RESUMO
We report on a 26-year-old patient with primary infertility since 3 years, when whilst undergoing an office laparoscopy to find out the causes of her infertility, the tip of a 10-year-old 10 mm optictrocar broke and fell in the abdomen. The patient was referred to our clinic to remove this foreign body after discovery of the breakage and loss of the trocartip in the abdomen. We discuss in this case report and literature review on the loss of parts of instruments in the abdomen during laparoscopy as well as the management of such complication and measures to their careful prevention. This case report shows and stresses the importance of security tests and proof of instruments before laparoscopy by the laparoscopic and operation theatre nurse, more especially when reusable instruments are used.
Assuntos
Corpos Estranhos/etiologia , Infertilidade Feminina/cirurgia , Complicações Intraoperatórias/etiologia , Laparoscópios , Cavidade Peritoneal , Adulto , Falha de Equipamento , Feminino , HumanosRESUMO
We evaluated the in vitro cytotoxicity of topotecan (TPT), versus cisplatin, etoposide (VP-16) and paclitaxel (PTX) in four squamous cell cancer cell lines of the cervix uteri and vulva. Four established human squamous cancer cell lines from the cervix uteri (A-431, Ca Ski and C-33) and vulva (CAL-39) were used. The cytotoxic effects of the agents were examined using the ATP-Tumor Chemosensitivity Assay (ATP-TCA). In addition to the single agents, the following combinations were tested: TPT+cisplatin, TPT+VP-16 and TPT+PTX. Three cell lines (C-33, Ca Ski and CAL-39) were highly sensitive to TPT, but one cell line (A-431) was less sensitive. Furthermore, the cytotoxic activity of TPT was superior to that of cisplatin in Ca Ski and C-33 cells, but inferior in CAL-39 and A-431. TPT was also more active than VP-16 in CAL-39 and Ca Ski. On the other hand, the cytotoxic activity of TPT was weaker than PTX in C-33, CAL-39 and A-431. TPT increased the cytotoxic activity of cisplatin and VP-16 in C-33, Ca Ski and A-431. However, synergistic features were observed only in A-431 cells. TPT also enhanced the cytotoxic activity of PTX in A-431 and Ca Ski. In CAL-39 and C-33, however, increased cytotoxic activity occurred only at higher drug concentrations, whereas antagonism was observed at lower drug concentrations. In conclusion, our results suggest that TPT has a significant cytotoxic effect on most squamous cell cancer cell lines which may be superior to cisplatin, VP-16 and PTX in some instances. Furthermore, TPT is likely to potentiate the cytotoxic activity of these agents in individual cell lines tested.
Assuntos
Antineoplásicos/toxicidade , Protocolos de Quimioterapia Combinada Antineoplásica/toxicidade , Carcinoma de Células Escamosas/tratamento farmacológico , Topotecan/toxicidade , Neoplasias do Colo do Útero/tratamento farmacológico , Neoplasias Vulvares/tratamento farmacológico , Trifosfato de Adenosina/análise , Cisplatino/administração & dosagem , Cisplatino/toxicidade , Ensaios de Seleção de Medicamentos Antitumorais , Inibidores Enzimáticos/toxicidade , Etoposídeo/administração & dosagem , Etoposídeo/toxicidade , Feminino , Humanos , Medições Luminescentes , Paclitaxel/administração & dosagem , Paclitaxel/toxicidade , Topotecan/administração & dosagem , Células Tumorais CultivadasRESUMO
We analyzed tumor tissues from 14 patients with invasive squamous cell carcinoma of the cervix for aberrations of chromosome 17 and p53 expression. All but 3 patients were negative for p53 protein expression, the protein being detected in 2 International Federation of Obstetrics and Gynecology stage IIa cancers and 1 stage Ib G3 carcinoma. Significant cytogenetic aberrations in the form of losses and gains of chromosome 17 were diagnosed in 9 and 7 patients, respectively. There was no correlation with tumor prognosis, clinical stage or histologic grade. According to most reports, almost all cervical carcinomas contain integrated human papilloma virus (HPV) and express E6 oncoproteins. Increasing evidence suggests that E6 protein interaction leads to p53 mutation in HPV-infected cervical epithelium. Since most cervical tumors are infected with HPV, and the tumors originate through p53 gene mutation caused by the said interaction, which leads subsequently to the overexpression of p53 oncoprotein, lack of the latter in the remaining 11 cervical tumors may either be the result of technical shortcomings, or the tumor may arise in such circumstances through a p53-independent pathway. On the other hand, 2 of 3 stage IIa cancers and 1 Ib G3 carcinoma were found to be p53 positive, thus supporting the notion that p53 inactivation is a relatively late event in the progression of cervical cancer.