Biomedical subjects
Publications and source records attributed to I Bearzi.
A case of pernicious anemia associated with multiple gastric carcinoids is reported. The neoplastic growth was composed of enterochromaffin-like (ECL) cells, and ECL cell hyperplasia was observed also in hyperplastic polyps, inside the fundic glands and in small nests lying in the lamina propria (microcarcinoidosis). The possible relation between pernicious anemia and ECL cell hyperplasia is discussed.
69 foci from 27 multifocal EGC are compared morphologically with 90 solitary EGC. In the multifocal group there was a preponderance of gross types IIa and IIb, Small and Minute carcinomas, an intramucosal growth pattern and a well differentiated intestinal histotype. Although the differences in gross type and tumor size are related in some measure to the stage of neoplastic growth at the time of diagnosis, the higher frequency of well differentiated intestinal carcinomas in multifocal EGC probably reflects a different histogenesis. This hypothesis seems to be borne out by the greater extent of intestinal metaplasia and the larger number of dysplastic foci detectable in the surrounding gastric mucosa.
Double contrast barium meal, endoscopy and histology of the duodenal bulb were blindly compared in 47 consecutive patients. The agreement in the judgement of normality of the mucosal surface between radiology and endoscopy was 78%. The agreement in the diagnosis of presence or absence of nodularity and thickened folds was respectively 91% and 87%. The findings of nodularity correspond to duodenitis with pyloric metaplasia or to heterotopic gastric mucosa, while the thickened folds correspond to duodenitis with pyloric metaplasia, Brunner's hyperplasia, lymphatic nodular hyperplasia or cystic glandular dilatation. The diagnostic errors in the radiological examinations in respect to endoscopy is quite important in the case of erosions.
Out of 5000 consecutive double-contrast examinations of the esophagus, 50 cases presented a diffuse finely granular or nodular appearance of the mucosa. Endoscopy was subsequently performed in 38 cases and biopsy in the majority of these. In 23 of the 38 verified cases the diagnosis was reflux esophagitis. In the other 15 cases the diagnoses were: candidal esophagitis (4), leukoplakia (2), glycogenic acanthosis (1), and diffuse leiomyomatosis (1). A normal mucosa was demonstrated in 7 cases. Our study indicates that a radiologically granular or nodular appearance of the esophageal mucosa often indicates reflux esophagitis and less commonly identifies diffuse lesions of variable origin.
This paper presents a case of Crohn's disease with associated small bowel adenocarcinoma. A polypoid area of gastric metaplasia was present and showed both fundic and pyloric features, the latter showing increasingly severe dysplasia and infiltrating adenocarcinoma containing many enterochromaffin cells, in which serotonin was demonstrated. At foci of granulomatous inflammation one observed a well differentiated sulfomucin secreting adenocarcinoma. Away from the metaplastic or inflammatory lesions there arose both a poorly and well differentiated sialomucin secreting adenocarcinoma. Multiple microfoci of adenocarcinoma and dysplastic changes of the ileal epithelium were present in the absence of any gross abnormality.
Benign tumors of the esophagus are rare. So far radiological examination has been useful in the diagnosis of fairly large benign tumors. In 4100 consecutive double-contrast studies we have found 22 incidental cases of protruded lesions of the esophagus with the appearance of submucosal tumor (8 cases) or polyp of the mucosa (14 cases). The lesions were small: 14 were less than 1 cm and 8 were between 1 and 3 cm. The histological data showed leiomyoma in the submucosal tumors and squamous papillomas in the polyps of the mucosa. A noteworthy feature is the unusual frequency of small squamous papillomas detected. The radiological diagnosis of benign tumors of the esophagus cannot be confined to large tumors in symptomatic patients but may include the accidental detection of small tumors. These call for histological verification and possibly endoscopic removal.
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The incidence as well as the morphologic features of early gastric cancer observed in 41 cases during the last 5 years are reported. The incidence of early gastric cancer was 9.11% among the total gastric carcinomas seen during the above period. As regards age and sex, the patients suffering with early as well as advanced gastric cancer revealed insignificant variation. With gastric biopsies, the diagnostic accuracy was 88.5%. There were multifocal lesion in 29.2% of cases with a total of 85 foci. Type IIc was the predominant macroscopic lesion, followed by type III. The antrum and the angularis of the lesser curvature were the main sites for early gastric cancer. The intestinal and well-differentiated types of early gastric cancer were the main histologic features seen. Diffuse type and submucosal lesions were more frequent in 6 (14.6%) cases observed with regional lymph node metastases. Our study revealed that there has been a gradual increase in the number of gastric biopsies, early gastric cancer, and the early:advanced gastric cancer ratio.
In 4538 double-contrast examinations of the upper gastrointestinal tract, 8 early gastric cancers (EGCs) were prospectively diagnosed before endoscopy. Four others were false negative cases, but retrospective analysis led to identification of the lesion in 3. The rate of EGC in radiologically diagnosed and verified cancers was found to be 10.6%. Gastric polyp rarely corresponded to EGC, whereas gastric ulcer more frequently corresponded to an EGC. Five of 12 EGCs were multifocal, with 21 satellite foci of carcinoma, of which 3 were probably radiologically identifiable as varioliform erosions. Routine double-contrast study appears valuable for detecting EGC, but the rate of false negative cases indicates that integration of radiologic, endoscopic, and cytologic data as well as accurate histopathologic study of the surgical specimen are needed to diagnose and characterize early gastric carcinoma.
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Bone marrow and spleen samples were studied biochemically to elucidate the nature of the material stored in the large histiocytes present in beta-thalassemic patients. Only the protein-bound N-acetylneuraminic acid (NANA) content of the spleen of homozygous beta-thalassemic patients was significantly higher than that of controls. In the bone marrow, which contained a large number of thalassemic storage cells, the lipid-bound NANA and the glucocerebroside showed a moderate increase, while the amount of protein-bound NANA was much greater than that in controls. These results, in agreement with ultrastructural and histochemical observations, differentiate thalassemic storage cells from other storage cells found in diseases characterized by an increased destruction of blood cells and suggest that there may also be an impairment of the sialoglycoprotein metabolism of the red blood cells in homozygous beta-thalassemia.
A comparative analysis of preC sequences of hepatitis B virus (HBV) in human hepatoma (hepatocellular carcinoma; HCC) tissues and non-tumoral liver samples from HCC patients was performed. Ten out of 17 HCC tissue samples exhibited an amino acid substitution at the level of the distal cysteine residue of the HBV preC region, while generation of a TAG translational stop codon was observed in 4 of these samples. Interestingly, substitution of the distal cysteine residue was not observed in non-tumoral liver (available from 8 of the 17 patients), thus suggesting either that a selection among different HBV variants occurs in HCC cells, or that modifications to the conformation and stability of the HBV capsid protein may play a role in the process of selection and escape of transformed liver cells.
The primary aim of this work was to investigate the ultrastructural morphology of the small intestinal mucosa in children affected by selective IgA deficiency (SIgAD). Absorptive tests and intestinal biopsies were performed in a group of nine children with SIgAD, none of them presenting with diarrhea. Biopsy specimens were processed for routine histology and scanning or transmission electron microscopy (SEM and TEM). By light microscopy, the jejunal mucosa appeared normal in all but one patient with patchy villous atrophy. By SEM, two further biopsies showed small areas of flat mucosa surrounded by villous ridges of nearly normal height. By TEM, four out of the nine mucosal specimens showed degenerative changes of the surface epithelium, including enlargement of the mitochondria, apical accumulation of primary and secondary lysosomes, and shortening and branching of the microvilli. These findings suggest that the small intestinal mucosa of children with SIgAD often shows pathological changes, some of which are recognizable only at the ultrastructural level. The study of biopsy specimens by SEM seems to be a useful diagnostic tool when patchy mucosal damage may occur, as in some of our patients with SIgAD.
Hereditary nonpolyposis colorectal cancer (HNPCC) is an inherited syndrome of cancer susceptibility caused by germ line mutations of genes participating in mismatch repair (MMR). Carriers of MMR gene mutations have an increased risk of colorectal cancers and cancer of other organs. Tumors of the endometrium represent the most frequent extracolonic malignancies in HNPCC. It has been suggested that women harboring MMR gene mutations have a higher risk of endometrial cancer than of colon cancer. Here, we describe an HNPCC patient with early-onset endometrial cancer and a strong familial history of endometrial tumors who harbored a germ line MSH2 splice site mutation (IVS9_2A>G). This mutation was responsible for abnormal messenger RNA processing, leading to the introduction of a premature stop signal and to the expression of a truncated MSH2 protein. In addition, the same mutation was associated with loss of MSH2 protein expression, high microsatellite instability, and PTEN inactivation. Although a direct relationship between the endometrial cancer susceptibility and the MSH2 mutation we found cannot be established, our observations, consistent with the work of other authors, suggest the involvement of germ line MSH2 abnormalities in endometrial tumor development and support the case for endometrial cancer screening in women from HNPCC families.
Hepatic fatty infiltration generally appears in a widespread form but it can occasionally involve the liver in an irregular way. As regards focal forms, nodular focal fatty infiltration (NFFI) has great importance regarding problems of differential diagnosis with benign and malignant focal pathology of the liver. Except for this aspect, NFFI has little clinical importance as it is mainly asymptomatic. We report a case of an acute bleeding of a big nodule of FFI which required an urgent hepatectomy.
Treatment of gastrointestinal stromal tumors (GIST) has been revolutioned by the recently discovered molecular mechanism responsible for the oncogenesis of this disease. In addition, due to the rapid progress at molecular and clinical level observed in the last few years, there is a need to review the current state of the art in order to delineate appropriate guidelines for the optimal management of these tumors. A panel of experts from several specialities, including medical oncology, surgery, pathology, molecular biology and imaging, were invited to participate in a meeting to present and discuss a number of pre-selected questions, and to achieve a consensus according to the categories of the National Comprehensive Cancer Network (NCCN) and the Standard Options Recommandations (SOR) of the French Federation of Cancer Centers. Generally, consensus points were from categories 2A of the NCCN and B2 of the SOR. Conventional histologic examination with immunohistochemistry for CD117, CD34, SMA, S-100 and desmin is considered standard. Molecular analysis for the identification of KIT and PDGFRA mutation may be indicated in CD117-negative GIST. Complete tumor resection with negative margins is the optimal surgical treatment. Adjuvant imatinib should be considered an experimental approach. Neoadjuvant imatinib is also experimental, although its use may be justified in unresectable or marginally resectable GIST. Imatinib should be started in metastatic or recurrent disease, and should be continued until progressive disease or drug intolerance. In these cases, sunitinib can be used. The optimal criteria for the assessment and monitoring of GIST undergoing imatinib therapy are not well known, but they should include reduction in tumor size and disease stabilization, as well as reduction of tumor density on CT scan and metabolic activity on PET scan.
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