KARACİĞER FONKSİYON TESTİ YÜKSEKLİĞİNİN NEDENİ: ÇÖLYAK HASTALIĞI

Year 2010, Volume: 11 Issue: 2, 35 - 37, 09.11.2010

İrfan Yavasoglu Adil Coskun İbrahim Meteoglu Vahit Yükselen Gürhan Kadıköylü Zahit Bolaman

Abstract

Çölyak hastalığı (ÇH) çevresel faktörün (gliadin) oluşturduğu bilinen tek otoimmun bozukluktur. Son yıllardaolguların %40'ında transaminaz yüksekliklerinin görülebileceği bildirilmektedir. On yedi yaşında bayan olgu 5yıldır olan halsizliğinin son 6 aydır artması şikayeti ile başvurdu. Diyare ve dispeptik yakınmalar tariflemiyordu.Muayene, solukluk dışında normaldi. ALP: 1026 IU/L (kemik kaynaklı), AST: 50 IU/L, ALT: 71 IU/L, GGT: 52IU/L, total bilirubin 1.93 mg/dL, direkt bilirubin 1,34 mg/dL, Anti HBs, HBsAg, Anti HCV, HAV Ig M negatif,hemoglobin: 7.7 gr/dl, ferritin: 2.92 ng/ml idi. Magnetik rezonans görüntüleme ile kolanjiopankreotikografisinormal, DEXA vertebral ölçümde T skoru: -5, Z skoru: -4.7 idi. Endomisial antikor (EMA) Ig A, anti Gliadinantikor IgA>200 RU/ml (>50 pozitif) veAnti-Gliadin antikor IgG 61.5 RU/ml pozitifti. Karaciğer biyopsisisindeparankimde fokal spoty nekroz ve kolestaz bulguları vardı. Endoskopik duodenal biyosisinde villuslarda atrofi,yüzey epitelyimunda yoğun intraepitelyal lenfosit varlığı, immunhistokimyasal boyamada intraepitelyallenfositlerin CD3 ve CD8 ile diffüz boyandığı, CD4 ve CD20 ile az sayıda lenfositin pozitif boyandığı gözlendi.Bulgular ÇH modifiye Marsh klasifikasyonuna göre Tip 3B ile uyumluydu. Olguya biyopsi ve antikordeğerlendirmesi ile ÇH tanısı kondu. Glutensiz diyet başlandı. Tedavinin birinci ayında ALP (büyüme çağındaolgu) yüksekliği dışında AST, ALT, GGT, bilirubin değerleri normal sınırlarda saptandı. Sonuç olarak karaciğerfonksiyon testi yüksekliğinin ayırıcı tanısında diyare olmasa da ÇH düşünülmelidir

Keywords

Çölyak Hastalığı, karaciğer fonksiyon testleri, glutensiz diyet

A Reason For High Liver Function Test Results: Celiac Disease

Abstract

Celiac disease (CD) is the only autoimmune disorder caused by an environmental factor (gliadin). Recently it has been reported that transaminase increase was seen in 40% of the cases.A17 years old female patient was admitted for increased weakness in the last 6 months, which she has been complaining for 5 years. She didn't have diarrhea or dyspepsia. Except paleness, her examination was normal. Biochemical test results were as follows;ALP:1026 IU/L (originating from bone), AST:50 IU/L, ALT:71 IU/L, GGT:52 IU/L, total bilirubin: 1.93mg/L, direct bilirubin:1.34 mg/dL, Anti-HBs, HbsAg,Anti HCV,HAVIgM were negative, hemoglobin: 7.7g/dL, and ferritin: 2.92 ng/ml. Cholangiopancreaticography with magnetic resonance imaging was resulted normal. In DEXA, vertebral measurement T score was -5 and Z score was -4.7. Endomysial autoantibody (EMA) IgA, anti gliadin antibody IgA>200 RU/ml (>50 positive), and anti gliadin antibody IgG 61.5 RU/ml were positive. Liver biopsy showed focal spotty necrosis and cholestasis in parenchyma. Endoscopic duodenal biopsy showed villous atrophy, intense intraepithelial lymphocytes in surface epithelium. Intraepithelial lymphocytes were dyed diffusely with CD3 and CD8 in immunohistochemical staining but few were dyed positively with CD4 and CD20. Findings were in agreement with type 3B according to modified Marsh classification for CD. She was diagnosed with CD according to biopsy and antibody evaluation.Agluten free diet was started. In the first month of treatment except ALP increase (she was in puberty), AST, ALT, GGT, bilirubin values were normal. In conclusion, even if no diarrhea,CDmust be thought in differential diagnosis of increased liver function tests.

Keywords

Celiac disease, liver function tests, gluten free diet

References

• 1. Green PH, Cellier C. Celiac disease. N Engl J Med 2007;357:1731-43.
• 2. NIH Consensus Development Conference on Celiac Disease. NIH Consens State Sci Statements 2004;21:1- 23.
• 3. Volta U. Pathogenesis and clinical significance of liver Injury in celiac disease. Clinic Rev Allerg Immunol 2009;36:62-70.
• 4. Duggan JM, Duggan AE. Systematic review: the liver in coeliac disease. Aliment Pharmacol Ther 2005;21:515-8.
• 5. Marsh MN. Gluten, major histocompatibility complex, and the small intestine. A molecular and immunobiologic approach to the spectrum of gluten sensitivity ('celiac sprue'). Gastroenterology 1992;102:330-54.
• 6. Volta U, Granito A, De Franceschi L, Petrolini N, Bianchi FB. Anti tissue transglutaminase antibodies as predictors of silent coeliac disease in patients with hypertransaminasaemia of unknown origin. Dig Liver Dis 2001;33:420-5.
• 7. Volta U, De Franceschi L, Lari F, Molinaro N, Zoli M, Bianchi FB. Coeliac disease hidden by cryptogenic hypertransaminasaemia. Lancet 1998;352:26-9.
• 8. Jacobsen MB, Fausa O, Elgjo K, Schrumpf E. Hepatic lesions in adult coeliac disease. Scand J Gastroenterol 1990;25:656-62.
• 9. Erkan T, Kutlu T, Yılmaz E, Çullu F, Tümay GT. Çölyak'li Türk çocukları nda HLA ile hipertransaminazemi ve Antigliadin düzeyi ilişkisi. Cerrahpaşa Tıp Dergisi 1998;29:38-42
• 10. Ojetti V, Fini L, Zileri Dal Verme L, Migneco A, Pola P, Gasbarrini A. Acute cryptogenic liver failure in an untreated coeliac patient: a case report. Eur J Gastroenterol Hepatol 2005;17:1119-21.