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Journals / Turkish Journal of Gastroenterology / 2003 / Cilt: 14 - Sayı: 4

Non-alkolik steatohepatit potogenezinde demir ve bakır birikiminin önemi

The importance of iron and copper accumulation in the pathogenesis of non-alcoholic steatohepatitis

Kemal AKIN
Ali Reşit BEYLER
Muhsin KAYA
Esra ERDEN
Pages
228–233
DOI
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⚡ TL;DR(Too Long; Didn't Read)

Conclusion: There was no correlation between hepatic iron and copper accumulation and the development of NASH.

📌 3 Key Takeaways

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Objective & Hypothesis:Background/aims: The pathogenesis of non-alcoholic steatohepatitis (NASH) is poorly understood.
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Key Findings & Data:Serum iron, serum iron binding capacity (SIBC), transferrin saturation, ferritin, ceruloplasmin, and 24-hour urinary copper level were measured.
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Conclusion & Impact:Conclusion: There was no correlation between hepatic iron and copper accumulation and the development of NASH.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Biyopsi · Yağlı karaciğer · Demir

Abstract

Background/aims: The pathogenesis of non-alcoholic steatohepatitis (NASH) is poorly understood. Hepatic iron and copper overload can directly cause lipid peroxidation and eventually hepatic damage. The aim of this study was to investigate the role of hepatic iron and copper accumulation in the development of NASH. Methods: Fifty-three patients with NASH were studied. All patients underwent liver biopsy. Clinical and biochemical variables were examined. Serum iron, serum iron binding capacity (SIBC), transferrin saturation, ferritin, ceruloplasmin, and 24-hour urinary copper level were measured. The presence of stainable iron and copper on liver biopsy specimen was investigated. Results: Serum iron level in 14 (26%) patients, SIBC in 2 (3.7%), ferritin level in 1 (1.9%) and transferrin saturation in 2 (3.7%) patients were elevated. One male patient had abnormality in serum iron metabolism showing the possibility of hemochromatosis. Slightly decreased serum ceruloplasmin level in 4 (7.5%) patients and slightly elevated 24-hour urinary copper amount in 6 (11%) patients were identified. No patients had the abnormality showing the possibility of Wilson disease. NASH was grade I in 25 (47%) patients, grade II in 20 (38%) and grade III in 8 (15%). Fourteen (26%) patients had no fibrosis, 31 (59%) patients had mild fibrosis. None of the patients had bridging or septal fibrosis or cirrhosis. No hepatic iron or copper staining was demonstrated in any patient. Conclusion: There was no correlation between hepatic iron and copper accumulation and the development of NASH.

Özet

Amaç: Non-alkolik steatohepatitin (NASH) patogenezi tam bilinmemektedir. Karaciğerde aşırı demir ve bakır birikimi direkt lipit peroksidasyonuna ve karaciğerde zedelenmeye yol açabilir. Bu çalışmanın amacı karaciğerde demir ve bakır birikiminin NASH gelişimindeki rolünü araştırmaktı. Yöntem: NASH tanısı almış 53 hasta çalışmaya alındı. Tüm hastalara karaciğer biyopsisi yapıldı. Hastaların klinik ve biyokimyasal özellikleri incelendi. Serum demir (Fe), serum demir bağlama kapasitesi (SDBK), transferrin saturasyonu (TS), ferritin, seruloplazmin, 24 saatlik idrar bakır düzeyi ölçüldü. Karaciğer biyopsisinde boyanabilen demir ve bakır varlığı araştırıldı. Bulgular: Serum Fe seviyesi 14 (%26) hastada, SDBK 2 (% 3,7), ferritin seviyesi l (%1,9) ve transferrin seviyesi 2 (% 3,7) hastada artmıştı. Bir erkek hastada hemokromatosis varlığını düşündüren serum Fe metabolizması bozukluğu bulguları vardı. Hafif azalmış serum seruloplazmin seviyesi 4 (%7,5) hastada ve hafif artmış 24 saatlik idrar bakır seviyesi 6 (%11) hastada saptandı. Hiçbir hastada Wilson hastalığını düşündürecek patolojik bulgu saptanmadı. NASH 25 (%47) hastada grade I, 20 (%38) hastada grade II, ve 8 (%15) hastada grade III düzeyindeydi. On dört (%26) hastada fibrosis saptanmadı. Otuz bir (%59) hastada hafif derecede fibrosis vardı. Hiçbir hastada köprüleşme şeklinde veya septal fibrosis veya siroz saptanmadı. Hiçbir hastanın karaciğer biyopsisinde demir veya bakır varlığı saptanmadı. Sonuç: Yaptığımız bu çalışmada karaciğerde demir veya bakır birikimiyle NASH gelişimi arasında herhangi bir ilişki saptanmadı.

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Cite This Article

AKIN, K., BEYLER, A. R., KAYA, M., ERDEN, E. (2003). Non-alkolik steatohepatit potogenezinde demir ve bakır birikiminin önemi. Turkish Journal of Gastroenterology, Cilt: 14 - Sayı: 4, 228–233. https://ajindex.com/articles/410478

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References (17)

  1. Ludwig J, Viggiano TR, McGill DB, et al. Nonalcoholic steatohepatitis. Mayo Clinic experiences with hitherto unnamed disease. Mayo Clin Proc 1980; 55: 434-8
  2. Reid AE. Nonalcoholic steatohepatitis. Gastroenterology 2001; 121: 710-23
  3. Bacon BR, Farahvash MJ, Janney CG, et al. Nonalcoholic steatohepatitis: an expanded clinical entity. Gastroenterology 1994; 107: 1103-9
  4. Matteoni CA, Younossi ZM, Gramlich T, et al. Nonalcoholic fatty liver disease: a spectrum of clinical and pathological severity. Gastroenterology 1999; 116: 1413-9
  5. Younossi ZM, Gramlich T, Bacon BR, et al. Hepatic iron and nonalcoholic fatty liver disease. Hepatology 1999; 30: 847-50
  6. Marchesini G, Birizi M, Morselli-Labate AM, et al. Association of nonalcoholic fatty liver disease with insulin resistance. Am J Med 1999; 107: 450-5
  7. Mendler MH, Turlin B, Moirand R, et al. Insulin resistance-associated hepatic iron overload. Gastroenterology 1999; 117: 1155-63
  8. Britton RS. Metal-induced hepatotoxicity. Sem Liv Dis 1996; 16: 3-12
  9. Angulo P, Keach JC, Batts KP, et al. Independent predictors of liver fibrosis in patients with nonalcoholic steatohepatitis. Hepatology 1999; 30: 1356-62
  10. Chitturi S, Weltman M, Farrell GC, et al. HFE mutations, hepatic iron, and fibrosis: ethnic-specific association of NASH with C282Y but not with fibrotic severity. Hepatology 2002; 36:142-9
  11. Myers BM, Prendergast FG, Holman R, et al. Alterations in hepatocyte lysosomes in experimental hepatic copper overload in rats. Gastroenterology 1993; 105: 1814-23
  12. George DK, Goldwurm S, Macdonald GA, et al. Increased hepatic iron concentration in nonalcoholic steatohepatitis is associated with increased fibrosis. Gastroenterology 1998; 114: 311-8
  13. Bonkovsky HL, Javaid Q, Tortorelli K, et al. Non-alcoholic steatohepatitis and iron: increased prevalence of mutations of the HFE gene in non-alcoholic steatohepatitis. J Hepatol 1999; 31: 421-9
  14. Groot MJ, Gruys E. Yellow discoloration in veal calves: the role of hepatic copper. Veterinary Record 1993; 132: 156-60
  15. Schilsky ML. Wilson disease: genetic basis of copper toxicity and natural history. Sem Liv Dis 1996; 16: 83-95
  16. Itoh S, Yougel T, Kawagoe K. Comparison between nonalcoholic steatohepatitis and alcoholic hepatitis. Am J Gastroenterology 1987; 82: 650-4
  17. Ruhl CE, Everhart JE. Determinant of the association of overweight with elevated serum alanine aminotransferase activity in the United States. Gastroenterology 2003;