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The Turkish Journal of Gastroenterology
2013, Volume 24, No 1, Pages 76-77
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A rare cause of elevated liver enzymes: Addison’s disease
Neslihan ÇUHACI1 , Aylin DEMİREZER2 , Didem ÖZDEMİR1 , Reyhan ERSOY1 , Osman ERSOY2 , Bekir ÇAKIR1
Departments of 1 Endocrinology and Metabolism and2 Gastroenterology, Yıldırım Beyazıt University, School of Medicine, Ankara
Keywords:
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Summary
Mildly elevated serum aminotransferase levels (<250 IU/L) occasionally may be due to endocrine diseases and disorders. Diabetes mellitus, hypothyroidism, and hyperthyroidism are well-recognized endocrine diseases that may cause increased serum aminotransferase activity. Olsson et al. first reported that Addison’s disease, another endocrine disease, may be another one of the reasons we see mildly elevated serum aminotransferase levels (1). To date, a total of 14 cases have been published in the literature (1-8). It is not clear why liver enzymes increase in Addison’s disease. Boulton et al. have suggested that chronic hypo-perfusion may be the underlying mechanism for the abnormal liver biochemistry values (2). Another hypothesis by Rizvi et al. has proposed that the liver test abnormalities may be due to an immunologic reaction within hepatic tissue (4). An alternative explanation is that apoptosis and necrosis of hepatocytes, induced by local release of cytokines by infiltrating lymphocytes, may occur. This phenomenon can be reversed by glucocorticoid replacement therapy (5). Here, we report a patient with Addison’s disease presenting with high serum liver transaminase levels, and normalization of these transaminases after administration of corticosteroid treatment. A 49 year old woman was admitted to the hospital with a two month history of weakness, fatigue, and increased skin pigmentation. On physical examination, she had hyperpigmentation on her hands, feet, and knees. Her laboratory tests showed low serum cortisol, 5.9 ug/dL (4.3-22.4 ug/dL) and increased adrenocorticotropic hormone (ACTH), >1250 pg/mL (0-46 pg/mL). Serum aspartate aminotransferase and alanine aminotransferase were 120 IU/L (5-34 IU/L) and 87 IU/mL (5- 49 IU/L), respectively. Also, serum aldosterone level was 40 pg/mL (70-300 pg/mL), renin level was 11 ng/mL (0.2-1.6 ng/mL). Increased skin pigmentation, low serum cortisol, and high ACTH levels suggested Addison’s disease and the diagnosis was confirmed by lack of cortisol response to 250 mcg ACTH stimulation test. 21-hydroxylase antibody was found to be positive. She was also evaluated for hypertransaminasemia. Serum alkaline phosphatase, gamma-glutamyl transferase, total bilirubin and albumin levels were all normal. Also, all viral hepatitis markers were negative. Tests for anti-smooth muscle antibody, anti mitochondrial antibody, and antinuclear antibody were all negative. Abdominal computed tomography showed no pathology within the liver and adrenal glands. After confirmation of Addison’s disease by ACTH stimulation test, corticosteroid therapy was initiated. Nearly two weeks after corticosteroid replacement therapy aminotransferase activity returned to normal, and continued to normalize for three months after replacement therapy (Table1). For patients with constantly elevated liver enzymes, extra-hepatic diseases have to be considered. Although rare, Addison’s disease should be kept in mind.
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  • Summary
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  • Introduction

  • Top
  • Summary
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  • Materials And Methods
  • Results
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  • Conclusion
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  • Case Presentation

  • Top
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  • Case Presentation
  • Results
  • Discussion
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  • References
  • Materials And Methods

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  • Case Presentation
  • Materials And Methods
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  • Discussion
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  • Top
  • Summary
  • Introduction
  • Case Presentation
  • Materials And Methods
  • Results
  • Discussion
  • Conclusion
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  • Top
  • Summary
  • Introduction
  • Case Presentation
  • Materials And Methods
  • Results
  • Discussion
  • Conclusion
  • References
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  • Top
  • Summary
  • Introduction
  • Case Presentation
  • Materials And Methods
  • Results
  • Discussion
  • Conclusion
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    1. Olsson RG, Lindgren A, Zettergren L. Liver Involvement in Addison ’s disease. Am j Gastroenterol 1990; 85:435-8. 2. Boulton R, Hamilton MI, Dhillon AP, et al. Subclinical Addison’s disease: a cause of persistent abnormalities in transaminase values. Gastroenterology 1995; 109:1324-7. 3. Castiella A, Etxeberria X, Ganzarain J, Aramburu V. Hypertransaminasaemia and Addison’s disease. Eur J Gastroenterol Hepatol 1998;10:891-2. 4. Rizvi AA, Kerrick JG. Liver involvement and abnormal variables in undiagnosed Addison’s disease. Endocr Pract 2001;7:184-8. 5. Milionis HJ, Dimos GA, Tsiara S, et al. Unexplained hypertransaminasaemia: a clue to diagnosis of Addison’s disease. Eur J Gastroenterol Hepatol 2002;14:1285-6. 6. Gurakuqi GC, Stadlbauer V, Stepan V, et al. Addison’s disease as a rare cause of chronically elevated liver enzymes. Z Gastroenterol 2006; 44:179–83. 7. Anagnostis P, Athyros VG, Vasiliadis T, et al. Should we consider Addison's disease in the differential diagnosis of persistent hypertransaminasemia? A case report. Acta Gastroenterol Belg 2011;74:95-6. 8. Özaslan E, Demirezer AB. Addison’s Disease: A rare cause of hypertransaminasaemia. Dig Dis Sci 2008;53: 3269-71.
  • Top
  • Summary
  • Introduction
  • Case Presentation
  • Materials And Methods
  • Results
  • Discussion
  • Conclusion
  • References
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