Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the prevalence of mesenteric artery stenoses (MAS) is high, symptomatic chronic mesenteric ischemia (CMI) is rare. The collateral network in the mesenteric circulation, a remnant of the extensive embryonal vascular network, serves to prevent most cases of ischemia. This explains the high incidence of MAS and relative rarity of cases of CMI. The number of affected vessels is the major determinant in CMI development. Most subjects with single vessel mesenteric stenosis do not develop ischemic complaints. Our experience is that most subjects with CA and SMA stenoses with abdominal complaints have CMI. A special mention should be made on patients with median arcuate ligament compression (MALS). There is ongoing debate whether the intermittent compression, caused by respiration movement, can cause ischemic complaints. The arguments pro and con treatment of MALS will be discussed. The clinical presentation of CMI consists of postprandial pain, weight loss, and an adapted eating pattern caused by fear of eating. In end-stage disease more continuous pain, diarrhea or a dyspepsia-like presentation can be observed. Workup of patients suspected for CMI consists of three elements: the anamnesis, the vascular anatomy and proof of ischemia. The main modalities to establish mesenteric vessel patency are duplex ultrasound, CT angiography or MR angiography. Assessing actual ischemia is still challenging, with only tonometry and visual light spectroscopy as tested candidates. Treatment consists of limiting metabolic demand, treatment of the atherosclerotic process and endovascular or operative revascularisation. Metabolic demand can be reduced by using smaller and more frequent meals, proton pump inhibition. Treatment of the atherosclerotic process consists of cessation of smoking, treatment of dyslipidemia, hypertension, hyperglycaemia, and medication with trombocyte aggregation inhibitors.
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PMID:Diagnosis and treatment of chronic mesenteric ischemia: An update. 2839 88

End stage renal disease (ESRD) population account for 1.9 per patient year of hospital admissions annually. ESRD population are at increased risk of bleeding secondary to use of anticoagulation during hemodialysis and uremia induced platelet dysfunction. Gastrointestinal bleeding accounts for 3-7% of all deaths in ESRD population. Lower gastrointestinal bleeding refers to blood loss from a site in the gastrointestinal tract distal to the ligament of Treitz. It is usually suspected when a patient complains of hematochezia. It is different from patients presenting with hematemesis that suggests bleeding from upper gastrointestinal tract. Common causes of lower gastrointestinal bleed include diverticulosis, ischemia, hemorrhoids, neoplasia, angiodysplasia, and inflammatory bowel disease. ESRD patients are known to retain phosphate alone or in combination with calcium which has been associated with high mortality. Sevelamer is a phosphate binder used widely in ESRD population. The known side effects of sevelamer include metabolic acidosis, vomiting, nausea, diarrhea, dyspepsia, abdominal pain, constipation, flatulence, fecal impaction, and skin rash. We are reporting a unique case of a 56-year-old female with end stage renal disease on sevelamer hydrochloride who presented with gastrointestinal bleeding and underwent a right hemicolectomy found to have sevelamer-induced mucosal ulceration and crystal deposition in the colonic mucosa. This case report highlights the fact that, with widespread use of this medication in the patients with chronic kidney diseases, physicians should be aware of this underrecognized entity in the differential diagnosis of gastrointestinal bleed in ESRD patients.
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PMID:Colonic Mucosal Ulceration and Gastrointestinal Bleeding Associated with Sevelamer Crystal Deposition in a Patient with End Stage Renal Disease. 2968 71


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