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

Vitamin D has been proposed as a risk factor of ischaemic heart disease. In 12 patients with acute myocardial infarction the major circulating vitamin D metabolite, 25-hydroxy-cholecalciferol (25-HCC), did not show any fluctuations during the first 4 days after onset of symptoms. The serum 25-HCC level was then measured in 128 patients consecutively admitted because of chest pain, 53 of whom had myocardial infarction and 75 had angina pectoris. The values found did not differ from those measured in 409 normal persons. The seasonal variations of serum 25-HCC were less pronounced in heart patients than in normals, probably due to less sun exposure in the summer months. The levels of serum 25-HCC did not correlate with the concentrations of serum cholesterol, glycerides, calcium or magnesium. Low serum calcium and magnesium were observed in all patients. Serum calcium was further reduced in the course of acute myocardial infarctions while serum parathyroid hormone rose significantly. We conclude that patients with ischaemic heart disease are not ingesting or producing in their skin elevated amount of vitamin D.
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PMID:Vitamin D and ischaemic heart disease. 74 75

An enzyme-linked immunosorbent assay (ELISA) has been developed for human manganese-superoxide dismutase (Mn-SOD), using a specific monoclonal antibody raised against the purified enzyme. The Mn-SOD molecule comprises four identical sub-units and this permitted the development of a symmetrical assay, using the same monoclonal antibody as both capture and detector. The assay offers a specific, sensitive and convenient means of measuring immunoreactive Mn-SOD in human sera. Under optimum conditions, the sensitivity of the assay permits the detection of 2-200 ng of purified Mn-SOD from human liver. The mean serum Mn-SOD levels of normal healthy males and females were 99.8 +/- 24.8 (mean +/- SD) and 88.8 +/- 20.8 (mean +/- SD), respectively. A high level of the enzyme was found in the sera of patients with acute myocardial infarction as well as malignant diseases such as acute myeloid leukemia, primary hepatoma and gastric cancer. This is the first report of an ELISA using a monoclonal antibody specific for a distinct epitope of Mn-SOD.
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PMID:Serum-manganese-superoxide dismutase: normal values and increased levels in patients with acute myocardial infarction and several malignant diseases determined by an enzyme-linked immunosorbent assay using a monoclonal antibody. 231 2

Tissue-type plasminogen activator (t-PA) is a plasma serine protease that catalyzes the initial and rate-limiting step in the fibrinolytic cascade. t-PA is widely used as a thrombolytic agent in the treatment of acute myocardial infarction. However, its use has been impaired by its rapid hepatic clearance from the circulation following intravenous administration. Studies with both rat hepatoma MH1C1 cells (G. Bu, S. Williams, D. K. Strickland, and A. L. Schwartz, 1992. Proc. Natl. Acad. Sci. USA. 89:7427-7431) and human hepatoma HepG2 cells (G. Bu, E. A. Maksymovitch, and A. L. Schwartz. 1993. J. Biol. Chem. 28:13002-13009) have shown that binding of t-PA to its clearance receptor, the low density lipoprotein receptor-related protein/alpha 2-macroglobulin receptor, is inhibited by a 39-kD protein that copurifies with this receptor. Herein we investigated whether administration of purified recombinant 39-kD protein would alter t-PA clearance in vivo. We found that intravenous administration of purified 39-kD protein to rats prolonged the plasma half-life of 125I-t-PA from 1 min to approximately 5-6 min. The plasma half-life of t-PA enzymatic activity was similarly prolonged following intravenous administration of purified 39-kD protein. In addition we found that the 39-kD protein itself was rapidly cleared from the circulation in vivo. Clearance of 125I-39-kD protein was a biphasic process with half-lives of 30 s and 9 min and the liver was the primary organ of clearance. Preadministration of excess unlabeled 39-kD protein slowed 125I-39-kD protein clearance in rats in a dose-dependent manner, suggesting that specific clearance receptors were responsible for this process. Administration of increasing doses of unlabeled 39-kD protein along with labeled 39-kD protein resulted in a decrease in the amount of labeled 39-kD protein associating with the liver and a concomitant increase in the amount of labeled 39-kD protein associating with the kidneys, indicating two clearance mechanisms exist for the 39-kD protein.
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PMID:39-kD protein inhibits tissue-type plasminogen activator clearance in vivo. 834 26

Thirty patients with primary hepatocellular carcinoma or liver metastases were entered into a program of chemoembolization with cisplatin, lipiodol, and escalating doses of thiotepa. Doses of cisplatin were 100/m2, and thiotepa doses ranged from 9 mg/m2 to 24 mg/m2. Two of three patients with ocular melanoma had partial responses in the liver metastases for 3+ and 16 months. In patients with either hepatocellular carcinoma (15 patients) or primary cholangiocarcinoma of the liver (three patients), there were two partial responses, for 22 and 33 months. Five patients had minor responses: four with a 40% reduction in tumor and one with a mixed response. There were four early deaths, which involved sepsis in two patients, respiratory failure in one, and acute myocardial infarction in one. Otherwise, toxicity was tolerable and reversible and included abdominal pain and transient elevation of serum creatinine, bilirubin, and transaminases. Less common toxicities included ototoxicity and peripheral neuropathy. Chemoembolization of the liver with cisplatin, thiotepa, and lipiodol can produce responses, but toxicity can be significant. The recommended starting phase II dose for future studies is thiotepa 24 mg/m2 and cisplatin 100 mg/m2.
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PMID:A phase I study of chemoembolization with cisplatin, thiotepa, and lipiodol for primary and metastatic liver cancer. 1044 Jan 93

A 71 year old patient presented with a non-ST segment elevation acute myocardial infarction. The echocardiogram showed several masses attached to the interatrial septum. Several days after admission the patient died. A postmortem examination found a large hepatocarcinoma with intravascular and intracardiac metastases and several myocardial infarctions of different ages. The infarctions had been caused by coronary paradoxical embolisms through a patent foramen ovale and contained neoplastic cells from the liver carcinoma, which had not been diagnosed. The cause of death was a massive pulmonary embolism.
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PMID:Acute myocardial infarction caused by paradoxical tumorous embolism as a manifestation of hepatocarcinoma. 1508 77

Hepatitis B surface antigen positivity (HBsAg(+)) was believed to be an exclusion for kidney donation. However, in the presence of an organ shortage, allocation of kidneys from HBsAg(+) donors to recipients with anti-HBsAb(+) might be allowed. We examined the 10-year outcomes of kidney transplants (KT) from HBsAg(+) donors to natural or vaccine-induced anti-HBsAb(+) recipients (Group 1). Hepatitis B hyperimmune globulin (HBIG) and lamivudine were not used at any time. We compared the 10-year outcomes of patients who had HBsAg(+) prior to KT and received kidneys from HBsAg(-) donors (Group 2). The endpoint was patient survival determined by Kaplan-Meier and Cox proportional hazard methods. A total of 41 patients were transplanted from 1991-1997. There were 14 Group 1 patients and 27 Group 2 patients. Anti-HBsAb titer ranged from 10 to >1000 mIU/mL. Actuarial 10-year patient survivals were 92.8% and 62.5% for Group 1 and Group 2. Only 1 patient in Group 1 died; this case was due to an acute myocardial infarction. Eleven deaths occurred among Group 2; they were due to chronic active hepatitis (n = 5), hepatoma (n = 3), acute fibrosing cholestatic hepatitis (n = 1), and stroke (n = 2). More than 2 times elevated ALT occurred among 45% of Group 2 but none in Group 1. No patients in Group 1 had positive HBsAg and HBV DNA at last follow-up. Four patients in Group 2 displayed seroconversion to positive HBeAg after KT. Secondary analysis examining the impact of KT on patient life expectancy (from the start of dialysis until last follow-up) used Cox regression, revealing that KT was significantly associated with an increased risk for death within 12 months after transplantation (RR = 30, P = .005) but a decreased risk for death thereafter (RR = .03, P = .005) for Group 2. However, KT did not have significant impact on the risk for death within the first year for Group 1 (P = .61). Our results showed that the 10-year survival of KT from HBsAg(+) donors to recipients with anti-HBsAb(+) was good. This was not associated with evidence of active liver disease. The presence of HBsAg(+) in donors thus should not be considered an exclusion for kidney donation for anti-HBsAb(+) recipients.
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PMID:Ten-year follow-up of kidney transplantation from hepatitis B surface antigen-positive donors. 1924 16

Transarterial chemoembolization has been widely used to treat unresectable hepatocellular carcinoma. Various complications have been reported, but they have not included acute myocardial infarction. Acute myocardial infarction results mainly from coronary artery occlusion by plaques that are vulnerable to rupture or from coronary spasm, embolization, or dissection of the coronary artery. It is associated with significant morbidity and mortality. We present a case report that describes a patient with hepatocellular carcinoma who underwent transarterial chemoembolization and died subsequently of acute myocardial infarction. To our knowledge, there has been no previous report of this complication induced by transarterial chemoembolization for hepatocellular carcinoma. This case illustrates the need to be aware of acute myocardial infarction when transarterial chemoembolization is planned for the treatment of hepatocellular carcinoma, especially in patients with underlying coronary artery disease.
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PMID:An unusual complication following transarterial chemoembolization: acute myocardial infarction. 1973 Sep 38

A 60-year-old man with liver cirrhosis caused by hepatitis C, who was receiving warfarin anticoagulation following acute myocardial infarction, was diagnosed with advanced hepatocellular carcinoma and multiple lung metastases, and began treatment with sorafenib 200 mg daily. From the treatment's start to 14 and 63 days later, sorafenib was increased to 400 mg and 600 mg, respectively. After increasing the quantity to 600 mg, he had an increase in PT-INR values and experienced a lower-extremity hemorrhage. For the patient with liver cirrhosis, who is receiving warfarin, PT-INR values might be elevated during the early period of sorafenib treatment dosage as for the increase in quantity. Therefore, when increasing dosage, a frequent measurement of PT-INR and a careful follow-up for PT-INR is necessary.
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PMID:[Gastrointestinal hemorrhage associated with concurrent use of sorafenib and warfarin for hepatocellular carcinoma]. 2199 74

The early results of liver transplantations (OLT) in patients with advanced hepatocellular carcinoma (HCC) were poor because of frequent tumor recurrence. However, OLT has significant, theoretical advantage that it removes both the tumor and the organ that is at a risk of malignancy. The Japanese law on organ transplantation limited the availability of cadaveric liver donors until its revision on July 17, 2011. ABO-incompatible OLT was formerly contraindicated because performed anti-A/B antibodies on recipient endothelial cells raised the risk of antibody-mediated humoral graft rejection. We have herein described four successful cases of steroid withdrawal among adult patients who underwent living donor OLT from ABO-incompatible donors. In addition, we transplanted a liver from a living donor into an ABO-incompatible recipient on August 9, 2004. The 55-year-old man with HCC due to hepatitis B virus (HBV) a cirrhosis had a Child-Pugh score of C, and Model for End-stage Liver Disease score of 22. Two tumors greater than 5 cm, exceeded the Milan criteria. His des-gamma-carboxy prothrombin level was 6 mAu/mL, and alpha-fetoprotein, 18.78 ng/mL. Antirejection therapy included multiple perioperative plasmaphereses and splenectomy; with an immunosuppressive regimen consisting of tacrolimus, methylprednisolone, and mycophenolate mofetil. The maintenance dose of immunosuppression did not differ from that of ABO-identical cases. After transplantation, we used intrahepatic arterial infusion therapy with prostaglandin E1 (PG E1). The patient had complications of portal vein thrombosis, hepatic artery thrombosis, and acute myocardial infarction, which were treated by interventional radiology in the posttransplantation period. We controlled the HBsAb titer by administering hepatitis B immunoglobulin and lamivudine (200 IU/L doses) for 1 year after OLT and 100 IU/L doses thereafter. As a result, the patient achieved long-term, disease-free graft survival without steroids. He currently has good liver function and leads a normal lifestyle. Our results suggested the feasibility of controlling antibody-mediated humoral rejection and other complications in living donor liver transplantations into ABO-incompatible adults via intrahepatic arterial PG E1 infusion splenectomy, and plasmapheresis with regular immunosuppression. Withdrawal of steroids, HBV vaccination, and lamivudine, an nucleoside analog reverse transcriptase inhibitor, have achieved long-term (7 years) survival without recurrent HBV infection or tumor.
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PMID:Long-term recurrence-free survival after liver transplantation from an ABO-incompatible living donor for treatment of hepatocellular carcinoma exceeding Milano criteria in a patient with hepatitis B virus cirrhosis: a case report. 2241 70