Prothrombotic states in portal vein thrombosis and Budd-Chiari syndrome in India: A systematic review and meta-analysis

Giri, Suprabhat; Angadi, Sumaswi; Varghese, Jijo; Sundaram, Sridhar; Bhrugumalla, Sukanya

doi:10.1007/s12664-023-01400-5

Cited by 4 publications

(1 citation statement)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, authors observed a trend toward a higher prevalence of the prothrombin G20210A mutation in patients with cirrhosis and PVT, but it was not statistically significant (OR, 2.93; 95% CI, 0.94–9.07) [ 24 ]. Another recent meta-analysis was performed on the prevalence of acquired and hereditary thrombophilia among Indian patients with non-cirrhotic PVT [ 25 ], thus showing PC deficiency in 10.7%, Janus kinase 2 (JAK-2) mutation in 8.5%, and antiphospholipid antibodies (APLA) in 7.5% [ 25 ].…”

Section: Risk Factors For Portal Vein Thrombosismentioning

confidence: 99%

Portal Vein Thrombosis: State-of-the-Art Review

Boccatonda,

Gentilini,

Zanata

et al. 2024

JCM

View full text Add to dashboard Cite

Background: Portal vein thrombosis (PVT) is a rare disease with an estimated incidence of 2 to 4 cases per 100,000 inhabitants. The most common predisposing conditions for PVT are chronic liver diseases (cirrhosis), primary or secondary hepatobiliary malignancy, major infectious or inflammatory abdominal disease, or myeloproliferative disorders. Methods: PVT can be classified on the basis of the anatomical site, the degree of venous occlusion, and the timing and type of presentation. The main differential diagnosis of PVT, both acute and chronic, is malignant portal vein invasion, most frequently by hepatocarcinoma, or constriction (typically by pancreatic cancer or cholangiocarcinoma). Results: The management of PVT is based on anticoagulation and the treatment of predisposing conditions. The aim of anticoagulation in acute thrombosis is to prevent the extension of the clot and enable the recanalization of the vein to avoid the development of complications, such as intestinal infarction and portal hypertension. Conclusions: The treatment with anticoagulant therapy favors the reduction of portal hypertension, and this allows for a decrease in the risk of bleeding, especially in patients with esophageal varices. The anticoagulant treatment is generally recommended for at least three to six months. Prosecution of anticoagulation is advised until recanalization or lifelong if the patient has an underlying permanent pro-coagulant condition that cannot be corrected or if there is thrombosis extending to the mesenteric veins.

show abstract

Section: Risk Factors For Portal Vein Thrombosismentioning

confidence: 99%

Portal Vein Thrombosis: State-of-the-Art Review

Boccatonda,

Gentilini,

Zanata

et al. 2024

JCM

View full text Add to dashboard Cite

show abstract

Venous thromboembolism risk in adults with hereditary thrombophilia: a systematic review and meta-analysis

Alnor,

Gils,

Vinholt

2024

Ann Hematol

View full text Add to dashboard Cite

This systematic review and meta-analysis assesses venous thromboembolism (VTE) risk in adults with hereditary thrombophilia, including Factor V Leiden (FVL) mutation, prothrombin G20210A (FII) mutation, compound heterozygosity, protein C (PC), protein S (PS), and antithrombin (AT) deficiency. Eligibility criteria included studies suitable for quantitative synthesis with extractable information on VTE risk in adults (> 15 years). There were no restrictions on VTE type, location, or occurrence. Two authors reviewed all studies and extracted data from 107 publications, encompassing 107,130 individuals (21,560 experiencing VTE). We used a random effects model and calculated odds ratios (ORs) with 95% confidence intervals (CIs). The highest risk was associated with homozygous FVL (OR 5.58, 95% CI 4.61–6.74), homozygous FII (OR 5.16, 95% CI 3.12–8.52), and compound heterozygosity (OR 4.64, 95% CI 2.25–9.58). In contrast, VTE risk was lowest for FVL heterozygosity (OR 2.97, 95% CI 2.41–3.67) and FII heterozygosity (OR 2.21, 95% CI 1.70–2.87), whereas PC (OR 3.23, 95% CI 2.05–5.08), PS (OR 3.01, 95% CI 2.26–4.02), and AT deficiency (OR 4.01, 95% CI 2.50–6.44) demonstrated an intermediate VTE risk. These results highlight an increased risk of venous thromboembolism in adults with hereditary thrombophilia. However, the risk for patients with PC, PS, and AT deficiency appears to be lower than previously stated, likely due to varying thrombogeneity of the underlying genetic mutations. Further research addressing this aspect of VTE risk in hereditary thrombophilia is imperative to improve patient management. Trial registration PROSPERO registration number CRD42022376757.

show abstract

Thrombophilia testing in splanchnic venous thrombosis: Decoding a conundrum

Shukla,

Harindranath

2023

Indian J Gastroenterol

View full text Add to dashboard Cite

Prothrombotic states in portal vein thrombosis and Budd-Chiari syndrome in India: A systematic review and meta-analysis

Cited by 4 publications

References 51 publications

Portal Vein Thrombosis: State-of-the-Art Review

Portal Vein Thrombosis: State-of-the-Art Review

Venous thromboembolism risk in adults with hereditary thrombophilia: a systematic review and meta-analysis

Thrombophilia testing in splanchnic venous thrombosis: Decoding a conundrum

Contact Info

Product

Resources

About