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Open Medicine
|
2010
|
vol. 5
|
issue 5
535-537
EN
Patients with liver metastases from squamous cell head and neck cancer (SCHNC) are usually treated with chemotherapy and are not evaluated for eventual liver-directed treatment. However, the potential benefits from liver surgery for the patients with hepatic-only metastases from SCHNC generally remain undefined. We report a patient with late liver-only metastases from squamous cell glottic cancer treated with resection of the liver metastases followed by adjuvant platinum-based chemotherapy plus cetuximab. The patient died 25 months after resection of the hepatic metastases from widespread hepatic and pulmonary recurrence. The literature data as well as this case demonstrates the capability of liver surgery to prolong survival in patients with hepatic metastases from SCHNC.
EN
A wide range of molecular markers and different types of cells in liver are possible factors for progression of non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH) development of liver fibrosis. We investigated biopsies from 57 patients with NASH. The material was obtained from livers and was proceed immunohistochemistry antibodies against CD68 and TGF-beta 1. In addition, biopsies were evaluated for iron content. Macrophages/-positive/could be found in all 57 cases. The number of macrophages in the sinusoids correlated with the degree of portal fibrosis:64.% of the patients with mild or intensive fibrosis had high infiltration with CD68-positive cells, while 100% of the patients without fibrosis hadlow infiltration (χ2=8.56; p=0.003). In specimens we, 69.% of patients with different degree of fibrosis expressed TGF-β1 in their portal tracts, and 100% of patients without fibrosis did demonstrate expression of the protein (χ2=23.7; p<0.001). Hepatic iron was found in 100% (9) of patients with intensive fibrosis vs. 10.3% of the patients mild fibrosis (χ2=23.4; p<0.001). Our results suggest that the macrophages and macrophage-derived TGF-beta1 are the major factors responsible for development of fibrosis and progression of chronic liver disease.
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