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Acute portal vein thrombosis in noncirrhotic patients–different prognoses based on presence of inflammatory markers: a long-term multicenter retrospective analysis
Autoři | |
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Rok publikování | 2019 |
Druh | Článek v odborném periodiku |
Časopis / Zdroj | SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY |
Citace | |
www | http://dx.doi.org/10.1080/00365521.2019.1677768 |
Doi | http://dx.doi.org/10.1080/00365521.2019.1677768 |
Klíčová slova | Acute portal vein thrombosis; hemato-oncologic disease; prothrombotic factors |
Popis | Background: Portal vein thrombosis (PVT) is a partial or complete thrombotic occlusion of the portal vein and is rare in noncirrhotic patients. Patients and methods: 78 adult patients with noncirrhotic acute PVT without known malignity were evaluated. Patients with initial CRP level 61–149 mg/l were excluded. Results: Patients were divided into two groups–the first one (33 patients) was characterized with signs of inflammation and CRP over 149 mg/l. The second group (45 patients) was without signs of inflammation and CRP level less than 61 mg/l. The frequency of prothrombotic hematologic factors was statistically significantly different in levels of factor VIII and MTHFR 677 C mutation. All patients from both groups underwent the same oncologic and hemato-oncologic screening which was positive in 23 patients (51.1%) in the group without signs of inflammation. In the group of patients with clinical and laboratory signs of inflammation oncologic and hemato-oncologic screening was positive only in 1 patient (3.0%). Complete portal vein recanalization was achieved in 19.2%, partial recanalization in 26.9%. Conclusions: Patients with clinical signs of inflammation and acute PVT have a low risk of malignancy in contrast to patients without signs of inflammation and acute PVT, which have a high risk of oncologic or hemato-oncologic disease. Patients with negative hemato-oncologic screening should be carefully observed over time because we expect they are at higher risk for the development of hemato-oncologic disease, independent from the presence and number of procoagulation risk factors. |