+1: 40. Viral markers were all negative, including hepatitis C virus RNA by polymerase chain reaction. Ultrasound with Doppler study of the hepatic vessels was unremarkable. A liver biopsy showed marked portal and lobular inflammation with numerous plasma cells, zone 3 hepatocyte necrosis, rosetting, and mild fibrosis without bile duct damage. The patient was started on steroids and azathioprine and her liver function normalized. She is receiving glatiramer acetate (Copaxone, Teva Pharmaceutical Industries, Petach Tikva, Israel) for MS. Interferon- may cause autoimmune complications in- cluding thyroiditis, myasthenia gravis, lupus erythematosus, rheumatoid arthritis, and Raynaud’s phenomenon (1). Pa- tients on interferon- may develop anti–smooth muscle and antinuclear antibodies (2), and one case of AIH has been reported during treatment with interferon beta-1b (3). Inter- ferons, both  and , prevent apoptosis of activated T-cells during inflammation and expand the pool of memory cells. This has been linked to development of chronic inflamma- tion and autoimmunity (4). Physicians treating MS with interferon- should be aware of this potentially serious complication. Although elevation of transaminases is common in patients with MS during interferon- treatment, current guidelines recommend inter- ruption of treatment only for increases greater than five times the initial values (1). In my opinion, AIH should be excluded before and during treatment for any liver test abnormalities, and patients should be referred to liver cen- ters as soon as AIH is suspected. Andrea Duchini, M.D. Baylor College of Medicine Houston, Texas REFERENCES 1. Walther EU, Hohlfeld R. Multiple sclerosis. Side effects of interferon beta therapy and their management. Neurology 1999; 53:1622–7. 2. Speciale L, Saresella M, Caputo D, et al. Serum autoantibodies presence in multiple sclerosis patients treated with beta-inter- feron 1a and 1b. J Neurovirol 2000;6(suppl 2):S57– 61. 3. Durelli L, Bongioanni MR, Ferrero B, et al. Interferon treatment for multiple sclerosis: Autoimmune complications may be le- thal. Neurology 1998;50:570 –1. 4. Akbar AN, Lord JM, Salmon M. IFN-alpha and IFN-beta: A link between immune memory and chronic inflammation. Im- munol Today 2000;21:337– 42. Reprint requests and correspondence: Andrea Duchini, M.D., Michael E. DeBakey Department of Surgery, Baylor College of Medicine, 6550 Fannin, Suite 1661, Houston, TX 77030. Received Sep. 28, 2001; accepted Oct. 12, 2001. Acquired and Hereditary Thrombotic Risk Factors in Patients With Acute Mesenteric Vein Thrombosis TO THE EDITOR: We read with interest the article by Amitrano et al. (1) regarding the prevalence of thrombo- philic genotypes in patients with acute mesenteric vein thrombosis (MVT). A thrombophilic genotype was found in nine of 12 patients (75%), whereas four of 12 (33.3%) had multiple genetic prothrombotic disorders, suggesting that factor V Leiden, prothrombin 20210A mutation, and TT677 methylenetetrahydrofolate reductase polymorphism are im- portant predisposing factors in the pathogenesis of MVT. Several acquired and hereditary prothrombotic disorders have been reported to be associated with MVT (2). Re- cently, new thrombophilic genes have been discovered, and consequently, the percentage of idiopathic vein thrombosis is constantly decreasing (3). On the other hand, we have shown that colon ischemia is associated with hypercoagu- lable states, probably leading to thrombotic occlusion of small mesenteric vessels supplying the colon (4). We report our experience in four patients with acute MVT admitted to our hospital during the last 2 yr. These patients were all evaluated for the prevalence of both acquired and genetic prothrombotic disorders; they were assessed for the presence of protein C, protein S, and antithrombin deficien- cies; resistance to activated protein C; anticardiolipin anti- bodies; anti–2-glycoprotein I antibodies; lupus anticoagu- lant; factor V Leiden; the G20210A prothrombin gene mutation; and the TT677 methylenetetrahydrofolate reduc- tase gene mutation. Two of the patients had both superior MVT and portal vein thrombosis. One patient also had thrombosis of the hepatic veins (Budd-Chiari syndrome). In all cases the diagnosis was confirmed by colored Doppler Table 1. Results of Thrombophilic Screening in Patients With MVT Patient Age Sex PC Deficiency PS Deficiency AT Deficiency APCR aCL, a2GPI LAC Factor V Leiden G20210A TT677 Other Thrombophilic Risk Factor 1 41 M No No No No No No No No No Thrombo- cythemia 2 36 M No No No No No No No No No No 3 75 M No No No No No No Hetero- zygous Hetero- zygous No No 4 46 M Yes Yes No No No No No No No No a2GPI = anti–2-glycoprotein antibodies; aCL = anticardiolipin antibodies; APCR = resistance to activated protein C; AT = antithrombin; G20210A = mutation G20210A of prothrombin gene; LAC = lupus anticoagulant; PC = protein C; PS = protein S; TT677 = mutation TT677 of methylenetetrahydrofolate reductase. 768 Letters to the Editor AJG – Vol. 97, No. 3, 2002