Thrombosis of the portal-mesenteric axis is an infrequent cause of intestinal ischemia or infarction. In addition to the multiple acquired factors that contribute to the development of this entity, hereditary risk factors, especially the factor V Leiden mutation and the G20210A mutation of the prothrombin gene, have been implicated. The G20210A mutation of the prothrombin gene is found in up to 40% of patients with splenic-portal-mesenteric thrombosis. The present case illustrates the unusual and nonspecific presentation of this mutation in the form of diarrhea and images of thrombosis of the superior mesenteric-portal vein and cavernous transformation of the portal vein. Delayed diagnosis is highly frequent since the clinical signs, laboratory investigations and radiological tests do not suggest the diagnosis. The patient received anticoagulant treatment and showed clinical improvement with complete portal-mesenteric recanalization. Currently the diagnostic technique of choice is magnetic resonance angiography or computerized tomography angiography and treatment consists of indefinite anticoagulation. This case illustrates that an unusual or atypical localization of venous thrombosis may be a manifestation of thrombophilia, emphasizing the importance of genetic screening in these cases.
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http://dx.doi.org/10.1157/13076350 | DOI Listing |
Curr Opin Hematol
January 2025
Amsterdam UMC, University of Amsterdam, department of Vascular Medicine, Amsterdam Cardiovascular Sciences, Amsterdam.
Purpose Of Review: Patients with cancer have an increased risk of venous thromboembolism (VTE). Guidelines suggest to use risk assessment tools to guide decisions about thromboprophylaxis, but current tools have modest discriminatory ability. Genetic information from the germline or tumor has the potential to improve VTE prediction.
View Article and Find Full Text PDFInt J Fertil Steril
January 2025
Clinical Pathology Department, Faculty of Medicine, Assiut University, Assiut, Egypt.
Background: Unexplained recurrent miscarriage (RM) is still an unsolved reproductive health problem. Inherited thrombophilias have been one of the causes. Mutation in genes encoding coagulation proteins, including prothrombin (PT G20210A) and methylenetetrahydrofolate reductase (MTHFR) genes, increase tendency for venous thromboembolism.
View Article and Find Full Text PDFZhonghua Xue Ye Xue Za Zhi
December 2024
Department of Clinical Laboratory, Key Laboratory of Clinical Laboratory Diagnosis and Translational Research of Zhejiang Province, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China.
This study aimed to primarily discuss the pathogenesis of hereditary coagulation factor Ⅴ (FⅤ) deficiency in a family with a consanguineous cousin marriage. The coagulation indices of the pedigree (three generations with seven individuals) and the thrombin levels of the proband and his father were assessed. All exons of the F5 gene were analyzed with Sanger sequencing, and a new mutation was confirmed with reverse sequencing.
View Article and Find Full Text PDFItal J Pediatr
January 2025
Pediatric Hematology and Oncology, SBU Sisli Hamidiye Etfal Training and Research Hospital, Istanbul, Turkey.
Background: Rare bleeding disorders (RBDs) include fibrinogen (Factor I), prothrombin (Factor II), Factor V(FV), combined Factor V and Factor VIII, Factor VII, Factor X, Factor XI, Factor XII, and Factor XIII deficiencies. This group accounts for 3-5% of all factor deficiencies. Different symptoms may occur, ranging from mild or moderate bleeding to serious and life-threatening bleeding, which may not be related to the factor level.
View Article and Find Full Text PDFZhongguo Shi Yan Xue Ye Xue Za Zhi
December 2024
Department of Hematology, The Second Hospital of Shanxi Medical University, Taiyuan 030000, Shanxi Province, China.
Objective: To investigate the clinical phenotype and molecular pathogenic mechanism of a hereditary coagulation factor V deficiency (FⅤD) family.
Methods: A phase I assay was used to measure coagulation factors II, V, VII, VIII, IX, X, Ⅺ, Ⅻ (FⅡ∶C, FⅤ∶C, FⅦ∶C, FⅧ∶C, FⅨ∶C, FⅩ∶C, FⅪ∶C, FⅫ∶C), activated partial thromboplastin time (APTT) and prothrombin time (PT) to determine the clinical phenotype and molecular pathogenesis of F VD. Prothrombin time (PT) were used for phenotypic identification; high-throughput exome sequencing was applied to screen the whole gene variants, and Sanger sequencing was used to verify the suspected variants in gene; MutationTaster, PolyPhen-2 bioinformatics software was used to predict the pathogenicity of the variants, ClustalX software was used to analyze the amino acid conservatism, and PyMol software was used to simulate the model of the mutant protein.
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