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• W2000921170 abstract "Portal vein thrombosis (PVT) is a rare cause of portal hypertension. Its diagnosis has been facilitated by improvements in imaging techniques, in particular Doppler sonography. The prevalence is about 1% in the general population, but much higher rates are observed in patients with hepatic cirrhosis (7%, range 0.6-17%), particularly those who also have hepatocellular carcinoma (HCC) (35%). The most common causes of PVT are myeloproliferative disorders, deficiencies of anticoagulant proteins, prothrombotic gene mutations, cirrhosis with portal hypertension, and HCC. Its development often requires the presence of two or more risk factors (local and/or systemic), e.g., a genetically determined thrombophilic state plus an infectious episode or abdominal surgery. It is clinically useful to distinguish between cirrhotic and noncirrhotic forms. Portal vein thrombosis is also traditionally classified as acute or chronic, but this distinction is often difficult. Color Doppler ultrasound is the first-line imaging study for diagnosis of PVT; magnetic resonance angiography and CT angiography are valid alternatives. The main complications are ischemic intestinal necrosis (in acute PVT) and esophageal varices (in chronic cases); the natural history of the latter differs depending on whether or not the thrombosis is associated with cirrhosis. The treatment of choice for PVT has never been adequately investigated. It is currently based on the use of anticoagulants associated, in some cases, with thrombolytics, but experience with the latter agents is too limited to draw any definite conclusions. In chronic thrombosis (even forms associated with cirrhosis), anticoagulant therapy is recommended and possibly, beta-blockers as well. Naturally, treatment of the underlying pathology is essential.SommarioLa trombosi portale rappresenta una causa rara di ipertensione portale che oggi viene diagnosticata con maggior facilità per l'affinamento delle metodiche di imaging, in particolare quelle ecografiche. La prevalenza è dell'1% circa, del 7% (0,6–17%) nella cirrosi epatica, del 35% circa nell'epatocarcinoma. Le cause più comuni di trombosi portale sono: i disordini mieloproliferativi, il deficit di proteine anticoagulanti, le mutazioni geniche protrombotiche, la cirrosi con ipertensione portale, l'epatocarcinoma. Per lo sviluppo di trombosi portale è spesso necessaria la presenza di due o più fattori, locali e sistemici, come uno stato trombofilico su base genetica e un episodio infettivo o un intervento chirurgico addominale. È utile clinicamente dividere la trombosi portale in cirrotica e non-cirrotica. La trombosi portale è inoltre tradizionalmente classificata in acuta e cronica, ma spesso è difficile distinguerle. L'indagine di primo livello per la diagnosi di trombosi portale è rappresentata dall'eco-color-Doppler; in alternativa possono essere usate angio-RM e angio-TC. Le conseguenze della trombosi portale sono rappresentate principalmente dalla necrosi intestinale ischemica nelle forme acute e dalle varici esofagee, che hanno una storia naturale diversa a seconda della presenza o meno di cirrosi, nelle forme croniche. Non vi sono studi adeguati sulla terapia della trombosi portale, che attualmente consiste nell'anticoagulazione, a cui può essere associata la trombolisi, sulla quale non vi è però casistica adeguata. Nella trombosi cronica è indicata l'anticoagulazione, probabilmente anche nella cirrosi, ed eventualmente il beta-bloccante. Ovviamente importante è la terapia della patologia di base." @default.
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• W2000921170 date "2007-03-01" @default.
• W2000921170 modified "2023-09-26" @default.
• W2000921170 title "Thrombosis of the portal venous system" @default.
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• W2000921170 doi "https://doi.org/10.1016/j.jus.2007.02.007" @default.
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