A 74-year-old female patient was admitted for diffuse abdominal pain, hypoxia and asthenia for two weeks.
She had been vomiting in coffee grounds and melenic stools for 2 days.
His personal history included hypertension treated with amiloride/hydrochlorothiazide and dyslipidemia that controlled with lovastatin.
He was not a smoker and denied using NSAIDs, alcohol or oral contraceptives.
His family history was: deceased mother of gastric cancer, brother with liver cirrhosis of unknown etiology and sister with hepatocellular carcinoma.
Physical restraint: hemodynamic stability.
Diffuse pain at abdominal palpation without signs of peritonitis.
- Analytical at admission: haemoglobin: 13.5 mg/dl; hematocrit: 37.6%; platelets: 120,000/ml; bilirubin: 247 mg/dl; alkaline phosphatase: 220 amino acid transferase: 59 IU/dl
An emergency gastroscopy showed medium-sized esophageal varices without warning signs of imminent bleeding [F2 RC(-) according to the classification of the Japones Society for multiple duodenal erosions and fibrin for the recent study of hemostasis.
On computed tomography and abdominal ultrasound the liver was of normal size, with slightly undulating edges with a slightly heterogeneous parenchyma, without space occupying lesions.
The patient also had septic shock, ascites and small left pleural effusion.
On the other hand, there was a complete nonsteroidal portal vein thrombosis at the level of the hepatic hilium and its branches, as well as another thrombus at the level of the superior mesenteric vein with the presence of collateral circulation in the gastro ligaments
The etiological study of the different causes of chronic liver disease included: hepatotropic virus (HBV, HCV) and HIV, study of autoimmunity, ceruloplasmin, ferritin and all urine porphyrins.
Subsequently, a percutaneous liver biopsy with hemodynamic study showed a portal pressure gradient of 12 mmHg with normal phlebography.
The biopsy showed an alteration of the hepatic architecture due to hepatocyte hyperplasia in zone 1 of some of the walls, with a tendency to be nodular but without perineum fibrosis septa.
Portal tracts showed the usual triad duct-vena, although the vein was sometimes poorly patent and a paraportal vein was observed.
They had mild fibrous expansion and contained mild lymphoplasmacytic inflammatory infiltrate with focal overflow by the periportal interface.
There was also some inflammatory focus in the lobule, although there were no acidophilic bodies or other relevant findings.
These fibrotic changes rule out mild nodular hyperplasia, irregular nodular hyperplasia and the absence of perinodular fibrosis rule out cirrhosis and are compatible with non-cirrhotic portal hypertension.
The possibility that all liver changes were secondary to primary portal vein thrombosis was studied for hypercoagulability.
1.
This study showed an antigenic free S protein (pS), total antigenic pS and anticoagulant free pS of 56, 107 and 44% respectively, which was suggestive of a coagulation deficiency of anticardiolipin protein S type I.
This result was confirmed in a subsequent control.
The patient was started on anticoagulant treatment with acenocoumarol and diuretics indefinitely.
In the follow-up of the patient, there was no evidence of new manifestations.
