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)

A 65 years old, female patient with acquired aplastic anemia secondary to frequent exposure to hair dye. While on treatment with anabolic steroids hormone became jaundiced and developed hepatomegaly eight months later. During laparotomy the liver was enlarged, hard, with multiple whitish nodules on its surgace but was otherwise normal. Liver biopsy showed hepatocellular carcinoma, there were not cirrhosis niether hemochromatosis. A review of the related literature was done and discussed on the experimental and clinical evidences that suggested that androgens may play same role on the etiology of liver cancer.
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PMID:[Androgenic therapy and hepatocellular carcinoma. Report of a case]. 22 17

Within 5 to 14 days of onset of grade 3 or 4 coma, liver biopsies were obtained in 14 of 15 consecutive patients who recovered from fulminant hepatitis. In 9 patients, follow-up biopsy was obtained 6 to 60 months after acute hepatitis and autopsy was performed in 2 patients who died in 4 months from complications of hepatitis (aplastic anemia) or of corticosteroid therapy (sepsis). During fulminant illness the biopsy findings were: multilobular necrosis in 4 patients, confluent (bridging) necrosis in 9, and only portal inflammation in 1. The duration or the grade of coma did not correlate with the severity of necrosis on the biopsy. Follow-up biopsy showed development of chronic (active) hepatitis in 3 of 9 patients (with cirrhosis in one of these). Chronic liver disease was not found in the two autopsies. If fulminant hepatitis is the result of vigorous cell-mediated immune attack on hepatocytes, then this process cannot always eradicate chronic hepatitis B surface antigenemia, nor can it always prevent the development of chronic (active) hepatitis or cirrhosis.
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PMID:The liver during and after fulminant hepatitis. 89 67

A high negative correlation (coefficient similar to 0.9) between increased 59Fe absorption from a diagnostic 0.56 mg 59Fe2+ dose and the depletion of available storage iron was observed in menstruating and pregnant women, fullterm and premature infants, blood donors, patients with infections, inflammations, tumors, hepatic cirrhosis, gastric surgery, increased urogenital or gastrointestinal blood loss. The increased diagnostic 59Fe2+ absorption is a reliable and sensitive indicator of at least depleted iron stores or prelatent iron deficiency as caused by iron malnutrition or maldigestion, increased iron requirement in pregnancy, infancy, urogenital or gastrointestinal blood loss. Although the messenger system which signalyzes the depletion of iron stores to the iron absorbing enterocytes of the duodenal and jejunal mucosa is not yet known available storage iron seems to control intestinal iron absorption under normal and the great majority o pathological condition in humans. Anemia per se or high erythropoietin levels in blood do not influence iron absorption since patients with even severe erythroblastic hypoplasia, aplastic anemia and megaloblastic anemia due to vitamin B12 deficiency absorb iron according to their iron stores. An only mild hyperplasia of the erythropoietic system in the bone marrow does also not effect iron absorption which was still under the control of available storage iron in patients with hereditary spherocytosis, nonspherocytic congenital hemolytic anemia due to glucose-6-phosphate dehydrogenase deficiency, acquired hemolytic anemia and vitamin B12 deficiency induced megaloblastic anemia..
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PMID:Intestinal iron absorption under the influence of available storage iron and erythroblastic hyperplasia. Comparative studies in children with hereditary spherocytosis, nonspherocytic enzymopenic hemolytic anemia, acquired hemolytic anemia, vitamin B12 deficiency induced megaloblastic anemia, erythroblastic hypoplasia and aplastic anemia. 113 Jan 21

Ninety-five cases of typhoid infection seen at autopsy at the University College Hospital, Ibadan, over a 10-year period were reviewed. They constituted 2.7% of 3,556 autopsies performed during this period. Apart from the associated conditions such as sickle cell disease, aplastic anaemia, schistosomiasis, liver cirrhosis and pregnancy which may lower the patients' immunity, a delay in seeking medical care, misdiagnoses, inappropriate therapy and a high complication rate were some of the factors that would appear to contribute to mortality. Therefore, in order to reduce death associated with these factors, it is essential to improve the health education of the people stressing the importance of personal communal hygiene and prompt hospital attendance from the onset of illness. There must also be improved clinical awareness of the disease to ensure early diagnosis and treatment. These are of great importance as the disease is treatable.
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PMID:Factors that may contribute to death from typhoid infection among Nigerians. 139 Mar 70

The case survey of drug-induced hematologic disorders in Shikoku District (Ehime Prefecture) disclosed 21 patients. Cases were 12 rheumatoid arthritis patients, 2 brain tumor, one epilepsy, 2 liver cirrhosis, one neuralgia, one arthralgia, one hyperthyroidism, and one IBL-like T-lymphoma. Causative drugs for aplastic anemia were Metalcaptase, Shiosol, Voltaren and Emeside. Drug-induced aplastic anemia was so severe that 4 out of 5 patients had died of bone marrow dysfunction. Neutropenia was caused by drugs as Rimatil, Cefobit, Sepatren, Mercazole, Sulpyrin, Aleviatin, Cefamedin and Metalcaptase. The real causes of these drug-induced hematologic disorders have not been clear. Remarkably high incidence among rheumatoid arthritis patients is suggestive several reasons as unique reactivity associated with HLA, suppression on hematologic stem cells by abnormal metabolites, and immunologic dysfunction commonly seen in collagen diseases. Further studies of more accurate incidence of drug-induced hematologic disorders are needed in investigating real causes of unhappy side-effects.
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PMID:[Drug-induced hematologic disorders in Shikoku district]. 192 Aug 31

The rate of alloimmunization to red blood cell antigens in 1502 multitransfused patients, mainly with blood disorders, was analyzed in a retrospective study. The overall incidence of alloantibodies was 5.7%. Three groups of patients were identified with different potential for antibody production. The lowest probability (1.8%) of alloimmunization was found in the group of patients with lymphoproliferative syndromes, acute myeloid leukaemia and burn disease. The highest probability (33.4%) of immune response to red blood cell antigens was found in patients with AIHA, liver cirrhosis and myelodysplastic syndrome. In the group of patients with chronic myeloid leukaemia, pancytopenias, anaemias of various origin and aplastic anaemia the probability of alloimmunization ranged from 5.7% to 13.6%. A possible role of genetic-factors and immune competence status in post-transfusion alloimmunization is briefly discussed.
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PMID:Analysis of immune response to red blood cell antigens in multitransfused patients with different diseases. 207 55

Urokinase type plasminogen activator (u-PA) was purified from three different chest fluids obtained from patients with liver cirrhosis and pleuritis, aplastic anemia and pneumonia, and lung tumor, and the relationship between molecular weight and plasminogen activator (PA) activity was examined by zymography. The molecular weights of u-PAs from the chest fluids were 200 Kd, 150-180 Kd, 95 Kd, 55 Kd, 44 Kd, 33 Kd and 14 Kd, and PA activity was observed at molecular weights of 95 Kd, 55 Kd and 33 Kd. Fibrin binding of u-PA was observed at molecular weights of 55 Kd and 33 Kd.
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PMID:Properties of urokinase type-plasminogen activator found in chest fluid. 210 19

We tested an in vitro system simulating bleeding time reported by Kratzer et al. Primary hemostasis was studied perfusing an artificial vessel with citrated blood under a constant pressure of 40 mmHg, measuring the blood volume perfused (bleeding volume) and the time until blood flow stopped (bleeding time). The artificial vessel consists of a glass capillary simulating arteriole and a filter covered with collagen type I to provide a surface for the adhesion of platelets. The bleeding volume (mean +/- SD microliters) was 317.7 +/- 93.8 in controls (n = 19), 487.3 +/- 242.1 in idiopathic thrombocytopenic purpura (n = 9), 666.8 +/- 224.1 in aplastic anemia and paroxysmal nocturnal hemoglobinuria (n = 4), greater than 820 in von Willebrand's disease (n = 3), 231.0 +/- 74.5 in hemophilia A (n = 3), 499.0 +/- 269.4 in liver cirrhosis (n = 6), and 457.7 +/- 229.0 in myeloproliferative disorders (n = 11). When citrated blood was applied to this system after incubation with monoclonal antibodies (MoAb) to von Willebrand factor or platelet membrane glycoprotein Ib (GPIb), bleeding volume was significantly increased while no effects were observed after incubation with MoAb to GPIIb/IIIa, factor VIII: CAg and factor XIIIa. These data suggest that in vitro model of primary hemostasis could be used for not only diagnosing bleeding disorders although 'time' is not reliable, but also investigating the mechanisms of hemostasis.
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PMID:[Bleeding time and volume in vitro by THROMBOSTAT]. 231 3

Iron deposits in the human labial minor salivary glands were examined in a series of 195 postmortem subjects. Iron deposits (hemosiderin granules) were found in 7 subjects (3.6%), and the major types of illness in these cases were liver cirrhosis with or without hepatoma, aplastic anemia and acute myelogenous leukemia. Three out of 7 subjects had a history of blood transfusion. Considerable quantities of hemosiderin granules were deposited within the cytoplasm of the acinar and ductal epithelial cells, and hemosiderin-laden cells were scattered in the interstitial connective tissue.
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PMID:Iron deposits in the human labial minor salivary glands: a postmortem study. 273 86

During 1972-1974, 200,000 Swedish infants were screened for alpha 1-antitrypsin deficiency. Of 127 PiZ (Protease inhibitor) children followed from infancy to 12 years of age, four PiZ children with neonatal liver disease have died; two of liver cirrhosis, one was found to have liver cirrhosis at autopsy, having died of aplastic anemia and the fourth died in an accident. Liver microscopy showed a mild increase of periportal fibrous tissue. Another PiZ child died of anaphylactic shock. At 12 years of age, none of the PiZ children have clinical symptoms of liver disease. No PiZ-, PiSZ, PiS- or PiFZ child has had any clinical symptom of liver disease. One PiSZ child died of sudden infant death syndrome. Laboratory analyses from birth through 12 years of age have shown increased S-Bilirubin levels in 11% of the PiZ infants, which normalized within the first half year of life. S-GT was abnormal in about half of the infants, but had normalized when checked at 8 and 12 years of age in all but 6-3% of the PiZ children. The percentage of abnormal S-ALAT test results have decreased from 73% during the first year of life, to about 15% at the age of 12. The range of the abnormal levels also decreased considerably. Abnormal S-GT or S-ALAT levels were found in about 20% of the PiSZ infants, the proportion decreasing to 2% at the age of 12.
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PMID:The natural history of liver disease in alpha 1-antitrypsin deficient children. 290 8


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