Résumé
Objective To summarize the diagnostic and therapeutic experiences for multiple insulinoma. Methods Clinical data of 34 cKsefl of multiple insulinoma treated in Peking Union Medical College Hospital between 1984 and 2007 were analyzed retrospectively. Results Multiple insulinoma was identified in these 34 cases for 37 instances.Malignant insulinoma was found in 2 cases.Three cases suffered from postoperative recurrent multipie tumors.35.3% cases belonged to MEN1;13.5% cases were of insulinoma combined with islet hyperplasia;43.2% cases had 3 or more than 3 insulinomas;Fifteen cases (40.5%)had had a misdiagnosis.45.2%tumors were smaller than 1 cm in diameter:88.9%multiple insulinonla located at the body and tail of the pancreas.Enucleation of multiple tumors was performed for 48.7 percent of cases. Conclusions Most multiple insulinomas were small,it was difficult for preoperative examination to locate all the tumors therefore.Being on the alert against multiple insulinoma and such measures as careful exploration,intraoperative blood glucose determination.fine needle aspiration biopsy,frozen sections helps to avoid missing multiple imuhnoma.
Résumé
Several molecular and genetic changes have been found in pituitary adenomas. We looked for correlations between these changes and the degree of invasiveness of the tumors. The invasiveness of 11 pituitary adenomas was graded by Hardy classification. We examined the retinoblastoma gene (RB1.20 on chromosome 13q) and the region around the MEN1 locus (chromosome 11q13.1-5) for loss of heterozygosity. Also examined are p53 mutations using single strain conformation polymorphism, p53 protein overexpression using immuno cytochemistry, homozygous deletions of p15 and p16 by polymerase chain reaction, and cellular proliferative activity using MIB-1 antibody. Six tumors (54.5%) had an LOH at either RB1.20 or the MEN1 locus. LOHs were found more frequently in Grade 4 and stage E tumors (72% and 67%) than in Grade 3 and stage D tumors (25% and 40%). However, no mutation or overexpression of p53 was found. No homozygous deletions of p15 or p16 were identified. The cell proliferative index ranged from 0 to 3%. LOH at 11q13 and 13q may be valuable in predicting the invasiveness of pituitary adenomas.