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)

In patients with cirrhosis, the etiocholanolone test showed a decrease in the bone marrow granulocyte reserve; in all the cases studied, the baseline counts of peripheral granulocytes were normla. The mechanisms leading to such a defect are explained.
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PMID:Defect of bone marrow granulocyte reserve in liver cirrhosis evaluated with etiocholanolone. 10 Oct 15

Chronic alcoholics who had been drinking heavily until admission for withdrawal from alcohol were studied to determine their level of granulocyte function, immunoglobulin concentration, and complement system activity. Although most had some mild derangement in results of liver function tests, serum albumin concentrations were normal, and there was no clinical evidence of malnutrition or cirrhosis. Granulocyte adherence was slightly depressed in two subjects (52.4% and 54.1%; normal, 76.0% +/- 12%), although mean adherence for the group was normal. Mean chemotaxis was significantly below normal (2,103 vs. 7,943 counts per min), and the impairment was related to a defect or inhibitor in the serum of patients. Phagocytic activity was less than half that of control subjects in two alcoholics, but mean values were not depressed. Bactericidal activity was normal in all. Serum concentrations of immunoglobulins and total hemolytic complement activity were above the normal range for the group. The general inhibition of chemotaxis or the occasional defects in other granulocyte functions may contribute to the difficulty that alcoholics have with infection.
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PMID:Granulocyte function and levels of immunoglobulins and complement in patients admitted for withdrawal from alcohol. 73 54

Opsonic glycoprotein, alpha 2-HS-glycoprotein concentration was studied in the serum of 753 patients with various hematological, malignant, immunological, metabolic, endocrine and liver diseases and 68 healthy controls. Decreased serum alpha 2-HS-glycoprotein levels were detected in patients with acute leukemias, chronic granulocyte and myelomonocyte leukemias, lymphomas, myelofibrosis, multiple myeloma, metastatizing solid tumors, systemic lupus erythematosus, rheumatoid arthritis, acute alcoholic hepatitis, fatty liver, chronic active hepatitis, liver cirrhosis, acute and chronic pancreatitis, and Crohn's disease. Elevated levels were measured in patients with B and NANB/C hepatitis. Further decreased levels were observed in some groups with secondary infections. Serum alpha 2-HS-glycoprotein levels are affected by many factors, influencing the synthesis and elimination of the protein. The detection of serum alpha 2-HS-glycoprotein concentration has no specific diagnostic value as a marker for tumors or other diseases, however, its determination can be useful for the assessment of a non-specific regulator of the host defence.
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PMID:[Diagnostic value of the determination of serum alpha2-HS-glycoprotein]. 140 55

The influence of pentoxifylline on normal and diseased neutrophil function has been studied in vitro. In high concentrations pentoxifylline stimulated human neutrophil chemotaxis toward both bacterial oligopeptides and complement components. Pentoxifylline was also shown in vitro to restore the normal chemotactic capacity of neutrophils from patients with known functional defects, i.e. myelodysplastic syndromes, lazy leucocyte syndrome, juvenile parodontitis, hyper-IgE-syndrome and liver cirrhosis. Pentoxifylline was also shown to strongly inhibit the release of primary and secondary granule release of granulocytes. Moreover, pentoxifylline inhibits both basal and stimulated neutrophil adhesion to both aortic and pulmonary artery calf endothelium. The mechanism whereby pentoxifylline exerts this action is not adequately understood. While our results partially imply interference of pentoxifylline with neutrophil cyclic AMP and/or prostaglandin metabolism, down-regulation of neutrophil functional antigen (e.g. CD11, CD18) expression seems to play a key role in the observed drug effects. Finally, these results indicate that pentoxifylline may be useful in the treatment of granulocyte mediated diseases and symptoms.
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PMID:In vitro modulation of normal and diseased human neutrophil function by pentoxifylline. 197 92

Excessive ethanol intake may affect the intestinal mucosa functionally and morphologically. The ethanol effect could partly be the result of inflammatory mechanisms, possibly reflected by an enhanced local granulocyte turnover. This study investigated habitual alcoholics by segmental perfusion of the jejunum and analysed the perfusion fluid content of granulocyte granule constituents. The mean jejunal secretion rate of myeloperoxidase (MPO), a neutrophil granule constituent, was 152 (26) (SE) ng/min/40 cm jejunal segment in the controls (n = 16). The MPO secretion rate in non-cirrhotic habitual alcoholics (n = 7) was on average 450 (103) ng/min and significantly increased compared with controls (p less than 0.001). In contrast alcoholics with cirrhosis (n = 6) had normal MPO secretion rate. The mean secretion rate of eosinophil cationic protein (ECP), an eosinophil granule constituent, was in the controls 77 (15) ng/min/40 cm jejunal segment. Corresponding values in non-cirrhotic and cirrhotic alcoholics were 141 (38) and 130 (93) ng/min, respectively (ns). The data suggest an enhanced neutrophil granulocyte turnover in the jejunum in alcoholics, possibly contributing to the ethanol induced affection of the small bowel. The lack of increased neutrophil activity in cirrhotic alcoholics may reflect a role of the liver for granulocyte activity.
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PMID:Neutrophil and eosinophil involvement of the small bowel affected by chronic alcoholism. 285 4

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

Twenty per cent of 60 patients with cirrhosis (55 alcoholic patients) had neutropenia (defined as neutrophil polymorphonuclear (NP) count under 2,000/mm3). The authors tried to define the mechanism of this neutropenia and compared it with the acute bone marrow cytotoxicity of alcohol. They found that bone marrow neutrophil colony growth was normal in 7 cases of cirrhosis compared to 7 controls (with and without cirrhotic serum incubation). On the other hand, the granulocyte response to hydrocortisone test was less marked than in controls. This result suggests involvement of the late maturation process of NP and delayed release from bone marrow.
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PMID:[Granulopoiesis in the alcoholic and cirrhotic patient. Exploration of neutropenia in cirrhosis using bone marrow cultures and a hydrocortisone test]. 402 8

Blood granulocyte-macrophage progenitor cells (CFU-GM) and myeloid differentiation were studied in 16 patients with hepatic cirrhosis by culturing blood mononuclear cells in semisolid and in liquid medium. The numbers of CFU-GM from normal and cirrhotic subjects were not significantly different, even when increased numbers of monocyte-macrophagic colonies and decreased numbers of granulocytic colonies were observed in cirrhotic patients. Significantly reduced granulocytic growth and increased monocyte-macrophagic cell growth were found in liquid culture of cirrhotic patients. These data seem to indicate that in hepatic cirrhosis, besides granulocyte sequestration within the spleen, there is a disorder of granulocytic versus monocyte-macrophagic differentiation.
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PMID:Blood granulocyte-macrophage progenitor cell concentrations and differentiation in vitro in patients with hepatic cirrhosis. 644 23

So as to assess the effects of lithium carbonate on peripheral leucocyte levels of hepatic cirrhosis patients, 10 cirrhotic patients were studied with less than 4,500 leukocytes per cubic ml and without contraindications for lithium salts that were administered for three weeks at a dose of 90 mg daily. At the end of each week total peripheral leukocytes, differential formula, platelet count and serum lithium concentration determinations were made. In the basal stage, total leukocyte average was 3,400 +/- 527 (X +/- DE) and granulocyte average was 2,090 +/- 341. After the first week of lithium treatment a significant increase was observed in total leukocyte and granulocyte levels whose averages at the end of the third week of treatment were 4,800 +/- 1,052 (p less than 0.01) and 3,694 +/- 1,003 (p less than 0.001) respectively. There was no correlation between the magnitude of leukocyte increase and serum lithium levels obtained that ranged from 0.28 and 1.32 mEq/l. Three patients showed transient gross tremor and two suffered hepatic coma. We can conclude that lithium carbonate increases peripheral leucocytes at the expense of neutrophilia in patients with secondary granulocytopenia and hypersplenism resulting in liver cirrhosis.
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PMID:Effects of lithium carbonate on leucocytes of hepatic cirrhosis patients. 679 6

Transient granulocytopenia and lymphopenia may occur in acute alcoholics without splenomegaly, cirrhosis, infection, and megaloblastic anemia due to folate deficiency. The bone marrow in granulocytopenic patients is frequently hypocellular with few mature granulocytes, and the functional marrow granulocyte reserve is reduced. These findings suggest a depressed granulopoietic activity in these patients. The mechanism by which alcohol suppresses granulopoiesis remains unclear. Direct toxicity of alcohol on granulopoietic stem cells and increased individual susceptibility to the toxic effect of alcohol may be important factors. Alcohol also causes functional impairment of granulocytes (adherence, motility, and chemotaxis), macrophages (motility and phagocytosis), and lymphocytes (blastogenic transformation and development of delayed dermal hypersensitivity reaction), probably by perturbation of the cell membrane resulting in an increased intracellular cyclic AMP level.
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PMID:Effects of alcohol on granulocytes and lymphocytes. 737 52


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