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- Trouble-makers in cytologic interpretation of the uterine cervix
- Eunah Shin, Jaeeun Yu, Soon Won Hong
- J Pathol Transl Med. 2023;57(3):139-146. Published online May 15, 2023
- DOI: https://doi.org/10.4132/jptm.2023.04.25
- 3,374 View
- 335 Download
- 2 Web of Science
- 2 Crossref
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Abstract
PDF - The development and standardization of cytologic screening of the uterine cervix has dramatically decreased the prevalence of squamous cell carcinoma of the uterine cervix. Advances in the understanding of biology of human papillomavirus have contributed to upgrading the histologic diagnosis of the uterine cervix; however, cytologic screening that should triage those that need further management still poses several difficulties in interpretation. Cytologic features of high grade intraepithelial squamous lesion (HSIL) mimics including atrophy, immature metaplasia, and transitional metaplasia, and glandular lesion masquerades including tubal metaplasia and HSIL with glandular involvement are described with accentuation mainly on the differential points. When the cytologic features lie in a gray zone between the differentials, the most important key to the more accurate interpretation is sticking to the very basics of cytology; screening the background and cellular architecture, and then scrutinizing the nuclear and cytoplasmic details.
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- Pitfalls in Gynecological Cytology: Review of the Common and Less Frequent Entities in Pap Test
Danijela Vrdoljak-Mozetič, Snježana Štemberger-Papić, Damjana Verša Ostojić, Roberta Rubeša, Marko Klarić, Senija Eminović
Acta Cytologica.2024; 68(3): 281. CrossRef - Cytological features of human papillomavirus‐infected immature squamous metaplastic cells from cervical intraepithelial neoplasia grade 2
Mitsuaki Okodo, Kaori Okayama, Koji Teruya, Ruku Shinohara, Shuichi Mizuno, Rei Settsu, Yasuyoshi Ishii, Masahiko Fujii, Hirokazu Kimura, Mizue Oda
Journal of Medical Virology.2023;[Epub] CrossRef
- Pitfalls in Gynecological Cytology: Review of the Common and Less Frequent Entities in Pap Test
Original Articles
- Correlation of the Intestinal Metaplasia Subtypes and Gastric Carcinoma.
- Hwa Eun Oh, Mee Ja Park, Jong Sang Choi
- Korean J Pathol. 1997;31(12):1272-1281.
- 1,730 View
- 18 Download
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Abstract
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- Helicobacter pylori, loss of basement membrane, atrophy, type III intestinal metaplasia, adenomatous polyposis coli (APC) gene mutations and altered p53 function were believed as a factor to develop the gastric adenocarcinomas. To investigate the incidence and prevalence of Helicobacter pylori, intestinal metaplasia and atrophy, 120 gastrectomy specimens collected from patients with gastric adenocarcinoma (100 cases) and non-neoplastic conditions (20 cases) were studied. Intestinal metaplasia can be classified as type I (complete), type II (incomplete, sulfomucin-negative) and type III (incomplete, sulfomucin-positive) by Filipe and Jass. The incidence of intestinal metaplasia of gastric adenocarcinoma was 96% compared with the incidence of 75% in non-neoplastic conditions. The type I and type II were more common than type III and were present in both non-neoplastic conditions (75%) and adenocarcinoma (74%). In contrast, type III intestinal metaplasia was seen in only 20% of intestinal metaplasia-positive cases, all of which (22 of 22) were from patients with adenocarcinoma. The high specificity of type III intestinal metaplasia might be acceptable for screening purposes, but its sensitivity of 22% for gastric adenocarcinoma is low. Helicobacter pylori were detected in 96% of adenocarcinoma cases and 100% of non-neoplastic cases. Atrophy was detected in 50% of non-neoplastic cases and in 57% of adenocarcinoma cases. The data thus confirms a significant relation between incomplete sulfomucin-secreting intestinal metaplasia (type III) and gastric carcinoma, especially intestinal type (p<0.01). Thus, the type III intestinal metaplasia should be considered a risk factor and its presence in a biopsy specimen should prompt close surveillance.
- Mechanisms of Acinar Cell Deletion in Rat Pancreas Following Experimental Duct Ligation.
- Sang Pyo Kim, Kun Young Kwon, Sang Sook Lee, Chai Hong Chung
- Korean J Pathol. 1989;23(1):51-64.
- 1,673 View
- 17 Download
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Abstract
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- This study was carried out to investigate the mechanisms of acinar cell deletion, leading to the pancreatic atrophy of rat pancreas after experimental duct ligation. Fifty-seven male Sprague-Dawley rats, maintained on a stock diet, weighing 200 gm, in average, were divided into 2 experimental groups. Group 1. Control group. Six rats. Abdominal cavity was opened and closed without further treatment. Group 2. Fifty-one rats. Animals were treated with partial ligation of the pancratic ducts according to the procedure developed by Hultquist followed by sequential sacrifices at: 1 hour (3 rats), 3 hours (3 rats), 6 hours (6 rast), 12 hours (3 rats) and 24 hours (8 rats); 2 days (8 rats), 3 days (3 rats), 4 days (3 rats) and 5 days (5 rats); 1 week (3 rats), 2 weeks (3 rats) and 8 weeks (3 rats); after partial ligation was extirpated and examined by both light and electron microscopy. The results obtained were as follows: Light microscopically, noted were an interstitial edema and focal necrosis of the pancreatic tissue along with fine vacuolization and depletion of the zymogen granules in the acinar cell cytoplasms and condensation of the acinar cell nucleus. These changes were observed by 2 days after ligation. At about the same time, one can observe the dense body, identified to be apoptotic body, in the acinar cell which were found to be decreased in quantity. By 5 days after ligation, no recognizable acinar cells left in the collagenous stroma except intercalated ducts. Conspicuous stroma except intercalated ducts. Conspicuous stromal hyalinization, thereafter. Electron microscopically (TEM and SEM), nuclear condensation and margination toward the nuclear membrane was noted by 6 hours after duct ligation. By 24 hors sporadic membrane-bounded apoptotic bodies appeared in the acinar cells, the number of which reaching to the peak by 3 days after ligation. These apoptotic bodies were found to be phagocytosed by either intraepithelial mononuclear phagocytes or adjoining acinar cells. It can be concluded, therefore: That orderly remodeling of pancreatic exocrine tissue during atrophy is effected by rapid deletion of acinar cells by apoptosis.
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