Rubio C A, Kanter L, Björk J, Poppen B, Bry L
Department of Gastrointestinal Pathology, Karolinska Institute, , Stockholm, Sweden.
Jpn J Cancer Res. 1996 Jan;87(1):109-12. doi: 10.1111/j.1349-7006.1996.tb00208.x.
A patient having familiar adenomatosis polyposis and an ileo-rectal anastomosis developed a flat mucosal lesion in the rectum. A punch biopsy revealed a villous adenoma with high-grade dysplasia. The subsequent surgical specimen indicated that the flat villous adenoma was rich in Paneth cells. Special stains included lysozyme muramidase (to visualize Paneth cells), MIB1 proliferation monoclonal antibody and single and multilabel immunohistochemistry for Paneth cells. Other methods included transmission electron microscopy and quantification with an image quantifier (Program Optilab 2.1) of lysozyme-stained Paneth cells. The subjective evaluation of hematoxylin-eosin-stained preparations demonstrated that the Paneth cells were mainly located in the lower half of the villi. Sections labeled with a specific stain (lysozyme muramidase) revealed more Paneth cells in the villi and electron microscopy showed even more in lysozyme-negative areas. Obviously some migrating dysplastic Paneth cells had retained their characteristic granules on their way towards the tip of the villi. Quantitative studies indicated that the lysozyme muramidase-positive material accounted for 41% of the adenomatous tissue. MIB1 revealed intense cell proliferation at the base of the adenoma and in the entire slopes of the villi. Despite the wide distribution of Paneth cells in intestinal metaplasia of the stomach, in the normal small intestine and in the large bowel with chronic inflammatory diseases, it is surprising that tumors arising in Paneth cells are extremely rare. The causes of the apparent natural resistance of Paneth cells to tumor development deserve to be investigated. This is the first case of Paneth cell-rich flat adenoma of the rectum in the literature.
一名患有家族性腺瘤性息肉病且行回肠 - 直肠吻合术的患者，直肠出现了扁平黏膜病变。穿刺活检显示为高级别发育异常的绒毛状腺瘤。后续手术标本表明，扁平绒毛状腺瘤富含潘氏细胞。特殊染色包括溶菌酶（用于观察潘氏细胞）、MIB1增殖单克隆抗体以及针对潘氏细胞的单标和多标免疫组化。其他方法包括透射电子显微镜检查以及使用图像定量仪（Program Optilab 2.1）对溶菌酶染色的潘氏细胞进行定量分析。苏木精 - 伊红染色制剂的主观评估表明，潘氏细胞主要位于绒毛的下半部分。用特异性染色剂（溶菌酶）标记的切片显示绒毛中有更多潘氏细胞，电子显微镜检查发现在溶菌酶阴性区域甚至更多。显然，一些迁移的发育异常的潘氏细胞在向绒毛顶端迁移的过程中保留了其特征性颗粒。定量研究表明，溶菌酶阳性物质占腺瘤组织的41%。MIB1显示腺瘤底部和绒毛整个斜坡处有强烈的细胞增殖。尽管潘氏细胞在胃的肠化生、正常小肠以及患有慢性炎症疾病的大肠中广泛分布，但令人惊讶的是，起源于潘氏细胞的肿瘤极为罕见。潘氏细胞对肿瘤发生具有明显天然抗性的原因值得研究。这是文献中首例直肠富含潘氏细胞的扁平腺瘤病例。
