Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined hematopoietic disorders in 74 patients with various malignancies. The proportions of patients with anemia in the case of esophageal carcinoma, gastric carcinoma, colorectal carcinoma, hepatoma, and pancreatic carcinoma were 75%, 87.5%, 77%, 64% and 87.5%, respectively. Hypochromic microcytic anemia was mainly observed in showed patients with carcinoma of the gastro-intestinal tract which showed severe bleeding. The major proportion of patients with hepatoma and pancreatic carcinoma showed normochromic normocytic anemia. The WBC count was usually within the normal range except for patients with liver cirrhosis or generalized metastasis who showed decreased WBC counts. The mean lymphocyte count in the peripheral blood, which is thought to be correlated with the prognosis of cancer patients, was less than 1,500/microliter except for patients with gastric carcinoma, whose five-year survival rate was 28.6%. Monocytosis was mainly observed in patients with colorectal carcinoma and pancreatic carcinoma, accounting for 24.5% of the total cases. This finding may suggest some relationship between cancer and monocytes. Thrombocytosis was seen in patients with severe bleeding, but thrombocytopenia was seen in patients with liver cirrhosis. Most cancer patients showed normo-cellular marrow and normal M/E. We also examined the ferrokinetics and ferritin levels in cancer patients.
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PMID:[Hematological disorders in malignancy]. 301 96

In 67 patients (mean age 51 years, range 26-79), at diagnosis of primary haemochromatosis (PH), grade III or IV liver iron overload was present in all cases, cirrhosis in 85%, transferrin saturation greater than 80% in 75%, serum ferritin greater than 1000 micrograms/l in 84%, and overt diabetes in 48%. Alcohol intake was greater than 150 g/day in 11 patients; six were chronic hepatitis B surface antigen (HBsAg) carriers. HLA-A3 and B7 antigens were present in 64% and 23% versus respectively 22% (p less than 0.01) and 9% (p less than 0.025) in controls. Iron overload was found in the stomach, duodenum, skin and bone marrow in 57, 43, 45 and 59% of the patients studied. Sixty-three patients were followed for 1-260 months (median 24); 43 received regular iron-depleting treatment and 20 did not because of liver failure, cancer or refusal. Cumulative survival was 79%, 67% and 61% at 1, 4 and 10 years, respectively. Ten patients died from hepatocellular carcinoma and two from extrahepatic cancer. The early high mortality rate was due to some cases of advanced disease or cancer. Cumulative survival in the regularly treated group was 95% at 1 year and 91% at 4 and 10 years, which was higher than in the untreated group.
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PMID:Clinical, biochemical and histological features of primary haemochromatosis: a report of 67 cases. 302 81

Surgically resected specimens, consisting of tumor and adjacent non-neoplastic liver tissue, were obtained from 40 patients with primary liver cancer at Zhong Shan Hospital, Shanghai Medical University, the People's Republic of China, between March 1983 and July 1984. All were hepatocellular carcinomas (HCC), one being admixed with cholangiocarcinoma. The relationship of hepatitis B virus (HBV) markers with iron and ferritin was evaluated in liver tissues from patients with primary liver cancers. The serum HBsAg (Hepatitis B surface antigen) positive rate was 80.0% (32/40). Cirrhosis was observed in 97.5% (39/40). HBsAg was identified in 82.5% (33/40) of uninvolved liver, and 35.0% (14/40) of HCC tissues (P less than 0.001). HBcAg (hepatitis B core antigen) was detected in 25.0% (10/40) of liver, and 7.5% (3/40) of HCC tissues (P less than 0.05). Stainable iron was found in 65.0% (26/40) of unaffected livers, and 10.0% (4/40) of HCC tissues (P less than 0.001). Ferritin was demonstrated in 75% (30/40) of non-neoplastic liver, and 40% (16/40) of HCC tissues (P less than 0.001). Twenty-two of 33 HCC patients (66.7%) with HBsAg positive cells in their livers also showed stainable iron. Of 16 patients positive for ferritin in HCC cells, iron was found in only two. Iron was found in nine of ten patients with HBcAg in non-neoplastic hepatocytes (P = 0.056); a finding compatible with the hypothesis that iron accumulates in cells replicating HBV. The other results indicate that: immunohistologic ferritin in HCC is not due to increased stainable iron; tumor cells may produce ferritin; polyclonal antibodies to human liver ferritin react better with non-neoplastic hepatocytes than with HCC cells; the high prevalence of HBsAg and cirrhosis in HCC suggests that HBV plays a major etiologic role in hepatocarcinogenesis in China; and one case of HCC is attributed to Schistosoma japonicum infestation via cirrhosis.
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PMID:Iron, ferritin, hepatitis B surface and core antigens in the livers of Chinese patients with hepatocellular carcinoma. 302 1

In this paper the clinical usefulness of CEA and ferritin in the diagnosis of pancreatic cancer was pointed out. CEA was found to be increased in 51% of patients with pancreatic cancer; it was also abnormal in 22% of chronic pancreatitis and 31% of extra-pancreatic diseases. In patients with metastatic pancreatic cancer CEA was found to be more elevated than in those with localized tumor. CEA correlated with the age of the subjects in all material; in liver cirrhosis with IgG and in extra-pancreatic gastro-intestinal malignancies with alkaline-phosphatase. Ferritin was found to be increased in 73% of pancreatic cancer patients; it was also abnormal in 40% of chronic pancreatitis and in 38% of extra-pancreatic diseases. Patients with chronic pancreatitis studied during a relapsing phase all had elevated serum ferritin. We can conclude that neither CEA nor ferritin are useful indices of pancreatic malignancy, due to the lack of sensitivity or specificity. Both are influenced by several factors: CEA mainly by age and liver dysfunction, ferritin by the presence of an acute inflammation with cell necrosis.
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PMID:Limits of CEA and ferritin in the diagnosis of pancreatic cancer. 320 64

Acquired hemosiderosis resulting from massive iron deposits in various organs, including heart, liver, and pancreas, may lead to architectural and functional disturbances of these organs. Even though iron overload can occur in nonuremic as well as in uremic individuals, the dialysis patient is at particular risk for developing hemosiderosis. Many dialysis patients receive exogenous iron from either oral iron therapy or blood transfusions. In addition, these patients seem to be at high risk for retaining iron. A diagnosis of excess iron deposition should be considered if the patient has unexplained cardiomyopathy, hepatic cirrhosis, proximal myopathy, diabetes mellitus, arthropathy, or immune dysfunction such as listeriosis. Several techniques are available for determining iron overload. Diagnostic tests include measuring serum ferritin levels, staining bone marrow preparations for excess iron, measuring tissue hemosiderin concentrations, magnetic resonance imaging, and the deferoxamine (DFO; Desferal) "challenge test." The simplest treatment for iron overload in nonuremic patients is removal of iron by venesection. However, in patients in whom venesection is not feasible, the chelating agent DFO can effectively remove excess iron. In the dialysis patient, DFO therapy can be combined with either dialysis or hemoperfusion to remove the iron-DFO complex that would otherwise be removed by the kidney. DFO therapy in the nondialyzed individual has proven to be successful, but before treatment, the benefits of the treatment must be weighed against possible adverse side effects such as cataracts, changes in color vision, and anaphylaxis. In the dialysis patient, indications for iron removal are less clearly defined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Management of iron overload in dialysis patients. 329 89

We report two sisters with neonatal hemochromatosis (NHC), including the first documented survivor. Characterized by excessive parenchymal iron in liver, pancreas, heart, and other organs, but little iron in the spleen, bone marrow, or other sites of the reticuloendothelial system, NHC is rarely reported and has been uniformly fatal. The first infant (case 1) presented with neonatal hypoglycemia, coagulopathy, and mild hyperbilirubinemia; she rapidly deteriorated and died of multisystem failure. Autopsy showed cirrhosis. Her sister (case 2) presented similarly; liver biopsy showed giant cell hepatitis, which is consistent with idiopathic neonatal hepatitis (INHP). However, iron staining revealed that case 1 had extensive iron deposits in the liver, pancreas, heart, thymus, and bone, but none in bone marrow or spleen. Case 2 had grade 4 liver iron staining, normal bone marrow iron, elevated serum ferritin and transferrin saturation, and HLA-A3 haplotype. At 16 months of age, the growth, development, and serum measures of iron status in case 2 were normal; liver biopsy showed fibrosis, negative iron staining, and normal tissue iron concentration. NHC is compatible with survival, has clinicopathologic features that overlap with INHP, and may frequently be misdiagnosed as INHP. A prospective study is needed to determine the incidence and natural history of NHC--a disorder that may be more common than is currently recognized.
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PMID:Familial neonatal hemochromatosis with survival. 333 84

The immunoenzyme method was used to measure serum ferritin levels in 55 patients with haemolymphopathies and advanced solid tumours. Patients were divided into five groups according to tumour type. 50 healthy subjects and 12 patients with cirrhosis of the liver were also studied. In 76% of the cancer patients ferritin levels were significantly higher than in the control group of healthy subjects (p less than 0.01). Only 8 of the patients studied had primary or secondary liver tumours. None of the cancer patients showed clinical or blood chemical signs of current acute or chronic liver disease. Furthermore 13 of the cancer patients had severe anaemia and were given multiple transfusions during hospitalisation. All the groups studied showed a significant (p less than 0.01) increase in mean ferritinaemia levels compared to the healthy control groups. There was also a significant difference between the mean value encountered in the liver cancer and cirrhosis groups. Both groups also showed significantly higher levels than the control group. In contrast no significant differences were noted between the mean values encountered in the individual cancer groups by means of variance analysis.
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PMID:[Serum ferritin levels in patients with hemolymphopathies and solid neoplasms in an advanced phase: a comparison with healthy subjects and liver cirrhosis patients]. 354 40

We studied 29 patients with thalassaemia major who had received intensive chelation for between 6.2 and 8.8 years. All patients had normal oral glucose tolerance tests before subcutaneous chelation therapy was introduced and 22 of 29 patients had normal liver function tests. At the end of the period of study 12 patients still had normal oral glucose tolerance (7 with normal liver function tests and 5 with chronic active hepatitis). On the other hand, 11 patients had developed impaired glucose tolerance tests (3 patients had normal liver function tests, 5 with chronic active hepatitis and 3 with cirrhosis), and 6 patients had developed frank diabetes mellitus (one with chronic active hepatitis and 5 with cirrhosis). Patients with chronic active hepatitis showed 91% positivity for one or more hepatitis B markers whilst all patients with cirrhosis were positive. Ferritin levels before subcutaneous chelation in patients with normal oral glucose tolerance tests were lower than in those patients with abnormal oral glucose tolerance or diabetes (P less than 0.05) but none had normal serum ferritin levels. In addition, a positive correlation was found between glucose area under the curve after chelation therapy and serum ferritin levels (r = 0.47, P less than 0.01). It is apparent that long term chelation therapy does not prevent the development of abnormal oral glucose tolerance in chronically transfused patients. More intensive chelation therapy is needed to prevent tissue damage. Chronic liver disease may have an important role to play in the deterioration of glucose tolerance.
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PMID:The development of diabetes mellitus and chronic liver disease in long term chelated beta thalassaemic patients. 354 13

Serum ferritin levels in chronic liver diseases were measured by an enzyme-linked immunosorbent assay (ELISA) using two monoclonal antibodies (McAb) against placental ferritin. One of the McAbs (CM-H9) recognizes a specific placental-like isoferritin (PLF) only, while the other McAb (CM-G8) recognizes an isoform (CF) common to human placenta, liver and spleen. The different diseases studied were primary biliary cirrhosis (PBC-14 patients), chronic active hepatitis (CAH-12 patients), alcoholic cirrhosis (AC-18 patients) and cryptogenic cirrhosis (CRY-26 patients). Increased levels of both isoferritine were found in all these liver disorders, with an overall incidence of 80% for CF and 40% for PLF. The mean level of CF was significantly above normal in PBC, AC and CRY and that of PLF in PBC and CRY. Circulating placental-type isoferritins have not been previously described in patients with liver disorders. Our findings indicate that elevation of serum ferritin in liver diseases is caused by different isoferritin components.
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PMID:Placental type isoferritins in chronic liver diseases. 359 58

Primary hemochromatosis is a genetic disorder rarely recognized in childhood; its long-term consequences include cirrhosis and liver cancer. We report a family with primary hemochromatosis affecting three generations, including a 7-year-old child and a 29-month-old child; these are the youngest children with primary hemochromatosis yet reported. The pathophysiology, genetics, and clinical findings of this disorder are reviewed. Serum ferritin and transferrin saturation are useful screening tests; definitive diagnosis, however, depends on determination of hepatic iron content. A plan for evaluating and treating affected patients is proposed. Physicians caring for children must learn to recognize this potentially treatable disorder.
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PMID:Primary hemochromatosis in childhood. 365 74


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