Yoshinori Tsugawa

Calcified Carcinoma of the Stomach in a Hemodialysis Patient

Accessible online at: http://BioMedNet.com/karger Fig. 1. Unenhanced computed tomography of the abdomen showed a thickened gastric wall with miliary calcification and porcelain gallbladder. No liver metastases were seen. Dear Sir, Calcified carcinoma of the stomach has been considered to be rare [1, 2]. We report a rare case of calcified carcinoma of the stomach in a hemodialysis patient. A 52-year-old female with end-stage renal disease (ESRD) had been on hemodialysis for 11 years. Renal anemia was treated with recombinant human erythropoietin (rhEPO) in a weekly dose of 3,000 IU, although the hematocrit was 24%. The rhEPO weekly dose was increased up to 4,500 IU. The hematocrit increased up to 28.3%. However, the hematocrit then gradually decreased to 20%. Gastrointestinal endoscopic examination showed a Borrmann type I gastric carcinoma in the greater curvature of the antrum and a type 1 early carcinoma in the lesser curvature of the antrum. The serum calcium was 9.7 mg/dl and phosphate 6.9 mg/dl. The serum intact parathyroid hormone was 618 pg/ml. Computed tomography of the abdomen showed a thickened gastric wall with miliary calcifications within it (fig. 1). She underwent subtotal gastrectomy. Microscopic examination of the larger carcinoma revealed a mucinous adenocarcinoma. Findings of central degeneration and calcification were found in the carcinoma. The foci of calcification corresponded to degenerated areas. The other early carcinoma was a papillary adenocarcinoma without calcification. Extraskeletal calcifications of several types are common in patients with ESRD [3, 4]. Visceral calcifications are rather infrequently detectable during life. These calcifications mainly occur in heart, lungs, kidney and stomach [3–5]. The factors that predispose to this complication include an increase in the product of serum calcium and phosphate, overt secondary hyperparathyroidism, the presence of alkalosis, and local tissue injury [3, 4]. It is likely that both metastatic and dystrophic factors act together in patients with ESRD [3]. In the present case, the increase of product of serum calcium and phosphate, or parathyroid hormone in part might promote the calcification. However, microscopic examination showed that calcification existed in the center of the mucus produced by the adenocarcinoma. Kitagawa and Kimata [1] stated that mucinous adenocarcinoma has a tendency to cause tissue injury by expansive growth because of mucin secreted from carcinoma cells. It is suggested that the mechanism of calcification in this case might be dystrophic calcification rather than metastatic calcification. Several mechanisms of dystrophic calcification have been proposed. First, the solubility of secondary calcium phosphate varies inversely with pH [3]. Inadequate blood supply resulting from expansive growth might diminish cellular respiration with a concomitant diminished carbon dioxide production. This state of the environment toward the relative alkalinity would then promote calcium salt deposition [2]. Second, the mucin is a glycoprotein very similar to that present in the cartilage of the provisional zone of calcification and it thus has a propensity to calcification [2]. Whether visceral calcifications are accompanied by malignancy or not in patients with ESRD should be considered.