Serum α-Fetoprotein Levels in Patients with Chronic Hepatitis C : Relationships With Serum Alanine Aminotransferase Values, Histologic Activity Index, and Hepatocyte MIB-1 Scores

Goldstein, Neal S.; Blue, Deborah E.; Hankin, Rebecca C.; Hunter, Susan; Bayati, Nasser; Silverman, Ann L.; Gordon, Seymour

doi:10.1093/ajcp/111.6.811

Cited by 49 publications

(47 citation statements)

References 16 publications

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“…It increases as a result of ongoing inflammation, most probably secondary to cellular destruction or stimulation of AFP production by cytokines. Elevated serum AFP levels may also be due to altered hepatocyte-hepatocyte interaction and the loss of normal architectural arrangements [9]. The presence of hepatic inflammation and/or fibrosis may be the underlying cause of increased serum AFP levels in patients with severe fatty liver.…”

Section: Discussionmentioning

confidence: 99%

Serum α-fetoprotein levels in liver steatosis

Babali¹,

Çakal

Pürnak

et al. 2009

Hepatol Int

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Background Nonalcoholic fatty liver disease (NAFLD) is a common disorder and becoming a leading cause of cirrhosis in the western world. The monitoring of the disease is challenging and the prognostic importance of a-fetoprotein (AFP) level elevation in NAFLD remains uncertain. Methods Eighty-four patients were evaluated in the study. Patients with evidence of fatty liver in an abdominal ultrasonography performed for any reason were enrolled in the study. Degree of liver steatosis was graded into three groups. As a control group, patients without fatty liver or other liver diseases were included. All patients and controls were asked about prior hepatic diseases, consumption of alcohol, smoking, drug use, and a physical examination, biochemical analyses including liver function tests, different components of the metabolic syndrome, and the homeostasis model assessment-estimated insulin resistance (HOMA-IR) score were also performed. Results Body mass index, aspartate aminotransferase, alanine aminotransferase, glucose, insulin, and HOMA-IR in patients with NAFLD were higher than in control group. Triglyceride, total cholesterol, low-density lipoprotein, and high-density lipoprotein cholesterol levels were higher in NAFLD group than in control group. A statistically significant increase in AFP levels was noted in patients with NAFLD (4.09 ± 1.68) when compared with healthy controls (2.95 ± 0.41) (P \ 0.05). A statistically significant increase in AFP levels was noted in patients with grade 3 NAFLD (5.43 ± 1.51) when compared with grade 1 (2.92 ± 1.06) and grade 2 NAFLD groups (3.97 ± 1.45). Also, AFP was significantly higher in grade 2 NAFLD group than in grade 1 NAFLD group. AFP was correlated with NAFLD grade, but neither ALT nor AST showed correlation. According to multivariate analysis, correlation between NAFLD grade and serum AFP levels was independent from the other factors. Conclusion Patients with NAFLD have higher AFP levels than those without fatty liver changes. AFP levels rise as grade of liver steatosis increases. NAFLD should be among the differential diagnosis of elevated serum AFP levels.

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Section: Discussionmentioning

confidence: 99%

Serum α-fetoprotein levels in liver steatosis

Babali¹,

Çakal

Pürnak

et al. 2009

Hepatol Int

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“…It has a reported sensitivity of 39% to 65% and specificity of 65% to 94% and has multiple limitations when applied to patients with HCV (9 -11). Recently, high levels of AFP have been reported in HCV patients with fibrosis and necroinflammation resulting from the natural process of disease progression in HCV and unrelated to HCC (12,13 from the Hepatitis C Antiviral Long-term Treatment against Cirrhosis study, 27% of patients with HCV and cirrhosis had an AFP of >20 ng/mL in the absence of HCC, and AFP levels declined with antiviral therapy (14).AFP also seems to have reduced sensitivity for smaller tumors (15), and some authors argue that it has limited utility as a screening test (10). Recently, the American Association for the Study of Liver Diseases guidelines for HCC screening have recognized the overall poor performance of AFP and have removed it from the screening recommendations (16).…”

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confidence: 99%

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confidence: 99%

Serum Proteomics and Biomarkers in Hepatocellular Carcinoma and Chronic Liver Disease

Zinkin¹,

Grall

Bhaskar³

et al. 2008

Clinical Cancer Research

189

123

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Purpose: Proteomic profiling using surface enhanced laser desorption/ionization time of flight mass spectrometry (SELDI-TOF MS) enables the identification of biomarkers for cancer.We evaluated the sensitivity and specificity of SELDI-TOF MS for detection of established hepatocellular cancer (HCC) and compared it against a-fetoprotein (AFP), Lens culinaris agglutinin^reactive AFP (AFP-L3), and prothrombin induced by vitamin K absence-II (PIVKA-II). Experimental Design: Forty-one patients with HCC and 51 patients with hepatitis C cirrhosis were enrolled. Serum was analyzed by SELDI-TOF MS using three Ciphergen protein array types. Results: An 11-peak algorithm for HCC detection was identified. Using the AFP cutoff of 20 ng/mL, the sensitivity was 73% and the specificity was 71%. Using the AFP-L3 cutoff of 10% yielded a sensitivity of 63% and a specificity of 94%. Using the PIVKA-II cutoff of 125 milliabsorbance units (mAU), the sensitivity was 84% and the specificity was 69%. Overall, the sensitivity and specificity of SELDI-TOF MS for HCC were 79% and 86%, respectively. In multivariate analysis, the 11-peak SELDI profile was predictive of HCC independent of AFP, PIVKA, and AFP-L3. Among eight patients with the largest tumor size of <2 cm, SELDI-TOF MS correctly identified seven whereas AFP, AFP-L3, and PIVKA-II identified only three, one, and one, respectively. One of the 11 peaks in the SELDI-TOF MS 11-peak predictor from SELDI-TOF MS was identified as cystatin C. Conclusions: SELDI-TOF MS accurately distinguished patients with HCC from those with hepatitis C virus cirrhosis, was more accurate than traditional biomarkers in identifying small tumors, and should be further evaluated.The incidence of hepatocellular carcinoma (HCC) is on the rise in the United States (1 -3). Recently, El-Serag et al. showed that the incidence of HCC had increased from 1.8 per 100,000 to 2.5 per 100,000 over one decade and that nearly all of this increase was attributable to infection with hepatitis C virus (HCV; ref. 2). Once cirrhosis has developed, retrospective studies have suggested that patients will develop either hepatic decompensation or HCC at a rate of 2% to 7% per year (4 -8). The general practice among many physicians has been to screen for HCC using ultrasound and serum a-fetoprotein (AFP) levels at 3-month to 6-month intervals.However, even with this screening regimen, many patients still present with either large HCC (>5 cm) or multifocal HCC (more than three lesions) or HCC that has invaded the portal vein or other critical structures. The limitations of ultrasound, the primary radiologic screening modality under current use, include its operator dependence and its poor ability to differentiate malignant from benign nodules in the small cirrhotic liver. Although imaging with triphasic computed tomography scan and magnetic resonance imaging with i.v. gadolinium can improve the diagnostic accuracy, these techniques are time consuming and too expensive for widespread screening at the present time. Because outco...

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“…Malignite olmadan saptanan AFP düzey yüksekliğinin sebebi karaciğer fibroz ve sirozunda olduğu gibi; hepatositler arası iletişimin karaciğer parankim yapısındaki düzenin bozulmasından ve karaciğer doku kollapsından kaynaklanabilmektedir. 11 AFP seviyesi gebelikte karaciğer yapımına sekonder artmış saptanabilmektedir. Nitekim AFP gibi CA 19-9 seviyesi de bazı benign seyirli hastalıklarda artmış saptanabilmektedir.…”

Section: Discussionunclassified