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

Although venous air embolism is a known complication in medical practice in general, only a single case of upper gastrointestinal endoscopy complicated by venous air embolism with consecutive acute cardiovascular failure has so far been described in literature. Here we show that gastroscopy may be accompanied by massive, i.e. fatal venous air embolism. If a vessel in the gastrointestinal tract is exposed but does not collapse (in the case of a gastric ulcer, for example) air insufflated under pressure by the gastroscope may lead to a fatal air embolism. Our tests using a commercial gastroscope revealed that an overpressure of up to 43 kPa (kiloPascals) is reached without the rinsing function while an overpressure of up to 45 kPa is measured if the rinsing function is operated simultaneously. The maximum flow rates without resistance were 100 ml/min for rinsing liquid (purified water) and 2000 ml/min for air. Our results suggest that air insufflation by the gastroscope may result in a critical air embolism within very few seconds on condition that a connection with the vascular system exists. However, this complication is extremely rarely encountered. We propose that CO2 should be administered in place of air or alternatively the maximum pressure should be considerably reduced to avoid a fatal outcome in routinely performed gastroscopical examinations.
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PMID:Mechanism of fatal air embolism after gastrointestinal endoscopy. 958 99

We report a case of hypermagnesemia in a hospitalized patient after prolonged laxative use; due to preexisting impaired consciousness and digestive problems, the hypermagnesemia was difficult to detect until it almost became fatal. A 64-year-old man who was a patient at another hospital for treatment of head injury and gastric ulcer had developed circulatory collapse and was transferred to our hospital. Hypermagnesemia (serum magnesium concentration 11.0 mg.dl(-1)) was thought to be the cause of the circulatory collapse and treatments were successful. A magnesium laxative had been administered for more than a month at the previous hospital, but the patient's serum magnesium level was never measured. Care should be taken when a magnesium laxative is administered to patients who already have impaired consciousness and digestive problems that are early symptoms of hypermagnesemia.
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PMID:Circulatory collapse caused by unnoticed hypermagnesemia in a hospitalized patient. 1745 60

A 10-year-old female neutered boxer was presented with a five-week history of episodic collapse and melaena. Twenty-four-hour electrocardiograph (Holter) analysis revealed the collapsing episodes to coincide with episodes of paroxysmal ventricular tachycardia. Investigation of the dog's melaena revealed a gastric ulcer which was treated medically and an ileocaecal mass which was surgically excised. Histopathological examination of the mass was consistent with a neuroendocrine (carcinoid) tumour. The patient's recovery after surgery was unremarkable. At six-week follow-up, there had been no further episodes of melaena or collapse and repeat Holter analysis did not show any significant abnormalities. In this dog the gastric ulceration and paroxysmal ventricular tachycardia could be attributed to a paraneoplastic syndrome as a result of circulating vasoactive substances released by the tumour; this is supported by the evidence that all clinical signs resolved after surgical excision of the mass and the dog was clinically well 18 months after surgery.
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PMID:An intestinal neuroendocrine tumour associated with paroxysmal ventricular tachycardia and melaena in a 10-year-old boxer. 1761 58

CCN1 is a matricellular protein that activates many genes related to wound healing and tissue remodeling in fibroblasts, but its effect on epithelial cells remains unclear. This study examined the role of CCN1 in epithelial wound healing using rat gastric epithelial cells and rat stomach ulcer as in vitro and in vivo models, respectively. We found that CCN1 expression is highly upregulated in the epithelial cells adjacent to a wound and remains high until the wound is healed. Upregulation of CCN1 activates a transient epithelial-mesenchymal transition in the epithelial cells at the migrating front and drives wound closure. Once the wound is healed, these epithelial cells and their progeny can resume their original epithelial phenotype. We also found that CCN1-induced E-cadherin loss is not due to transcriptional regulation but rather protein degradation due to the collapse of adherens junctions, which is contributed by beta-catenin translocation. CCN1-activated integrin-linked kinase mediates this process. Finally, our in vivo study showed that locally neutralizing CCN1 drastically impairs wound closure, whereas local injection of recombinant CCN1 protein induces expression of vimentin and smooth muscle alpha-actin in normal gastric mucosal epithelial cells and accelerates re-epithelialization during ulcer healing. In conclusion, our study indicates that CCN1 can induce reversible epithelial-mesenchymal transition, and this feature may have great value for clinical wound healing.
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PMID:CCN1 induces a reversible epithelial-mesenchymal transition in gastric epithelial cells. 2045 73