ABSTRACT
BACKGROUND: Because of inaccuracies in clinical staging, endometrial adenocarcinoma is now a surgically staged disease. This study was done to determine the safety and efficacy of a laparoscopically assisted approach in the treatment and staging of this disease. METHODS: Using a retrospective chart review, we identified demographic characteristics, mean blood loss, operative findings, and complications of patients who had laparoscopically assisted staging and treatment for endometrial carcinoma from 1992 to 1997. RESULTS: Of 34 patients, 28 had laparoscopic surgical staging that included pelvic and para-aortic lymph node assessment, peritoneal washings, bilateral salpingo-oophorectomy, and total vaginal hysterectomy; 23 patients (82%) had stage I disease, 2 (7%) had stage II disease, and 3(11%) had stage III disease. Complications included herniation through a 5 mm port site, necessitating small bowel resection, and a fatal myocardial infarction 10 days postoperatively. CONCLUSION: Laparoscopic staging and treatment of endometrial carcinoma is appropriate in a select group of patients.
Subject(s)
Adenocarcinoma/secondary , Adenocarcinoma/surgery , Endometrial Neoplasms/pathology , Endometrial Neoplasms/surgery , Laparoscopy , Blood Loss, Surgical , Blood Transfusion , Female , Humans , Laparoscopy/adverse effects , Length of Stay , Lymphatic Metastasis , Medical Records , Middle Aged , Neoplasm Staging , Retrospective StudiesABSTRACT
The ratio of mtDNA and a nuclear reference gene was estimated by Southern blotting in the skeletal muscle DNA of a 3-year-old girl who suffered from congenital brain damage, focal epilepsy, hepatomegaly, malabsorption syndrome and severe myopathy. The signal ratio of mtDNA versus 18S rDNA was 22% of the mean value obtained from controls. No major deletions or insertions were found and the MERRF, MELAS and NARP mutations were ruled out. Mitochondrial DNA-encoded enzyme activities and mitochondrial respiration were reduced. The analysis of the NAD(P)H and flavoprotein redox states of intact fibres revealed the presence of mitochondrial dysfunction. In tissue sections a moderate elevation of type I and type II fibre diameter variation was detected, aberrant NADH- and succinate dehydrogenase staining and some ragged red fibres. This suggested that a mitochondrial disorder caused by a decrease in the amount of intact wild-type mtDNA was responsible for the severe myopathy.
