A 19 year old Hispanic male (AG) presented to the emergency department with a one week history of multiple episodes of coffee ground emesis combined with bright red blood. Past medical history included a four years history of heavy alcohol abuse, otherwise unremarkable. In the emergency department, AG had evidence of ongoing upper GI bleeding with unstable vital signs. Physical exam failed to demonstrate stigmata of chronic liver disease or splenomegaly. Lab results were consistent with iron deficiency anemia (Hgb 4.7, low iron, high TIBC, low ferritin). Additional lab work revealed an INR of 1.36, otherwise, normal hepatic function tests. An urgent upper endoscopy demonstrated portal hypertensive gastropathy with Grade II-III esophageal varices. The patient underwent esophageal variceal ligation without difficulty. Abdominal ultrasound revealed a coarse echotexture throughout the liver, mild splenomegaly and pelvic ascites. Lab evaluation for chronic liver disease including viral hepatitis panel (hepatitis A, B, C), alpha 1 antitrypsin, ceruloplasmin, liver- kidney microsomal antibody, ANA, smooth muscle antibody, ANCA, and alpha-fetoprotein were unremarkable. In addition, screening for schistosomiasis and other ova and parasites were negative. Serum drug and alcohol screening were negative. An ultrasound guided-paracentesis demonstrated a transudative ascites without evidence of malignancy. Liver biopsy showed noncirrhotic portal hypertension, mildly dilated sinusoids without significant fibrosis. Doppler ultrasound disclosed no evidence of thrombosis. Protein C and S were marginally low. Anti-thrombin III was normal. Factor V leiden, serum arsenic, and copper are still pending. This patient presented with variceal bleeding, anemia, splenomegaly with no clinical or pathological evidence of liver cirrhosis or schistomiasis. He has no family or personal history suggestive of hypercoagulable state. The prothrombin screen has been unremarkable. In addition, there is no history of hepatotoxic medication use. Therefore, most likely AG had a form of Idiopathic Portal Hypertension (IPH). IPH, characterized by gastroesophageal variceal bleeding, is not uncommon in young adults, who otherwise have little or no evidence of hepatic dysfunction. Treatments of variceal hemorrhage in patients with IPH are similar to those in patients who bleed from other causes. Although there have been no controlled trials in this setting, primary prophylaxis with a non-selective beta-blocker is reasonable.