SUMMARY Sections from 100 cervical biopsy specimens were studied by 12 consultant histopathologists to determine the robustness of the existing pathology terminology and classification. Analysis by K statistics showed good agreement in the diagnosis of CIN 3 and squamous carcinoma but an inability to distinguish accurately between the lesser grades of CIN.It is recommended that the classification be changed to low grade (present CIN 1 and 2) and high grade (present CIN 3) categories alone. There was very poor agreement in the identification ofcellular changes associated with human papilloma virus (HPV) infection.Several novel analytical methods of assessing the severity of uterine cervical intraepithelial neoplasia (CIN) have been proposed,'2 but histological assessment remains the basis for determination oftreatment, clinical management, and subsequent follow up of patients. Although clear criteria for the diagnosis and grading of CIN have been described,3 such assessments are subjective and prone to intra-and interobserver variation.45 The problems of histological assessment have been further complicated by the increasing recognition of human papilloma virus (HPV) infection"7 which may be an aetiological factor in the development of CIN.89 HPV infection may be indicated by koilocytosis and other changes that distort cellular appearances and so may apparently exaggerate the severity of the premalignant appearances ofthe cervical epithelium, particularly in the higher layers-making grading more difficult.It is reasonable that efforts should be made to establish the degree of confidence which can be given to the histological reporting of cervical biopsy lesions by pathologists and to determine the robustness of the existing terminology and classification. We describe the findings of a study of cervical biopsy specimens conducted by a group of 12 pathologists, all of consultant grade, but with varying degrees of experience.Accepted for publication 1 September 1988 Material and methods COMPOSITION OF PANELTwelve histopathologists were invited to join the study with a deliberate attempt by the organisers to obtain a composition representative of Scottish pathology as a whole. The members came from pathology laboratories in Aberdeen (n = 2), Dundee (n = 2), Edinburgh (n = 2), Airdrie (n = 1), Perth (n = 1), Stirling (n = 1) and Glasgow (n = 3) and varied in years of consultant experience (five to 25 years) and nature ofsubstantive post (university staffn = 5: NHS staff n = 7). All the members of the group had undertaken their postgraduate training in Scotland. CLASSIFICATION OF CERVICAL HISTOPATHOLOGYAt the initial meeting current cervical pathology terminology was reviewed and following discussion a proforma was designed for completion after examination of each slide in the circulation. This was modified in a minor way after the first circulation and the final form is shown in the figure. It was decided to keep the classification simple, but to relate it as closely as possible to everyday practice. The following ...
To identify the most accurate and useful panel to diagnose mesothelioma, we immunostained sections from 112 mesotheliomas, 18 adenocarcinomas, and 11 reactive pleural specimens with 13 antibodies. Positive results for mesotheliomas, adenocarcinomas, and reactive pleura, respectively, were CAM5.2, 111, 18, and 11; vimentin, 30, 3, and 3; HBME-1, 75, 10, and 8; thrombomodulin, 31, 2, and 2; calretinin, 43, 6, and 11; and CD44H, 68, 10, and 4. Positive results for adenocarcinoma markers in mesotheliomas and adenocarcinomas, respectively, were carcinoembryonic antigen, 1 and 15; LeuM1, 7 and 9; and Ber-EP4, 5 and 12. All reactive pleura were negative. Positive results for markers to help distinguish mesothelioma from reactive pleura in mesotheliomas, adenocarcinomas, and reactive pleura, respectively, were epithelial membrane antigen, 76, 17, and 6; p53, 78, 16, and 9; P-170 glycoprotein, 37, 4, and 2; and platelet-derived growth factor receptor beta, 31, 1, and 2. The differential diagnosis of mesothelioma from adenocarcinoma is based on negative markers. Individual mesothelial markers are of low sensitivity and specificity for mesothelioma. However, diagnostic accuracy is improved by the use of antibody panels. To date there are no antibodies that help distinguish mesothelioma from reactive pleura.
Our group had a satisfactory agreement on the distinction of mild from severe dysplasia and on microinvasive carcinoma without any discussion as to histopathological criteria to be used. Clinical management--review endoscopy, repeat cord stripping, radiotherapy and laryngectomy--is in general dependent on histological assessment. Thus the agreement on categories which underpin clinical management is reassuring. However, assessment of moderate dysplasia remains problematic. An attempt to utilize a two grade system--low grade from high grade dysplasia/CIS--may have merit. The implications of the terminology used must be agreed among pathologists and clinicians working closely within clinicopathological cancer groups.
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