Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 46-year-old woman with the CRST variant of scleroderma (calcinosis, Raynaud's phenomenon, sclerodactyly, and telangiectasis) was treated with a diphosphonate (disodium etidronate) in an effort to reduce her dystrophic calcifications or retard their progression. After 18 months of therapy, no improvement in her calcinosis was noted. In addition, she developed bloody diarrhea, epigastric burning, and weight loss during the last two months of Therapy. Upper gastrointestinal series revealed a gastric ulcer. Endoscopy with biopsy proved it to be benign. Gastric ulcerations has been seen in animals given disodium etidronate but only at much higher doses than are currently recommended for humans. Although a cause and effect relationship cannot be established with certainty in this patient, it is suggested since she was not receiving other ulcerogenic drugs chronically. This information may be important to other investigators of disodium etidronate.
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PMID:Appearance of a gastric ulcer during diphosphonate therapy in a woman with CRST syndrome. 41 Nov 74

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.
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PMID:Gastric mucosal calcinosis. Calcified aluminum phosphate deposits secondary to aluminum-containing antacids or sucralfate therapy in organ transplant patients. 844 8