RESUMO
AIM: Advanced pancreatic cancer has a bad prognosis, with a median overall survival (OS) no longer than 4-6 months. Since the end of last century, monotherapy with gemcitabine has remained the elective therapy, but new schedules are needed in order to improve these results. We aim to evaluate the efficacy of tegafur and levofolinic acid (LV) associated with gemcitabine, as well as its toxicity, progression-free survival and OS in advanced pancreatic cancer. PATIENTS AND METHODS: An open-label, multicentric, prospective, non-controlled trial was carried out on patients with advanced or disseminated pancreatic cancer. Gemcitabine 1250 mg/m² was administered on the 1st and 8th days of the cycle, tegafur 750 mg/m²/day for 21 consecutive days and LV 25 mg/day continuously, every 28 days, with a maximum of six cycles. The primary variable was tumour overall response rate (ORR). Secondarily, time to progression (TTP), OS and scheme toxicity were determined. RESULTS: Forty patients were recruited; the male/female ratio was 30:10, with a mean age of 61 years. Forty percent had a Karnofsky index of 90% or 100%. Only 11 patients (27%) completed the six cycles of treatment, but more than 50% received three or more cycles. Dose intensity was 89.56% for gemcitabine and 87.36% for tegafur. Efficacy ORR was 22.5% (CI 95%, 6-37%). TTP was 3.87 months (CI 95%, 2.1-5.6), time to treatment failure was 2.97 months (CI 95%, 2.43-4.67) and OS 6.3 months (CI 95%, 4-7). The chemotherapeutic combination was well accepted; most haematologic and non-haematologic toxicities were grade 1 or 2. The most prevalent grade 3/4 toxicities were asthenia (30%), liver biochemistry disorders (25%), diarrhoea (15%) and stomatitis (12%). CONCLUSIONS: The administration of gemcitabine, associated with oral tegafur and leucovorin, has activity against advanced pancreatic cancer, with an adequate toxicity profile.
Assuntos
Adenocarcinoma/tratamento farmacológico , Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem , Desoxicitidina/análogos & derivados , Neoplasias Pancreáticas/tratamento farmacológico , Tegafur/administração & dosagem , Adenocarcinoma/mortalidade , Adenocarcinoma/patologia , Administração Oral , Antineoplásicos/administração & dosagem , Antineoplásicos/efeitos adversos , Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Desoxicitidina/administração & dosagem , Desoxicitidina/efeitos adversos , Progressão da Doença , Feminino , Humanos , Leucovorina/administração & dosagem , Leucovorina/efeitos adversos , Masculino , Pessoa de Meia-Idade , Neoplasias Pancreáticas/mortalidade , Neoplasias Pancreáticas/patologia , Análise de Sobrevida , Tegafur/efeitos adversos , Resultado do Tratamento , GencitabinaRESUMO
Haemolytic uraemic syndrome (HUS) is a rare thromboembolic complication observed in patients with cancer. It is characterised by the clinical triad of acute renal failure, microangiopathic haemolytic anaemia and thrombocytopaenia. It may be associated with a variety of aetiologies, including chemotherapeutic agents such as mitomycin, cisplatin, bleomycin, 5-fluorouracil and, most recently, gemcitabine. We report a 70-year-old patient treated with gemcitabine who developed haemolytic uraemic syndrome.
Assuntos
Desoxicitidina/análogos & derivados , Síndrome Hemolítico-Urêmica/induzido quimicamente , Idoso , Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Carboplatina/administração & dosagem , Carcinoma/tratamento farmacológico , Carcinoma/patologia , Desoxicitidina/administração & dosagem , Desoxicitidina/efeitos adversos , Humanos , Masculino , Neoplasias da Bexiga Urinária/tratamento farmacológico , Neoplasias da Bexiga Urinária/patologia , Urotélio/efeitos dos fármacos , Urotélio/patologia , GencitabinaRESUMO
INTRODUCTION: Gastrointestinal stromal tumours (GIST) are mesenchymal tumours of the digestive tract originated in the interstitial cells of Cajal. They express the tyrosine kinase c-kit (CD117) activity receptor. Mutations in this receptor cause neoplastic development. Curative treatment continues to be radical resection of the tumour and is resistant to commonly employed chemotherapy regimens. Imatinib mesilate is a drug that inhibits c-kit activity expressed by GIST and its activity in these tumours has been demonstrated. MATERIAL AND METHODS: Retrospective study of all cases of leiomyoma, leiomyosarcoma, schwannoma, and stromal or mesenchymal tumors from 1989 to July 2004. C-kit and CD34 proteins were detected at immunohistochemical study in addition to the usual markers for mesenchymal tumours. RESULTS: 49 GISTs were diagnosed, 26 males and 23 females (mean age 64.1). Symptoms were digestive tract bleeding (n = 13), abdominal pain (n = 13), intestinal occlusion (n = 4) and others. The lesion was located in small bowel (n = 22), stomach (n = 19), rectum (n = 3), peritoneum (n = 2), esophagus (n = 1), omentum (n = 1), and retroperitoneum (n = 1). Forty-three of the 49 patients underwent surgery; radical resection was performed in 37 (75.5%) and palliative surgery in the other six (16.2%). Two of the patients that did not undergo surgery received chemotherapy. At the time of study, 28 (57.14%) patients remained alive, 23 (46.9%) of whom were disease- free and five (10.2%) were not. Nineteen (38.7%) patients died. CONCLUSIONS: The results of our series are similar to the others published. Before the year 2001, surgery was the only successful option for the GIST. Surgical resection continues being the best treatment to definitively cure this disease. Imatinib is used to treat not only resectable tumours, but even to allow the possibility to make a subsequent rescue surgery. On the other hand, Imatinib is used in the treatment of the metastatic disease.