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)

The causes of death of 79 patients with ankylosing spondylitis (AS) diagnosed between 1952 and 1959 were investigated. The basic cause of death was a cardiovascular disease in 35.4% of the patients, AS in 29.1%, violent death in 10.1%, malignancy in 8.9%, gastrointestinal diseases in 6.3%, pulmonary tuberculosis in 2.5%, urogenital diseases in 2.5%, respiratory diseases in 3.8% and diabetes mellitus in 1.3%. Only one patient had a lymphoma and another patient chronic lymphatic leukaemia despite the X-ray therapy that almost every patient received. The immediate cause of death was uraemia caused by renal amyloidosis in 18% of the cases. In addition, uraemia from renal amyloidosis was part of the basic cause of death or a contributory factor in 3.8%. Thus, uraemia caused by renal amyloidosis in one way or another affected the cause of death in 21.5% of the cases. This figure is considerably higher than those given in earlier works.
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PMID:Cause of death in 79 patients with ankylosing spondylitis. 745 21

The present case-control study was conducted in an effort to determine if work in the chemical industry is related to excesses of certain hematopoietic and lymphoid neoplasms. Cases who died from non-Hodgkin's lymphoma, multiple myeloma, and leukemia were matched by race, gender, age, year of death, and county of residence to controls who died from cardiovascular disease. A total of 618 (309 matched pairs) white male residents of Kanawha County, WV, aged 23-96, who had died between 1965 and 1990 were identified. Conditional logistic regression was conducted and yielded an association between chemical industry work and death due to non-Hodgkin's lymphoma, multiple myeloma, and lymphoid leukemia among subjects who died at age < 65. These results are consistent with the findings of previous studies linking work in chemical manufacturing to hematopoietic and lymphoid neoplasms, and indicate that the excesses may be related to the occupational exposures in men who died at younger ages.
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PMID:A case-control study of hematopoietic and lymphoid neoplasms: the role of work in the chemical industry. 940 35

We studied fifteen patients older than 80 years of age with acute myelogenous leukemia (AML) treated between 1984 and 1996. Among 15 cases of AML including 7 de novo cases and 8 from myelodysplastic syndrome (MDS) or hypoplastic leukemia, 14 patients had complications, including cardiovascular disease, diabetes mellitus or other malignancies. Although patients with de novo AML showed high peripheral WBC counts and higher cellularity of bone marrow than those from MDS or hypoplastic leukemia, it was difficult in some cases to distinguish these types of AML from hematological findings. Of the 6 AML cases, three had entered complete remission (CR) by a standard dose of combination chemotherapy (BHAC-DMP). One CR patient has had CR for more than 9 years now with good QOL. Among the 3 patients treated by low-dose Ara-C, one attained CR but only for a short period. Four other patients received BRM, such as G-CSF or Ubenimex, and 2 patients died without chemotherapy. Since AML at more than 80 years of age is a highly heterogenous disease, it would be reasonable to give antileukemic agents according to the individual patient's condition.
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PMID:[Treatment of acute myelogenous leukemia in patients more than 80 years old]. 923 61

Contraception selection poses special challenges to women with pre-existing medical problems and clinicians often lack the knowledge to counsel these women. The IUD represents an excellent option for many US women with medical problems. Because IUDs have no direct systemic effects other than increasing circulating immunoglobulins and possibly copper ions, they are unlikely to affect a woman's underlying disease process or to interact with medications used in disease treatment. Currently available IUDs may be appropriate for women with cardiovascular disease, diabetes mellitus with vascular disease, hematologic disorders, neurologic conditions, and psychiatric disorders. Other candidates for IUD use include women with a history of breast cancer or other hormone-sensitive cancers, active liver disease, hypertriglyceridemia, a sensitivity to hormonal contraception, and smokers over 40 years old. IUDs are contraindicated in women with diseases that increase their vulnerability to infection (e.g., AIDS, leukemia, and intravenous drug abuse), diseases or medications that produce profuse uterine bleeding, and conditions that distort the uterine cavity. Given the deleterious impact of unintended pregnancy on the clinical course of many diseases, information on contraception for women with pre-existing medical conditions should be more broadly disseminated among clinicians.
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PMID:Intrauterine device practice guidelines: medical conditions. 980 94

The majority of newly diagnosed patients are expected to survive Hodgkin's disease because of effective therapies established during past 30 years. Long-term observations from large populations of treated patients have disclosed a variety of late effects of the disease and its therapy have contributed morbidity and excess mortality to Hodgkin's disease survivors. Secondary cancers have continued to accrue, and the risk relative to the general population has increased to 6.4 (95% confidence intervals: 5.5 to 7.3) in updated experience at Stanford University. Risks are significantly elevated for leukemia (primarily after chemotherapy regimens containing alkylating agents); non-Hodgkin's lymphoma; and tumors of the lung, breast, soft tissues, bone, stomach, pancreas, salivary gland, thyroid, and cutaneous melanoma. Early cardiovascular disease has also been observed and numerically exceeds second cancers as a cause of death in patients with early stage Hodgkin's disease (49 v 47 cases). Pulmonary dysfunction, thyroid dysfunction, infertility, psychosocial changes, gastrointestinal problems, soft-tissue changes, alterations in immunity, and risks for infection have also affected some treated patients. As these problems have been recognized, treatment approaches have been modified over the last 10 to 15 years, and early data suggest a decrease in some treatment sequellae.
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PMID:Long-Term Complications of Treatment and Causes of Mortality After Hodgkin's Disease. 1071 80

Hyperhomocysteinemia, a risk factor for cardiovascular disease, is caused by nutritional and/or genetic disruptions in homocysteine metabolism. The most common genetic cause of hyperhomocysteinemia is the 677C-->T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene. This variant, with mild enzymatic deficiency, is associated with an increased risk for neural tube defects and pregnancy complications and with a decreased risk for colon cancer and leukemia. Although many studies have reported that this variant is also a risk factor for vascular disease, this area of investigation is still controversial. Severe MTHFR deficiency results in homocystinuria, an inborn error of metabolism with neurological and vascular complications. To investigate the in vivo pathogenetic mechanisms of MTHFR deficiency, we generated mice with a knockout of MTHFR: Plasma total homocysteine levels in heterozygous and homozygous knockout mice are 1.6- and 10-fold higher than those in wild-type littermates, respectively. Both heterozygous and homozygous knockouts have either significantly decreased S-adenosylmethionine levels or significantly increased S-adenosylhomocysteine levels, or both, with global DNA hypomethylation. The heterozygous knockout mice appear normal, whereas the homozygotes are smaller and show developmental retardation with cerebellar pathology. Abnormal lipid deposition in the proximal portion of the aorta was observed in older heterozygotes and homozygotes, alluding to an atherogenic effect of hyperhomocysteinemia in these mice.
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PMID:Mice deficient in methylenetetrahydrofolate reductase exhibit hyperhomocysteinemia and decreased methylation capacity, with neuropathology and aortic lipid deposition. 1118 67

Gingerols, the active components of ginger (the rhizome of Zingiber officinale, Roscoe), represent a potential new class of platelet activation inhibitors. In this study, we examined the ability of a series of synthetic gingerols and related phenylalkanol analogues (G1-G7) to inhibit human platelet activation, compared to aspirin, by measuring their effects on arachidonic acid (AA)-induced platelet serotonin release and aggregation in vitro. The IC(50) for inhibition of AA-induced (at EC(50)=0.75 mM) serotonin release by aspirin was 23.4+/-3.6 microM. Gingerols and related analogues (G1-G7) inhibited the AA-induced platelet release reaction in a similar dose range as aspirin, with IC(50) values between 45.3 and 82.6 microM. G1-G7 were also effective inhibitors of AA-induced human platelet aggregation. Maximum inhibitory (IC(max)) values of 10.5+/-3.9 and 10.4+/-3.2 microM for G3 and G4, respectively, were approximately 2-fold greater than aspirin (IC(max)=6.0+/-1.0 microM). The remaining gingerols and related analogues maximally inhibited AA-induced platelet aggregation at approximately 20-25 microM. The mechanism underlying inhibition of the AA-induced platelet release reaction and aggregation by G1-G7 may be via an effect on cyclooxygenase (COX) activity in platelets because representative gingerols and related analogues (G3-G6) potently inhibited COX activity in rat basophilic leukemia (RBL-2H3) cells. These results provide a basis for the design of more potent synthetic gingerol analogues, with similar potencies to aspirin, as platelet activation inhibitors with potential value in cardiovascular disease.
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PMID:Gingerols and related analogues inhibit arachidonic acid-induced human platelet serotonin release and aggregation. 1155 71

Exposures to extremely low-frequency electric and magnetic fields (EMF) emanating from the generation, transmission, and use of electricity are a ubiquitous part of modern life. Concern about potential adverse health effects was initially brought to prominence by an epidemiologic report two decades ago from Denver on childhood cancer. We reviewed the now voluminous epidemiologic literature on EMF and risks of chronic disease and conclude the following: a) The quality of epidemiologic studies on this topic has improved over time and several of the recent studies on childhood leukemia and on cancer associated with occupational exposure are close to the limit of what can realistically be achieved in terms of size of study and methodological rigor. b) Exposure assessment is a particular difficulty of EMF epidemiology, in several respects: i) The exposure is imperceptible, ubiquitous, has multiple sources, and can vary greatly over time and short distances. ii) The exposure period of relevance is before the date at which measurements can realistically be obtained and of unknown duration and induction period. iii) The appropriate exposure metric is not known and there are no biological data from which to impute it. c) In the absence of experimental evidence and given the methodological uncertainties in the epidemiologic literature, there is no chronic disease for which an etiological relation to EMF can be regarded as established. d) There has been a large body of high quality data for childhood cancer, and also for adult leukemia and brain tumor in relation to occupational exposure. Among all the outcomes evaluated in epidemiologic studies of EMF, childhood leukemia in relation to postnatal exposures above 0.4 microT is the one for which there is most evidence of an association. The relative risk has been estimated at 2.0 (95% confidence limit: 1.27-3.13) in a large pooled analysis. This is unlikely to be due to chance but, may be, in part, due to bias. This is difficult to interpret in the absence of a known mechanism or reproducible experimental support. In the large pooled analysis only 0.8% of all children were exposed above 0.4 microT. Further studies need to be designed to test specific hypotheses such as aspects of selection bias or exposure. On the basis of epidemiologic findings, evidence shows an association of amyotrophic lateral sclerosis with occupational EMF exposure although confounding is a potential explanation. Breast cancer, cardiovascular disease, and suicide and depression remain unresolved.
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PMID:Review of the epidemiologic literature on EMF and Health. 1174 9

Recent advances enable one to apply numerical techniques to anatomically-correct human models to compute current densities and electric fields in tissue due to exposure to electric fields, magnetic fields, or contact currents. These methods have proved to be informative in estimating exceedance of basic restrictions prescribed by exposure guideline organizations. To date, the analyses have been conducted with a resolution on the order of millimeters. However, these techniques have future roles to play at higher levels of resolution at those sites in target tissues suspected of transducing local electric fields into biological responses. Two specific cases in which high resolution "microdosimetry" would yield value involve (a) residential settings and childhood leukemia and (b) worker exposure and cardiovascular disease. Recent research suggests that residential contact currents on the order of microamperes can produce biologically significant dose (expressed as the local electric field) to the bone marrow of a child. Microdosimetry would focus on pluripotent progenitor cells resident in the marrow compartment, as well as anatomic features that distinguish a child's from an adult's marrow. Laboratory and epidemiologic research has suggested that magnetic field exposure may affect heart rate variability, a measure reflective of autonomic nervous system control of cardiac activity. Given the physical attributes of the central nervous system and the sites that could serve as substrates for field interactions, future microdosimetry addressing heart rate variability effects may be well-advised to focus on the electrically excitable dendritic arborizations of neurons. In both cases, microdosimetry will help shed light on primary interactions in tissue.
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PMID:Candidate sites of action for microdosimetry associated with exposure to extremely-low-frequency magnetic fields, electric fields and contact currents. 1219 52

A new method for assessing both current and historical occupational exposures to magnetic fields has been developed and used in health studies involving a cohort of electricity generation and transmission workers in England and Wales. The exposure values are derived by calculation from engineering and operational data about the power stations rather than from measurements. They are provided for each of 11 job categories for each year of operation of each power station represented in the cohort. The engineering data are used to determine the average magnetic fields in specified areas of work within the power station and then applied to information about the time spent in these areas by each of the job categories. The operational data are used to adjust the exposures for each year according to the power station output for the year. Earlier methods used measurements or the advice of panels of experts to provide exposure scores for a number of job categories across all power stations and years. Such methods were not able to distinguish exposures from different power facilities or during the different years of their operation. Measurement surveys at 10 power stations of the magnetic fields in the work areas gave confidence that the calculations were realistic. Exposure measurements on 215 workers at three power stations were compared in job groups with the exposures predicted by the method. The Pearson correlation coefficient was 0.86 and the slope and intercept of the line of best fit were 0.87 and 0.07 microT respectively. The method gives a good prediction of measured exposure and is being used for studies of occupational exposure to magnetic fields and leukaemia, and of cardiovascular disease, and a reanalysis of brain cancer.
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PMID:A method for assessing occupational exposure to power-frequency magnetic fields for electricity generation and transmission workers. 1458 20


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