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)

To elucidate the mechanism of anemia and leukopenia in the patients with liver cirrhosis, we investigated hematopoietic progenitor cell contents in their bone marrow, and the effects of their sera and blood mononuclear cells on hematopoietic progenitors from normal subjects. While there was no significant difference in the number of marrow CFU-E and BFU-E between the patients with liver cirrhosis and normal subjects, the number of marrow CFU-C was significantly reduced in liver cirrhosis patients. Patients' sera suppressed in vitro colony formation of normal CFU-E, BFU-E, and CFU-C, and the degree of suppression was well correlated with severity of anemia or granulocytopenia. In vitro colony formation of normal hematopoietic progenitor cells was not affected by blood mononuclear cells from liver cirrhosis patients. These results indicate that the appearance of humoral inhibitor(s) of hematopoietic progenitors plays a role in the development of anemia and granulocytopenia in liver cirrhosis.
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PMID:A study on the mechanism of anemia and leukopenia in liver cirrhosis. 341 79

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

The figures obtained in simultaneous radioimmunological assays of serum folate and vitamin B12 concentrations and erythrocyte folate concentration in 74 patients are presented. All these patients had a regular daily intake of over 80 g ethyl alcohol and presented an increase in mean blood cell volume. Most of the patients were males hospitalised with liver disease and/or anaemia. All were given bone narrow needle aspirations and liver biopsies. 46% of the patients presented a reduction in erythrocyte folates but vitamin B12 deficiency was rarely encountered. Megaloblastic transformation of the bone narrow was present in 56% of the alcoholics with reduced erythrocyte folates and in 10% of those with normal folate concentration. No correlation was found between serum and erythrocyte folate concentration and degree of liver damage. Serum vitamin B12 levels were higher in patients with cirrhosis. Inadequate diet was frequently found in the alcoholics with reduced folate concentrations. Due to variations in patient selection it is difficult to compare these data with those of other series but they do seem to confirm the hypothesis that the macrocytosis in most "healthy" alcoholics reflects a direct toxic action of the alcohol on erythropoiesis. In contrast folate deficiency is found among "derelict" chronic alcoholics in whom the vitamin deficiency has often not yet produced megaloblastosis of the bone marrow.
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PMID:[Macrocytosis, megaloblastosis and folate status in chronic alcoholics]. 358 23

The records of 54 patients with documented cirrhosis who underwent colectomy between January 1970 and January 1984 were studied to assess the operative risk and to determine the preoperative predictive risk factors. In-hospital mortality was 24 percent (13 patients), and postoperative complications occurred in 48 percent (26 patients). The risk of surgical intervention was significantly increased if encephalopathy, ascites, anemia, or hypoalbuminemia was present before operation. A simple operative risk index involving the presence of encephalopathy and ascites and the levels of hemoglobin and albumin is proposed to help distinguish a low-risk subgroup in whom postoperative mortality was 12.8 percent from a high-risk subgroup in whom postoperative mortality was 53.3 percent.
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PMID:The surgical risk of colectomy in patients with cirrhosis. 359 74

To reassess the need for repeat liver biopsies in patients receiving long-term methotrexate therapy, we reviewed the results of 15 biopsies in 14 such patients seen from 1979 to 1984 at the Medical University of South Carolina. Significant changes in liver histology were found in seven patients. These findings did not correlate with biochemical abnormalities, presence of anemia or obesity, or age when methotrexate therapy was initiated. Four of the 15 biopsies (27%) showed grade III or IV histologic changes (fibrosis or cirrhosis), which led to discontinuance of treatment. The single most significant factor predisposing to toxicity appeared to be the duration of therapy, though the cumulative doses, no patient with grade III or IV histology had been treated for less than five years. Thus, surveillance liver biopsies at suitable intervals are advisable once the patient has been treated for five years or more. Conversely, liver biopsies within the first five years of treatment with methotrexate appear not to be necessary, though these results should be confirmed in a larger patient group.
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PMID:Hepatotoxicity after long-term methotrexate therapy. 370 18

Porphyria cutanea tarda (PCT) may be associated with various neoplasma. Two additional cases are reported here. In the first case, a 58-year old alcoholic man had been presenting for two years with clinical signs of PCT. The diagnosis was confirmed by porphyrin assays in the urine. He also had cirrhosis of the liver. During a routine fibroscopy in search of oesophageal varices, a gastric adenocarcinoma was discovered by chance. Following partial gastrectomy the skin lesions of PCT improved dramatically within a few weeks, leaving only moderate cutaneous fragility. Urinary porphyrin assays performed 18 and 40 months after gastrectomy gave normal results, although no specific treatment had been prescribed. The second case concerns a 67-year old man, also alcoholic, with clinical and biochemical PCT. For the previous 12 months he had received chemotherapy (Adriamycin, then BCNU combined with melphalan, vincristine and prednisone) for multiple IgA K myeloma. The myeloma was active when PCT was diagnosed with, in particular, chronic anaemia. Treatment with chloroquine improved the cutaneous signs of PCT but had no effect on urinary porphyrins after 5 months. Comments PCT has been reported to be associated with cancers. The best known of these cancers is primary carcinoma of the liver (4, 27, 32), but its frequency is diversely evaluated depending on the diagnostic methods (e. g. patient autopsied or not) and on the selection of patients (age, duration of the disease).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Porphyria cutanea tarda and neoplasms. Apropos of 2 cases]. 380 Feb 18

A 41-year-old woman died within a few hours one morning due to massive rectal hemorrhage. At autopsy, complete liver cirrhosis, signs of portal hypertension, liquid blood in the entire colon, and high-grade anemia were detected. The source of bleeding was a ruptured submucosal varix in the sigmoid colon, which was almost invisible even microscopically and had been caused by portal hypertension. In the vicinity, and somewhat further away from the rupture site, numerous, greatly dilated veins with wall sclerosis and intimal thickening, as well as paravascular iron deposits, were found as indications that severe hemorrhages had already occurred earlier. To detect the source of bleeding, meticulous inspection and dissection with hematoxylin and eosin, elastica van Gieson, and iron staining, were necessary.
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PMID:[Fatal hemorrhage from ruptured varicose veins of the sigmoid colon in liver cirrhosis]. 387 49

Acute and chronic alcohol intoxication may lead to various types of corpuscular hemolytic anemias, irrespective of other coexisting organ damage such as liver cirrhosis. It also suppresses hemopoiesis in the bone marrow, leading to hyporegenerative anemia and to a pathogenetically unclear red cell macrocytosis, which in turn represents a sensitive and valuable index for occult alcoholism. Alcohol also suppresses platelet production. Acute intoxication may, furthermore, lead to reversible thrombocytopenia due to platelet sequestration. Platelet function is affected by alcohol both in vitro and in vivo, the defect being similar to that provoked by aspirin. The impaired host defense in chronic alcoholism is not yet adequately explained. It appears to be based on depression of bone marrow granulocyte reserve, granulocyte mobilization and granulocyte function, and also on impressive functional abnormalities of the lympho-plasmocellular system. The clinical relevance of alcohol-mediated hematological changes has not yet been sufficiently defined. It is certainly underestimated.
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PMID:[Alcohol and the blood]. 391 82

Occupational mortality in women who died in England and Wales from 1970 to 1972 was analysed. Many of the associations found were consistent with those that have been described for men, with high mortality ratios for cirrhosis in barmaids and publicans, for suicide in the medical and allied professions, and for respiratory disease in textile workers. Parity is a determinant of patterns of disease in working women, and the relative excess of cancer of the breast, ovary, and uterine body in professional and clerical workers probably reflected the high proportion of nulliparous women in these groups. Other associations may have reflected true occupational hazards; one observation requiring further attention was the high proportional mortality ratio for anaemia in textile and clothing workers. The description of the occupational mortality among women in England and Wales is hampered by the incomplete recording of information about women's occupations at registration of death. As women now constitute 40% of the workforce, often have their own specific occupations, and possibly also have their own diseases related to specific occupations it is time for the registrar's guidelines on the recording of women's occupation--last reviewed at the beginning of this century--to be revised.
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PMID:Occupational mortality among women in England and Wales. 392 19

Thirteen patients with Wilson's disease were compared with seven cirrhotic and 13 normal controls to define better the haematological abnormalities in this condition. Hypersplenism (anaemia, leukopenia, thrombocytopenia, and reduced red cell survival) commonly occurred in patients with both Wilson's disease and cirrhosis. These abnormalities correlated with splenic enlargement. Despite reduced haematocrits, red cell mass was greater in these two groups than in normal controls. Plasma volume and the body haematocrit/peripheral haematocrit ratios were also greater in patients with Wilson's disease and cirrhosis. Increased splenic sequestration of (51)Cr-tagged red blood cells was not demonstrated in any subjects. The hypersplenism in patients with Wilson's disease is similar to that found in patients with cirrhosis from other causes.
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PMID:Hypersplenism in Wilson's disease. 502 27


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