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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship between platelet count and aggregability was serially evaluated after splenectomy in patients with normosplenism and hypersplenism, and the results were compared with those found in patients undergoing only upper abdominal surgery. The preoperative count and aggregability of platelets were significantly suppressed in patients with cirrhosis of the liver, idiopathic portal hypertension, and prehepatic portal obstruction. However, the platelet aggregability of these patients markedly increased in accordance with the platelet counts after splenectomy. In the patients with normal splenic function preoperatively, splenectomy caused a simultaneous increase in platelet count and aggregability. The platelet function was not always reflected by the count in the patients with idiopathic thrombocytopenic purpura. On the other hand, in the control patients undergoing only laparatomy the platelet count substantially increased two weeks after operation, but platelet aggregability did not differ from the preoperative value. The present results suggest that additional factors for thromboembolism such as hypotension, acidosis, or stagnant blood flow should be avoided during the peak period of reactive thrombocytosis after splenectomy, and that an appropriate use of anticoagulants or inhibitors of platelet aggregation is recommended if and when necessary.
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PMID:Platelet aggregability after splenectomy in patients with normosplenism and hypersplenism. 56 40

Platelet abnormalities associated with hepatobiliary diseases include increased (thrombocytosis) and decreased (thrombocytopenia) numbers of platelets as well as abnormalities in function (thrombocytopathy or thrombasthenia). Hepatic diseases that are accompanied by platelet abnormalities include hepatitis, cirrhosis, portal hypertension, and neoplastic disorders both benign and malignant. The objective of this work is to examine the platelet abnormalities that occur with a variety of hepatobiliary disorders. Thrombocytosis is seen as a reactive entity following splenectomy. Thrombocytopenia is associated with hypersplenism, dysproteinemias and liver disease related disseminated intravascular coagulation (DIC). Qualitative platelet abnormalities are found in hepatic failure, liver diseases associated with high or low levels of lipid, and with medications given for a variety of hepatocellular diseases. Clinically common and significant platelet abnormalities associated with liver disease are thrombocytopenia secondary to portal hypertension and the thrombasthenias following metabolic changes and/or therapeutic interventions of liver disease.
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PMID:Platelet abnormalities in hepatobiliary diseases. 218 3

We report the first detailed study of hepatic morphology in 28 biopsies from 16 Greenland Eskimo children with fatal familial cholestatic syndrome. The changes were categorized as early, intermediate and late. In the early stage, until 5 months of age, changes were restricted to zone 3, consisting of cholestasis and rosette formation without fibrosis. In the intermediate stage, from 5 to 14 months, cholestasis persisted and rosette formation increased, both with further extension into zone 2. Perisinusoidal fibrosis developed, first in zone 3 and later in zone 1. The late stage, from 17 to 60 months, showed a further increase in cholestasis and rosette formation, and fibrosis of zones 3 and 1 in nearly all biopsies. Portal to portal and portal to central fibrosis was evident with resulting cirrhosis in 2 of 7 patients. The morphological features can be summarized as pure cholestasis with prominent rosette formation followed by zone 3 fibrosis, zone 1 fibrosis, and, cirrhosis. Other characteristics are the virtual absence of inflammation and the lack of anatomical abnormalities such as paucity of bile ducts. The changes and their progression resemble those of Byler disease. Clinical and biochemical features are also largely similar, except for the presence of thrombocytosis in many of the Eskimo patients.
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PMID:Fatal familial cholestatic syndrome in Greenland Eskimo children. A histomorphological analysis of 16 cases. 250 28

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

Although full blood counts (FBC) are among the most commonly performed laboratory tests, the contribution of routine FBCs to the diagnosis of new problems is controversial. This study represents a unique linkage of a consultant haematology team, reviewing all abnormal blood counts, to an organization providing ambulatory health care to 350,000 patients. The objective was to establish the underlying clinical disorders responsible for all abnormal FBCs during a 2-month period, and to estimate the impact of the haematology team on the diagnostic work-up and management of newly identified problems. 572 (2.55%) of the 22,454 FBCs were abnormal. Of these, 357 showed microcytosis, caused by iron deficiency (58%), thalassaemia minor (35%), inflammation (6%) or chronic renal failure (1%). The most common causes of normocytic anaemia (25 patients) were disseminated malignancy and acute blood loss; of macrocytosis (27 patients), chronic liver disease and cancer; of erythrocytosis (16 patients), chronic hypoxia; of thrombocytopaenia (48 patients), chronic liver disease and ITP; of thrombocytosis (47 patients), iron deficiency and inflammation; of leukopaenia or pancytopaenia (20 patients), cirrhosis and disseminated malignancy; and of leukocytosis (26 patients), chronic leukaemias in the elderly and infection in children. Major new haematological abnormalities were encountered in 0.24% of all blood counts, representing about one new diagnosis per day. Routine blood counts do contribute to the health care of a population. Screening for haematological disease through a central clinical laboratory covering a large high-risk ambulatory population offers a cost-effective way of searching for serious clinical problems, alerting the primary physicians of their existence, and offering advice in continued evaluation and problem management.
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PMID:The haematologist as watchdog of community health by full blood count. 779 88

Platelet glycocalicin (GC) is the extramembranous portion of GPIb alpha that can be rapidly cleaved by enzymes such as calpain, plasmin, trypsin, elastase, etc. Quantitative cleavage will ultimately result in an acquired Bernard-Soulier-like bleeding disorder, and circulating GC may act as a potential inhibitor of platelet adhesion. We have developed and standardized a new enzyme-linked immunosorbent assay (ELISA), which uses two monoclonal antibodies (mAbs), both of which bind to the amino-terminal 45-kD fragment of GC and inhibit platelet-von Willebrand interactions and the streptavidin-biotin system. First, the methodology was evaluated and standardized with special emphasis on the anticoagulant and the inhibitors (EDTA, prostaglandin E1 [PGE1], aprotinin, N-ethyl-maleimide), the mode of high-speed centrifugation (to avoid platelet microparticles), and the standards used (purified GPIb and GC). This assay was then used to analyze the GC levels of healthy subjects (2.04 +/- 0.46 micrograms/mL) and of patients with selected diseases. The results of patients with aplastic anemia and thrombocytosis confirmed that GC levels are clearly dependent on the platelet count, which was the basis for the introduction of the GC index, the standardization of GC for a platelet count of 250 x 10(9)/L. The GC index discriminates reliably patients with active immune thrombocytopenic purpura from those in remission. GC levels are elevated in patients on hemodialysis (3.62 +/- 0.75 micrograms/mL, P < .001). The high GC index (6.93 +/- 4.21, P < .001) in cirrhosis patients suggests an increased platelet turnover and/or abnormal proteolysis. In contrast to other groups, we have not found that recombinant tissue plasminogen activator (rtPA) treatment of patients with myocardial infarction increases GC levels. However, concentrations are elevated in leukemia and the highest levels found are approximately 40 micrograms/mL. These studies suggest that GC is a useful platelet marker in certain diseases, which directly reflects platelet damage and possibly platelet dysfunction.
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PMID:Glycocalicin: a new assay--the normal plasma levels and its potential usefulness in selected diseases. 829 32

The effect of the deleted form of hepatocyte growth factor (dHGF) on thrombopoiesis was studied in rats. When normal rats were injected with dHGF (0.5 mg/kg i.v. twice a day), the number of platelets increased to about 1.5-fold the initial level. In addition, the treatment with dHGF (0.5 mg/kg i.v. twice daily) significantly increased the number of platelets in rats with liver cirrhosis induced by carbon tetrachloride and phenobarbital. When dHGF was given to rats at a dose of 0.05 or 0.5 mg/kg from the beginning of the induction of dimethylnitrosamine liver cirrhosis to day 28, dHGF dose-dependently ameliorated thrombocytopenia and completely prevented it at a dose of 0.5 mg/kg. These results indicate that dHGF may be applicable to the treatment of thrombocytopenia associated with liver cirrhosis.
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PMID:Deleted form of hepatocyte growth factor (dHGF) increases the number of platelets in rats with liver cirrhosis. 929 89

To clarify the role of thrombopoietin (c-Mpl ligand, TPO) in 'hypersplenic' thrombocytopenia, we used an enzyme-linked immunosorbent assay to examine changes in serum TPO levels accompanied with splenectomy in 6 patients with liver cirrhosis, 4 patients with gastric cancer, and 2 patients with lymphoid malignancies. We also measured serum levels of other thrombopoietic cytokines such as interleukin-6 (IL-6) and erythropoietin. Platelet counts reached a maximum at day 14 after splenectomy in all subjects. In patients with liver cirrhosis, a lower elevation of platelet counts was observed compared with that in patients with gastric cancer. Serum TPO levels gradually elevated after splenectomy and reached a maximum 3.5 days after splenectomy in noncirrhotic patients, whereas peak serum TPO levels were delayed until day 7 in the cirrhosis group. IL-6 and erythropoietin showed similar kinetics between cirrhotic and noncirrhotic patients. These findings suggest that transient thrombocytosis after splenectomy may be associated with an alteration in the site of TPO catabolism by platelets from spleen to the blood and that deterioration of TPO production may play a role in thrombocytopenia in liver cirrhosis.
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PMID:Changes in serum thrombopoietin levels after splenectomy. 985 90

Thrombopoietin (TPO) deficiency has been proposed as an important etiologic factor for thrombocytopenia in advanced-stage liver disease. To clarify the contributions of platelet production, platelet consumption, coagulation activation, and splenic sequestration to thrombocytopenia in liver disease, we studied TPO serum levels and markers of platelet production, platelet activation, and coagulation activation before and 14 days after orthotopic liver transplantation (OLT) in 18 patients with advanced liver cirrhosis. Thrombocytopenia before transplantation occurred with low-normal serum levels of TPO, normal levels of platelet and coagulation activation markers, and no increase in bone marrow production of platelets. TPO serum levels increased significantly on the first day after OLT, preceding the increase of reticulated platelets by 3 days and peripheral platelets by 5 days. Normalization of the peripheral platelet count occurred in most patients within 14 days of OLT, irrespective of the change in spleen size assessed by computed tomography volumetry. Normalization of platelet counts was not hampered by a certain degree of platelet activation observed during the steepest increase in the peripheral platelet count. Bone marrow production of platelets increased significantly within 2 weeks of transplantation. Low TPO serum levels with low platelet counts and without platelet consumption suggests low TPO production in end-stage liver disease. The rapid increase in TPO serum levels after transplantation induces an increase in the bone marrow production of platelets. Decreased TPO production in the cirrhotic liver is an important etiologic factor for thrombocytopenia in liver disease that is rapidly reversed by transplantation.
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PMID:Thrombopoietin induces rapid resolution of thrombocytopenia after orthotopic liver transplantation through increased platelet production. 1064 88

We present the case of a 62 years male subjects, known with liver cirrhosis diagnosed in 2000 during a laparoscopy. The subject presented with important atypical abdominal pain, leucocytosis, thrombocytosis, small ascites; pneumatosis and hydro-aeric images of small intestine at abdominal X Ray, thickened bowel wall at CT-scan. Laparoscopy revealed mesenteric venous thrombosis, intestinal infarction and the standard surgical treatment was enterectomy. Mesenteric thrombosis may rarely occur in liver cirrhosis due to portal hypertension. This rare but severe complication is usually difficult to diagnose..
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PMID:[Abdominal pain in liver cirrhosis patient--an unusual case]. 1568 18


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