Current diagnostic pathology最新文献

A neoplastic proliferation of peripheral nerve sheath cells (Schwann cells, fibroblasts and perineurial cells) and ganglion cells in the colorectum may give rise to the mucosal or submucosal polyps. Depending upon the predominant cell types, these neurogenic polyps can be classified as schwannomas, granular cell tumours, neurofibromas, perineuriomas, mixed nerve sheath tumours, ganglioneuromas or paragangliomas. Morphologically, the neoplastic cells repeat or mimic the corresponding nerve sheath cells or neurons in terms of growth pattern, histology and immunoreactivity. They are uncommon, but the polyps can occur in any age group, although the vast majority of patients are adults. The polyps can be either solitary (most peripheral nerve sheath tumours) or multiple, especially if associated with systemic diseases (i.e. syndromes involving the peripheral nerve tissue). They are usually incidental findings or may be accompanied by gastrointestinal symptoms. Almost all colorectal neurogenic polyps are benign, and they rarely undergo malignant transformation unless they are part of a syndromatic manifestation. However, these polyps may cause a diagnostic problem during screening for colorectal cancer. An accurate diagnosis of these entities will help clinicians to make appropriate management decisions.

This paper outlines types of surgical neck dissection and describes practical aspects of producing an accurate histopathological assessment and report.

With the explosion in the number of screening colonoscopic procedures, pathologists have learned to recognize a host of non-neoplastic polyps that can be loosely categorized as those stemming from mucosal prolapse, hamartomatous lesions, incidental benign stromal polyps and polyps associated with systemic diseases. We briefly review solitary rectal ulcer syndrome, inflammatory cloacogenic polyps, diverticular disease-associated prolapse polyps, cap polyps, juvenile polyps, Peutz–Jeghers polyps, Cronkhite–Canada polyposis, elastosis, benign fibroblastic polyps, inflammatory fibroid polyps, pneumatosis, vascular lesions, filiform polyps, lymphoid polyps, malakoplakia, amyloidosis and endometriosis.

Radical prostatectomy gives the most accurate and detailed information available for determining prognosis and deciding about adjuvant therapy for prostate cancer. The consistency and reproducibility of observations from these specimens requires a standardised protocol for tissue fixation, sampling, embedding and processing. Although the publication of processing protocols in recent years has led to a convergence of opinions, differences still exist in methods of handling, sampling and processing specimens. In this review article, we incorporate the processing methods for radical prostatectomy addressed in the previous reports and propose a comprehensively standardised approach to evaluate radical prostatectomy specimens.

Several investigators have recently proposed the concept of a ‘serrated neoplastic pathway’ to account for the development of a subset of colonic carcinomas that lack chromosomal instability and loss of heterozygosity. This pathway putatively involves several pathogenetically related polyps, including some hyperplastic polyps, the recently described sessile serrated polyp, serrated adenoma and mixed polyp; and is characterised by early BRAF mutations, DNA hypermethylation and microsatellite instability. Most hyperplastic polyps and sessile serrated polyps harbour mutations in BRAF, one gene involved in the mitogen-activated protein kinase pathway, and abnormal DNA methylation. Presumably, these genetic changes are sufficient to potentiate widespread genomic hypermethylation that ultimately affects the promoter regions of key DNA repair genes, such as hMLH-1 and O⁶-methylguanine methyltransferase, thereby silencing them from transcription and leading to progressive microsatellite instability. The morphological evolution of non-dysplastic serrated lesions (hyperplastic and sessile serrated polyps) to serrated adenomas, mixed polyps and/or colorectal carcinoma is believed to reflect the accumulation of these genetic events. The purpose of this review is to describe the morphological and molecular features of colorectal serrated polyps and to present the available data supporting the concept of a serrated neoplastic pathway of colorectal carcinogenesis.

The management of the patient with an endoscopically removed malignant colorectal polyp is predicated on proper handling of the specimen and on the pathologist's histopathological interpretation. The steps of specimen handling are: (1) fixation, (2) gross examination and sectioning, (3) processing, and (4) endoscopic findings and type of removal. The histopathological parameters to be reported on are: (1) the status of the resection margin, (2) the grade of the cancer, and (3) the presence or absence of lymphovascular invasion. Polyps with grade I or II cancer, no lymphovascular invasion and a negative resection margin can be successfully treated by endoscopic polypectomy, whereas those with grade III cancer, lymphovascular invasion, or a positive/close margin require definitive surgical resection subsequent to endoscopic polypectomy. Potentially, new significant parameters for patient management are: (1) depth of invasion, (2) tumour budding, (3) lymphatic vessel density, and (4) cribriform histology. The pathology report must be clear and concise, indicating all relevant important parameters. Finally, the pathologist must differentiate invasive adenocarcinoma from intramucosal adenocarcinoma and ‘pseudoinvasion’.

Gastrointestinal polyps are common lesions that usually present singly or in small numbers. Although the term ‘multiple colorectal polyposis’ was originally applied to patients carrying at least 100 large intestinal adenomas, it has subsequently become broadened to include patients carrying multiple polyps regardless of their nature. Most of the non-adenomatous polyposis syndromes are hereditary. They can be classified according to the dominant type of polyp, their distribution in the gastrointestinal tract and their potential for the development of gastrointestinal cancers. This review summarises their main clinical, genetic and histopathological features.

There is a clinico-pathological continuum of infection-driven sepsis syndromes, the most severe being septic shock with multi-organ failure. The organ dysfunctions are due to inflammatory cytokines from remote sources (the site of infection) and constitute the systemic inflammatory response syndrome (SIRS). The common causes are Gram-positive and Gram-negative infections; the common infection sites are (in descending frequency) lung, blood stream, intra-abdominal disease, urological sepsis and surgical wounds; the commonest organ dysfunctions are systemic shock, kidney, lung, and heart. The differential diagnosis of severe sepsis includes disseminated malignancy, atherosclerosis, and haemophagocytic syndrome. New treatments for severe sepsis are being trialled to raise the poor survival rates in intensive care. The role of the autopsy is to describe carefully the organ lesions, provide microbiological evidence of infection, and to correlate these with the clinical features and therapeutic variables.