AI Article Synopsis
- Cavernous transformation of the portal vein (CTPV), also known as portal cavernoma, results from thrombosis in the portal vein, leading to occlusion and portal hypertension, but its exact cause is still unknown.
- Key clinical features include gastroesophageal variceal bleeding, splenomegaly, and portosystemic collaterals, with some individuals being predisposed due to deficiencies in natural anticoagulant proteins like protein C and antithrombin III.
- A case study discussed involves a nine-year-old boy diagnosed with CTPV due to these deficiencies, who was treated for anemia and varices, and was subsequently referred for a transjugular intrahepatic portosystemic shunt (T
Article Abstract
Cavernous transformation of the portal vein (CTPV), also known as portal cavernoma, is a sequelae of thrombosis in the portal vein causing its occlusion and portal hypertension. The etiology, however, remains unknown. Gastroesophageal variceal bleeding, splenomegaly, portosystemic collaterals, and ultimate hematologic abnormalities are among the prominent clinical features. Among the causes, predisposing an individual to CTPV is natural anticoagulant protein C and antithrombin III deficiencies. Determination of the etiology of CTPV may also give a direction toward the management plan to not only relieve the patient of the already developed complications but also to treat the primary cause of the pathology We discuss a case of a nine-year-old male child diagnosed as CTPV secondary to protein C and antithrombin III deficiency who was treated symptomatically for anemia and varices and was referred for transjugular intrahepatic portosystemic shunt (TIPS).
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6825486 | PMC |
| http://dx.doi.org/10.7759/cureus.5779 | DOI Listing |
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