False-negative cervical smears.
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Biomedical subjects
Publications and source records attributed to M E Boxer.
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AIMS: To determine the sensitivity of the partial rescreening method of rapid review for internal quality control of cervical cytology; to determine which staff members are most suited to undertake it; and to investigate the cell patterns of false negative smears previously detected by the method. METHODS: As a prospective study 9517 cervical smears were partially screened by four cytotechnologists using the 'step' method prior to conventional screening and the results compared with the final report. As a retrospective study 62 false negative smears that had been identified by the method over four years were reviewed. RESULTS: A detection rate for dyskaryosis of 86% (range 82-91%) was achieved. Sixteen abnormal smears were missed on conventional screening that had been detected by prescreening. Review of the 62 false negatives revealed three patterns: (1) scanty abnormal cells; (2) abundant dyskaryotic cells presenting as "microbiopsies"; and (3) abundant, readily recognisable abnormal cells. CONCLUSIONS: Partial rescreening enables the detection of errors due to both fatigue and misinterpretation. In this laboratory the method has, together with targeted full rescreening, reduced the false negative report rate from 5.0% to 0.4%. For laboratories using a rapid review method to reduce false negative reports, a prescreening trial is recommended in order (1) to select the most effective review method and the staff most suited to undertake it; and (2) to determine the laboratory's sensitivity with the method, as this is required for accurate estimation of the false negative rate.
Eleven surgically excised left atrial myxomas have been stained for factor VIII related antigen (VIII-RA) and actin by the peroxidase-antiperoxidase technique. Most tumour cells were negative for VIII-RA. However a population was identified forming cords and vascular channels which possessed a core or lining of tumour cells with an endothelial morphology which were positive. Tumour cells lining vessel-like invaginations of the surface also showed focal positive staining. The staining pattern for actin precisely mirrored that for VIII-RA. These findings support the established theory that cardiac myxomas arise from primitive endocardial or subendocardial mesenchymal cells with the potential to differentiate towards endothelial cells. They are incompatible with the theory that these tumours originate from cardiac endothelium.
Epithelial cell proliferation in the duodenum was investigated in 50 patients by incubating mucosal biopsy samples with tritiated thymidine, followed by autoradiography. Fifteen patients had a normal duodenum, 15 duodenal ulcer undergoing elective surgery, 10 perforated duodenal ulcer, and 5 severe non-ulcer-associated duodenitis. The mean crypt cell labelling index in the duodenal bulb of controls was 8.8 +/- 0.4% (mean +/- SEM), at the edge of perforated ulcers 19.1 +/- 2.0%, at the edge of elective ulcers 18.6 +/- 1.4%, and in biopsy specimens from non-ulcer-associated duodenitis 14.0 +/- 1.2%. The mean labelling index in the distal first part of duodenum of control patients was 9.1 +/- 0.8 similar to the values found in histologically normal specimens distal to ulcer or duodenitis. The results indicate active epithelial cell proliferation in both duodenal ulcer and duodenitis. There was no evidence of impairment of epithelial cell proliferation in duodenal ulcer patients.
Mucosal cell proliferation in the first part of the duodenum was studied in 24 patients using a tissue culture technique in which endoscopic biopsies were subjected to autoradiography after exposure to tritiated thymidine. Eight patients had a normal duodenum, eight had duodenal ulcer, and eight had symptomatic chronic non-specific duodenitis. The mean crypt labelling index (LI) in normal duodenum was 8.8 0.4% (SEM). Increased labelling indices of 15.6 +/- 1.7% were found near the edge of duodenal ulcers and 17.8 1.8% in duodenitis. Treatment with cimetidine reduced both the severity of duodenitis and the mean crypt LI. The LI of histologically normal duodenal mucosa distal to ulcer of duodenitis was similar to that of the control subjects' mucosa. The increased mucosal cell proliferation seen in severe duodenitis, either alone or associated with duodenal ulceration, suggested that erosions and ulcers arose when the crypts passed into 'high output failure' and were unable to compensate for further epithelial cell loss. There was no evidence in out study for a generalised failure of mucosal cell proliferation in duodenal ulcer or duodenitis.