Department of Oncology, Nanchang county people's hospital, Nanchang, China.
Department of Oncology, The Second Afiliated Hospital of Nanchang University, 1 Minde Road, Nanchang, China.
BMC Cancer. 2018 Apr 27;18(1):474. doi: 10.1186/s12885-018-4415-5.
Calcification in primary gastric cancer is very rare. In this report, we describe the computerized tomography (CT) changes in calcification in a patient with locally advanced signet-ring gastric cancer treated with chemotherapy.
A 49-year-old man presented with 5 months' history of abdominal pain, anorexia, and rapid weight loss. He had undergone Billroth-II subtotal gastrectomy for a bleeding gastric ulcer 30 years ago. Abdominal CT showed irregular thickening of the gastric wall and miliary calcifications. Histologic examination of specimen obtained by endoscopic biopsy showed poorly differentiated calcified signet-ring gastric cancer. The patient was clinically staged T4N2M0 and treated with docetaxel, cisplatin, and fluorouracil (DCF)/oxaliplatin and S-1 (XLOX)/S-1. After five cycles of chemotherapy, the general condition of the patient improved and tumor markers (CEA, CA125, CA199) decreased. However, follow-up CT scans showed continuing increase in the calcification.
To conclude, in this case report we have described the dynamic changes in calcification in a gastric cancer patient receiving chemotherapy. One explanation for the observed increase in calcifications could be that the ischemic necrosis resulting from chemotherapy creates an alkaline environment, which promotes deposition of calcium salts. Our theory needs to be confirmed with histological evidence from a large series of patients. Nevertheless, we hope that these findings will improve understanding of the mechanism of calcification in gastric cancer.
原发性胃癌中的钙化非常罕见。在本报告中，我们描述了一名局部晚期印戒细胞胃癌患者在接受化疗后钙化的计算机断层扫描（CT）变化。
一名 49 岁男性，因腹痛、食欲不振和体重迅速下降 5 个月就诊。30 年前，他因胃出血性溃疡接受了 Billroth-II 次全胃切除术。腹部 CT 显示胃壁不规则增厚和粟粒状钙化。内镜活检标本的组织学检查显示低分化钙化印戒细胞胃癌。患者临床分期为 T4N2M0，并接受多西紫杉醇、顺铂和氟尿嘧啶（DCF）/奥沙利铂和 S-1（XLOX）/S-1 治疗。化疗 5 个周期后，患者一般状况改善，肿瘤标志物（CEA、CA125、CA199）下降。然而，随访 CT 扫描显示钙化持续增加。
总之，在本病例报告中，我们描述了接受化疗的胃癌患者钙化的动态变化。钙化增加的一个解释可能是化疗引起的缺血性坏死产生碱性环境，促进钙盐沉积。我们的理论需要通过大量患者的组织学证据来证实。尽管如此，我们希望这些发现将有助于提高对胃癌钙化机制的理解。
