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Biomedical subjects

R H Riddell

Publications and source records attributed to R H Riddell.

At least 91 records · Page 5Linked to original sources
PubMed1986

Liver pathology following hepatic arterial infusion chemotherapy. Hepatic toxicity with FUDR.

The authors reviewed the liver histopathology and the clinical features of eight patients with liver metastases from colorectal cancer who were treated by hepatic arterial infusion chemotherapy (HAIC) via an implantable pump (Infusaid). Before HAIC, these patients had no evidence of hepatitis, and results of liver biopsies performed on three patients showed only minor morphologic alterations. All the liver tumors responded to HAIC, but all patients developed hepatitis. Clinical findings included nausea, vomiting, abdominal pain and jaundice. Serum transaminases, alkaline phosphatase and bilirubin levels were increased. Clinical observations suggested that 5-fluoro-2'-deoxyuridine (FUDR), the predominant drug given, was the hepatotoxic agent. Toxic effects were hepatocyte necrosis, steatosis, cholestasis, central vein sclerosis, and alterations in the portal triad. In addition, central vein lesions like those in veno-occlusive disease, and micronodular cirrhosis resembling that induced by alcohol, were encountered. Although individual susceptibility to FUDR appeared to vary, portal triad fibrosis was present in all eight cases and, together with central vein sclerosis and cirrhosis, appeared to be related to the dose and duration of HAIC.

Adult↗
PubMed1985

Adenomatous polyposis coli and multiple endocrine neoplasia type 2b. A pathogenetic relationship.

A young man presenting with Cushing's syndrome was found to have multiple endocrine neoplasia type 2b MEN 2b and adenomatous colonic polyposis with duodenal and gastric polyps. The entire syndrome of MEN 2b was present, including metastatic medullary carcinoma of the thyroid, a pheochromocytoma, and peripheral nerve abnormalities. The concurrence of these two inherited multiple neoplasia syndromes may reflect a common pathogenetic step in this patient.

Adenoma↗
PubMed1985

Dysplasia in Barrett's esophagus.

In a retrospective histological study, resected specimens obtained from 23 patients with adenocarcinoma in Barrett's esophagus (Group I) and endoscopic multiple (step) biopsies from 38 patients without carcinoma in Barrett's esophagus (Group II) were investigated for dysplastic changes. Dysplasia was most frequently found in the type of mucosa comprising intestinal metaplasia. There seem to be two pathways to dysplasia in Barrett's esophagus. In Group I dysplasia was found in 18 out of 23, and in Group II in 2 out of 38 patients. In Barrett's esophagus, dysplasia may be considered not only a precursor of carcinoma, but also a marker for coexisting carcinoma.

Adenocarcinoma↗
PubMed1985

Ulcerative colitis and colonic cancer. Problems in assessing the diagnostic usefulness of mucosal dysplasia.

To assess the association of mucosal dysplasia and colonic cancer in patients with ulcerative colitis and to avoid bias in biopsy interpretation that may have affected results of previous studies, the authors examined coded histology slides from colectomy specimens of 22 patients who had ulcerative colitis and colonic cancer and 22 patients who had ulcerative colitis but no colonic cancer. As expected, it was found that dysplasia occurred contiguous to each cancer. However, at a distance from the cancer (i.e., in histology blocks not containing cancer), some dysplasia was found (low or high grade) in 16/22 cases (73 percent), and high grade dysplasia in 11/22 cases (50 percent). These results suggest that there may be somewhat weaker association than previously reported between colonic cancer and dysplasia at a distance from the colonic cancer. Further, these results suggest that, in studies of dysplasia, it is important to avoid bias in biopsy interpretation and to describe sampling methods.

Adolescent↗
PubMed1984

Abnormal goblet cell glycoconjugates in rectal biopsies associated with an increased risk of neoplasia in patients with ulcerative colitis: early results of a prospective study.

A group of 18 patients with stable ulcerative colitis involving the entire colon for at least eight years was subjected to a biopsy of normal appearing rectal mucosa and followed prospectively over four years for the development of either dysplasia or cancer. Goblet cell glycoconjugate structure was examined in the rectal biopsies using fluorescein conjugated lectins. At the beginning of the study, 13 of the 18 patients had abnormalities of goblet cell mucin or cytoplasmic glycoconjugates in the rectal biopsies. Dysplasia subsequently developed in six and carcinoma in one of these patients. Among the five patients with normal lectin binding studies in the initial rectal biopsies, colonic dysplasia has subsequently developed in one. The abnormalities seen in the rectal goblet cells resembled in part those previously seen in immature and neoplastic colonic cells. The dysplastic tissues all contained the form of mucin which has been found in other neoplastic colonic tissues. This preliminary report after four years of prospective study suggests that abnormalities of glycoconjugate structure may be associated with, and may precede, neoplastic events in the setting of chronic ulcerative colitis.

Colitis, Ulcerative↗
PubMed1984

Dysplasia and cancer in ulcerative colitis: a soluble problem?

Now that many of the problems associated with the recognition, classification and terminology of dysplasia in ulcerative colitis have been overcome, the clinical effectiveness of such a classification needs to be investigated. Because dysplasia has been defined as an unequivocally neoplastic transformation of the epithelium which is capable of giving rise to an invasive carcinoma, it follows that in waiting for the development of dysplasia in patients at risk, there will always be an associated and as yet undefined incidence of invasive carcinoma already being present. Nevertheless, it is currently inappropriate to consider proctocolectomy before such changes develop. It is emphasised that waiting for high grade dysplasia to develop may lead to an unacceptably high level of associated invasive carcinoma. Also, because dysplasia is frequently focal, the changes of detecting it on random biopsy are directly proportional to the number of biopsies taken, and if found in flat mucosa it may be difficult to confirm the presence of such dysplasia by re-biopsy. Colectomy at this stage is aimed at cancer prevention rather than early cancer detection. Conversely, targeted biopsies of endoscopically visible plaques, nodules or other abnormalities, which may already be the superficial part of invasive carcinomas, offer the best hope of early detection of carcinoma. However, a proportion of these may have metastasised already; this is much more likely to have occurred if such a lesion is found at the first colonoscopy rather than in a patient in whom several surveillance colonoscopies have been carried out. Finally, the initial stages of many colitic cancers are undetectable endoscopically or radiologically but may be biopsied accidentally. All of these factors suggest that unexpected carcinomas will occur in any long-term prospective study. Surprisingly, most will not be lethal and they can be kept to a minimum if proctocolectomy is considered once unequivocal dysplasia is demonstrated on biopsy, particularly in parts of the world where large bowel cancer is already common. Data are required which assess accurately the risk of an invasive carcinoma being present or developing when epithelium indefinite for dysplasia, low grade dysplasia or high grade dysplasia are present both with and without an endoscopic abnormality being the source of the biopsy, and when such biopsies are obtained at the first or at subsequent colonoscopies. Only then can the risks of colectomy be weighed adequately against the likelihood of carcinoma already being present.(ABSTRACT TRUNCATED AT 400 WORDS)

Biopsy↗
PubMed1983

Dysplasia in inflammatory bowel disease: standardized classification with provisional clinical applications.

Assessment of epithelial dysplasia in ulcerative colitis has been hindered by inconsistencies in and disagreements about nomenclature and interpretation. To resolve these issues, pathologists from ten institutions participated in three exchanges of multiple slides and, following each exchange, in discussions of the results. A classification system for the epithelial changes that occur in ulcerative colitis was developed, which should be applicable to other forms of inflammatory bowel disease as well. The classification makes use of standardized terminology, addresses specific problem areas, and offers practical solutions. The reproducibility of the system was studied by means of examinations of both inter- and intra-observer variations. The clinical implications of the findings were incorporated into suggestions for patient management. The basis of the classification is that the term "dysplasia" is reserved for epithelial changes that are unequivocally neoplastic and may therefore give rise directly to invasive carcinoma. Specimens are categorized as negative, indefinite, or positive for dysplasia. The negative category includes all inflammatory and regenerative lesions and indicates that only continued regular surveillance is required. The indefinite category is applied to epithelial changes that appear to exceed the limits of ordinary regeneration but are insufficient for an unequivocal diagnosis of dysplasia or are associated with other features that prevent such unequivocal diagnosis. Clinically, it indicates that early repeat biopsy is often required to assess the changes more accurately. The positive category is divided into two subcategories: 1) high-grade dysplasia, for which colectomy should be strongly considered after confirmation of the diagnosis, and 2) low-grade dysplasia, which also requires confirmation and early repeat biopsy or colectomy, depending on other findings.

Biopsy↗
PubMed1983

Barrett's esophagus. Comparison of benign and malignant cases.

Using strict criteria for diagnosis, 23 patients having benign Barrett's esophagus, and 20 patients with adenocarcinoma arising in this epithelium have been analyzed. Evidence supports severe gastroesophageal reflux as a cause of Barrett's esophagus. Successful antireflux surgery leads to stabilization and possibly regression of the dysplasia in Barrett's epithelium, and can be followed by squamous epithelial regeneration in some. Antireflux surgery is advocated in all patients with Barrett's esophagus demonstrated to have abnormal reflux regardless of symptoms. The malignant potential of the columnar epithelium is higher in men who smoke, in patients with intestinal-type metaplasia who continue to have severe reflux, and in patients who develop dysplasia. In those with high grade dysplasia, the probability of carcinoma is high and esophagectomy should be seriously considered in the hopes that the pathological stage of the neoplasm is still favorable.

Adenocarcinoma↗
PubMed1982

Granulomatous mastitis: a report of seven cases.

The clinical history and histological features of seven cases of granulomatous mastitis are presented. The lesion occurs in young parous women as a tender extra-areolar breast lump. Histologically, non-caseating discrete granulomas are present, confined to breast lobules with, in three cases, coalescence of the granulomas and microabscess formation. Pathogenesis of the changes is discussed. It is thought that granulomatous mastitis is an entity morphologically distinct from duct ectasia/plasma cell mastitis and the commoner forms of granulomatous breast diseases.

Adult↗