancer. Radiother Oncol 2000; 56: 15767. McGibney C, Holmberg O, McClean B, Williams C, McCrea P, Sutton P, et al. Dose escalation of chart in non-small cell lung cancer: is threedimensional conformal radiation therapy really necessary? Int J Radiat Oncol Biol Phys 1999; 45: 33950. Armstrong J, Raben A, Zelefsky M, Burt M, Leibel S, Burman C, et al. Promising survival with three-dimensional conformal radiation therapy for non-small cell lung cancer. Radiother Oncol 1997; 44: 1722. Oda M, Wtanab Y, Shimizu J, Murakami S, Ohta Y, Skedo N, et al. Extent of mediastinal node metastasis in clinical stage I non-small cell lung cancer: the role of systematic nodal dissection. Lung Cancer 1998; 22: 2330. Hayakawa K, Mitsuhashi N, Saito Y, Nakayama Y, Furuta M, Sakurai H, et al. Limited field irradiation for medically inoperable patients with peripheral stage I non-small cell lung cancer. Lung Cancer 1999; 26: 137 Slotman BJ, Antonisse IE, Njo KH. Limited field irradiation in early stage T1-2N0 ; non-small cell lung cancer. Radiother Oncol 1996; 41: 414. Lung cancer study group. Effects of postoperative mediastinal radiation on completely resected stage II and stage III epidermoid cancer of the lung. N Engl J Med 1986; 315: 137781.
Abstract The evolving role of mitochondria as a target for many anticancer drugs e.g. platinum-based compounds, alkylating agents and anthracyclines ; prompted us to investigate their immediate effects on the mitochondrial respiratory chain. For this purpose, we used a phosphorescence analyzer that measures [O2] in solution. The [O2] of solutions containing an appropriate substrate and various cell lines, tumors from patients or beef heart submitochondrial particles SMPs ; declined almost linearly r 0: 99 ; function of time, indicating that the kinetics of cellular oxygen consumption were zero order. Rotenone inhibited respiration, confirming that oxygen was consumed by the respiratory chain. Exposure to a clinically relevant concentration of cisplatin 5 mM at 378 for 13 hr ; had no effect on the respiration in cells or in SMP. Higher cisplatin concentrations 1099 mM at 378 for 13 hr ; produced 25% inhibition. Incubations with 4-hydroperoxycyclophosphamide 50100 mM at 378 for 1 hr ; inhibited oxygen consumption in SMP % inhibition at 50 mM ; and in cells % inhibition at 50 mM ; Incubations 378 for 1 hr ; of SMP with doxorubicin 25100 mM ; and daunorubicin 25100 mM ; had no inhibitory effect on the respiration. By contrast, incubations 378 for 1 hr ; of cells with doxorubicin 520 mM ; and daunorubicin 220 mM ; produced significant inhibition. We conclude that cisplatin does not directly damage the energy converting mechanism of mitochondria. On the other hand, comparable exposures to alkylating agents and anthracyclines produce immediate and dose-dependent impairment of cellular respiration. # 2003 Elsevier Inc. All rights reserved and elidel.
Doxorubicin lawsuits
OTHER SUBJECTS Kirkendall, W. M., Liechty, R. D., and Culp, D. A.: Diagnosis and Treatment of Patients with Pheochromocytoma. Arch. Int. Med. 115: 529 May ; , 1965. The diagnostic and therapeutic aspects of pheochromocytoma, based on experience with 17 patients seen during a period of 23 years, were reviewed. Symptoms of anxiety, emotional disturbances, and convulsions were frequent. About half had hyperglycemia, glycosuria, or an abnormal glucose tolerance test. Signs of increased metabolism in the absence of an increased serum protein-bound iodine level or of an increased uptake of I131 by the thyroid gland were characteristic. Pharmacologic tests were of some value but, as others have found, false-positive and false-negative tests also occurred. Urine catecholamine levels were increased in all but one patient in whom. however, an abnormal level did occur following provocation with histamine. It is thought that preoperative treatment with blood transfusions or with the alpha adrenergic blocking agent phentolamine is of value in order to combat the chronic depletion of plasma volume resulting from prolonged catecholamine-induced venoconstriction and dronabinol.
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