A prospective evaluation of laparoscopic surgery for acute appendicitis over a 6-month period is reported. Sixty-five patients with signs and symptoms of appendicitis necessitating surgery were assigned to open (n = 36) or laparoscopic (n = 29) appendicectomy. Thirty-seven patients were female (22 open) and 28 were male (14 open). The median age was 24 (range 14-64) years for open appendicectomy and 18 (range 14-60) years for the laparoscopic procedure. The mean postoperative stay for open operation was 4.8 (range 1-21) days and for the laparoscopic route 2.2 (range 1-11) days (P < 0.05). Inflammation was confirmed histologically in 72 per cent of the open cases and in 74 per cent of the laparoscopic cases (P not significant). The wound infection rate was 11 per cent (n = 4) for open and 4 per cent (n = 1) for laparoscopic appendicectomy (P < 0.05). The median anaesthesia time was 52 (range 15-90) min for open appendicectomy and 48 (range 20-120) min for laparoscopic surgery (P not significant). After open appendicectomy patients had a median of 5 (range 2-12) intramuscular injections of analgesia compared with a median of 1 (range 0-5) in the laparoscopic group (P < 0.05). Two laparoscopic operations were converted to an open procedure. The results suggest that emergency laparoscopic appendicectomy should be explored further as an alternative to open surgery for acute appendicitis.

For a variety of technical reasons it is rarely possible to study cytogenetic abnormalities in ductal carcinoma in situ (DCIS) using traditional techniques. However, by combining molecular biology and computerized image analysis it is possible to carry out cytogenetic analyses on formalin‐fixed, paraffin‐embedded tissue, using comparative genomic hybridization (CGH). The purpose of this study was to identify the prevalence of chromosomal amplifications and deletions in high‐grade DCIS and to look specifically for unique or consistent abnormalities in this pre‐invasive cancer. Twenty‐three cases of asymptomatic, non‐palpable, screen‐detected, high‐grade DCIS were examined using CGH on tumour cells obtained from histology slides. All cases showed chromosomal abnormalities. A wide variety of amplifications and deletions were spread across the genome. The most frequent changes were gains of chromosomes 17 (13 of 23), 16p (13 of 23), and 20q (9 of 23) and amplifications of 11q13 (22 of 23), 12q 24.1–24.2 (12 of 23), 6p21.3 (11 of 23), and 1q31‐qter (6 of 23). The most frequent deletions were on 13q 21.3–q33 (7 of 23), 9p21 (4 of 23), and 6q16.1 (4 of 23). These findings indicate that high‐grade DCIS is, from a cytogenetic viewpoint, an advanced lesion. There was no absolutely consistent finding in every case, but amplification of 11q13 was found in 22 of the 23 cases. The precise significance of this is unknown at present. This region of chromosome 11q harbours a number of known oncogenes, including cyclinD1 and INT2. It is likely that many of these findings are the result of accumulated chromosomal abnormalities, reflecting an unstable genome in established malignancy. Copyright © 1999 John Wiley & Sons, Ltd.

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