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)

Total and unsaturated folate binding capacity (TFBC, UFBC) have been measured in sera of selective groups of patients to study the role of cell turnover, cell necrosis and the effect of pregnancy in determining their concentrations in blood. The mean value of TFBC in 35 normal sera was 151 +/- (SD) 53 pg/ml with a saturation of 88%. The TFBC was raised in chronic granulocytic leukemia (CGL), in acute hepatitis, in cirrhosis, and in pregnancy (third trimester). The normal mean value of TFBC was found in chronic lymphocytic leukemia (CLL) and inthe first trimester of pregnancy. The mean UFBC in the normal sera was 19 +/- 18 pg/ml. In all the pathological conditions studied the mean UFBC was significantly greater than normal and it was particularly high in CGL (85 +/- 78 pg/ml).
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PMID:Serum folate binding capacity in leukemias, liver diseases and pregnancy. 10

Serum vitamin B12 and vitamin B12 binding proteins (transcobalamins, TCS) were determined in patients with malaria, amoebic liver abscess, carcinoma of the liver, infectious hepatitis, cirrhosis and chronic myelocytic leukemia (CML) as well as in 60 blood donor subjects. Serum vitamin B12 in patients with infectious hepatitis, cirrhosis and CML were higher than that of the normal subjects. The values of unsaturated vitamin B12 binding capacity (UBBC) in patients with carcinoma of the liver, infectious hepatitis, cirrhosis were lower while that of patients with CML were higher than that of the normal subjects. A markedly increased TCI and decreased TCII was observed in patients with CML while these changes was much less in patients with other liver diseases. The difference was possibly due to a flooding of vitamin B12 from damaged liver cells into the circulation and the decreased synthesis of transcobalamins in patients with liver diseases while the increased granulocytes, the source of TCI, was much increased in patients with CML.
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PMID:Vitamin B12 and vitamin B12 binding proteins in liver diseases. 60 23

Portal hypertension with varices developed in 18/675 patients with chronic myeloid leukaemia (CML) in a randomized trial comparing busulphan with busulphan and thioguanine. All 18 had received the drug combination and none busulphan alone (P less than 0.0001). Ascites was also seen significantly more often in the combination arm (P less than 0.05). These results strongly suggest that the addition of thioguanine was responsible for the development of portal hypertension. The histological features were predominantly those of non-cirrhotic portal hypertension--either idiopathic portal hypertension with minimal morphological abnormalities, nodular regenerative hyperplasia or in two cases leukaemic infiltration only was noted. Cirrhosis was present in 3/16 cases studied. Both treatment groups developed abnormal liver function tests during the chronic phase, but particularly with progression of the disease. During chronic phase abnormalities were significantly more frequent in those receiving busulphan and thioguanine-alkaline phosphatase (P less than 0.02), transaminases (P less than 0.04), bilirubin (P less than 0.05), multiple abnormalities (P less than 0.01). The development of portal hypertension was often associated with abnormalities of these tests; however, lack of specificity precludes their use as a predictor of subsequent clinical problems. Thioguanine confers no survival advantage in this disease. In view of its hepatotoxicity it should not be used routinely for maintenance of control in chronic phase CML.
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PMID:Thioguanine used in maintenance therapy of chronic myeloid leukaemia causes non-cirrhotic portal hypertension. Results from MRC CML. II. Trial comparing busulphan with busulphan and thioguanine. 195 75

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

Splenomegaly was evaluated by a 0.1 T MR system using multi-echo SE image. (TR = 1500 msec., TE = 40, 80 and 120 msec.) Calculated measurement of T2 relaxation time was obtained. Material consists of 32 cases including 14 liver cirrhosis, 3 chronic myelocytic leukemia, 1 malignant lymphoma and 14 normals. 1) T2 value of normal spleen measured 113.7 +/- 5.68 msec. 2) Splenomegaly due to congestion had the prolonged T2 value of 122.6 +/- 10.25 msec. 3) T2 value of splenomegaly with malignant cell infiltration such as leukemia and lymphoma were shorter than normal spleen. Good histological correlation was obtained in MRI findings of splenomegaly due to congestion and malignant cell infiltration.
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PMID:[MRI of splenomegaly]. 223 8

We present 3 cases of juvenile chronic granulocytic leukemia in which there are histological changes in the liver of both portal and bridging fibrosis, with fibrosis around central veins, the latter being confirmed by quantitative measurement. We stress the histological differences from cirrhosis, nodular regenerative hyperplasia, and veno-occlusive disease and describe the evidence which favors an etiology from the leukemic infiltration rather than chemotherapy.
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PMID:Hepatic fibrosis in juvenile chronic granulocytic leukemia: an unusual finding in three cases. 234 56

Of 501 patients with chronic myeloproliferative diseases (c-MPD) 18 developed thrombosis of major abdominal vessels including 6 with hepatic vein thrombosis (Budd-Chiari syndrome). The complication was seen in 14 of 140 (10%) patients with polycythemia vera (PV), 3 of 23 (13%) patients with essential thrombocythemia (ET), 1 of 106 (1%) patients with idiopathic myelofibrosis (IMF), and none of 232 patients with chronic myelogenous leukemia (CML). Leading symptoms and signs were abdominal pain, progressive splenomegaly, widening abdominal girth, ascites, venous collaterals, and nausea and vomiting. The diagnostic modalities with highest specificity were angiography and explorative laparotomy. A causal relationship between the thrombotic event and hematocrit, thrombocyte count, or hemostatic abnormalities at the time of diagnosis could not be established. Detailed laboratory tests of platelet function and coagulation and fibrinolytic parameters of 5 surviving patients did not show any specific defect. Despite medical and surgical intervention, 39% of the patients died within 2 months after diagnosis of the thrombosis. The majority of the survivors developed further complications like liver cirrhosis with portal hypertension and esophageal varices or the short bowel syndrome after extensive bowel resection for mesenterial infarction.
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PMID:Budd-Chiari syndrome and thrombosis of other abdominal vessels in the chronic myeloproliferative diseases. 279 52

In animal models of cancer, an elevation of T1 and T2 in uninvolved tissues and in the blood of tumor bearing animals has been termed "the systemic effect." This study reports T1 values in sera of human patients from Genoa, Italy, with several types of cancer and non-cancerous diseases. T1 values were significantly elevated over normal controls (1628 +/- 113 ms) in colorectal cancers (1725 +/- 149 ms) and stomach cancers (1817 +/- 219 ms). However a systemic effect was not demonstrated in acute myeloid leukemia, chronic lymphatic leukemia, chronic myeloid leukemia, or plasma cell myeloma, or in pancreatic and lung cancers. Noncancerous states of cirrhosis, chronic hepatitis, and monoclonal gammapathies did not show a T1 elevation. In general, T1 values of sera correlated with protein content of the sera; however, a disproportionate contribution of gamma-globulin protein on water proton relaxation times was observed in several cases.
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PMID:The systemic effect of cancers on human sera proton NMR relaxation times. 608 32

Three patients who developed symptomatic, autoimmune-mediated thyroid dysfunction during treatment with interferon-alpha (IFN-alpha) for chronic active hepatitis C with liver cirrhosis, age-related macular degeneration with foveal involvement, and chronic myelogenous leukemia, respectively, are described. The first two patients developed autoimmune hypothyroidism that required thyroxine replacement, and the third developed autoimmune thyroiditis with transient thyrotoxicosis. The clinical manifestations were protean, and required a high index of suspicion for diagnosis, the failure of which led to significant morbidity. A literature review revealed that the mean incidence of IFN-alpha induced thyroid dysfunction was 6%. Spontaneous resolution occurred in more than half with discontinuation of IFN-alpha treatment. Hypothyroidism was induced more frequently than hyperthyroidism. At least one positive thyroid autoantibody titer was found in 17% of patients receiving IFN-alpha. Risk factors for developing thyroid dysfunction with IFN-alpha treatment were female sex, underlying malignancy or hepatitis C, higher doses of IFN-alpha for longer durations, combination immunotherapy (especially with interleukin-2), and the presence of thyroid autoantibodies prior to or during treatment.
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PMID:Interferon-alpha induced thyroid dysfunction: three clinical presentations and a review of the literature. 945 33

Congenital generalized lipodystrophy (CGL, Berardinelli-Seip syndrome) is a rare autosomal recessive disorder with a clinical presentation of paucity of adipose tissue, muscular hypertrophy, organomegaly, and insulin-resistant diabetes. A 4-month-old Taiwanese female infant had hepatosplenomegaly and low body weight gain despite a voracious appetite. Hypermetabolism, hyperhidrosis, loss of subcutaneous fat, muscular hypertrophy, acanthosis nigricans, hypertrichosis, and marked hypertriglyceridemia were also noted. Liver histology revealed fatty change and portal-to-portal bridging fibrosis. Clinical features, serum biochemistry, and liver histology were compatible with the diagnosis of CGL. She was given a special diet characterized by calorie restriction and partial substitution of long-chain triglycerides with medium-chain triglycerides. The serum triglyceride concentration subsequently decreased. This present case suggests that extensive fatty infiltration and subsequent cirrhosis of the liver may be the earliest complication of CGL.
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PMID:Congenital generalized lipodystrophy in a 4-month-old infant. 1169 79


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