PHILIPPE HALFON, PHARM, M.D., PH.D. “
“A 71-year-old woman was referred for a second opinion before hospice with progressive abdominal pain, fullness, diarrhea, and weight loss. A workup revealed ascites and esophageal varices. Imaging selleckchem showed seven liver lesions that were suspicious for hepatocellular carcinoma (HCC) on a computed tomography scan (Fig. 1A), and follow-up magnetic resonance imaging revealed arterial enhancement followed by washout. A tissue sample was compatible with well-differentiated HCC (CD34 and glutamine synthetase positivity, reticulin loss, and isolated vessels); the background liver

revealed hepatoportal sclerosis without cirrhosis (Fig. 1B). A further review of the abdominal scan revealed a dilated inferior mesenteric vein (IMV) due to an arteriovenous malformation (AVM), which was confirmed by angiography (Fig. 1C). There was no evidence of trauma or prior surgery. There was no endoscopic evidence of ischemia or a superficial AVM in the terminal ileum or ascending Apoptosis inhibitor colon, and biopsies were normal. She underwent transhepatic mesenteric

venous coil embolization, which reduced the IMV flow and the main portal venous pressure from 46 to 26 mm Hg. Shortly after the procedure, there was significant improvement in her diarrhea and abdominal pain. Four months later, the ascites had fully resolved, and she had gained weight. Furthermore, abdominal imaging demonstrated complete resolution of the hepatic lesions (Fig. 1D). AVM arteriovenous malformation HCC hepatocellular carcinoma IMV inferior mesenteric vein. This is the first known case in which an intra-abdominal AVM produced (1) chronic intestinal ischemia and diarrhea from arteriovenous shunting of blood; (2) noncirrhotic, presinusoidal portal hypertension with varices and ascites; and (3) multiple hepatic nodules suspicious

for HCC (all of which completely resolved 3-oxoacyl-(acyl-carrier-protein) reductase after venous embolization). Splanchnic AVMs commonly involve the hepatic or splenic artery, but IMV involvement is rare.1 Mesenteric AVMs alter vascular flow, reduce the distal arterial pressure, and increase the proximal venous pressure.2 This bypasses the capillary bed and induces a form of mesenteric steal syndrome, which results in abdominal pain, weight loss, diarrhea, and nonocclusive ischemic colitis. Several reports describe inferior mesenteric arteriovenous fistulas resulting in clinically significant arteriovenous shunting.3–5 The symptoms correlate with the amount of blood shunted and the length of time for which the malformation has been present. Hyperdynamic flow from AVMs can also result in presinusoidal portal hypertension. Ascites, varices, and splenomegaly are well-described complications of mesenteric AVMs,1, 6 and arterialization of the portal venous system can significantly increase hepatic blood inflow.