Agustos 2020
Nonalkolik yagli karaciger hastaliginda histolojik progresyon ile klinik ve laboratuvar parametrelerin iliskisi
The relationship between clinical and laboratory parameters and histological progression in nonalcoholic fatty liver disease
- Ana Sayfa
- Sayılar
- Agustos 2020
- Nonalkolik yagli karaciger hastaliginda histolojik progresyon ile klinik ve laboratuvar parametrelerin iliskisi...
Özet
Giris ve Amaç: Nonalkolik steatohepatit nonalkolik yagli karaciger hastali- ginin ilerleyici bir formudur. Nonalkolik steatohepatit, zamanla siroz ve hepatosellüler karsinomaya sebep olabilir. Bu çalismada nonalkolik yagli karaci- ger hastaligi tanili olgularda zamanla karaciger histolojisindeki degisikliklerin arastirilmasi ve histolojik progresyonla iliskli klinik ve laboratuvar degiskenlerin saptanmasi amaçlanmistir. Gereç ve Yöntem: Bu çalismada 1994-2009 yillari arasinda hepatoloji veri tabanina kayitli toplam 783 nonalkolik yagli karaciger hastalikli olgu retrospektif olarak tarandi. En az 2 yil arayla yapi- lan 2 karaciger biyopsisi olan 29 hasta çalismaya alindi. Vücut kitle indeksi, glukoz intoleransi veya diyabetes mellitus varligi, karaciger fonksiyon testi dahil biyokimyasal parametreler kaydedildi. Nonalkolik yagli karaciger hastaligi aktivite skoru steatoz, lobüler inflamasyon ve hepatosellüler balonlasma skorlarinin toplami ile hesaplandi. Fibroz skorlari ayri rapor edildi. Bulgular: Ortalama yas 45.2±11 yil, olgularin 17’si (%58.6) erkekti. Basvuruda ortalama vücut kitle indeksi 29.5±4 kg/m2, 15’i (%51.7) fazla kilolu, 12’si (%41.4) obezdi. Toplam 11’inde (%37.9) diyabetes mellitus, 6’sinda (%20.7) glukoz intoleransi vardi. Aspartat aminotransferaz düzeyi ortalama 51±36 IU/ml, alanin aminotransferaz düzeyi ortalama 79±50 IU/ml, albümin ortalama 4.5±0.4 gr/dL, trigliserit ortalama 197±106 mg/dL saptandi. Hastalarin 14’ünde (%48.3) “nonalkolik steatohepatit” ve 6’sinda (%20.6) basit steatoz vardi. Egzersiz ve diyet önerisiyle kontrol biyopsi için medyan takip araligi 4.8 yil (2-9 yil) saptandi. Kontrol biyopsi aninda vücut kitle indeksi ortalama 29.6±4 kg/m2, aspartat aminotransferaz ortalama 38.8±14 IU/ml, alanin aminotransferaz ortalama 59.2±32 IU/ml, 13’ünde (%44.8) diyabetes mellitus ve 7’sinde (%24.1) glukoz intoleransi saptandi. Ikinci karaciger biyopsilerinde nonalkolik yagli karaciger hastaligi aktivite skoru; 9 (%31) hastada ilerlemis, 17’sinde (%58.6) gerilemis, 3’ünde (%10.3) ayni bulundu. Fibrozis skorunda ise 6 (%20.1) hastada ilerleme, 3 (%10.3) hastada ise iyilesme gö- rüldü. Nonalkolik yagli karaciger hastaligi aktivite skoru ilerlemesiyle baslangiç yasi arasinda negatif, baslangiç vücut kitle indeksi ile pozitif korelasyon saptandi, sirasiyla (r=-0.370, p=0.047 ve r=0.485, p=0.007). Fibrozis skoru ilerlemesiyle, baslangiç yasi arasinda negatif, baslangiç vücut kitle indeksi ile pozitif ve kontrol biyopsileri anindaki aspartat aminotransferaz düzeyiyle pozitif korelasyon saptandi, sirasiyla (r=-0.503 p=0.005; r=0.382 p=0.04 ve r=0.546 p=0.007). Sonuç: Basit yaglanma yasla ve yüksek vücut kitle indeksi ile iliskili olarak nonalkolik steatohepatite progrese olabilir. Genç yastakiler, yüksek vücut kitle indeksi ve aspartat aminotransferaz düzeyinde yükseklik olanlar fibrozis progresyonu açisindan daha riskli bulunmustur.
Abstract
Background and Aims: Nonalcoholic steatohepatitis is the progressive form of nonalcoholic fatty liver disease and can cause cirrhosis and hepatocellular carcinoma. We aimed to investigate the changes in liver histology and determined the relationship between histologic progression and clinical and laboratory parameters in patients with nonalcoholic fatty liver disease. Materials and Methods: We retrospectively screened 783 patients with nonalcoholic fatty liver disease who had enrolled in the hepatology database between 1994 and 2009. Among the 783, there were 29 patients with two liver biopsies performed at least two years apart. Body mass index, presence of glucose intolerance or diabetes, and biochemical parameters including liver function test were noted. Nonalcoholic fatty liver disease activity score was the sum of steatosis, lobular inflammation, and hepatocellular ballooning scores. The fibrosis scores were reported separately. Results: Mean patient age was 45.2±11years, and 17 (58.6%) patients were men. Mean body mass index was 29±4 kg/m2, and 15 (51.7%) patients were overweight and 12 (41.4%) were obese. Twelve (41.4%) patients had diabetes mellitus and five (17.2%) patients had glucose intolerance. Mean aspartate aminotransferase level was 51±36 IU/ml, mean alanine aminotransferase level was 79±50 IU/ml, mean albumin level was 4.5±0.4 g/dL, and mean triglyceride level was 197±106 mg/dL at baseline. Fourteen (48.3%) patients had nonalcoholic steatohepatitis and six (20.6%) patients had simple steatosis. The patients followed the recommended exercises and diet for therapy, and control liver biopsies were performed. The median follow-up duration was 4.8 years (2–9). Mean body mass index was 29.6±4 kg/m2, mean aspartate aminotransferase level was 38.8±14 IU/ml, and mean alanine aminotransferase was 59.2±32 IU/ml. Thirteen (44.8%) patients had diabetes mellitus and seven (24.1%) had glucose intolerance at the time when their control biopsies were collected. According to nonalcoholic fatty liver disease activity score, nonalcoholic steatohepatitis progression was detected in 9 (31%) patients, while improvement was detected in 17 (58.6%) patients. In control liver biopsies, nonalcoholic fatty liver disease activity score remained the same in three (10.3%) patients. Six (20.1%) patients experienced progression and three (10.3%) patients showed improvement in fibrosis scores in the control biopsies. Regarding the basal parameters, age was negatively correlated and body mass index was positively correlated with the nonalcoholic steatohepatitis progression (r=?0.370, p=0.047 and r=0.485, p=0.007, respectively). The progression of fibrosis scores was negatively correlated with baseline age and positively correlated with baseline body mass index and aspartate aminotransferase levels when control biopsies were taken (r=?0.503, p=0.005; r=0.382, p=0.04; and r=0.546, p=0.007, respectively). Conclusion: Simple steatosis may progress to nonalcoholic steatohepatitis in patients with younger age and high body mass index. Patients with younger age and higher body mass index at baseline and higher aspartate aminotransferase at the time of collecting the control biopsies were more likely to experience progression of liver fibrosis.
