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ABSTRACT: Langerhans cell histiocytosis (LCH) is a rare disease of unknown etiology characterized by oligoclonal proliferation of Langerhans cells. The diagnosis of LCH is complicated by the fact that it may involve multiple organ systems and its clinical presentation and course varies, ranging from an isolated to a multisystem disease. We report a 35-year-old male with LCH involving multiple systems, including the bones, lungs, spleen, liver and bile ducts, whose first clinical presentation was liver dysfunction. The patient was diagnosed following a skull biopsy that revealed infiltration of Langerhans cells. However, a liver biopsy revealed sclerosing cholangitis (SC) with no signs of Langerhans cell infiltration, and the clinical manifestations of the involved organs were atypical, leading to a delayed diagnosis. The patient was in partial remission following chemotherapy. In conclusion, findings of this case may aid our understanding of the pathophysiology of LCH and in improving its diagnosis and treatment.
Oncology letters 02/2012; 3(2):391-394. · 0.11 Impact Factor
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Chinese medical journal 10/2010; 123(19):2750-2. · 0.86 Impact Factor
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ABSTRACT: There has been much progress in antiviral therapy for chronic hepatitis B; however, antiviral therapy for hepatitis B in special populations is still very challenging. Here, we review antiviral therapy for hepatitis B in special populations, including children and pregnant patients, patients with hepatitis-B-related cirrhosis, patients with acute hepatitis B and chronic hepatitis B surface antigen carriers who receive immunosuppressive or cytotoxic therapy. Major advances have been made in antiviral therapy for hepatitis B in these special populations because of recent increasing availability of oral nucleoside/nucleotide analogues that are well-tolerated and highly effective; however, the findings are mostly based on small uncontrolled short-term studies. More well-designed clinical studies on antiviral therapy for hepatitis B in these special populations are urgently needed to obtain more evidence-based high-quality data.
Antiviral therapy 01/2010; 15(8):1067-75. · 3.16 Impact Factor
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ABSTRACT: Radiofrequency ablation (RFA) followed by transarterial chemoembolization (TACE) for unresectable primary liver cancer (PLC) has not been widely discussed. In this study, the outcome of the combination of RFA with TACE was retrospectively evaluated.
From May 2003 to March 2008, 127 consecutive PLC patients with a median age of 56.4 +/- 8.8 years underwent RFA plus TACE. All patients were deemed to have unresectable PLC based on their tumor characteristics. The maximal diameter of the tumor was between 1.5 cm and 10.0 cm. Twenty-six cases with small (<or= 3.0 cm), 33 with medium (3.1 - 5.0 cm), and 68 with large (> 5.0 cm) tumors were included in this study. RFA was performed using a RITA Medical Systems expandable electrode device, which was followed by first-time TACE administration one to two months later.
Technical success of RFA was achieved in all 127 patients with no severe treatment-related complications. RFA was performed percutaneously in 16 (13.5%) cases, by laparoscopic approach in 19 (15.7%), and through laparotomy in the remaining 92 (72.4%). RFA response was classified as complete ablation in 48 cases, nearly complete ablation in 28, and partial ablation in 51. The total 1-, 2-, and 3-year survival rates after RFA were 83.1%, 55.7%, and 43.7%, respectively. The survival rates at 3 years were 78.6%, 28.1%, and 0 for complete ablation, nearly complete ablation, or partial ablation groups, respectively. Three-year disease-free survival rates for the complete ablation and nearly complete ablation groups were 50.3% and 21.3%, respectively. RFA response and liver function were significant variables influencing survival time as analyzed using the Cox regression model.
RFA could be the first-line exterminate treatment for unresectable PLC, and TACE following RFA may assist in eradicating the peripheral viable tissue and micro-metastasis.
Chinese medical journal 04/2009; 122(8):889-94. · 0.86 Impact Factor
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ABSTRACT: Urotensin II (UII) is a relatively novel peptide that functions as a potent vasoactive mediator throughout the human body, and also possesses mitogenic and fibrogenic potential. Recent reports showed increased plasma levels of UII in human cirrhotic populations; these levels were correlated with the severity of the disease. We therefore hypothesized that the blockade of UII signaling would arrest the progression of hepatic fibrosis in a rat model of cirrhosis. Cirrhosis was induced in rats by carbon tetrachloride. SB-710411 was used as the UII antagonist. Treatment lasted 8 weeks. Plasma hyaluronic acid (HA) and laminin (LN) were evaluated by radioimmunoassay, and plasma UII was determined by ELISA for the quantity of hydroxyproline (Hyp) in the liver tissues. Fibrosis was assessed histologically. The activated hepatic stellate cells (HSCs) were assessed by α-smooth muscle actin innunostaining. The relative mRNA expression of UII/G protein-coupled receptor (UT), collagen I, collagen III, transforming growth factor β1 (TGF-β1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in the liver was determined by real-time reverse transcriptase-polymerase chain reaction. Western blot analysis was used to assess liver levels of UT. The mitogenic activity of UII on HSC-T6 cells was also evaluated. Animals with cirrhosis showed increased plasma UII. UII/UT mRNA expression was up-regulated in the liver. Plasma levels of UII were also positively correlated with HA, LN and Hyp. In vivo, treatment with SB-710411 significantly reduced fibrosis development and down-regulated the profibrogenic cytokines TGF-β1 and TIMP-1. In vitro, UII induced the proliferation of HSCs. This mitogenic effect was significantly inhibited by 10-3 M SB-710411 (p<0.05). These data suggest that the selective blockade of UT has an arresting effect on fibrosis progression in vivo, and inhibits UII-mediated HSC proliferation in vitro.
Molecular Medicine Reports 2(6):953-61. · 0.42 Impact Factor
