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At least 19 recordsLinked to original sources
PubMed1994

[Partial portal vein and mesenteric vein thrombosis in familial protein S deficiency].

Protein S, a vitamin-K dependent glycoprotein is a cofactor of protein-C system, which acts as an inhibitor of the plasmatic coagulation. Protein-S congenital deficiency results in recurrent venous thromboses, atypical locations in portal and mesenteric veins are possible. In our patient the partial thrombosis of the portal vein was diagnosed by computed tomography and angiography. Small bowel ischaemia due to mesenteric vein thrombosis required segmental resection. Post-operatively the patient was heparinized and later phenprocoumon was applied to a long-term therapy.

Adult↗
PubMed1998

Budd-Chiari syndrome, portal vein and mesenteric vein thrombosis in a patient homozygous for factor V Leiden mutation treated by TIPS and thrombolysis.

We present the first case of Budd-Chiari syndrome in association with portal and mesenteric vein thrombosis in a patient homozygous for the factor V Leiden mutation. She was treated by transjugular intrahepatic portosystemic stent (TIPS) placement followed by local thrombolytic therapy. Venous outflow from the liver was established and the thrombi in the portal and mesenteric veins were lysed completely. This therapeutic approach may be used for such patients with this severe thrombotic event, who generally have a poor prognosis.

Adult↗
PubMedDate not supplied

Aneurysms of the portal vein and superior mesenteric vein.

Only scattered reports of portal vein and superior mesenteric vein aneurysms appear in the literature. Case reports of three patients with portal vein and superior mesenteric vein aneurysms diagnosed by computed tomography (CT) and gray-scale, color Doppler, and duplex Doppler sonography are presented. In one case, an isolated portal vein aneurysm was demonstrated. In the second case, an aneurysm of the portal vein and superior mesenteric vein resulting in biliary ductal dilatation was observed. In the third case, an isolated superior mesenteric vein aneurysm was found. None of the patients had a history or clinical evidence of underlying liver disease, pancreatitis, or other disease states that would predispose them to the development of aneurysms. The clinical presentations, possible etiologies, and imaging features of portal vein and superior mesenteric vein aneurysms are reviewed. The value of CT and sonography in the detection and characterization of these rare aneurysms is discussed.

Adult↗
PubMed1981

Antithrombin III deficiency appearing as mesenteric vein thrombosis.

Mesenteric vein thrombosis is a relatively uncommon but devastating problem. Absence of any of the generally accepted etiologic factors of mesenteric vein thrombosis has lead to the diagnosis of "primary" mesenteric vein thrombosis in 25-55% of all cases. In this report we identify a young man with antithrombin III deficiency presenting as "primary" mesenteric vein thrombosis with massive bowel infarction. It again raises the possibility that other cases of "primary" mesenteric vein thrombosis may have been associated with this coagulopathy. Factors influencing antithrombin III levels are discussed in relation to diagnosis of the familial deficiency state in a patient with mesenteric vein thrombosis. The association of intra-abdominal venous occlusion and antithrombin III deficiency is emphasized.

Adult↗
PubMed1996

Unusual alpha-adrenoceptor subtype in canine saphenous vein: comparison to mesenteric vein.

1. We investigated the nature of the adrenoceptors in the dog saphenous vein (DSV) and dog mesenteric vein (DMV) to determine the nature of the unexpected interactions of phenylephrine and methoxamine with rauwolscine in the DSV, i.e. the ability of the putative alpha 2-adrenoceptor antagonist to inhibit competitively contractions to these alpha 1-agonists. Radioligand binding studies were performed in parallel with contractility studies. 2. Functionally, in the DSV, phenylephrine and methoxamine-induced, contractions were antagonized by rauwolscine with Schild slopes of -0.52 and -0.46, respectively and apparent pA2 values of 8.5 and 9.2, respectively. Such antagonism was not observed in the DMV. In the DSV, prazosin competes for [3H]-rauwolscine binding sites with a high and a low affinity binding site (Ki of 1.49 +/- 0.65 and 94.7 +/- 51 microM, n = 6, respectively). 3. Pretreatment with 100 microM chloroethylclonidine (CEC) for 15 min abolished [3H]-prazosin binding in microsomes from both veins and reduced binding (Bmax) of [3H]-rauwolscine in microsomes by 55.1 +/- 0.8% (n = 3) in the DSV but did not affect the Bmax in the DMV. CEC pretreatment in the venular rings denuded of endothelium caused persistent contraction in the DSV but not in the DMV. In the DSV, CEC appeared to interact with a single [3H]-rauwolscine binding site. In both the DSV and the DMV, CEC (100 microM) caused a significant shift in the EC50 values for phenylephrine and methoxamine. Maximum responses in the DMV were significantly attenuated while those in the DSV were unaffected when total tension was considered. 4. Studies of the functional interactions of the DSV and the DMV with WB 4101 or 5-methylurapidil (5-MU) suggested the presence of alpha 1D-adrenoceptors in the DSV and alpha 1A-adrenoceptors in the DMV. The receptors inactivated by CEC in the DMV and DSV may represent some or all of the receptors with properties of alpha 1D and alpha 1A-receptors present in the two veins. Studies of radioligand binding interactions of these two antagonists with [3H]-prazosin, were consistent with the presence of some alpha 1D-receptors in DSV and alpha 1A-receptors in DMV. These findings raise questions about the selectivity of CEC in differentiating alpha 1-adrenoceptor subtypes. 5. B-HT 920 caused contractions in the DSV smaller than those to the alpha 1-agonists but the maximum was not affected by CEC pretreatment. The EC50 values were shifted to the left after CEC. In radioligand binding studies, B-HT 920 competition for [3H]-rauwolscine binding was not significantly affected by CEC pretreatment. 6. These results suggest the presence of unusual alpha-adrenoceptors in the DSV. In addition to alpha 2-adrenoceptors, receptors recognizing rauwolscine as well as prazosin, WB 4101, phenylephrine and methoxamine and susceptible to inactivation by CEC are present. They appear to be, in part, unusual alpha 1D-adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed2001

[Superior mesenteric vein syndrome: a case of duodenal stenosis caused by atypical malposition of the superior mesenteric vein].

Cases in which mesenteric vessels lead to stenosis of the duodenum are very rare. Several cases have been reported of patients suffering from stenosis of the last third of the duodenum due to a malpositioning of the superior mesenteric artery or the left renal vein. We report a 78-year-old patient who was suffering from dyspepsia, pain in the upper abdominal region, nausea, and vomiting. The medical history revealed that the patient had undergone a subtotal gastrectomy according to Billroth II at the age of 19 because of similar complaints. In the last 20 years the patient had to be laparotomized several times for ileus of the small intestine. Now the patient presented abdominal complaints with nausea and pressure in the upper abdominal region. Assuming an efferent-loop syndrome and adhesions, the patient was laparotomized. We discovered malpositioning of the superior mesenteric vein, leading to stenosis of the superior part of the duodenum. In fact, 60 years ago surgeons performed a duodenojejunostomy, circumvening the stenosis of the duodenum. With a "delay of 60 years", we then performed a subtotal gastrectomy according to Billroth II. The postoperative course was uneventful; the patient had no complaints and increased in body weight. To our knowledge, this is the first time that a stenosis of the duodenum due to malpositioning of the superior mesenteric vein has been observed.

Aged↗
PubMedDate not supplied

Prothrombotic disorders in patients with mesenteric vein thrombosis.

Mesenteric vein thrombosis (MVT) is uncommon condition. The purpose of this study was to assess prevalence of prothrombotic disorders in these patients. Eleven patients with MVT were screened for protein C, protein S, and antithrombin III deficiencies. Gene analysis was performed by polymerase chain reaction. A prothrombotic disorder was detected in 9 (81.8%) patients. Factor V Leiden, methylenetetrahydrofolate reductase TT677, and prothrombin G20210A mutations were found in 2 (18.2%), 2 (18.2%), and 5 patients (45.4%), respectively. Protein S, protein C, and antithrombin III deficiencies were present in 1, 1, and 2 patients, respectively. Four patients (36.3%) had combined defects. Thus, prothrombotic disorders may have a causative role in the pathogenesis of MVT, and these patients must be screened for these disorders.

Adult↗
PubMed2001

High prevalence of thrombophilic genotypes in patients with acute mesenteric vein thrombosis.

OBJECTIVES: Mesenteric vein thrombosis is a rare but severe abdominal emergency, often requiring intestinal resection. New genetic prothrombotic defects such as factor V Leiden, the prothrombin transition G20210A, and the methylenetetrahydrofolate reductase TT677 genotype have been described in association with venous thrombosis. Our goal was to assess prevalence and clinical significance of genetic thrombophilia in mesenteric vein thrombosis. METHODS: Twelve patients with acute mesenteric vein thrombosis were compared with 431 healthy people from the same geographical area. The factor V Leiden, the prothrombin transition G20210A, and the methylenetetrahydrofolate reductase TT677 genotype were identified by polymerase chain reaction and restriction analysis. RESULTS: A thrombophilic genotype was present in 9 patients (75%): the methylenetetrahydrofolate reductase TT677 genotype was present in 6 (50%), the factor V Leiden in 3 (25%), and the prothrombin transition G20210A in 3 (25%). Combined mutations were present in 4 (33%) patients. CONCLUSIONS: The factor V Leiden, the prothrombin transition G20210A, and the methylenetetrahydrofolate reductase TT677 genotype are important predisposing factors in the pathogenesis of mesenteric vein thrombosis. Their identification bears strong clinical implications for management of patients with mesenteric vein thrombosis.

Acute Disease↗
PubMedDate not supplied

Effects of portal vein stenosis and superior mesenteric vein ligation on mesenteric venous pressure and porta-systemic shunting in the rat.

We studied the relative contributions of splanchnic congestion and porta-systemic shunting to the maintenance of experimental portal venous hypertension. Three groups of rats were prepared: portal vein-stenosed, superior mesenteric vein-ligated and sham operated. Though elevated in both operated groups compared to controls, mesenteric venous pressure was highest in the portal vein-stenosed animals (PV vs SMV vs Sham: 19.6 +/- 1.3 vs 15.6 +/- 0.7 vs 13 +/- 0.6; p < .05 PV and SMV vs Sham, and PV vs SMV) despite the presence of 50% porta-systemic shunting in the portal vein-stenosed animals. Shunting was negligible in the other two groups. Peripheral plasma glucagon and vasoactive intestinal peptide (VIP) levels were similar in all three groups. We conclude that mesenteric congestion alone plays a minor role in the pathogenesis of portal hypertension, which may instead be related to the porta-systemic shunting of vasoactive substances other than glucagon and VIP.

Animals↗
PubMedDate not supplied

Importance of a medical treatment in mesenteric vein thrombosis (MVT).

Mesenteric vein thrombosis (MVT) and particularly superior mesenteric vein thrombosis (SMVT) can induce 5 to 15 percent of mesenteric and intestinal infarctions in a small and large bowels. The thrombotic process can be idiopathic or consecutive to inherited or acquired thrombophilic states. The clinical diagnosis of this event remains difficult and requires always specific imaging investigation to treat as soon as possible. Its evolution and mortality rate are quite different than these observed in arterial mesenteric ischemic accident. Medical treatment with thrombolytic, anticoagulant, antiplatelet and antispasmodic agents, initiated promptly after precocious diagnosis is able not only to prevent surgical procedure but also to reduce significantly the mortality and recurrence rate of this venous thrombotic event.

Anticoagulants↗
PubMed1986

Endothelium-dependent changes in the response to vasoconstrictor substances of isolated dog mesenteric veins.

In dog mesenteric vein strips, contractions induced by histamine relative to those induced by 5 mM Ba++ were potentiated by removal of endothelium. The induced contractions were potentiated by AA861, a lipoxygenase inhibitor, and methylene blue, a guanylate cyclase inhibitor, to an appreciably greater extent in the strips with endothelium than in those with damaged endothelium. Indomethacin did not potentiate the contraction induced by histamine. Cimetidine potentiated the contraction in control strips and those without endothelium to a similar extent whereas chlorpheniramine suppressed the contraction. Contractile responses to acetylcholine, norepinephrine, serotonin and prostaglandin (PG) F2 alpha were not potentiated by removal of endothelium. It may be concluded that histamine activates histaminergic receptors, possibly H1 but not H2, in endothelial cells and results in a release of vasodilator substance produced by lipoxygenase, which accumulates cellular cyclic GMP and relaxes mesenteric veins. The H1 and H2 receptors in smooth muscle cells appear to be responsible for contractions and relaxations, respectively. Acetylcholine, norepinephrine, serotonin and PGF2 alpha do not seem to release vasodilator substances from endothelium in an amount sufficient to cause significant relaxations of venous smooth muscle.

Animals↗
PubMed2002

Asymptomatic chronic intestinal ischemia caused by idiopathic phlebosclerosis of mesenteric vein.

Phlebosclerosis of the mesenteric vein is a rare condition causing chronic intestinal ischemia, it has only been reported in Japan. A 56-year-old man with liver cirrhosis and hepatic tumor presented with phlebosclerosis of mesenteric vein without any abdominal symptoms. He was admitted for examination of suspected hepatic tumor. Abdominal plain x-ray films and computed tomography revealed calcification of the mesenteric vein. Barium enema revealed narrowing and thumbprinting from the cecum to transverse colon. On colonoscopic examination, blue-black vessels were visible in the terminal ileum, and hyperemic nodular mucosa with small irregular ulcers surrounded by dark purple mucosa was found from the cecum to transverse colon. The etiology of mesenteric vein phlebosclerosis is unknown, although a physical mechanism rather than inflammatory changes appear to be involved in this rare and usually progressive condition of chronic intestinal ischemia.

Calcinosis↗
PubMed1994

[Mesenteric infarct in acute mesenteric vein thrombosis].

Mesenteric venous thrombosis is an infrequent but distinct form of intestinal ischemia. We report 2 cases of acute mesenteric venous thrombosis, treated successfully by carrying out intestinal resection and postoperative anti-coagulation (Heparin, Sintrom). Both patients were diagnosed in the operating room. Improvements in computed tomography may identify patients earlier in their clinical course, heparin has both a primary therapeutic role in early disease and a postoperative adjunctive role in advanced disease. With such care, these patients can expect an acceptable prognosis.

Adult↗
PubMed1984

Mesenteric vein thrombosis: CT identification.

Superior mesenteric vein thrombosis was identified on computed tomographic scans in six patients. In each case, contrast-enhanced scans showed a high-density superior mesenteric vein wall surrounding a central filing defect. Four of the six patients had isolated superior mesenteric vein thrombosis. A fifth patient had associated portal vein and splenic vein thrombosis, and the sixth patient had associated portal vein and inferior vena cava thrombosis. The diagnosis of superior mesenteric vein thrombosis was confirmed by angiography in two patients and by surgery in a third. One of the six patients had acute ischemic bowel disease. The other five patients did not have acute ischemic bowel symptoms associated with their venous occlusion. This study defines the computed tomographic appearance of mesenteric vein thrombosis. A dense venous wall surrounding a central lucency representing blood clot was present in all six cases.

Humans↗