Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Laparoscopic findings of nine patients with chronic schistosomiasis japonica were analyzed and compared to hepatic ultrasonograms, computed tomography (CT) scans and histological findings from the same patients. In all nine patients laparoscopy revealed yellowish, small speckles, approximately 50 microm in diameter, sparse or clustered over the liver surface, which were later found to represent subcapsular calcified ova of Schistosoma japonicum. While the liver surface was almost smooth in mild schistosomiasis, multiple whitish markings and irregular, relatively wide, groove-like septums were seen in more advanced cases. In severe schistosomiasis block-like formations of variable size, separated by groove-like depressions, made the liver surface appear like a tortoise shell. In moderate or severe schistosomiasis ultrasonography revealed spotted high echoes and CT scans demonstrated network patterns and lineal calcified spots. The liver surface of chronic schistosomiasis japonica without re-infection appeared stable without change over time but with a tendency to improve. Hepatocellular carcinoma was initially recorded in two of the nine patients and follow-up revealed a further two with the same diagnosis. However, all these four cases also had chronic hepatitis C (HCV). Hepatocellular carcinoma was not detected in patients without viral hepatitis, indicating that hepatic viral infection is more important than schistosomiasis in promoting the development of hepatocellular carcinoma.
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PMID:Laparoscopic diagnosis and clinical course of chronic schistosomiasis japonica. 1099 28

Background: The studies carried out on hepatocellular carcinoma (HCC) are scarce in Egypt. Nevertheless, they presumed an upward trend for HCC among chronic liver disease (CLD) patients. The objectives of this research were to determine the trend of HCC, the possible risk factors implicated in its development and the population attributable risk of HCVAb and HBsAg positivity for HCC. Methods: Medical records of all patients attending Cairo Liver Center during the years 1992-1995 were reviewed to determine the sociodemographic characteristics, HCVAb, HBsAg and HCC status. Prospectively, 200 HCC cases' stored sera as well as 120 healthy control were tested for aflatoxin B(1) quantitatively and qualitatively. Results: HCC accounted for 4.7% (321/6850) of CLD patients included in the study. HCVAb positive cases were strikingly high (71.1%) and HBsAg positive cases were reported in 22.4% of patients. There was an annual significant rise of HCC ranging from 3.6% in 1992 to 5.3% in 1995. HCC was significantly more prevalent among old age groups (60 years) than younger age groups. The impact of gender and past history of schistosomiasis on HCC was not proved by this study. HCVAb and HBsAg positivity were the two significant independent risk factors for HCC. The population attributable risk percent has shown that HCC cases attributed to HCVAb positivity accounted for 51.1%; while HBsAg positivity only explained 21.3% of cases. Aflatoxin B(1) was detected in 17% of HCC cases compared to 9.4% of healthy control. Risk ratio=2(95%). Conclusion: HCC is showing an increasing trend among our patients. Its development is mainly due to high rates of HCVAb and HBsAg positivity. HBsAg positive patients were at double risk to develop HCC and HCVAb positive patients were at 1.6 more risk. The high prevalence of HCVAb positivity renders its contribution to the development of HCC over seven-fold higher than HBsAg positivity. Short and long term health strategies are crucial to prevent and control HCC in Egypt.
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PMID:Prevalence and epidemiological features of hepatocellular carcinoma in Egypt-a single center experience. 1116 41

Advances in imaging technology and development of liver-specific contrast agents have significantly increased the role of radiology in the detection and characterization of processes diffusely involving the liver. Tailored magnetic resonance imaging (MRI) sequences allow an accurate detection of many storage and metabolic diseases, such as iron overload disorders and steatosis (fatty liver). Faster scanning techniques available with both computed tomography (CT) and MRI provide, by assessing contrast dynamics, sufficient information for the characterization of diffuse neoplastic and vascular disorders. Characteristic changes in attenuation on CT, signal intensity on MRI, and enhancing features can be used to diagnose specific diffuse diseases such as candidiasis, diffuse/multifocal hepatocellular carcinoma, and schistosomiasis. Although an overlap in imaging findings still exists, familiarity with the imaging features of uncommon disorders such as Wilson's disease, amyloidosis, and sarcoidosis may be diagnostic in the proper clinical setting. This review focuses on the current role of imaging in the detection and characterization of diffuse liver disorders. Recent developments that have amplified the role of noninvasive diagnostic evaluation of these conditions are especially highlighted.
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PMID:Imaging of diffuse liver disease. 1143 72

Hepatocellular carcinoma is associated with liver fibrosis. Murine schistosomiasis infection offers a model to study hepatic fibrogenesis. Single-stranded phosphorothiate oligodeoxynucleotides containing the TGF-beta regulatory element have been shown to regulate the transcription of this gene and effectively inhibit collagen synthesis in primary fibroblasts isolated from schistosomiasis-induced hepatic granulomas. While the single-stranded oligos did not decrease collagen and non-collagen protein synthesis below control levels, their double-stranded modified and unmodified counterparts did. Competitive cold oligodeoxynucleotide gel mobility shift analysis using control fibroblast nuclear extract demonstrated that the single-stranded oligos diminished binding of the TGF-beta activator protein to the TGF-beta regulatory element while the double-stranded oligos totally inhibited this binding. TGF-beta element containing single-stranded phosphorothioate oligodeoxynucleotides and their double-stranded counterparts may be successful therapeutic agents to inhibit hepatic fibrogenesis and associated hepatocellular carcinoma.
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PMID:Rational basis for oligodeoxynucleotides to inhibit collagen synthesis in lung fibroblasts and primary fibroblasts from liver granulomas of Schistosoma mansoni-infected mice. 1217 45

Immunological factors are important in the pathogenesis of a wide spectrum of hepatobiliary diseases. Using flow cytometry, we determined the changes in lymphocyte subsets and natural killer cells in 123 individuals (81 patients with liver disease and 42 healthy volunteers). The liver diseases included periportal fibrosis (PPF, 10 patients), liver cirrhosis (LC, 31 patients), and hepatocellular carcinoma (HCC, 40 patients). Schistosomiasis and viral hepatitis B and C were the putative etiological agents of liver diseases. Immunophenotyping by indirect immunofluorescence was conducted using monoclonal antibodies to CD3 (T-lymphocytes), CD4 (helper/inducer T-cells), CD8 (suppressor/cytotoxic T-cells), and CD57 (natural killer cells) cell surface markers. Immunophenotyping of PPF patients showed no significant changes in all markers compared with the healthy controls. However, there was a significant decrease ( P<0.01) in CD3 and CD4 T-cells, and a highly significant increase ( P<0.001) in CD57 T-cells in patients with LC or HCC. In addition, LC and HCC patients showed no significant change in CD8 T-cells compared with controls. In conclusion, the progression of liver diseases is associated with a dysregulation of cellular immune responses. T-lymphocytes and natural killer cells may play a role in the immunopathogenesis of liver cirrhosis and HCC.
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PMID:Dysregulation of blood lymphocyte subsets and natural killer cells in schistosomal liver cirrhosis and hepatocellular carcinoma. 1464 34

Three hundred and forty-nine autopsy cases of schistosomiasis japonica were divided into two groups, based on the pathomorphology. Frequent regressive hepatic lesions such as active schistosomal lesion and destruction of limiting plates characterized the first group. The second group showed reparative hepatic lesions such as regeneration of the collapsed parenchyma, newly formed limiting plates and subsequent narrowing and disappearance of fibrous septa. Complications of liver cirrhosis and hepatocellular carcinoma related to viral hepatitis B and/or C also increased. Clonorchiasis was consistently found in both groups.
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PMID:A historical view of schistosomiasis japonica in the Chikugo river basin. What can we learn from autopsy? 1466 90

The natural history of hepatitis C virus (HCV) infection has a highly variable course. Many patients develop chronic infection, with its consequent risk of cirrhosis, liver failure and hepatocellular carcinoma. A key question is whether patients at high risk of disease progression can be distinguished from those with relatively benign disease course. The disease progression is influenced by other factors such as duration of infection, age at infection, sex, co-infection with hepatitis B virus (HBV), Epstein Bar virus (EBV), cytomegalovirus (CMV), the level of HCV viraemia and its type. Other endemic infections in the community as bilharziasis may have a role in progression of the condition to serious complications. These factors are correlated with newly proposed grades and stages of the disease. The studied (109) cases were divided into 6 groups according to the concomitant infection with HCV. The result proved that groups 1, 3 & 5 had a higher level of viraemia than other groups, and to be the high-risk groups as 56.4% and 34.6% were in G2S2 and G3S3, respectively. All cases of liver cell dysplasia and hepatocellular carcinoma in this study were seen in these groups. The conclusion showed that these factors play an important role in the progression of HCV infection. Death of the patients of this progressive condition occurs in younger age and is more due to liver failure than to HCC.
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PMID:HCV and associated concomitant infections at Sharkia Governorate, Egypt. 1512 52

Hepatitis C virus (HCV) is the leading cause of chronic liver disease worldwide with a prevalence of approximately 14% in Egypt. IL-10 is a cytokine produced by Th2 cells. It down-regulates the proinflammatory response and modulates hepatic fibrogenesis. IL-12 is produced by antigen presenting cells. It promotes Th1 cell response and has many antiviral properties. Data concerning the Th-1/Th-2 balance in chronic hepatitis C (CH-C) are rather conflicting. Using ELISA, we assessed serum IL-10 and IL-12p40 levels in 66 Egyptian patients with HCV-related liver illness (CH-C, cirrhosis, and HCC), and their relationship to disease activity. Our results showed that spontaneous IL-10 was undetectable in patients with CH-C, HCC or controls. Only 5/22 (23%) of patients with cirrhosis showed detectable levels of IL-10. IL-12p40 was elevated in the patient groups compared to controls (p= 0.01, p= 0.01, p= 0.05 in CH-C, cirrhosis and HCC, respectively). The presence of IL-12p40 was associated with HCV level of viremia and serum AST. Serum ALT level was significantly associated with the level of IL-12p40. IL-12p40 was unrelated to liver histology or fibrosis. We concluded that in the Egyptian patients an augmentation of IL-12p40 and a suppression of IL-10 are both found. Whether this pattern is related to HCV genotype 4, or to the presence of schistosomiasis would need to be further investigated.
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PMID:IL-10 and IL-12p40 in Egyptian patients with HCV-related chronic liver disease. 1571 17

Hepatitis B and C viruses (HBV and HCV) have been associated with hepatocellular carcinoma (HCC). Recently, a novel DNA virus was isolated from a patient with posttransfusion hepatitis of unknown etiology and designated TT virus (TTV). To examine whether this virus is associated with HCC, we investigated sera from 82 Egyptian patients with histopathologically-diagnosed HCC. All subjects underwent serological investigations for detection of hepatitis B surface antigen (HbsAg), hepatitis B core antibody (HbcAb) and anti-HCV. Detection of TTV-DNA was performed by semi-nested polymerase chain reaction (PCR) using TTV-specific primers. TTV-DNA was detected in 28% of the patients. Age, gender, risk factors and biochemical liver functions did not significantly differ between TTV-DNA positive and negative patients. TTV was detected in 27.1% of patients with HCV-HCC, 25% of HBV-HCC, 66.7% of dual HCV and HBV infection and 40% of those with non-B, non-C-HCC (NBNC-HCC). It is concluded that, in this the cohort of Egyptian patients with HCC, TTV infection is common and is not associated with HCV, HBV, NBNC-HCC, history of schistosomiasis or blood transfusion.
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PMID:TT virus infection among Egyptian patients with hepatocellular carcinoma. 1571 18

The molecular clock has been a very powerful tool in looking back at the epidemic spread of HCV infection in the United States (US) and Japan, as well as in Egypt. This analysis estimates that the growth of the US HCV genotype 1a (HCV-1a)-infected population occurred around 1960, at least 30 years later than the widespread introduction of HCV-1b into the Japanese population. In Japan, the estimated effective number of HCV infections indicated a rapid exponential growth in the 1920s among patients with schistosomiasis, which coincides with injection treatment for schistosomiasis since 1921 in previously schistosomiasis-endemic areas. In Egypt, the spread of HCV-4a would have increased exponentially during the 1940s through 1980, which was also consistent with the duration of intravenous antimony campaigns for the treatment of shistosomiasis in that country. The implications are that Japan has set the model for HCV-related HCC, and that the high HCC incidence in Japan might be replicated by the rest of the world as their HCV-infected population ages and the duration of HCV infection approaches that currently observed in Japan.
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PMID:Tracing the evolution of hepatitis C virus in the United States, Japan, and Egypt by using the molecular clock. 1623 67


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