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)

A 50-year-old male with unresectable hepatocellular carcinoma (HCC) had a hypercalcemic crisis with a serum calcium concentration of 7.8 mEq/zeta, without any evidence for bone metastases or parathyroid lesions. The hypercalcemia was thought to be due to increased renal reabsorption of calcium and increased bone resorption, which was probably caused by humoral factors derived from the HCC, some being parathyroid hormone-like factors. Since conservative therapy for hypercalcemia was not sufficiently effective and was accompanied by progressive exacerbation of ascites and leg edema, transcatheter arterial chemo-embolization (TACE) was performed. On the following day, serum calcium concentration decreased from 6.3 mEq/zeta to the normal range, although serum alpha-fetoprotein levels decreased only slightly. Thereafter hypercalcemia did not develop for about 4 weeks. The results demonstrated that TACE can be effective for humoral hypercalcemia of HCC.
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PMID:Transcatheter arterial chemo-embolization for humoral hypercalcemia of hepatocellular carcinoma. 283 39

The Japanese Ministry of Health and Welfare Research Committee on Aberrant Portal Blood Flow carried out an epidemiological survey and clinical study on Budd-Chiari syndrome in 1990. In the primary survey for determining the prevalence of the disease, a questionnaire was sent to all major hospitals throughout Japan and 160 cases seen in 1989 were compiled. More epidemiological details were obtained in 87 of these 160 cases. The number of patients with Budd-Chiari syndrome in this country was estimated to be about 300 (prevalence of 2.4/million) with about 20 new cases occurring every year. In the clinical study, 157 authentic cases of Budd-Chiari syndrome studied in 15 years (1975-89) were analyzed. There were 87 males (average age, 36.4 years) and 70 females (46.5 years), and the average period from the likely onset to the first medical consultation was 6.6 years, suggesting that these patients were mostly chronic cases. The main clinical features were hepatomegaly, leg edema, ascites and venous dilatation over the trunk. Abdominal pain was recorded in only four (2.5%). There were 16 (10.2%) with known identifiable etiologies. Of the patients 93% showed an obstructing lesion of various thickness in the hepatic portion of the inferior vena cava. Only nine (5.7%) had hepatic vein obstruction without caval lesions. Thus, the majority of Budd-Chiari syndrome patients in Japan are idiopathic, having an obstructing lesion in the inferior vena cava. The main causes of 33 deaths (21%) were liver failure, variceal bleeding and hepatocellular carcinoma. Hepatocellular carcinoma occurred in 10 (6.4%) in the 15-year period. However, the incidence of Budd-Chiari syndrome among all cases of hepatocellular carcinoma was less than 1% in the survey made by the Liver Cancer Study Group of Japan.
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PMID:Epidemiological and clinical features of Budd-Chiari syndrome in Japan. 775 74

Here we report an autopsy case with anti-neutrophil antibodies (ANCA) associated vasculitis accompanied by autoimmune hepatitis and hepatocellular carcinoma. A 69-year-old woman was admitted to Tokyo Metropolitan Ohtsuka Hospital in October 1995 because of leg edema. She had presented cough in 1990 and diagnosed as interstitial pneumonia, esophageal varices and liver chirosis. On admission, laboratory data showed mild anemia, hypoproteinemia, and marked gammagloblinemia. IgM-HA antibody, HBs antigen, HBs antibody, HCV antibody and HDV antibody were negative. Anti-nuclear antibody, anticentromere antibody, anti-neutrophil cytoplasmic antibody against myeloperoxidase and cathepsin G (MPO-ANCA and cathepsin G), rheumatoid factor and direct coombs test were positive. Serum level of AFP and CEA were elevated. Ultrasonography and computed tomography of abdomen scowed liver chirosis and tumor in left lobe of liver. The diagnosis of liver chirosis based on autoimmune hepatitis and Interstitial pneumonia was made with clinical course, laboratory findings and radiographic findings although liver biopsy was not performed. She complained of bloody stool due to ulcer of the large intestine, and died of liver failure which progressed rapidly. The autopsy findings detected that pulmonary fibrosis, liver fibrosis with multiple hepatocellular carcinoma, necrotizing crescentic glomerulonephritis, and vasculitis of small artery inn colon. This was the first report of MPO-ANCA associated vasuculitis complicated with autoimmune hepatitis and hepatocellular carcinoma. Clinical significance of ANCA and immunogenetic background of these diseases were discussed.
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PMID:[An autopsy case of anti-neutrophil cytoplasmic antibodies associated vasculitis accompanied by autoimmune hepatitis and hepatocellular carcinoma]. 917 69

A case of pedunculated hepatoma which was preoperatively diagnosed as non-functioning adrenal tumor is reported. A 48-year-old man presented to our hospital for further examination of remittent fever and leg edema. Abdominal ultrasonography, computed tomographic scan and magnetic resonance imaging showed a right suprarenal mass, its continuity of liver was uncertain. Tumor vessels were visualized on selective right adrenal arteriography and right adrenal function and serum alpha-fetoprotein were normal. Preoperative diagnosis was non-functioning right adrenal tumor. On operation, the dissection between the tumor and the inferior part of liver was easy. Pathological diagnosis was hepatocellular carcinoma with sarcomatous change. Difficulty of preoperative diagnosis of pedunculated hepatoma is discussed.
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PMID:[A case of pedunculated hepatoma suspected of adrenal tumor]. 1044 83

Budd-Chiari syndrome (BCS) is a disorder caused by occlusion of the hepatic vein or inferior vena cava. The clinical presentation include abdominal pain, hepatomegaly, ascites, leg edema, collateral venous dilatation of the body trunk, and portal hypertension. In addition, BCS can cause hepatocellular carcinoma (HCC) in some patients, although its pathogenesis is not yet completely understood. The average reported time lag from diagnosis of BCS to full-blown HCC ranges from several years to several decades. Hepatic carcinogenesis in patients with BCS perhaps reflects a prolonged and persistent liver injury in that it occurs in the primary inferior vena cava obstruction rather than the primary hepatic vein thrombosis. Among patients with BCS, membranous obstruction of the vena cava (MOVC) usually presents an insidious and chronic illness, whereas primary hepatic vein thrombosis presents an acute or subacute illness. We experienced a case of a patient with BCS, which progressed rapidly that HCC developed only nine months after the diagnosis of BCS. The factors causing this rapid progression are still unclear and remain to be investigated.
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PMID:Rapidly progressing Budd-Chiari syndrome complicated by hepatocellular carcinoma. 1461 90

A 58-year-old man ingested an herbal preparation of Ajuga nipponesis Makino, as recommended in folk medicine for the treatment of hepatoma. He developed profound gastrointestinal upset immediately, and decreasing urine output and bilateral leg edema over the following 2 days. Notable laboratory findings included elevated levels of blood urea nitrogen, creatine, bilirubin, and hepatic transaminases. Deterioration of renal function was noted during hospitalization and he died 11 days after ingesting the herbal preparation. Two other healthy individuals also consumed the same herbal preparation at the same time but developed only vomiting and diarrhea. One or more of the four major components of Ajuga nipponesis Makino may be responsible for the renal toxicity found in our patient.
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PMID:Ajuga nipponensis Makino poisoning. 1625 41

Sirolimus (SRL) is an mTOR inhibitor that has been shown, in contrast to calcineurin inhibitors (CNI), to inhibit cancers in experimental models. Since February 2005, we introduced SRL in liver transplant patients in group a, in whom the primary disease was hepatocellular carcinoma (HCC) associated with hepatitis B virus (HBV), hepatitis C virus (HCV), alcoholic or autoimmune liver cirrhosis, and group b, HCC-negative patients who developed posttransplantation cancers de novo. Of 18 patients in group a, 11 received SRL ab initio (subgroup a1), starting for 10 patients at 66.1+/-29.2 days after surgical healing and after 10 days in 1 case; the remaining 7 patients (subgroup a2) received SRL at 31.2+/-24.2 months. Three patients in group b, included 1 with Kaposi's sarcoma, 1 with bladder cancer, and 1 with thyroid cancer. In this group, SRL was introduced at 80.8+/-40.4 months. In all patients but one, who received a single 5 mg loading dose, SRL was started at 2 mg/d and adjusted to 6 to 8 ng/mL blood levels. CNI drugs, present as primary therapy, were gradually tapered to low levels and eventually stopped. The following observations were drawn from this initial experience: (1) 4/21 (19.0%) patients had to discontinue SRL because of early and late side effects: thrombocytopenia (n=2) and headache with leukopenia and leg edema associated with knee joint arthralgia (n=2); (2) 14 patients (11 in group a and 3 in group b) are still on SRL monotherapy; (3) 1 HCC recurrence and 1 de novo pancreatic adenocarcinoma were observed at 14 and 16 months, respectively (at the time of transplantation, both patients were beyond the MIlan HCC criteria), and (4) 1 patient, from subgroup a1, died after 99 days due to pneumonitis and possible relation to SRL lung toxicity. In conclusion, SRL appeared to be an effective immunosuppressant that could be used as monotherapy in liver transplant patients. Any conclusion on SRL anticancer effects can only come from randomized large studies after long follow-up.
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PMID:Sirolimus therapy in liver transplant patients: an initial experience at a single center. 1867 98

Case 1 was operated for HCC in September, 2002. After then TAE was performed two times for remnant liver recurrence. A year later, huge recurrence of left liver and tumor thrombus in IVC and PV were detected. After starting oral UFT administration, AFP lever went down within normal limit and tumor thrombus and early enhancement disappeared by CT scan. But after about a year, AFP level went up and TAE was performed two times, the patient died in July, 2007. Case 2 was operated for HCC in August, 2004. Re-operation was performed for recurrence of remnant liver in January, 2006. But recurrence was detected and TAE was performed in November. Ascites and leg edema appeared in June, 2007. Many recurrences of right liver, tumor thrombus in right hepatic vein and hilar hepatic lymph node were detected, UFT administration was started. After then, AFP level went down and tumor size reduced markedly by CT scan. We presents two cases effectively treated by oral UFT administration.
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PMID:[Two cases of advanced hepatocellular carcinoma (HCC) effectively treated by oral UFT administration]. 1901 43

Budd-Chiari syndrome is defined as hepatic venous outflow obstruction at any level from the small hepatic veins to the junction of the inferior vena cava and the right atrium independent of the underlying disease. We report here a 40-year-old male patient who complained of abdominal fullness and bilateral lower leg edema for 1 month. A physical examination disclosed bilateral lower leg edema. Abdominal sonography revealed a small amount of ascites with thrombosis of the inferior vena cava and right hepatic vein. Viral hepatitis marker tests showed positive hepatitis B surface antigen. Tumor markers showed elevated serum a-fetoprotein levels. Computed tomography and magnetic resonance imaging confirmed hepatocellular carcinoma with inferior vena cava and right hepatic vein thrombosis. Therefore, hepatocellular carcinoma with Budd-Chiari syndrome was diagnosed. The patient was treated with intravenous heparin, which was then changed to oral warfarin. Although it is relatively rare, clinicians should be aware of hepatocellular carcinoma with Budd-Chiari syndrome when leg edema occurs without hypoalbuminemia in patients with chronic hepatitis B, because these patients are in the high-risk group for developing hepatocellular carcinoma. Regular follow-up of chronic hepatitis B, including biochemical and sonography surveillance, should be performed.
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PMID:Hepatocellular carcinoma with presentation of budd-Chiari syndrome. 2017 89

We report two cases of Budd-Chiari syndrome. Case 1: A 57-year-old man presented with leg edema and esophageal varices. Cavography showed obstruction of the inferior vena cava with antiphospholipid syndrome. Further, the patient showed positive serology for hepatitis C virus and consumed large quantities of alcohol. Percutaneous transluminal angioplasty was performed on this patient and anticoagulants administered; leg edema and esophageal varices were ameliorated although liver biopsy showed cirrhosis without evident congestion. More than 9 months since the diagnosis, restenosis of the inferior vena cava has not occurred. Case 2: A 73-year-old woman presented abdominal pain but no edema or varices. Cavography showed membranous obstruction of the inferior vena cava which required no therapy. Manifestation of portal hypertension was not present and liver function was maintained although liver biopsy showed obvious congestion. These cases showed untypical features against histopathology, and careful observation will be required for emergence of hepatocellular carcinoma.
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PMID:Budd-Chiari syndrome: two cases with different courses. 2149 Aug 97


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