Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Vibrio parahemolyticus is a halophilic marine vibrio commonly associated with outbreaks of acute gastroenteritis which also sometimes causes serious wound infection. It is an uncommon cause of septicemia. A few reports suggest that patients with chronic liver disease and leukemia are more susceptible. A case of liver cirrhosis with septicemia caused by this organism is discussed. The patient's condition rapidly deteriorated, and he died 12 hours after admission.
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PMID:Septicemia caused by Vibrio parahemolyticus: a case report. 829 34

The mortality pattern among 999 Danish patients who had been subjected to angiography of the carotid artery with the alpha-ray emitting X-ray contrast media Thorotrast during the period 1935-47 was assessed by record linkage with the National Death Registry through 1989. Standardized mortality ratios (SMR) were calculated relative to the general population. The overall SMR was increased by 18 times during the first 3 years after Thorotrast injection. This rate reflects the often serious, underlying neurological conditions for which angiography was performed, however, mortality was increased by 3-4 fold even for the follow up period after the first 3 years. The increase in mortality was evident for all categories of cause of death, the SMR being 11.1 (95% confidence interval (CI) 7.1-16.4) for cirrhosis of the liver, 4.7 (4.1-5.3) for cancer, 1.6 (1.3-1.9) for cardiac disease, 3.3 (2.6-4.2) for cerebrovascular diseases, 3.9 (3.3-4.5) for other natural causes, and 4.4 (3.4-5.6) for violent causes (including suicides). The SMR was generally related positively to young age at injection, to time since injection, and to the amount injected. The excess mortality can be explained only partially by underlying neurological conditions and by diseases known to be induced by Thorotrast (cirrhosis and cancer of the liver, leukaemia and other haematological diseases), and it is suggested that unspecific effects induced by the alpha-radiation of Thorotrast may have contributed.
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PMID:Pattern of mortality among Danish thorotrast patients. 832 49

A cancer-associated, high-molecular-weight glycoprotein antigen (6B3.Ag) recognized by monoclonal antibody 6B3 was purified from culture medium of human large cell lung carcinoma cell line (HLC-2) and characterized biochemically and immunochemically. The 6B3.Ag was purified more than 1,200-fold with a yield of 30% by salting out, precipitation by acidification at pH 4.5, and chromatographies on Sepharose 4B and concanavalin A-Sepharose. The molecular weight of 6B3.Ag is approximately 1,000,000 and the molecule is a homodecamer of 94,000 subunits. The 6B3.Ag is a glycoprotein containing 22.9% sugars, consisting of both N- and O-glycoside chains. The N-terminal 19 amino acids were determined and only 4 out of 19 amino acid residues were different from those of an antigen, L3, secreted by lung carcinoma cell line Calu-1. The serum level of 6B3.Ag was determined in normal adults as well as patients with various diseases by enzyme-linked immunosorbent assay. The mean serum level of 6B3.Ag was 3.1 micrograms/ml, ranging from 1.6 to 6.2 micrograms/ml in 131 healthy adults. When the cut-off value was set at 6.2 micrograms/ml, the incidence of positive values in the sera was elevated not only in malignant diseases such as hepatoma (73%) and leukemia (62%), but also in benign diseases such as chronic hepatitis (42%) and liver cirrhosis (63%). While the incidence of positive values was elevated in advanced liver diseases, namely, chronic hepatitis, liver cirrhosis and hepatoma, the cancer specificity of 6B3.Ag did not appear to be high.
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PMID:Detailed characterization of a high-molecular-weight glycoprotein secreted by lung cancer cells. 840 67

The behavior of plasma von Willebrand factor (vWF) in patients with acute leukemia (n = 5), decompensated cirrhosis (n = 10), and acute pancreatitis (n = 5) was investigated to evaluate whether the systemic proteolytic states associated with these diseases had affected the structure and function of the molecule. vWF antigen and, to a lesser degree, ristocetin cofactor activity in patient plasma were high. Multimeric analysis of plasma vWF revealed loss of high molecular weight multimers. The subunit composition and proteolytic pattern of vWF immunopurified from patient plasmas and reduced were studied by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis followed by transblotting and probing with monoclonal antibodies that distinguish cleavages caused by plasmin from those caused by other proteases. There was marked reduction of the relative concentration of the native vWF subunit of 225 Kd in all patient groups, indicating heightened cleavage of the protein. The concentrations of 189- and 140-Kd vWF fragments, normally present in plasma, were increased in cirrhosis and pancreatitis but not in leukemia. Novel fragments, ranging in size from less than 225 to approximately 120 Kd were present in leukemia and cirrhosis, including plasmin-generated fragments of 176 and 145 Kd. These data indicate that in clinical conditions in which there is heightened proteolysis vWF is degraded in vivo by plasmin and other proteases. Degraded vWF may be less effective than native vWF in supporting primary hemostasis, thereby being a cofactor in the multifactorial bleeding diathesis accompanying systemic proteolytic states.
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PMID:Degradation of von Willebrand factor in patients with acquired clinical conditions in which there is heightened proteolysis. 842 64

To investigate the pathophysiological role of thrombopoietin (TPO) in thrombopoiesis, we measured its serum levels in 15 healthy individuals, 84 patients with various hematological diseases and 2 patients with liver cirrhosis using an enzyme immunoassay procedure. The TPO level was 0.84 +/- 0.40 f mol/ml in normal individuals. TPO levels were considerably elevated in patients with myelosuppression after intensification chemotherapy of acute leukemia in complete remission (postchemotherapy group; n = 18; 18.46 +/- 9.70 f mol/ml). When the data of normal individuals and the postchemotherapy group were combined, TPO levels were inversely correlated with the platelet count in this combined group. We compared these data of normal individuals and the postchemotherapy group with various hematological disease states. In aplastic anemia (n = 13; 16.03 +/- 9.44 f mol/ml), acute lymphoblastic leukemia (n = 5; 10.36 +/- 5.57 f mol/ml), malignant lymphoma (n = 6; 2.79 +/- 2.27 f mol/ml), multiple myeloma (n = 3; 3.34 +/- 0.20 f mol/ml) and chronic lymphocytic leukemia (n = 2; 1.71 +/- 3.91 f mol/ml), the relationship of serum TPO levels and platelet counts was almost the same as in the combined group with normal individuals and the postchemotherapy group. However, the TPO levels were slightly higher in myeloproliferative disorders (n = 12; 1.99 +/- 1.47 f mol/ml) and lower in acute myelogenous leukemia (n = 8; 2.27 +/- 1.25 f mol/ml), hypoplastic leukemia (n = 3; 2.76 +/- 2.23 f mol/ml), myelodysplastic syndrome (n = 2; 0.42 +/- 0.60 f mol/ml), liver cirrhosis (n = 2; 1.50 +/- 0.92 f mol/ml) and idiopathic thrombocytopenic purpura (n = 12; 2.08 +/- 1.41 f mol/ml), when compared to the regression line for the combined group with normal individuals and postchemotherapy group. These findings suggest that TPO might play an important role in regulation of the platelet count in normal and pathological conditions.
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PMID:Serum thrombopoietin level in various hematological diseases. 888 96

It has been suggested that organic solvent exposure may contribute to an increased risk of blood disorders, neurological, liver and renal disease, and cancer. A meta-analysis has been performed of 55 published mortality studies which involved solvent exposure and provided standardised mortality ratios (SMR) or relative risk (RR). The combined results showed the overall SMR to be 86.7 (95% confidence interval [Cl] = 83.7-89.9), while that for all sites of cancer was 92.3 (Cl = 87.5-97.4). Risk of death from leukaemia was increased (SMR = 112.2, Cl = 101.6-146.9) as was that from cancer of liver and biliary passages (SMR = 119.7, Cl = 104.4-137.2), even though the risk of death from cirrhosis was reduced (SMR = 81.5, Cl = 68.1-97.4). No excess risk of death from other diseases has been found. The favourable mortality might be from a "healthy worker effect', but the increase in death from liver cancer in the absence of excess deaths from cirrhosis is biologically plausible and justifies further investigation. The increase in mortality from leukaemia is likely to have been associated with exposure to benzene.
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PMID:A meta-analysis of mortality among workers exposed to organic solvents. 891 47

An acute transient swelling of the parotid glands is recorded after general anaesthesia in orthopaedic surgery. The first differential diagnosis is bacterial parotitis; other causes of gland enlargement are viral infections, lymphoma, leukemia, sarcoidosis, Sjogren's syndrome, malnutrition cirrhosis, vomiting, and poor oral hygiene. Excluding the above mentioned conditions, the most probably factors involved in our case are drugs used for anaesthesia, congestion of the venous drainage of the gland because of parasympathetic stimula during tracheal intubation and head positioning during surgery.
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PMID:[Transitory swelling of a parotid gland following general anesthesia. Description of a case]. 891 36

Results from a prospective mortality surveillance of 3803 refinery and petrochemical workers at a Shell Oil Company facility in Louisiana are presented. This report includes employees who worked more than 6 months before January 1, 1994 and pensioners who were alive as of January 1, 1973. Vital status was ascertained through 1993. Regardless of the comparison population used to calculate expected numbers (United States, Louisiana, or the surrounding tri-parish area), significantly fewer deaths were observed for all causes combined, all malignant neoplasms, heart disease, nonmalignant respiratory disease, and cirrhosis of the liver among male employees after 10 or more years' latency. With the United States as comparison, the all causes combined standardized mortality ratio (SMR) was 0.72 (95% confidence interval [CI] = 0.65 to 0.79), and the SMR for all cancer was 0.75 (95% CI = 0.61 to 0.92). The brain cancer rate for this group was nonsignificantly increased, with five observed deaths and three expected deaths, whereas mortality from leukemia was consistently lower than expected. The overall favorable mortality experienced by employees at this refinery and chemical plant is probably a result of a combination of factors, such as the healthy worker effect, relatively low risks related to the workplace, and the beneficial effects of continuing employment.
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PMID:A mortality study of oil refinery and petrochemical employees. 917 90

Cigarette smoking has been clearly and unambiguously identified as a direct cause of cancers of the oral cavity, oesophagus, stomach, pancreas, larynx, lung, bladder, kidney and leukaemia, especially acute myeloid leukaemia. Additionally, cigarette smoking is a direct cause of ischaemic heart disease (the commonest cause of death in western countries), respiratory heart disease, aortic aneurysm, chronic obstructive lung disease, stroke, pneumonia and cirrhosis and cancer of the liver. Cigarette smoking can kill in 24 different ways and, although smoking protects against several fatal and non-fatal conditions, the adverse effect of smoking on health is largely negative. In developed countries as a whole, tobacco is responsible for 24% of all male deaths and 7% of all female deaths: these figures rise to over 40% in men in some countries of central and eastern Europe and to 17% in women in the United States. The average loss of life of smokers is 8 years. Among United Kingdom doctors followed for 40 years, overall death rates in middle age were about three times higher among doctors who smoked cigarettes as among doctors who had never smoked regularly. About half of all regular cigarette smokers will eventually be killed by their habit. The important information is that it is never too late to stop smoking: among United Kingdom doctors who stopped smoking, even in middle age, there was a substantial improvement in life expectancy. World-wide, smoking is killing three million people each year and this figure is increasing. In most countries the worst is yet to come, since by the time the young smokers of today reach middle or old age there will be about 10 million deaths/year from tobacco. Approximately 500 million individuals alive today can expect to be killed by tobacco, 250 million of these deaths will occur in middle age. Tobacco is already the biggest cause of adult death in developed countries. Over the next few decades tobacco could well become the biggest cause of adult death in the world. For men in developed countries, the full effects of smoking can already be seen. Tobacco now causes one-third of all male deaths in middle age (plus one fifth in old age). Tobacco is a cause of about half of all male cancer deaths in middle age (plus one-third in old age). Of those who start smoking in their teenage years and keep on smoking, about half will be killed by tobacco. Half of these deaths will be in middle age (35-69) and each will lose an average of 20-25 years of non-smoker life expectancy. In non-smokers in many countries, cancer mortality is decreasing slowly and total mortality rapidly. The war against cancer is being won slowly: the effects of cigarette smoking are holding back this victory. Lung cancer now kills more women in the United States each year than breast cancer. For women in developed countries, the peak of the tobacco epidemic has not yet arrived. Tobacco now causes almost one-third of all deaths in women in middle age in the United States. Although it has only 5% of the world's female population, the United States has 50% of the world's deaths from smoking in women. Tobacco smoking is a major cause of premature death. Throughout Europe, in 1990 tobacco smoking caused three quarters of a million deaths in middle age (between 35 and 69). In the Member States of the European Union in 1990 there were over one quarter of a million deaths in middle age directly caused by tobacco smoking: there were 219700 in men and 31900 in women. There were many more deaths caused by tobacco at older ages. In countries of central and eastern Europe, including the former USSR, there were 441200 deaths in middle age in men and 42100 deaths in women. There is a need for urgent action to help contain this important and unnecessary loss of life. In formulating Recommendations, the European Cancer Experts Consensus Committee recognised that Tobacco Control depends on various parts of society and not only on the individual.
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PMID:Cancer, cigarette smoking and premature death in Europe: a review including the Recommendations of European Cancer Experts Consensus Meeting, Helsinki, October 1996. 919 26


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