Gastric Mucosal Calcinosis Research Articles

S2541 A Rare Case of Erosive Gastritis and Melena Related to Gastric Mucosal Calcinosis

S2541 A Rare Case of Erosive Gastritis and Melena Related to Gastric Mucosal Calcinosis

Calcinose de la muqueuse gastrique

The gastric mucosal calcinosis is a benign condition corresponding to calcium deposits in the gastric mucosa. A 39-year-old women, with an history of transplantation, transplant rejection and hemodialysis, treated with corticosteroids and calcium/phosphoremic supplements, had chronic diarrhea. Gastroduodenal fibroscopy found an atypical atrophic gastritis appearance with small focal whitish deposits in the gastric mucosa. Histological examination revealed brown and gray-bluish crystalline deposits in superficial chorion, stained by Von Kossa, leading to a diagnosis of gastric mucosal calcinosis. This lesion can be categorized as systemic, dystrophic, iatrogenic and idiopathic. In our observation, gastric mucosal calcinosis was probably mixed, linked to renal disorders, and mainly to exogenous phosphocalcic drug intakes. The gastric mucosal calcinosis is commonly found in kidney transplant patients reaching a frequency of 15 to 29%.

S3144 Recurrent Dyspepsia Secondary to Gastric Mucosal Calcinosis GMC

S3144 Recurrent Dyspepsia Secondary to Gastric Mucosal Calcinosis GMC

S3030 Gastric Mucosal Calcinosis in a Patient With End-Stage Renal Disease (ESRD), Eucalcemia, and Euphosphatemia

INTRODUCTION: Gastric Mucosal Calcinosis (GMC) is calcific deposition in the gastric mucosa that is only rarely observed on routine biopsies. The four broad categories of visceral calcinosis that may include gastric mucosa are metastatic, iatrogenic, dystrophic, and idiopathic. Occasionally gastric calcinosis can be encountered on upper endoscopy as irregular nodularity as described in this case. CASE DESCRIPTION/METHODS: We present a case of a 47-year-old caucasian male with a past medical history of end-stage renal disease on hemodialysis. The patient presented with non-healing right lower extremity wounds after a trans-metatarsal amputation. He developed hematochezia overnight with a drop in hemoglobin and hematocrit requiring blood transfusions. An endoscopy was done to find the cause which showed diffuse moderate inflammation characterized by congestion (edema) and erythema. Granularities were found in the entire examined stomach. Biopsies were taken for histology which revealed gastric mucosal calcinosis. The patient’s blood chemistry showed a Creatinine of 3.73, Calcium of 9.4, Magnesium of 1.7, Phosphorus of 4.3, and BUN of 21. On a 6-month analysis of his labs before the biopsy, he was found to be eucalcemic and euphosphatemic. He had no known underlying malignancy, had no history of chronic antacid use and 1,25-Hydroxy Vitamin D was found to be low. The patient’s hematochezia was later found to be a result of angiodysplasias in the cecum and was treated with argon laser. DISCUSSION: Calcific deposits in gastric mucosa are relatively rare and are a consequence of four main etiologies that include metastatic, iatrogenic, dystrophic, and idiopathic disease processes. Among these, metastatic calcinosis is the most common. Multiple primary factors have been shown to be associated with the pathogenesis of gastric mucosal calcinosis. These mainly include hypercalcemia and/or hypophosphatemia, elevated BUN in the setting of eucalcemia, organ transplants, gastric ulcers, chronic atrophic gastritis, and gastric neoplasms. In general, most cases of GMC are detected postmortem or on bone scintigraphy. GMC is rarely seen on endoscopy with biopsy showing white 1–2 mm nodules in a background of the thinned atrophic gastric mucosa.Figure 1.: Granularities in the entire examined stomach.

S3015 A Case of Gastric Mucosal Calcinosis

S3015 A Case of Gastric Mucosal Calcinosis

Lanthanum deposition in the gastric mucosa

Lanthanum carbonate is a phosphate binding agent used for the management of hyperphosphataemia in patients with chronic renal failure. Cases of lanthanum deposition within the gastrointestinal tract, first recognised in gastric mucosa, have been reported since 2015. However, lanthanum deposition remains a relatively novel entity with potential for under-recognition and confusion with a variety of other processes. This case study reports a case of lanthanum deposition involving the gastric mucosa in a renal transplant patient. Biopsies taken from the gastric antrum demonstrated appearances of reactive gastropathy together with an accumulation of histiocytes, including occasional multinucleated forms, containing deposits of amphophilic to brown finely granular to coarse material within the superficial lamina propria. The differential diagnosis included gastric mucosal calcinosis, iron therapy-induced gastric injury, an infectious aetiology, or the accumulation of exogenous materials related to medications including resins/crystalloids. Investigation of the patient’s medication history revealed oral lanthanum carbonate use; this finding taken in conjunction with the morphologic findings was most in keeping with lanthanum deposition. The identification of lanthanum deposition in gastric biopsies is important as the long-term consequences are currently unknown, and the use of this medication is increasing.

Gastric Mucosal Calcinosis

Gastric Mucosal Calcinosis

Gastric Mucosal Calcinosis

Gastric Mucosal Calcinosis

Gastric Mucosal Calcinosis

Background: Gastric mucosal calcinosis (GMC) is a rarely encountered disease characterized by calcific deposition in the gastric mucosa which was known to be associated with organ transplantation, end-stage renal disease, hypercalcemia, hyperphosphatemia, gastric neoplasia, medications such as antacids containing aluminum, sucralfate and bismuth, and so on. We describe incidentally found 23 cases of GMC. Methods: We identified 23 cases of GMC from July 2004 to June 2011 from pathology department records. All available inpatient and outpatient medical records including laboratory data were reviewed. Results: 23 cases (9 male and 14 femal: median age of 65.2, range 34-85) were found incidentally by upper gastrointestinal endoscopic biopsy. The microscopic examination showed multifocal basophilic calcific material just beneath the surface epithelium. 14 patients (60.9%) were taking tripotassium dicitrato bismuthate in variable duration from one week to four years, 5 patients (21.7%) were taking aluminum containing antacid and 2 patient (8.7%) were taking both of them. 1 patient (4.3%) showed hypercalcemia with increased parathyroid hormone. The patients had no history of renal insufficiency, organ transplantation or gastric malignancy and had variable symptoms according to other comorbid gastrointestinal diseases, in example, gastritis, gastroesophageal reflux disease, and functional dyspepsia. The endoscopic findings were hyperemia, edema, chalky or salty-white plaque in common and other frequently accompanying feature was spontaneous bleeding. However, endoscopic finding of 2 pateints (8.7%) showed gastric polyp which confirmed GMC pathologically. There was no difference of endoscopic findings between different etiologies. Follow up endoscopy which was available in 8 patients (34.8%) from two months to two years after stopping offending medication showed disappearance of previous noted GMC. Conclusion: Gastric mucosal calcinosis can develop in normal tissue because of altered serum or mucosal biochemical environment associated with therapeutic measures and can be reversed after abstinence of the offending medication.

Gastic Mucosal Calcinosis Associated With Gastrointestinal Bleeding

Purpose: Gastric mucosal calcinosis (GMC) is a rare cause of gastrointestinal bleeding, and usually an incidental finding on endoscopy. Histopathology characteristically reveals deposits of irregular, amorphous microcalcifications in the gastric mucosa. GMC is classified as metastatic, dystrophic or idiopathic. Metastatic calcinosis is the most common, occurring in the setting of abnormal calciumphosphate metabolism, and resulting in deposition of calcium salts. We report a case of gastric mucosal calcinosis associated with overt gastrointestinal bleed. Case: A 59 year old Hispanic man presented with 1 week of black stools. Past medical history included end stage renal disease on hemodialysis for 8 years, atrial fibrillation on anticoagulation, diabetes, and coronary artery disease. He denied nausea, vomiting, hematemesis, or abdominal pain. No NSAID use other than daily aspirin was reported. Vital signs on presentation were unremarkable. Physical exam was notable for pale conjunctiva, soft, non-tender abdomen, and melena on rectal exam. Laboratory tests revealed hemoglobin of 5.9 g/dL (baseline 10 g/dL), creatinine 5.87 mg/dL, corrected calcium 9.3 mg/dL, phosphorus 3.4 mg/dL, calcium-phosphate product 31, and INR 2.8. The patient received 2 units of packed red blood cells and 4 units of fresh frozen plasma with appropriate response. EGD showed thickened antral folds (Figure 1), which were further evaluated with endoscopic ultrasound showing hyperechoic foci and shadowing with intact gastric layers (Figure 2). Histopathology of thickened folds showed foveolar hyperplasia and histiocytes in the lamina propria containing calcium deposits. Von Kossa stain confirmed calcium deposition (Figure 3). Steiner stain was negative for Helicobacter pylori. No other source of bleeding was identified on repeat EGD, colonoscopy, and capsule endoscopy. At 4 months follow up, patient has had no further bleeding.Figure 1Figure 2Figure 3Conclusions: The presentation above is suggestive of upper GI bleed secondary to gastric mucosal calcinosis in the setting of end stage renal disease. GMC has been rarely reported as a cause of GI bleeding. This case emphasizes that gastric mucosal calcinosis should be considered as a possible GI bleeding source especially in the clinical setting of chronic kidney disease.

Gastric Mucosal Calcinosis: A Rare Cause of Bleeding

A52-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 antrumwith 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

Gastric mucosal calcinosis

Gastric mucosal calcinosis

A Rare Case of Gastric Mucosal Calcinosis

A Rare Case of Gastric Mucosal Calcinosis

Gastric mucosal calcinosis

Gastric mucosal calcinosis

Gastric Mucosal Calcinosis in a Patient with Abdominal Pain

Purpose: Background: Calcification of the gastric mucosa (gastric mucosal calcinosis) is a rare condition and is usually found incidentally on upper endoscopy. It is most frequently associated with conditions which cause hyperphosphatemia and hypercalcemia. In patients with chronic renal disease, it may be representative of impending systemic calcinosis. We herein report a case of gastric mucosal calcinosis in an otherwise healthy patient with abdominal pain. To our knowledge, such a presentation has not been described. Case Description: A 33 year-old female with no significant past medical history was referred for outpatient evaluation of worsening post-prandial epigastric pain of several months duration. She had intermittent headaches for which she used intermittent Excedrin®. Her only other medication was an oral contraceptive pill daily; no calcium-containing products. Physical Examination was notable for minimal epigastric tenderness but otherwise was unremarkable. Recent hepatic panel and serum chemistries (including calcium and phosphate) were normal. Upper endoscopy was significant for diffuse linear whitish plaques in the gastric antrum which did not wash off. Biopsy of these areas revealed gastric mucosal calcification and marked reactive changes. No Helicobacter pylori, inflammation, or metaplasia were seen. Stains for Congo red and PAS were additionally negative. Discussion: Gastric mucosal calcinosis is an extremely uncommon condition with a reported incidence of less than 0.1%. It has been described in association with chronic renal disease, hyperparathyroidism, gastric cancer, solid organ transplant recipients, and aluminum-containing antacids and sucralfate. Gastric mucosal calcinosis has been classified as metastatic, dystrophic, or idiopathic. In metastatic calcification, elevated serum calcium and phosphate lead to calcium salt deposition in normal gastric mucosa. Other organs including the lungs, kidneys and heart can also be affected. Multiple myeloma, tumor lysis syndrome, hyperparathyroidism, end-stage renal disease, and hypervitaminosis D are associated with this pattern. In dystrophic calcification, serum electrolytes are normal and calcium salt deposition occurs in damaged or inflamed gastric tissue. Peptic ulcer disease and malignancy are examples of associated conditions. The precise significance of gastric mucosal calcinosis in association with other diseases is unclear. Our patient was placed on omeprazole 20 mg daily and reported improved symptoms at follow-up.

Drug-induced pathology of the upper gastrointestinal tract

Drugs can produce a wide range of pathology in the upper gastrointestinal tract. Often, the injury pattern is non-specific. Pill-induced oesophagitis usually affects the mid oesophagus. In the stomach, many drugs, particularly non-steroid anti-inflammatory drugs (NSAIDs), can cause ulcers, erosions or reactive gastropathy. Some drugs produce specific injury patterns that can be recognized by pathologists. Proton pump inhibitors cause parietal cell hyperplasia and fundic gland polyps. Kayexalate may cause erosions or ulcers, with ‘mosaic’ crystals within the exudate. Patients taking iron tablets may develop reactive gastropathy with iron deposits in the lamina propria. Similarly, gastric mucosal calcinosis refers to deposits of calcium in the superficial lamina propria; antacids are one possible cause. Colchicine causes variable injury, and interference with microtubule assembly results in mitotic arrest. Hepatic arterial infusion chemotherapy may cause gastroduodenal ulcers associated with marked epithelial atypia that can be mistaken for carcinoma. Recognition of these histological patterns enables pathologists to make a diagnosis of drug-induced upper gastrointestinal injury and potentially to identify the specific agent responsible.

Gastric Mucosal Calcinosis

Generally, gastric mucosal calcinosis (GMC) is only rarely encountered in routine biopsies. GMC may be classified as dystrophic, metastatic, or idiopathic. Metastatic calcification represents the most frequently encountered subtype, and refers to the deposition of calcium salts on largely normal tissues in the setting of an abnormal serum biochemical environment (hypercalcemia, hyperphosphatemia, and/or an elevated CaxPO4 product). In contrast, dystrophic calcification implies calcification in inflammed, fibrotic, or otherwise altered tissue in the setting of a normal biochemical environment. The gastric mucosa, along with the kidneys and lungs, are preferential sites for metastatic calcification, a finding that has been attributed to the relative intracellular alkalinity at these sites. In addition to the wide variety of hypercalcemia and/or hyperphosphatemia-causing clinical conditions, GMC has also been associated with atrophic gastritis, hypervitaminosis A, organ transplantation, gastric neoplasia, uremia with eucalcemia/euphosphatemia, and the use of aluminum-containing antacids, citrate-containing blood products, isotretinoin, and sucralfate. Although GMC has rarely been associated with epigastric pain and/or dyspepsia, most come to clinical attention owing to their accumulation of bone-seeking radiopharmaceuticals or represent a postmortem finding. The precise significance or mechanistic basis for GMC remains to be elucidated. However, their presence in gastric biopsies should be reported, as they may serve as an indicator for generalized metastatic calcification, especially in organs where they may be fatal, such as the heart. Furthermore, some examples of systemic calcification are reversible with normalization of biochemical parameters, which highlights the need for pathologists to report this finding when encountered in a premortem gastric biopsy.

Gastric mucosal calcinosis in renal transplant patients

Gastric mucosal calcinosis in renal transplant patients

Gastric Mucosal Calcinosis

We have noticed calcium deposits (gastric mucosal calcinosis, or GMC) in the superficial gastric mucosa of 28 organ transplant patients (OTPs) (11 liver, seven bone marrow, four kidney, three kidney/pancreas, two heart, and one each of liver and kidney transplant) who underwent endoscopic biopsies. The deposits were tinctorially similar to cytomegalovirus inclusions, ranged from 40 to 250 mu in diameter, and were present just beneath the surface epithelium at the tips of the foveolae. An x-ray microanalysis showed that these mucosal deposits contained the elements aluminum, phosphorus, calcium, and chlorine. Clinical chart review showed that all OTPs with GMC were taking aluminum-containing antacids or sucralfate. Review of biopsies from gastric ulcer patients found GMC in a significantly smaller percentage than in transplant patients (32.7% vs. 5.1%, p < 0.0002). In addition, all three ulcer patients with calcified deposits were chronic renal failure patients on long-term aluminum-containing antacid therapy. Gastric mucosal calcinosis appears to be caused by aluminum phosphate accumulation secondary to antacid or sucralfate therapy in organ transplant patients. The presence of GMC in OTPs and chronic renal failure patients rather than other gastric ulcer patients is most likely due to the longer duration of therapy with aluminum-containing compounds in the former two patient groups. The clinical relevance of GMC remains to be seen. In theory, however, accelerated bone demineralization via loss of phosphates and absorption of aluminum in the gastrointestinal tract may be a consequence of long-term aluminum-containing antacid or sucralfate therapy.