Current diagnostic pathology最新文献

Neonatal liver biopsy is most frequently performed in the setting of conjugated hyperbilirubinaemia. In order to provide a differential diagnosis, the biopsy can be assigned to one of four histological patterns: biliary, neonatal/giant cell hepatitis, paucity of intrahepatic bile ducts and bland cholestasis. Within each category, clues can be sought to narrow the differential diagnosis still further. Potential aetiologies, emphasizing the most common and including the iatrogenic changes of total parenteral nutrition, are discussed, with a brief consideration of concepts in aetiopathogenesis.

This article provides an illustrated personal view of the British Society for Clinical Cytology's (BSCC) proposal to modify their terminology for reporting cervical cytology. The BSCC did not propose any major changes but moved closer to the two-tier Bethesda system for reporting pre-cancerous changes as high-grade and low-grade. Certain principles of reporting cytology that were intended in the original BSCC terminology are reinforced and difficult areas of borderline nuclear change are clarified. Revisiting the old terminology has drawn attention to errors and omissions in existing descriptions of dyskaryosis; this term is still used although its definition has been refined. This article will describe and illustrate different manifestations of dyskaryosis, with emphasis on its recognition as such, and its distinction from a wide variety of reactive changes. The illustrations draw widely on one of the author's (LT's) extensive experience with both types of liquid-based cytology preparations, which will now be the predominant methods of cell preparation in the UK.

The smear test for cervical screening has been around for over 50 years; however, there is still worldwide variation regarding screening age limits and intervals. This article will review the literature and present new analyses of UK Audit data and international cancer registry data to address the issues of when to start and stop screening and how often to screen. A rational approach to determining screening policy should take into account the underlying rate of cervical cancer, the absolute difference in effectiveness of screening at different intervals, and the costs of screening, including side effects of treatment.

Infection with high-risk human papillomaviruses (HPV) is the major risk factor for the development of cervical neoplasia. It is therefore reasonable to propose that the identification of these viruses may be helpful in the context of cervical screening. High-risk HPV infection is strongly associated with cervical neoplasia, particularly if persistent and present in women over the age of 35 years. Therefore, tests for HPV in the context of cervical cytology only need to identify high-risk HPV types. The strengths of HPV testing are high sensitivity and negative predictive value, indicating that the absence of HPV may be of more clinical value than its presence. However, the clinical application of HPV testing should be evaluated in the context of specific populations. HPV testing may have a role in: (i) primary screening; (ii) the assessment of women with mildly abnormal smears; (iii) post-treatment follow-up; and (iv) quality control of cervical cytology. HPV vaccination, if implemented, is likely to alter the epidemiological characteristics of HPV infection and cervical neoplasia. The effects of vaccination on HPV prevalence, HPV-type distribution and HPV-associated neoplasia will need to be monitored closely.

Cervical cancer, a potentially preventable disease, remains the second most common malignancy in women worldwide. Current screening protocols rely on the Pap smear test, which has a reported false-negative rate of 15–50%. Advances in automation of cervical cytology have resulted in improved cell preservation techniques and overall high-quality cellular material that is suitable for molecular analysis. The current focus is primarily on the use of molecular biomarkers as adjuncts to existing screening procedures. These biomarkers include human papillomavirus (HPV) and the host cell regulatory molecules, minichromosome maintenance proteins, Cdc6 (a cell division cycle protein) and p16(INK4A) tumour suppressor protein. Developments in micro-array technology and its application to the study of cervical cancer have greatly expanded the list of differentially regulated genes known to be involved in cervical cancer. This will help to unravel the pathogenesis of HPV infection and dysplastic progression, and ultimately improve treatment of cervical intra-epithelial neoplasia and cervical cancer.

Anal canal pathology, particularly infections and tumours, has recently come into prominence, mainly because of human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome. This review provides a framework for diagnostic pathologists who may encounter anal canal tumours. A summary of embryology, anatomy and terminology is provided by way of background. Important points of distinction between the surgical, anatomic and histologic anal canal are highlighted. Squamous carcinomas and their precursor lesion, anal intra-epithelial neoplasia, are the most common primary epithelial abnormalities seen in the anal canal. In addition, there is a predilection for HIV-positive homosexual men with co-existent human papillomavirus (HPV) infection to develop squamous carcinomas. The more proximal the tumour is in the anal canal, the greater the association with basaloid morphology and HPV infection.

Adenocarcinomas are uncommon and may arise from the anal transitional zone, anal glands or fistulous tracts, which may or may not be associated with long-standing Crohn's disease.

The immunohistochemical profiles and separation from morphologically similar tumours are provided in this article. In addition, the role of new molecular markers is discussed in relation to tumour behaviour and therapeutic options.

Barrett's oesophagus (BO) is a major risk factor for the development of oesophageal adenocarcinoma. Oesophageal adenocarcinoma is preceded by pre-malignant epithelial changes, i.e. low-grade dysplasia and high-grade dysplasia. Endosocopic surveillance programmes have been implemented to monitor these pre-malignant changes. In the last decade, much effort has been invested in non-invasive, low-risk, ablative techniques for elimination of BO as an alternative for oesophagectomy, which confers substantial morbidity and mortality. The rationale for ablative elimination of BO is to reduce or abolish the risk of malignant progression. However, at present, there is no convincing evidence that this risk is truly diminished. Residual or recurrent glands are commonly found after ablation and can be detected next to or underneath (neo)squamous epithelium. Moreover, molecular abnormalities associated with malignant progression have been detected in these glands. This review addresses histopathological aspects of oesophageal biopsy specimens after ablation of BO.

Teeth develop from oral cavity lining epithelial cells and cranial neural crest-derived ectomesenchymal cells. In a sequence of interactive processes, these cells develop into enamel-forming ameloblasts and dentine-producing odontoblasts. Odontogenic tumours are derived from these tooth-forming tissues, either the epithelial or the ectomesenchymal or both. Their behaviour varies from neoplastic to hamartomatous. Recently, the classification and nomenclature of odontogenic tumours has been updated. These new views will be incorporated in this article where appropriate.