Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000727 (acute abdomen)
 3,084 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elevated plasma homocysteine is an acknowledged risk factor for arteriosclerotic occlusive disease, but little clinical evidence is available regarding its role in acute arterial thrombosis in the absence of an underlying lesion. A 45-year old man presented with an acute abdomen. A magnetic resonance arteriogram (MRA) showed occlusion of the superior mesenteric artery. At exploration, necrotic ileum was resected and the superior mesenteric artery was thrombectomized, restoring normal mesenteric flow. The plasma homocysteine level was 98.8 mmol/L, more than eight times the normal level. No embolic source was identified and an MRA and contrast arteriogram showed no residual occlusive disease in the superior mesenteric artery. Additional studies documented pernicious anemia, which was treated with cobalamin (vitamin B12) injections. This case provides further evidence of an association between hyperhomocysteinemia and acute arterial thrombosis. Hyperhomocysteinemia can result from easily correctible vitamin B12, B6, or dietary folate deficiencies. Plasma homocysteine levels should be determined in young individuals with acute arterial thrombosis whenever a hypercoagulable state is suspected.
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PMID:Homocysteine-associated acute mesenteric artery occlusion treated with thrombectomy and bowel resection. 1126 92

We report a 23-year-old man who presented with acute abdomen. At laparotomy, he was diagnosed to have superior mesenteric artery thrombosis, with consequent extensive intestinal gangrene extending from the proximal jejunum till the mid transverse colon. He subsequently developed dry gangrene of the digits. Further evaluation showed that he had marked hyperhomocysteinemia. The gangrenous bowel was resected, and the homocysteine level normalized with folic acid supplementation. He is well at 1-year follow up. His brother, who was asymptomatic, was also detected to have hyperhomocysteinemia, which responded to folic acid.
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PMID:Hyperhomocysteinemia presenting as superior mesenteric artery thrombosis. 1587 60

Remodeling by its very nature implies synthesis and degradation of extracellular matrix components (such as elastin, collagen, and connexins). Most of the vascular matrix metalloproteinase (MMP) are latent because of the presence of constitutive nitric oxide (NO). However, during oxidative stress peroxinitrite (ONOO-) activates the latent MMPs and instigates vascular remodeling. Interestingly, in mesenteric artery, homocysteine (Hcy) decreases the NO bio-availability, and folic acid (FA, an Hcy-lowering agent) mitigates the Hcy-mediated mesentery artery dysfunction. Dimethylarginine dimethylaminohydrolase-2 (DDAH-2) and endothelial nitric oxide synthase (eNOS) increases NO production. The hypothesis was that the Hcy decreased NO bio-availability, in part, activating MMP, decreasing elastin, DDAH-2, eNOS and increased vasomotor response by increasing connexin. To test this hypothesis,the authors used 12-week-old C57BJ/L6 wild type (WT) and hyperhomocysteinemic (HHcy)-cystathione beta synthase heterozygote knockout (CBS+/-) mice. Blood pressure measurements were made by radio-telemetry. WT and MMP-9 knockout mice were administered with Hcy (0.67 mg/ml in drinking water). Superior mesenteric artery and mesenteric arcade were analyzed with light and confocal microscopy. The protein expressions were measured by western blot analysis. The mRNA levels for MMP-9 were measured by RT-PCR. The data showed decreased DDAH-2 and eNOS expressions in mesentery in CBS-/+ mice compared with WT mice. Immuno-fluorescence and western blot results suggest increased MMP-9 and connexin-40 expression in mesenteric arcades of CBS-/+ mice compared with WT mice. The wall thickness of third-order mesenteric artery was increased in CBS-/+ mice compared to WT mice. Hcy treatment increased blood pressure in WT mice. Interestingly, in MMP-9 KO, Hcy did not increase blood pressure. These results may suggest that HHcy causes mesenteric artery remodeling and narrowing by activating MMP-9 and decreasing DDAH-2 and eNOS expressions, compromising the blood flow, instigating hypertension, and acute abdomen pain.
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PMID:Mesenteric vascular remodeling in hyperhomocysteinemia. 2107 54