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)

Two cases, one of leukemia and one of a trophoblastic testicular teratoma, are described in which hypoglycemia occurred as a terminal event. The rarity of this association with these types of malignancy, together with possible mechanism, is discussed in a brief review of the literature.
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PMID:Fatal hypoglycemia after cytotoxic chemotherapy: a report of two cases and a review of the literature. 38 6

Two patients are described with asymptomatic low blood glucose and excessive in vitro consumption of glucose by leukocytes before separation of the serum for assay. This may be a more common problem than is appreciated and need not be associated with leukemia or extreme leukocytosis. The circumstances that allow this avoidable type of artifactual hypoglycemia may also produce factitious euglycemia during evaluation of suspected diabetes mellitus.
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PMID:Leukocytosis and artifactual hypoglycemia. 57 9

Growth hormone (GH) secretion was studied in 15 children at various times after treatment for acute lymphatic leukaemia. Impaired GH responses both to hypoglycaemia and to Bovril were found in 4 children. 13 of the children had been given prophylactic cranial irradiation of either 2500 rads in 10 fractions or 2400 rads in 20 fractions. The reduction in GH responses in those given the former dose was highly significant compared with the reduction in those given the latter dose. However, other differences between the two groups included the length of time since cranial irradiation and the chemotherapy used. The main cause of the GH deficiency is not yet clear, but we conclude that it may occur in children treated successfully for acute lymphatic leukaemia.
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PMID:Growth hormone deficiency after treatment of acute leukaemia in children. 106 58

Leukaemia and its associated therapy result in pathophysiological peculiarities relevant to anaesthesia. Leukaemic patients suffer from anaemia, coagulation disorders, and the consequences of immunosuppression. In addition, some patients show infiltrations of the oropharynx, potentially resulting in difficult intubation and/or pharyngeal haemorrhage. Mediastinal masses can induce complete airway obstruction during general anaesthesia. Patients with a white blood cell count (WBC) greater than 100,000/mm3 (hyperleukocytosis) can suffer from the leukostasis syndrome with acute respiratory failure as well as cerebral vascular occlusions and bleeding due to increased blood viscosity and disturbed microvascular perfusion. Since this syndrome may be triggered by surgery, the WBC should be reduced prior to general anaesthesia in patients with hyperleukocytosis. To avoid development of the leukostasis syndrome, transfusion of packed red cells should be restricted in these patients. Hyperleukocytosis can simulate in-vitro hypoxaemia due to the excessive oxygen consumption of the mass of leukaemic blood cells during routine blood gas analysis. Therapy of leukaemia can lead to the tumor-lysis syndrome with hyperuricaemia, hyperphosphataemia, hyperkalaemia, hypocalcaemia, and hypoglycaemia, and may induce acute renal failure. Since drug interactions have only been evaluated for the combination of two or three drugs, interactions of cytotoxic agents with anaesthetics can hardly be predicted because of the large number of drugs simultaneously administered to leukaemic patients. The heart and lungs are target organs for the acute or chronic side effects of cytotoxic drugs, resulting in non-cardiogenic pulmonary oedema (e.g., cytosine-arabinoside), lung fibrosis (e.g., bleomycin), or arrhythmias and cardiac failure (e.g., adriamycin). The severity of these side effects depends on pre-existing organ disease and only in part on drug dosage. Only HLA- and CMV-compatible blood components should be administered to leukaemic patients. Hyperleukocytosis and the first days of cytotoxic treatment represent relative contraindications to general anaesthesia.
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PMID:[Pathophysiologic and anesthesiologic characteristics of patients with leukemia]. 152 54

Growth hormone was given to 13 children (nine boys, four girls) with acute leukaemia who had undergone treatment with cyclophosphamide and total body irradiation before bone marrow transplantation. Mean age at total body irradiation and bone marrow transplantation was 9.0 years (range 3.7-15.8). Endocrinological investigation was carried out at a mean of 2.0 years (range 0.4-4.0) after bone marrow transplantation. Peak serum growth hormone responses to hypoglycaemia were less than 10.0 micrograms/l (less than 20.0 mU/l) in 10, 10.5 micrograms/l (21.0 mU/l) in one, greater than 16.0 micrograms/l (greater than 32.0 mU/l) in two patients. Mean age of the patients at the start of growth hormone treatment was 12.2 years (range 5.8-18.2). The mean time between total body irradiation and bone marrow transplantation and the start of growth hormone treatment was 3.2 years (range, 1.1-5.0). Height velocity SD score (SD) increased from a mean pretreatment value of -1.27 (0.65) to + 0.22 (0.81) in the first year, +0.16 (1.11) in the second year, and +0.42 (0.71) in the third year of treatment. Height SD score (SD) changed only slightly from -1.52 (0.42) to -1.50 (0.47) in the first year, to -1.50 (0.46) in the second year, and -1.74 (0.92) in the third year. Measurement of segmental proportions showed no significant increase in subischial leg length from -0.87 (0.67) to -0.63 (0.65) in the first year, to -0.58 (0.70) in the second year, and -0.80 (1.14) in the third year of treatment. Our data indicate that children who have undergone total body irradiation and bone marrow transplantation respond to treatment with growth hormone in either of two dose regimens, with an increase in height velocity that is adequate to restore a normal growth rate but not to 'catch up', and that total body irradiation impairs not only spinal but also leg growth, possibly by a direct effect of irradiation on the epiphyses and soft tissues.
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PMID:Growth hormone treatment of growth failure secondary to total body irradiation and bone marrow transplantation. 205 88

To focus attention on the problem of infant mortality in Lebanon, data were compiled on infant mortality from 1978 to 1986 at the American University of Beirut Medical Center. Causes of death are analyzed for 602 males and 398 females. 54.9% deaths occurred at 1 month of age and 77.4% died within the 1st year. Autopsies were performed on .7%. 37.7% of all neonatal deaths were due to neonatal diseases such as hyaline membrane disease, asphyxia neonatorum, immaturity, necrotizing enterocolitis, hemorrhage, hemolysis, meconium aspiration, and kernicterus. Better prenatal care would reduce this group, or the administration of corticosteroids to the mother 24-48 hours prior to delivery, as well as rapid resuscitation at birth and prevention of the 5 curses: hypoxemia, hypoglycemia, hypothermia, hypotension, and acidosis. Although unavailable in Lebanon, administration of surfactants through an endotracheal tube would also help. Infections constitute 25.1% of deaths; many are preventable through adequate public health measures and strict personal hygiene, i.e., diseases such as sepsis, pneumonia, meningitis, gastroenteritis, hepatitis, encephalitis, and 1-2 cases of the following: diphtheria, measles, peritonitis, tetanus, tuberculosis, cytomegalis inclusion, herpes, parathyphoid, pertussis, poliomyelitis, and shigellosis. Congenital diseases were 21.6%. In utero diagnosis could prevent some diseases and in utero treatment is possible for hydrocephalus and hydronephrosis. Screening programs postnatally could lead to treatment. 5.9% were malignancies such as leukemia, lymphoma, brain tumors, histocytosis, Wilm's tumor, Ewing sarcoma, and Hodgkin's disease. Early diagnosis is critical if mortality is to be reduced in this group, but medical advances are still needed. 2.9% are miscellaneous diseases such as poisoning, rheumatic diseases, marasmus, Reye's syndrome, nephrosis, rickets, and epilepsy. Most of these diseases are preventable, except for rheumatic inflammation of the heart. Recommended necessary steps to reduce infant mortality are: prenatal care, diagnosis and screening, intrauterine surgery; resuscitation and intensive care centers with modern equipment and trained personnel; national vaccination and screening programs; adequate public health measures and hygiene; parental education; and well-equipped hospitals to serve all regardless of income level.
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PMID:Pediatric mortality: an avoidable tragedy. 251 28

A total of 37 children (24 male, 13 female) who had been treated for leukaemia with chemotherapy and 24 Gy cranial irradiation, and who were disease free for at least 18 months, were commenced on somatrem at a mean of 7.6 years (range, 4.8-12.1 years) after leukaemia diagnosis because of growth rate below the 25th centile for bone age. Peak GH response to provocation (exercise, arginine, insulin hypoglycaemia) was less than 20 milliunits/litre in 27 children (deficient group) and 20 milliunits/litre or more in 10 children (non-deficient group). The mean height SD decrease from diagnosis of leukaemia to commencement of somatrem was 1.98, 86% of the children decreasing by more than 1 SD. Those who were tall for age at leukaemia diagnosis and females were more severely affected. Mean (+/- SD) height velocity increased on somatrem from 2.7 +/- 1.1 to 6.6 +/- 2.2 cm/year during the first 6 months (n = 25), and to 6.0 +/- 1.7 cm/year during the first 12 months (n = 19). No difference in growth response was seen between the sexes or between the deficient and non-deficient groups. Catch-up growth occurred for the first 6 months only. It is concluded that children with a low growth rate after treatment of leukaemia should be considered for GH therapy irrespective of the results of GH provocative tests.
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PMID:Growth and growth hormone therapy of children treated for leukaemia. 319 30

Seventeen children (11 M, 6 F) with acute leukaemia and myeloproliferative disorders were investigated for growth and endocrine dysfunction. All had undergone bone marrow transplantation prepared with cyclophosphamide and single fraction total body irradiation (900-1000 cGy) between 1.5 and 3.8 (mean 2.2) years previously. The majority of children exhibited growth failure, which was of multiple aetiology. Ten patients, of whom eight had had previous prophylactic cranial irradiation, had evidence of growth hormone deficiency based on the reduced growth hormone response to insulin induced hypoglycaemia. Three patients had evidence of hypothalamic damage as shown by their growth hormone response to 200 micrograms GHRH (1-29) NH2 intravenously. Gonadal failure was common, assessed clinically, and biochemically by basal gonadotrophin and sex steroid concentrations. All four girls of adolescent age (10.6-14.1 years) had ovarian failure requiring sex steroid replacement. Of the eight boys of adolescent age (12.3-18.3 years), two had testicular failure requiring sex steroid supplements. Both of these had had previous testicular irradiation. Five others had compensated gonadal failure, and one had normal Leydig cell function. Abnormalities of the TSH response to TRH occurred in 10 patients but only three had overt hypothyroidism. Unlike growth hormone deficiency, gonadal and thyroid dysfunction showed no correlation with previous cranial radiotherapy.
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PMID:The effect of total body irradiation and bone marrow transplantation during childhood and adolescence on growth and endocrine function. 332 61

Cellular glucose-metabolizing enzymes and acetylcholinesterase (AChE) have been utilized as biochemical markers of mononuclear cell (MNC) leukemia maintained by serial cell transplantation in F344 rats. We have evaluated the sensitivity and reproducibility of these tumor markers in comparison to other diagnostic criteria of leukemia. Weanling rats were injected with 2 X 10(7) leukemic spleen MNC and sampled at 6, 35, 63, and 83 days. At 6 days, the glycolytic enzyme activities from spleen that decreased were believed to be residual activity from injected leukemic MNC. Glycolytic enzyme activities in spleen MNC were normal at 35 days and no changes in blood MNC enzyme activity occurred at 6 days or 35 days. At 63 days, prior to clinical evidence of leukemia, glucose-metabolizing enzymes from spleen MNC changed, and there were decreases in AChE from both blood and spleen MNC that progressively decreased at 83 days, when there was depressed body weight, splenomegaly, elevated WBC, depressed RBC, hypoglycemia, hyperbilirubinemia, and elevated serum enzyme levels. Separation of leukemic MNC from blood and spleen enhances sensitivity of cellular enzyme responses and provides a reproducible model to study biochemical markers correlated with severity of leukemia.
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PMID:Biochemical markers for Fischer rat leukemia in a cell transplant model. 347 32

Following the observation, in a patient with leukemia, of a factitious hypoglycemia that was related to in vitro glucose consumption by leukocytes, a study of glucose fall in vitro in the blood of 17 patients with leukemia of various types and with various grades of leukocytosis was undertaken. Results show that in vitro glucose consumption is linked to the intensity of leukocytes concentration, and is independant of the type of leukocyte. Factitious hypoglycemia may thus frequently occur in patients with high blood leukocyte count. This phenomenon, that was previously described, is again of interest to day because many laboratories do not yet use any more glycolysis inhibitors that partially inhibit it. Indeed, these inhibitors interfere with measures of other biological parameters that are simultaneously determined in autoanalysers.
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PMID:[In vitro glucose consumption in severe hyperleukocytosis. A cause of factitious hypoglycemia]. 630 97


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