Portal hypertension is defined as an increase in pressure within the portal venous system caused by an obstruction located at the suprahepatic, intrahepatic, or infrahepatic level. In our setting, intrahepatic portal hypertension is predominant, mainly due to post-viral cirrhosis. The objective was to determine whether intrahepatic block and cirrhosis remain the predominant causes of portal hypertension, or whether other etiologies should be considered, and to highlight the key role of endoscopy in the diagnosis and management of related complications.

This is a monocentric retrospective and prospective study conducted over a 36-month period, from February 2022 to February 2025. All patients presenting with portal hypertension were included and underwent clinical evaluation, as well as biological, radiological, and endoscopic assessments.

Among the 192 patients included, the mean age was 60.2 years (range: 15–97 years). The study population consisted of 100 men (52%) and 92 women (48%), with a male-to-female ratio of 1.1.Clinically, upper gastrointestinal bleeding was the initial presenting symptom in 49.8% of cases. Physical examination revealed an abnormal liver in 46% of patients, ascites in 25.5%, splenomegaly in 24.7%, collateral venous circulation in 15.3%, jaundice in 9.3%, and hepatic encephalopathy in 6.8%.

Endoscopic evaluation showed that 93% of patients had portal hypertension–related lesions. Esophageal varices were grade III in 49%, grade II in 29%, and grade I in 14%. Gastro-esophageal varices (GOV) were observed in 37%, isolated gastric varices (IGV) in 10%, ectopic varices in 3%, and signs of portal hypertensive gastropathy in 52%. Red wale signs were present in 45% of patients.

Regarding therapeutic management, 56% of patients underwent esophageal variceal ligation, with a mean of 2.6 sessions per patient. Biological glue injection was performed in 6% of cases, and argon plasma coagulation in 3%. Somatostatin was administered in 13% of patients, and 82% were treated with beta-blockers.

Among the etiologies of intrahepatic portal hypertension, hepatic cirrhosis accounted for 65.6% (n=126). The underlying causes were: hepatitis C virus–related cirrhosis in 20.8% (n=41), hepatitis B virus–related cirrhosis in 7.3% (n=14), cirrhosis of indeterminate origin in 29% (n=15), alcoholic cirrhosis in 8.9% (n=17), primary biliary cholangitis in 7.8% (n=15), primary sclerosing cholangitis in 2% (n=4), and autoimmune hepatitis in 3.6% (n=7).Non-cirrhotic intrahepatic causes included porto-sinusoidal vascular disorders (PSVD) in 17.7% (n=34) and portal system compressions in 2.6% (n=5), due to compressive metastases, hepatic cysts, or giant hepatic hemangioma.Portal vein thrombosis etiologies included thrombophilia (1.6%), malignant hematologic disorders (1.6%), tumoral invasion of the portal vein trunk (1%), and idiopathic portal cavernoma (4.1%). Etiologies of Budd–Chiari syndrome included celiac disease in 1% (n=2) and hyperhomocysteinemia in 0.5% (n=1). The cause remained unidentified in 2.6% of cases (n=5)

Cirrhosis remains the leading cause of portal hypertension in our population, although non-cirrhotic etiologies such as PSVD, portal vein thrombosis, and Budd–Chiari syndrome are also significant. The high prevalence of endoscopic lesions confirms the central role of endoscopy in both diagnosis and management of complications. A systematic etiological assessment remains essential to guide appropriate care.