Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of hepatic inflammatory myofibroblastic tumor in a 26-year-old African American man who presented with right upper quadrant pain, weight loss, and fatigue during the previous year. Hepatomegaly was found on physical examination. Laboratory findings were significant for mild normocytic, normochromic anemia and elevated erythrocyte sedimentation rate. Imaging studies showed 2 contiguous masses suspicious for malignancy. A left partial hepatectomy was performed; the preoperative differential diagnosis was for angiosarcoma and hepatocellular carcinoma. The resected liver specimen showed 2 contiguous, firm, tan-white nodules that microscopically represented a proliferation of spindled myofibroblast cells set in an inflammatory and collagenized background. The spindle cells were strongly reactive for smooth muscle actin but negative for ALK-1. The morphologic and immunophenotypic findings, coupled with the clinical presentation, were consistent with an inflammatory myofibroblastic tumor of the liver.
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PMID:Inflammatory myofibroblastic tumor of the liver. 1709 Feb

Inorganic arsenic is clearly a human carcinogen causing tumors of the skin, lung, urinary bladder, and possibly liver (IARC, 2004). At the time of construction of this monograph, the evidence for arsenic as a hepatocarcinogen in humans was considered controversial and in rodents considered insufficient. However, recent data has accumulated indicating hepatocarcinogenicity of arsenic. This forum reevaluates epidemiology studies, rodent studies together with in vitro models, and focuses on the liver as a target organ of arsenic toxicity and carcinogenesis. Hepatocellular carcinoma and hepatic angiosarcoma, have been frequently associated with environmental or medicinal exposure to arsenicals. Preneoplastic lesions, including hepatomegaly, hepatoportal sclerosis, fibrosis, and cirrhosis often occur after chronic arsenic exposure. Recent work in mice clearly shows that exposure to inorganic arsenic during gestation induces tumors, including hepatocellular adenoma and carcinoma, in offspring when they reach adulthood. In rats, the methylated arsenicals, dimethylarsinic acid promotes diethylnitrosamine-initiated liver tumors, whereas trimethylarsine oxide induces liver adenomas. Chronic exposure of rat liver epithelial cells to low concentrations of inorganic arsenic induces malignant transformation, producing aggressive, undifferentiated epithelial tumors when inoculated into the Nude mice. There are a variety of potential mechanisms for arsenical-induced hepatocarcinogenesis, such as oxidative DNA damage, impaired DNA damage repair, acquired apoptotic tolerance, hyperproliferation, altered DNA methylation, and aberrant estrogen signaling. Some of these mechanisms may be liver specific/selective. Overall, accumulating evidence clearly indicates that the liver could be an important target of arsenic carcinogenesis.
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PMID:Liver is a target of arsenic carcinogenesis. 1856 22

Primary hepatic angiosarcoma (PHA) is a rare malignancy that carries a poor prognosis, accounting for less than 2% of all primary hepatic tumors. It is reported to be associated with chronic exposure to environmental carcinogens, but the majority of patients were still with unknown etiology. For patients with PHA often present with nonspecific symptoms and its rapid progression, accurate and early diagnosis is difficult and necessary. We described a 41-year old woman with no history of exposure to toxic chemicals having intermittent abdominal distention for 1 month. Imaging examinations showed multiple nodules with different sizes throughout markedly enlarged liver and spleen. Liver histology showed majority of necrotic lesions with foci of atypical cells, which displayed immunoreactivity for endothelial markers CD31, CD34 and FLi-1, supporting the diagnosis of angiosarcoma. She was finally diagnosed as PHA concomitant with spleen metastases through imaging technology combined with the histopathologically results. Then the patient showed a rapidly worsening clinical course. Finally the patient received liver transplantation and splenectomy. Unfortunately, the patient died of infection in 35 days after liver transplantation.
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PMID:Primary hepatic angiosarcoma with spleen metastases in an adult woman: a case report and literature review. 3196 72


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