Hyperhomocysteinemia and the MTHFR C677T mutation in Budd‐Chiari syndrome

Li, Xiaomei; Yue, Wei; Huang, Hao; Hao, Yubin; He, Liyun; Li, Jingdong; Mei, Biao; Wang, Suyun; Wang, Chao; Wang, Junxiang; Zhu, Junzhen; Liang, Jin-Quan

doi:10.1002/ajh.10149

Cited by 59 publications

(45 citation statements)

References 30 publications

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“…A recent study from Northern India 29 demonstrated the importance of an interaction between genetic and acquired risk factors in HVT, but in contrast to our findings, FVL was found to be the most common (17%) inherited risk factor. Our findings are compatible with those of a Chinese study 30 suggesting that both genetic hemochromatosis and the homozygous C677T mutation in the MTHFR gene are important risk factors for HVT.…”

Section: Mesenteric Vein Thrombosissupporting

confidence: 92%

Thrombophilia and abdominal vessel thrombosis in a Greek University hospital: A five year experience

Starakis¹,

Mazokopakis²,

Mougiou³

et al. 2010

Gastroenterol Insights

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Section: Mesenteric Vein Thrombosissupporting

confidence: 92%

Thrombophilia and abdominal vessel thrombosis in a Greek University hospital: A five year experience

Starakis¹,

Mazokopakis²,

Mougiou³

et al. 2010

Gastroenterol Insights

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“…Prevalence of heterozygote MTHFR gene mutation in patients with venous thrombosis is similar to healthy controls suggesting that this mutation is not an important prothrombotic factor [24] . It has been shown that homozygote MTHFR mutation, one of the causes of hyperhomocystinaemia (risk factor for vascular disease), is a risk factor for venous thrombosis [19,24] . None of the patients in the present study were homozygous for the MTHFR mutation.…”

Section: Discussionmentioning

confidence: 70%

Risk factors of thrombosis in abdominal veins

Dutta¹,

Chacko²,

George³

et al. 2008

WJG

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AIM:To estimate the prevalence of inherited and acquired thrombophilic risk factors in patients with abdominal venous thrombosis and to compare the risk factor profiles between Budd-Chiari syndromes (BCS) and splanchnic vein thrombosis (SVT). METHODS: In this retrospective study, 36 patients with abdominal venous thrombosis were studied. The patients were divided into Budd-Chiari group (hepatic vein, IVC thrombosis) and splanchnic venous thrombosis group (portal, splenic, superior mesenteric veins) based on the veins involved. Hereditary and acquired thrombophilic risk factors were evaluated in all patients. RESULTS: Twenty patients had SVT, 14 had BCS, and 2 had mixed venous thrombosis. Ten patients (28%) had hereditary and 10 patients (28%) acquired thrombophilic risk factors. The acquired risk factors were significantly more common in the SVT group

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“…36 Homocysteine is often elevated due to a vitamin deficiency (vitamin B12, vitamin B6 and folate), chronic disease (chronic liver disease, chronic kidney disease, hypothyroidism) or due to a genetic variant in the methylenetetrahydrofolate reductase (MTHFR). The MTHFR mutation has been found to increase the risk of BCS; 37 the exact prevalence of hyperhomocysteinemia is difficult to assess in BCS because homocysteine is often increased during chronic liver disease. 38 Oral contraceptive use is a frequent risk factor for BCS.…”

Section: Myeloproliferative Neoplasia (Mpn)mentioning

confidence: 99%

Budd‐Chiari syndrome

Martens

Nevens

2015

UEG Journal

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Budd-Chiari syndrome (BCS) is a rare and potentially life-threatening disorder characterized by obstruction of the hepatic outflow tract at any level between the junction of the inferior vena cava with the right atrium and the small hepatic veins. In the West, BCS is a rare hepatic manifestation of one or more underlying prothrombotic risk factors. The most common underlying prothrombotic risk factor is a myeloproliferative disorder, although it is now recognized that almost half of patients have multiple underlying prothrombotic risk factors. Clinical manifestations can be diverse, making BCS a possible differential diagnosis of many acute and chronic liver diseases. The index of suspicion should be very low if there is a known underlying prothrombotic risk factor and new onset of liver disease. Doppler ultrasound is sufficient for confirming the diagnosis, although tomographic imaging (computed tomography (CT) or magnetic resonance imaging (MRI)) is often necessary for further treatment and discussion with a multidisciplinary team. Anticoagulation is the cornerstone of the treatment. Despite the use of anticoagulation, the majority of patients need additional (more invasive) treatment strategies. Algorithms consisting of local angioplasty, TIPS and liver transplantation have been proposed, with treatment choice dictated by a lack of response to a less-invasive treatment regimen. The application of these treatment strategies allows for a five-year survival rate of 90%. In the long term the disease course of BCS can sometimes be complicated by recurrence, progression of the underlying myeloproliferative disorder, or development of post-transplant lymphoma in transplant patients.

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Hyperhomocysteinemia and the MTHFR C677T mutation in Budd‐Chiari syndrome

Abstract: Hyperhomocysteinemia (HH) is a factor that predisposes individuals to thrombosis

Cited by 59 publications

References 30 publications

Thrombophilia and abdominal vessel thrombosis in a Greek University hospital: A five year experience

Thrombophilia and abdominal vessel thrombosis in a Greek University hospital: A five year experience

Risk factors of thrombosis in abdominal veins

Budd‐Chiari syndrome

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