Szachnowicz Sergio, Cecconello Ivan, Iriya Kiyoshi, Marson Allan Garms, Takeda Flávio Roberto, Gama-Rodrigues Joaquim José
Department of Gastroenterology, Faculty of Medicine, University of São Paulo, São Paulo, SP, Brazil.
Clinics (Sao Paulo). 2005 Apr;60(2):103-12. doi: 10.1590/s1807-59322005000200005. Epub 2005 Apr 26.
Barrett's esophagus is the substitution of squamous epithelium of the distal esophagus by columnar epithelium. Intestinal metaplasia in Barrett's esophagus is considered to be the main risk factor for the development of adenocarcinoma. Diffuse adenocarcinoma and Barrett's esophagus without intestinal metaplasia are rare, and reports on the subject are scarce.
To estimate the prevalence of adenocarcinoma in 297 patients with Barrett's esophagus, during the period of 1990 to 2002, and in 13 patients undergoing surgery, to conduct detailed macroscopic and microscopic analysis, with performance of immunohistochemical tests for p53 and Ki67, correlating the type of tumor with its adjacent epithelium.
In our patients with Barrett's esophagus, there was a prevalence of 5.7% of adenocarcinoma. The tumors developed only when the Barrett's esophagus segment was long (>3.0 cm). Tumors were located close to the squamous-columnar junction. The histological study revealed 2 patients (15.4%) with Barrett's esophagus adjacent to a tumor with gastric metaplasia without the presence of intestinal metaplasia. Tumors were classified according to Nakamura's classification (23% differentiated pattern, and 77% undifferentiated pattern) and to Lauren's classification (61% intestinal and 39% diffuse). The difference is due to the migration of microtubular and foveolar tumors of undifferentiated (gastric) pattern in Nakamuras classification to the Lauren's intestinal type. The immunohistochemical test for Ki67 was strongly positive in all the patients, thus evidencing intense cell proliferation in both the columnar epithelium and tumor. Expression of p53 was negative in 67% of the adjacent columnar epithelia and 42% of the tumors, without any correlation between the tissue types.
Adenocarcinoma develops from mixed columnar epithelium, either intestinal or gastric, showing both the gastric and the intestinal patterns; thus, tumors can also grow in columnar epithelium without intestinal metaplasia. Barrett's esophagus should be followed up for the possibility of progression to malignancy, especially when the segment is longer than 3 cm.
巴雷特食管是远端食管的鳞状上皮被柱状上皮替代。巴雷特食管中的肠化生被认为是腺癌发生的主要危险因素。弥漫性腺癌和无肠化生的巴雷特食管很少见,关于这方面的报道也很稀少。
评估1990年至2002年期间297例巴雷特食管患者以及13例接受手术患者中腺癌的患病率,进行详细的大体和显微镜分析,并进行p53和Ki67的免疫组化检测,将肿瘤类型与其相邻上皮相关联。
在我们的巴雷特食管患者中,腺癌患病率为5.7%。肿瘤仅在巴雷特食管段较长(>3.0 cm)时发生。肿瘤位于鳞状柱状交界处附近。组织学研究显示,2例患者(15.4%)的巴雷特食管与伴有胃化生而非肠化生的肿瘤相邻。肿瘤根据中村分类法(23%为分化型,77%为未分化型)和劳伦分类法(61%为肠型,39%为弥漫型)进行分类。差异是由于中村分类法中未分化(胃)型的微管和小凹肿瘤向劳伦肠型的迁移。所有患者的Ki67免疫组化检测均呈强阳性,从而证明柱状上皮和肿瘤中均有强烈的细胞增殖。p53在67%的相邻柱状上皮和42%的肿瘤中表达为阴性,组织类型之间无任何相关性。
腺癌由肠型或胃型混合柱状上皮发展而来,呈现胃型和肠型两种模式;因此,肿瘤也可在无肠化生的柱状上皮中生长。应随访巴雷特食管恶变的可能性,尤其是当食管段长度超过3 cm时。