Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A deficient erythrocyte pyruvate kinase observed in a patient with congenital non-spherocytic anaemia was characterized by the following properties: very low activity in haemolysates, decreased thermal stability, slightly increased urea denaturation, high affinity for PEP, poor FDP activation, normal ATP inhibition, decreased affinity for ADP, normal pH of optimal activity, and presence of an abnormal slow-moving component in this layer polyacrylamide gel electrophoresis. The patient was probably double heterozygous for two different deficient mutants of erythrocyte pyruvate kinase.
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PMID:A deficient pyruvate kinase with an electrophoretically slow-moving component. 1 93

The prognostic significance of age, sex, ethnic origin and various laboratory data was studied retrospectively in 69 patients with multiple myeloma using conventional statistical tests and the multiple regression computerized analysis. The conventional statistical analysis confirmed that age, anemia, uremia, hypoalbuminemia, hyperglobulinemia, hyperuricemia and IgA lambda type myeloma were associated with a poor prognosis. The multiple regression analysis indicated that age and blood urea nitrogen levels were the only variables which significantly affect the survival of patients with multiple myeloma. A correlation was found between blood urea nitrogen levels and other laboratory data of apparent prognostic value. The differences between our results and those of other authors are discussed and it is suggested that they may, in part, be due to the fact that the interplay between the various prognostic variables was not exposed in other studies.
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PMID:Prognostic factors in multiple myeloma: a retrospective study using conventional statistical methods and a computer program. 10 Oct 12

NZB x OUW F1 hybrid mice were treated with thiamphenicol at 25, 50 and 250 mg/kg/day from the time of their first positive antinuclear antibody test until their death. Untreated mice fed the same diet served as controls with body weight, mortality and renal disease patterns conforming to published reports of the biology of the BW mice. Regular testing of urine and bloodm and detailed postmortem examinations showed (a) that with increasing drug dose levels heavy proteinuria was almost eliminated and blood urea concentrations significantly lowered; (b) that in treated and untreated mice moderate to severe anaemia developed, apparently unrelated to the degree of uraemia; (c) that changes in renal function did not correlate with antinuclear antibody activity, nor did the drop in packed cell volume correlate with fixed or free circulating antierythrocyte autoantibody positivity; (d) that histological analysis of renal changes showed that at the highest dose level glomerular lesions were minimal. Thus the prolonged treatment with thiamphenicol reduced the severity of the spontaneous renal disease and resulted in a significant extension of lifespan.
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PMID:Thiamphenicol and lupus nephritis. The effects of long-term therapy on kidney function and pathology: a pilot study. 15 49

The protective and curative effects of dietary iron and ascorbic acid on chronic (180 days) cadmium toxicity in rats were examined. Growth retardation and anemia were observed in rats fed a diet containing 50 ppm of cadmium for 180 days; during this period the contents of iron in the liver, kidney, spleen, testis, intestine, and tibia decreased and the zinc contents of the liver and kidney increased, but the calcium content of bone did not change. Addition of 400 ppm of iron and 1% of ascorbic acid to the cadmium-containing diet overcame the growth retardation and anemia due to cadmium toxicity and reduced the tissue levels of cadmium; however, it did not restore the zinc contents in the liver, kidney, and bone to normal. Similar effects were observed when these compounds were added to cadmium containing diet for 90 days after feeding the cadmium diet alone for 90 days. The glutamic-pyruvic transminase and glutamic-oxaloacetic transminase activities in the plasma of rats fed the cadmium diet increased significantly and these increases were prevented by supplementing the diet with iron and ascorbic acid. Glucose, urea, and alkaline phosphatase in the plasma and glycogen in the liver were not changed by feeding the cadmium diet for 180 days. These results indicate the long-term effectiveness of supplementing the diet with iron and ascorbic-acid for preventing and curing dietary cadmium toxicity in rats.
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PMID:Long-term effectiveness of dietary iron and ascorbic acid in the prevention and cure of cadmium toxicity in rats. 21 Jun 49

Dose-response relationships between blood lead levels and toxic effects have been evaluated in 160 lead workers in two smelters and a chemicals plant. Blood lead levels ranged from 0.77 to 13.51 mumol/litre (16-280 microgram/dl). Clinical evidence of toxic exposure was found in 70 workers (44%), including colic in 33, wrist or ankle extensor muscle weakness in 12, anaemia (Hgb less than 8.69 mumol/litre (Hb/4) or 14.0 gm/dl) in 27, elevated blood urea nitrogen (greater than or equal to 7.14 mmol/litre or 20 mg/dl) in 28, and possible encephalopathy in two. No toxicity was detected at blood lead levels below 1.93 mumol/litre (40 microgram/dl). However, 13% of workers with blood lead levels of 1.93 to 3.81 mumol/litre (40-79 microgram/dl) had extensor muscle weakness or gastrointestinal symptoms. Anaemia was found in 5% of workers with lead levels of 1.93-2.85 mumol/litre (40-59 microgram/dl), in 14% with levels of 2.90 to 3.81 mumol/litre (60-79 microgram/dl), and in 36% with levels greater than or equal to 3.86 mumol/litre (80 microgram/dl). Elevated blood urea nitrogen occurred in long-term lead workers. All but three workers with increased blood urea nitrogen had at least four years occupational lead exposure, and nine had received oral chelation; eight of this group had reduced creatinine clearance, and eight had decreased renal concentrating ability. These data support the establishment of a permissible biological limit for blood lead at a level between 1.93 and 2.90 mumol/litre (40-60 microgram/dl).
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PMID:Occupational lead poisoning in the United States: clinical and biochemical findings related to blood lead levels. 50 43

Wistar rats were exposed to atmospheres containing O (control) or 5000 ppm vinyl chloride monomer (VCM), 7 h/day, 5 days/week, for a period of 52 weeks. After 4, 13, 26 and 52 weeks each time 10 rats/sex/group were killed and subjected to extensive examinations. The present paper deals with growth, mortality, haematology, clinical chemistry and organ weights. Slight growth retardation throughout the experimental period and high mortality in the second half of the study were observed in VCM-exposed animals. Some of the haematological parameters and biochemical blood parameters were slightly influenced by VCM after an experimental period of 52 weeks only. Blood clotting time was generally slightly shorter in VCM-exposed rats than in controls. There were minor indications of increased potassium contents of the blood serum in VCM-exposed animals during the first half of the test period. The kidneys were adversely affected by VCM as appeared from increased blood urea nitrogen levels and relative kidney weights. After 52 weeks increased weights of heart and spleen, and slight signs of anaemia were noticed in VCM-exposed rats. The present study did not produce obviously suitable parameters for early diagnosing "VCM-disease" in man.
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PMID:One-year time sequence inhalation toxicity study of vinyl chloride in rats. I. Growth, mortality, haematology, clinical chemistry and organ weights. 51 69

Patients with chronic renal failure and on chronic intermittent hemodialysis have several metabolic risks such as retention of urea and other products of nitrogen metabolism, catabolism, acidosis, edema, dehydration, hyper- and hypotension, hyperkalemia, renal osteopathy, and renal anemia. Uremic coma is usually avoided by balanced nutritional therapy and treatment with hemodialysis. A dietary regimen containing protein with high amounts of essential amino acids is an important part of treatment. In patients on chronic hemodialysis disorders of protein and amino acid metabolism are caused by either deficiency of essential ingredients of the food or by the metabolic defects due to chronic uremia.
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PMID:[Dangers of a wrong diet in patients with renal insufficiency in the predialytic state or during chronic hemodialysis]. 55 61

Lymphocytic thyroiditis was induced in young Wistar rats by feeding them the immunosuppressive compound frentizole [1-(6-methoxy-2-benzothiazolyl)-3-phenyl urea] for 1 year. About half of the rats given 0.060 and 0.150% frentizole in the diet had lymphocytic thyroiditis. The incidence of thyroiditis was low in the group given the high dose because of severe anemia and hepatic disease which resulted in increased mortality. Reversibility of the thyroid lesion was indicated by reduced incidence rates at 15 and 18 months after treatment was stopped at 1 year. The thyroiditis was characterized by interstitial infiltrates of many lymphocytes and plasma cells and fewer macrophages with mild degenerative changes in the follicular epithelium. This inflammatory cell infiltrate was generally diffuse but occasionally was multifocal, particularly in thyroid glands of rats late in the reversibility phase of the study. The inflammatory cell infiltrate caused the thyroid glands to be several times normal size. Sera from rats with lymphocytic thyroiditis contained hemagglutinating antibody against rat perfect correlation between the presence of anti-thyroglobulin antibody and enlarged thyroid glands. Fine granular deposits of IgG and complement were identified in some areas of the follicular basement membrane. We concluded that the lymphocytic thyroiditis was immunologically mediated, at least in part, by anti-thyroglobulin antibody.
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PMID:Rat lymphocytic thyroiditis associated with ingestion of an immunosuppressive compound. 58 90

Erythrocyte life span was determined in 19 children with chronic renal failure on conservative treatment and in 12 children on regular hemodialysis. Erythrocytes were labeled with 111Indium. Blood loss was measured using a special counting chamber. Erythrocyte life span decreased with increasing blood urea nitrogen. Blood loss into the intestine and into the dialysis equipment was found to be a major cause for anemia of children with chronic renal failure. Daily intestinal blood loss amounted to 6 ml/m2 BSA on conservative treatment and 11 ml/m2 on hemodialysis. Mean blood loss in the dialysis equipment was 8 ml/m2 per dialysis, almost half being lost in the connecting tubing systems.
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PMID:Hemolysis and blood loss in children with chronic renal failure. 58 79

Three patients with a relatively mild form of beta O-thalassemia who did not require regular blood transfusions are described. Globin synthesis was studied by gel filtration and urea-carboxymethylcellulose chromatography of stroma-free hemolysates prepared from peripheral blood and bone marrow cells labeled in vitro with 14C-leucine. gamma/alpha Synthetic ratios in peripheral blood were in the same range as in patients with the severe clinical form of beta O-thalassemia, while gamma/alpha synthetic ratios in bone marrow cells were higher than in that group of patients. The size of the free alpha-chain pool measured in one case was smaller than in other patients with "classical" Cooley anemia. It is concluded that the severity of the clinical course in beta O-thalassemia does not correlate with the imbalance in alpha verus gamma chain synthesis in peripheral blood and is determined by the synthetic ratio in bone marrow cells, where the bulk of hemoglobin synthesis takes place.
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PMID:Beta O-thalassemia intermedia. 66 61


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