Appleyard et al. Journal of Medical Case Reports 2010, 4:311 http://www.jmedicalcasereports.com/content/4/1/311 C A S E R E P O R T Autoimmune hepatitis triggered by nitrofurantoin: a case series Sally Appleyard, Ruma Saraswati, David A Gorard* JOURNAL OF MEDICAL CASE REPORTS Open Access Abstract Introduction: Drugs can occasionally trigger the onset of autoimmune liver disease. Case presentation: Three Caucasian women (aged 65, 42 and 74 years old) who were receiving long-term nitrofurantoin as prophylaxis against recurrent urinary tract infections developed hepatitic liver disease. Serological auto-antibody profiles and liver histology appearances were consistent with autoimmune hepatitis. Two of the patients presented with jaundice, and one required a prolonged hospital admission for liver failure. In all three patients nitrofurantoin was withdrawn, and long-term immunosuppressive therapy with prednisolone and azathioprine or mycophenolate was given. The patients responded well, with liver biochemistry returning to normal within a few months. Conclusions: Although nitrofurantoin rarely causes autoimmune hepatitis, this antimicrobial is increasingly used as long-term prophylaxis against recurrent urinary tract infection. General practitioners and urologists who prescribe long-term nitrofurantoin therapy should be aware of this adverse effect. Introduction Autoimmune liver disease is a not uncommon cause of chronic hepatitis in women. Although autoimmune destruction usually occurs without an identifiable trig- ger, some drugs including methyldopa [1] and minocy- cline [2] are associated with autoimmune liver disease. The antimicrobial nitrofurantoin has also rarely been implicated in autoimmune hepatitis. We report here three patients with hepatitis in whom nitrofurantoin was felt to be etiologically important. Case 1 A 65-year-old Caucasian retired police woman devel- oped non-specific symptoms of abdominal discomfort, nausea and lethargy. She later became jaundiced, with dark urine and pale stools. She had a past history of irri- table bowel syndrome, chronic lumbar back pain and recurrent urinary tract infection. Her drug history included mebeverine 135 mg thrice daily, dosulepin 25 mg daily, lansoprazole 30 mg daily, nitrofurantoin 50 mg daily for six years, occasional paracetamol and inhaled salbutamol, and intermittent fluconazole for * Correspondence: david.gorard@buckshosp.nhs.uk Wycombe Hospital, Queen Alexandra Road, High Wycombe, Bucks HP11 2TT, UK groin candidiasis. She took no herbal remedies or unprescribed supplements and had not drunk any alco- hol for more than 20 years. On examination she was jaundiced, had a tender liver edge and mild ankle edema, but no other peripheral stigmata of liver disease. Initial blood tests revealed deranged liver function with bilirubin 649 μmol/L (nor- mal range 4-21), alanine transaminase 1322 U/L (10-35), and alkaline phosphatase 227 U/L (40-150). Albumin was low at 28 g/L (35-50), but her coagulation screen was normal. Full blood count, electrolytes and renal function were normal, with a platelet count of 196 × 109/L. Serological testing for hepatitis A, hepatitis B and hepatitis C was negative. Liver ultrasound revealed unre- markable appearances of the liver and biliary system, with no evidence of gallstones or biliary dilatation. Immunological tests demonstrated positive smooth mus- cle antibody and positive anti-nuclear antibody homoge- nous staining pattern at a titre of 1 in 320. There was an accompanying hyper-gammaglobulinemia with ele- vated IgG at 21.8 g/L (normal range 5.8-14) and normal IgA and IgG levels. Double stranded DNA antibodies, anti-mitochondrial antibodies and liver/kidney microso- mal antibodies were not detected. © 2010 Appleyard et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.