IMAGE OF THE MONTH Gastric Mucosal Calcinosis: A Rare Cause of Bleeding Meagan Gray, Andrew Brock, and Nilesh Lodhia Digestive Disease Center, Gastroenterology and Hepatology, Medical University of South Carolina, Charleston, South Carolina
52-year-old man with end-stage renal disease on hemodialysis presented with coffee-ground emesis and black stools. The physical examination revealed pale conjunctivae but was otherwise unremarkable. The laboratory analysis was significant for hemoglobin 4.4 g/dL, creatinine 7.8 mg/dL, and normal calcium and phosphorus (8.7 mg/dL and 2.5 mg/dL, respectively). The esophagogastroduodenoscopy revealed multiple smooth, nonbleeding nodules measuring 3–5 mm in diameter, extending radially in linear rows throughout the antrum with an overlying clot (Figure A). Two similar lesions were noted in the second portion of the duodenum (Figure B). Biopsies showed benign gastric and small bowel mucosa with calcinosis (Figure C). The bone scan demonstrated radiotracer within the region of the stomach, also compatible with calcinosis. The computed tomography scan was significant for mitral annular calcification and scattered pancreatic parenchymal calcifications. The patient did not have any risk factors for chronic pancreatitis. A review of laboratory studies over the past year revealed a persistently elevated parathyroid hormone as well as frequent hyperphosphatemia with occasional hypercalcemia. Two sessions of argon plasma coagulation, 14 days apart, were performed on the gastric lesions. No other endoscopic therapy was undertaken. After 8 months of follow-up, the patient did not have further bleeding. Gastric mucosal calcinosis (GMC) is a rare disorder typically encountered incidentally on routine biopsy or at autopsy. Metastatic calcification is the most common cause of GMC and occurs in the setting of abnormal calcium-phosphate metabolism. Hypercalcemia and/or hyperphosphatemia cause the deposition of calcium salts
A
Clinical Gastroenterology and Hepatology 2014;12:xxii
in otherwise normal tissue.1 Calcification preferentially occurs in gastric, kidney, heart, and lung tissue, likely because of their relative intracellular alkalinity.2 Cardiac and pulmonary calcifications are associated with significant and sometimes fatal consequences3; however, the natural history of gastric calcinosis is not entirely clear. Less commonly, GMC occurs from the deposition of calcium salts on inflamed or fibrotic tissue. This is referred to as dystrophic calcification and can be seen in conditions such as atrophic gastritis and gastric neoplasia. Finally, medications, such as isotretinoin and sucralfate, have also been associated with GMC. Given our patient’s hyperphosphatemia and multiorgan calcification, the etiology of his calcinosis was likely metastatic. To our knowledge, this is the first report in the literature of bleeding directly attributable to gastric calcinosis. It appears as if argon plasma coagulation may be effective in treating this rare entity.
References 1.
Gorospe M, Fadare O. Gastric mucosal calcinosis. Clinicopathologic considerations. Adv Anat Pathol 2007;14:224–228.
2.
Mulligan RM. Metastatic calcification. Arch Pathol 1947; 43:177–230. Kuzela DC, Huffer WE, Conger JD, et al. Soft tissue calcification in chronic dialysis patients. Am J Pathol 1977;86:403–424.
3.
Conflicts of interest The authors disclose no conflicts. © 2014 by the AGA Institute 1542-3565/$36.00 http://dx.doi.org/10.1016/j.cgh.2013.10.007
52-year-old man with end-stage renal disease on hemodialysis presented with coffee-ground emesis and black stools. The physical examination revealed pale conjunctivae but was otherwise unremarkable. The laboratory analysis was significant for hemoglobin 4.4 g/dL, creatinine 7.8 mg/dL, and normal calcium and phosphorus (8.7 mg/dL and 2.5 mg/dL, respectively). The esophagogastroduodenoscopy revealed multiple smooth, nonbleeding nodules measuring 3–5 mm in diameter, extending radially in linear rows throughout the antrum with an overlying clot (Figure A). Two similar lesions were noted in the second portion of the duodenum (Figure B). Biopsies showed benign gastric and small bowel mucosa with calcinosis (Figure C). The bone scan demonstrated radiotracer within the region of the stomach, also compatible with calcinosis. The computed tomography scan was significant for mitral annular calcification and scattered pancreatic parenchymal calcifications. The patient did not have any risk factors for chronic pancreatitis. A review of laboratory studies over the past year revealed a persistently elevated parathyroid hormone as well as frequent hyperphosphatemia with occasional hypercalcemia. Two sessions of argon plasma coagulation, 14 days apart, were performed on the gastric lesions. No other endoscopic therapy was undertaken. After 8 months of follow-up, the patient did not have further bleeding. Gastric mucosal calcinosis (GMC) is a rare disorder typically encountered incidentally on routine biopsy or at autopsy. Metastatic calcification is the most common cause of GMC and occurs in the setting of abnormal calcium-phosphate metabolism. Hypercalcemia and/or hyperphosphatemia cause the deposition of calcium salts
A
Clinical Gastroenterology and Hepatology 2014;12:xxii
in otherwise normal tissue.1 Calcification preferentially occurs in gastric, kidney, heart, and lung tissue, likely because of their relative intracellular alkalinity.2 Cardiac and pulmonary calcifications are associated with significant and sometimes fatal consequences3; however, the natural history of gastric calcinosis is not entirely clear. Less commonly, GMC occurs from the deposition of calcium salts on inflamed or fibrotic tissue. This is referred to as dystrophic calcification and can be seen in conditions such as atrophic gastritis and gastric neoplasia. Finally, medications, such as isotretinoin and sucralfate, have also been associated with GMC. Given our patient’s hyperphosphatemia and multiorgan calcification, the etiology of his calcinosis was likely metastatic. To our knowledge, this is the first report in the literature of bleeding directly attributable to gastric calcinosis. It appears as if argon plasma coagulation may be effective in treating this rare entity.
References 1.
Gorospe M, Fadare O. Gastric mucosal calcinosis. Clinicopathologic considerations. Adv Anat Pathol 2007;14:224–228.
2.
Mulligan RM. Metastatic calcification. Arch Pathol 1947; 43:177–230. Kuzela DC, Huffer WE, Conger JD, et al. Soft tissue calcification in chronic dialysis patients. Am J Pathol 1977;86:403–424.
3.
Conflicts of interest The authors disclose no conflicts. © 2014 by the AGA Institute 1542-3565/$36.00 http://dx.doi.org/10.1016/j.cgh.2013.10.007
