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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five hundred ninety-three nonstress tests were performed on 41 obstetric patients, at gestational ages ranging from 20 to 40 weeks. Diagnoses included 10 cases of prematurity, six cases of diabetes mellitus, five cases of collagen-vascular disease, five cases of poor obstetric history, three cases of cardiac arrhythmia, and one case each of asthma, polyhydramnios, leukemia, nonimmune fetal hydrops; and eight volunteers were without high-risk factors. All neonates had a 5-minute Apgar score greater than 8; 29 neonates weighed greater than or equal to 2500 gm, 12 weighed less than 2500 gm, and four weighed less than 1500 gm. One neonate died of prematurity, and one was small for gestational age. There were no congenital anomalies. There was a significant difference in the number of reactive nonstress tests and nonreactive nonstress tests between the 20- to 24-week, 24- to 28-week, 28- to 32-week, and 32- to 36-week gestational age groups. The increased incidence of nonreactive nonstress tests at earlier gestational ages may have clinical implications.
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PMID:The relationship of the nonstress test to gestational age. 390 68

The use of 111Indium oxine as a platelet label for the performance of platelet life-span studies has been examined. Platelet life-span in normal subjects varied between 8 X 10 and 10 X 36 d. Patients with primary thrombocythaemia had clearly reduced platelet life-span whether or not they presented with vascular occlusion and this abnormality persisted after reduction of the platelet count to normal by busulphan therapy. Patients with similarly elevate platelet counts due to chronic granulocytic leukaemia or after splenectomy had platelet life-span values in the normal range. Plasma beta-TG levels could not be used to predict platelet life-span in these groups of patients. Measurement of platelet life-span using 111Indium labelled platelets is a useful technique in the examination of platelet function in occlusive vascular disease.
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PMID:Measurement of platelet life-span in normal subjects and patients with myeloproliferative disease with indium oxine labelled platelets. 624 Feb 80

Hemorrhage from brain tumor was confirmed clinically, surgically, or on autopsy in 94 of 1861 cases (5.1%) treated during the past 18 years: 49 of 311 pituitary adenomas (15.8%) and 45 of 1550 other brain tumors (2.9%). The higher incidence of hemorrhage from pituitary adenoma was statistically significant (p less than 0.001). In brain tumors other than pituitary adenoma, the incidence of hemorrhage was significantly higher in the patients under 14 years old (17 of the 322 cases, 5.3%) than in the patients over 15 years old (28 of the 1228 cases; 2.3%) (p less than 0.001). Nineteen patients showed no evidence of clinical symptoms related to bleeding. Twenty-six patients had a definite history of an acute episode that suggested sudden bleeding. In 11 of these, the apoplectic syndrome was the initial presenting symptoms. The incidence of hemorrhage was not statistically correlated with sex. The hemorrhage was intratumoral in 30 cases, intracerebral in 7, subarachnoid in 7, and subdural in 1. The tumors were supratentorial in 36 cases, pineal in 1, and infratentorial in 8. Primary and metastatic choriocarcinoma and primary embryonal carcinoma seemed to cause hemorrhage most frequently. The following precipitating factors were found in 7 of the 17 patients aged under 14: ventricular drainage in 2, ventriculoperitoneal shunt in 2, carotid angiography in 1, head injury in 1, and leukemia in 1. Seven of the 17 patients under 14 years old died of massive bleeding from the tumor. Unless there is evidence of vascular disease such as cerebral aneurysm, vascular malformation, or hypertensive cerebrovascular disease, intracranial hemorrhage should be suspected of being due to a brain tumor.
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PMID:Spontaneous intracranial hemorrhage caused by brain tumor: its incidence and clinical significance. 709 93

Rapidly accumulating evidence suggests that a proportion of patients with acquired immunodeficiency syndrome (AIDS) develop hypertensive pulmonary vascular disease reminiscent of primary pulmonary hypertension. As an initial step to explore the link between AIDS and hypertensive pulmonary vascular disease, the present study determined whether pulmonary hypertension is present in a well-characterized murine model of retrovirus-induced immunodeficiency. In agreement with previous reports, mice infected with the LP-BM5 murine leukemia virus developed polyclonal B and T cell activation followed by progressive and severe B and T cell immunodeficiency. At 12 wk postinfection, when persistent immunodeficiency was established, mice were anesthetized, and right ventricular systolic pressure was determined in open-chest, mechanically ventilated animals. Mean right ventricular systolic pressure was 14.7 +/- 1.3 mm Hg in control animals and was increased significantly to 22.5 +/- 3.2 mm Hg in virus-infected mice. Right ventricular hypertrophy was also present in infected mice as evidenced by a 27% increase in the ratio of right to left ventricular weights; there were no group-dependent differences in the left ventricular to total-body weight ratio. Morphometric evaluation indicated that medial thickness in muscularized pulmonary arteries, expressed as a percentage of the external diameter, was 9.6 +/- 0.4% in control lungs and increased to 14.4 +/- 0.5% in lungs from infected animals. Qualitative histopathologic analysis suggested increased perivascular collagen deposition in lungs from infected animals relative to control animals. Unlike AIDS patients with pulmonary hypertension, infected mice did not exhibit plexiform lesions or intimal fibrosis of the pulmonary arteries.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary hypertension in a murine model of the acquired immunodeficiency syndrome. 802 49

The strain and developmental parameters that control susceptibility to murine leukemia virus (MuLV)-induced intracerebral hemorrhages and infarction were studied using the endothelial cell tropic MuLV TR1.3. Inoculated animals displayed an absolute age dependence on the development of intracerebral vascular disease; however, other genetic determinants affected the timing and magnitude of susceptibility to neurologic disease. BALB/c mice were susceptible to neurologic disease only when inoculated prior to Day 4 postpartum. In contrast, Swiss/NIH and C3H/HeN mice consistently showed a less virulent phenotype and were only susceptible when infected prior to Day 3 postpartum. These studies demonstrate that susceptibility to TR1.3 murine leukemia virus-induced neurologic disease is regulated by age- and strain-dependent factors encoded within cerebral endothelial cells.
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PMID:Intracerebral hemorrhages and infarction induced by a murine leukemia virus is influenced by host determinants within endothelial cells. 805 64

In a population based register of stroke (n = 536) compiled in Perth, Western Australia during an 18 month period in 1989-90, 60 cases (11%) of primary intracerebral haemorrhage were identified among 56 persons (52% men). The mean age of these patients was 68 (range 23-93) and 46 (77%) events were first ever strokes. The crude annual incidence was 35 per 100,000, with a peak in the eighth decade, and a male predominance. Deep and lobar haemorrhages each accounted for almost one third of all cases. The clinical presentations included sudden coma (12%), headache (8%), seizures (8%), and pure sensory-motor stroke (3%). Primary intracerebral haemorrhage was the first presentation of leukaemia in two cases (both fatal) and it followed an alcoholic binge in four cases. 55% had a history of hypertension. 16 (27%) patients, half of whom had a history of hypertension, were taking antiplatelet agents, and one patient was taking warfarin. There were only two confirmed cases of amyloid angiopathy. The overall 28 day case fatality was 35%, but this varied from 100% for haemorrhages in the brainstem to 22% for those in the basal ganglionic or thalamic region. Other predictors of early death were intraventricular extension of blood, volume of haematoma, mass effect, and coma and severe paresis at onset. Although based on small numbers, these data confirm the heterogeneous nature of primary intracerebral haemorrhage, but they also suggest a different clinical spectrum of this type of stroke in the community compared with the experience of specialist neurological units.
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PMID:Spectrum of primary intracerebral haemorrhage in Perth, Western Australia, 1989-90: incidence and outcome. 805 17

Disseminated infection with the rapidly growing mycobacteria Mycobacterium chelonae and Mycobacterium fortuitum is uncommon. Only eight cases were diagnosed at Duke University Medical Center (Durham, NC) over the last 14 years. We identified 46 other cases by review of the medical literature since 1960. We categorized these 54 cases into three groups according to underlying disease and outcome. Group 1 comprised patients with no identified immune defect, a kidney transplant, collagen vascular disease, or chronic renal failure; these patients usually presented with skin involvement and responded well to antimicrobial therapy (survival rate, 90%). Group 2 comprised patients with cell-mediated immune deficiency, lymphoma, or leukemia; they presented with widespread, multiorgan involvement and severe illness. The survival rate in this group was only 10%. Patients in group 3 (who had other underlying diseases) had intermediately severe illnesses and intermediate responses to therapy. These groups provide the basis for an understanding of disseminated infection secondary to rapidly growing mycobacteria and of the profound effect that unresolved immunosuppression has on survival.
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PMID:Disseminated infection with rapidly growing mycobacteria. 851 48

Factors that predispose to infection in general, of course, may predispose to infection with anaerobes. Included in this category are diabetes mellitus, neutropenia, hypogammaglobulinaemia, malignancy, splenectomy, collagen vascular disease, cytotoxic drug therapy, corticosteroid therapy and other immunosuppression. However, even with these situations there may be certain, more specific, associations: anaerobic cholecystitis and anaerobic osteomyelitis in diabetics, neutropenic colitis, and the increased incidence of local anaerobic infections associated with carcinoma of the lung, colon and uterus. Conditions that lead to decreased redox potential more specifically predispose to infection with anaerobes. Included in this category are obstruction and stasis, tissue anoxia, tissue destruction, vascular insufficiency, prior aerobic infection, burns, foreign body implantation, and calcium salts in a wound (in association with fractures). Other specific clinical situations that predispose to anaerobic infections include leukaemia; oral, gastrointestinal, and female pelvic surgery; trauma at other sites; childbirth; aspiration pneumonia; human and animal bites; and therapy with agents with poor activity against anaerobes (e.g. aminoglycosides, quinolones). AIDS patients appear to be predisposed to severe periodontal disease and its complications.
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PMID:Host factors predisposing to anaerobic infections. 851 53

Congenital errors of folate metabolism can be related either to defective transport of folate through various cells or to defective intracellular utilization of folate due to some enzyme deficiencies. Defective transport of folate across the intestine and the blood-brain barrier was reported in the condition 'Congenital Malabsorption of Folate'. This disease is characterized by a severe megaloblastic anaemia of early appearance associated with mental retardation. Anaemia is folate-responsive, but neurological symptoms are only poorly improved because of the inability to maintain adequate levels of folate in the CSF. A familial defect of cellular uptake was described in a family with a high frequency of aplastic anaemia or leukaemia. An isolated defect in folate transport into CSF was identified in a patient suffering from a cerebellar syndrome and pyramidal tract dysfunction. Among enzyme deficiencies, some are well documented, others still putative. Methylenetetrahydrofolate reductase deficiency is the most common. The main clinical findings are neurological signs (mental retardation, seizures, rarely schizophrenic syndromes) or vascular disease, without any haematological abnormality. Low levels of folate in serum, red blood cells and CSF associated with homocystinuria are constant. Methionine synthase deficiency is characterized by a megaloblastic anaemia occurring early in life that is more or less folate-responsive and associated with mental retardation. Glutamate formiminotransferase-cyclodeaminase deficiency is responsible for massive excretion of formiminoglutamic acid but megaloblastic anaemia is not constant. The clinical findings are a more or less severe mental or physical retardation. Dihydrofolate reductase deficiency was reported in three children presenting with a megaloblastic anaemia a few days or weeks after birth, which responded to folinic acid. The possible relationship between congenital disorders such as neural tube defects or dihydropteridine reductase deficiency and disturbances of folate metabolism are discussed. Neurological symptoms present in most of these congenital disorders highlight the role of folate in the central nervous system.
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PMID:Congenital errors of folate metabolism. 853 63

A 61-year-old man without hypertension was admitted for unconsciousness. Brain CT showed multiple cerebral hemorrhage of the left frontal lobe and right occipital lobe. The hemoglobin was 7.0 g/dl, the platelet count 7,000, the white-cell count 7,600 with erythroblasts, and the fibrinogen 327 mg/dl. No disseminated intravascular coagulation was found. Bone marrow examination demonstrated 69.2% erythroblasts including abnormal types of nucleus, 12.8% myeloblasts, 12.8% neutrophils, 0.8% monocytes, 4% lymphocytes, and 0.4% reticulocytes. Chromosomal examination showed 7 of 20 bone marrow cells were variously abnormal. A diagnosis of erythroleukemia with major karyotype aberrations (MAKA) was made. The patient died 5 days after admission. Histologically, cerebral hemorrhagic lesions showed complete necrosis, but neither invasion of leukemic cells nor amyloid angiopathy. We suspected that the cause of cerebral hemorrhage was severe loss of platelets. This is a rare case of erythroleukemia found after multiple cerebral hemorrhage. As a cause of cerebral hemorrhage in an old man without hypertension, one should consider not only cerebral amyloid angiopathy but also leukemia.
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PMID:[A case of erythroleukemia found after multiple cerebral hemorrhage]. 868 93


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