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)

Diethylene glycol monomethyl ether (DEGME) has been selected as a replacement anti-icing additive for ethylene glycol monomethyl ether (EGME) in Navy jet aircraft fuel. This experiment was performed to determine whether DEGME produced similar toxicity to EGME following dermal exposure. Male guinea pigs were dermally exposed to 1.00, 0.20, 0.04, or 0 (control) g/kg/day DEGME for 13 weeks, 5 days/week, 6 hr/day. Another group of animals was similarly exposed to 1.00 g/kg/day EGME. Body weights as well as testicular and splenic weights were reduced as a result of exposure to EGME, DEGME-exposed animals exhibited decreased splenic weight in the high- and medium-dose (1.00 and 0.20 g/kg/day) exposure groups only. Hematologic changes in EGME-exposed animals included mild anemia with increased erythrocytic mean corpuscular volumes and a lymphopenia with increased neutrophils. Similar hematological changes were not observed in any animals exposed to DEGME. Serum creatine kinase activity was increased in animals exposed to EGME, and serum lactate dehydrogenase activity was increased in EGME and 1.00 g/kg/day DEGME-exposed animals. In general, DEGME produced minimal toxicological changes following dermal exposure, whereas the toxicological changes observed following similar exposure to EGME were much more profound.
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PMID:A subchronic dermal exposure study of diethylene glycol monomethyl ether and ethylene glycol monomethyl ether in the male guinea pig. 369 23

A patient who developed chronic salicylism associated with salicylate therapy for treatment of juvenile rheumatoid arthritis is described, and the clinical presentation and treatment of chronic salicylism are reviewed. A 5 1/2-year-old boy was receiving aspirin 150/mg/kg/day for treatment of juvenile rheumatoid arthritis. While on salicylate therapy, the patient developed tachypnea and became increasingly hyperthermic, lethargic, and disoriented. The patient developed a maculopapular rash, weakness, and a decreased level of consciousness during the 11 days before admission to the hospital. Physical examination and laboratory determinations revealed that the patient had hypoprothrombinemia, hypoglycemia, and severe hepatic encephalopathy secondary to long-term salicylate toxicity. The patient was treated for hypoglycemia, electrolyte imbalances, thrombocytopenia, and anemia and was discharged after 24 days. Diagnosing chronic salicylism with hepatic dysfunction was difficult because the symptoms are similar to those of stage I to stage II Reye's syndrome. Liver enzymes, including aspartate aminotransferase (also called SGOT), alanine aminotransferase (also called SGPT), alkaline phosphatase, and lactate dehydrogenase, may be elevated in juvenile arthritis patients with hepatic dysfunction. Liver dysfunction usually improves when salicylate therapy is discontinued. Supportive therapy should always be used in symptomatic patients. Children on long-term, high-dose salicylate therapy should be monitored closely, and baseline liver function tests should be performed. The clinical effectiveness of administering sodium bicarbonate in attempts to alkalinize urine and increase salicylate elimination is controversial. In patients with juvenile rheumatoid arthritis who develop chronic salicylism, careful analysis of the patient's medication history, laboratory values, and clinical presentation are necessary to rule out Reye's syndrome.
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PMID:Chronic salicylism in a patient with juvenile rheumatoid arthritis. 370 82

An early sign of erythroblastic leukemia in rat was nodule formation in the spleen. Hyperplastic foci of stem cells, indistinguishable histologically from leukemic stem cells, were found in the red pulp whereas the malpighian corpuscles were uninvolved. Anemia is a normal phenomenon in immature rats and the spleen of the prepubertal rat possesses considerable hemopoietic potential. Pulse-doses of 7, 8, 12-trimethylbenz(a)anthracene prevented the physiologic hematological development of maturing rats and was associated with subsequent development of leukemic stem cells in the red pulp of the spleen. Significant enzyme changes were observed in leukemic spleens. Compared with the spleens of normal littermates, the concentration of lactate dehydrogenase rose while that of malate dehydrogenase fell; the content of alkaline phosphatase rose whereas acid phosphatase fell. Increased alkaline phosphatase activity in leukemic spleen was attributed to nonleukemic foci of myelopoiesis.
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PMID:Leukemia evoked with 7,8,12-trimethylbenz(a)anthracene in rat. I. Changes in spleen and thymus. 528 70

The involvement of the brain, lungs and kidneys was studied in a lethal rat malaria. Lewis inbred rats were infected with Plasmodium berghei K173. The disease proved fatal within 10-14 days. Parasitaemia showed an increase of up to 43% parasitised red blood cells on Day 10 p.i. The haematocrit decreased from 50% to 12%. The systolic blood pressure dropped from 99 to 56 mmHg. The lactate dehydrogenase activity rose to 2,543 U/l. BUN and serum creatinine doubled during the course of the disease. The transaminases increased tenfold and the cholinesterase decreased from 943 U/l to 271 U/l. Morphologically the kidneys showed an immune complex glomerulo-nephritis with a normal tubulo-interstitial system. The brain, heart and lungs were normal by light microscopic examination. Marked anaemia and shock were the main causes of death in the above-mentioned specimen rat, showing that the course of the disease is significantly different from lethal infections in humans with Plasmodium falciparum who show severe pulmonary, renal and cerebral complications.
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PMID:Causes of death in lethal rat malaria. 661 21

The protean manifestations of Legionnaires' disease are described in an analysis of 12 sporadic cases. Two forms of the disease have been delineated. One variant (Group A) consisted of six patients who had a mild form of non-progressive pneumonia with minimum extra-pulmonary involvement. Six patients (Group B) were differentiated by rapidly progressive pulmonary infiltrates, severe hypoxia and respiratory failure, plus a higher frequency of band neutrophils and extra-pulmonary manifestations. Particularly notable were evidence of severe myositis (elevated creatinine phosphokinase and lactate dehydrogenase), anaemia, and neurological findings which included alterations in the sensorium, meningitis, and convulsions. Cerebrospinal fluid (CSF) abnormalities were seen frequently in patients with neurological manifestations, and necropsy findings in one patient suggested that the Legionnaires' bacillus was capable of producing a fatal leucoencephalitis. Renal findings included haematuria, proteinuria and oliguric renal failure. Hepatic transaminases (SGPT, SGOT) were elevated in six patients and serum bilirubin was abnormal in five. Alkaline phosphatase values were normal to minimally elevated. The gastrointestinal symptoms commonly considered to be a frequent initial manifestation of Legionnaires' disease were rare in this series. Recommendations for instituting empirical therapy, based upon recognition of a clinical syndrome which should suggest the diagnosis of Legionnaires' disease, are included.
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PMID:The protean manifestations of Legionnaires' disease. 663 Oct 29

A case of Coombs' positive anemia in a man who had procainamide-induced lupus erythematosus syndrome is reported. The patient had a hemoglobin of 4.3 gm/dl and reticulocytopenia (3.1% corrected). Serum lactate dehydrogenase and haptoglobin levels were normal, and total bilirubin was only slightly elevated. Two other reported cases of procainamide-induced hemolytic anemia have demonstrated similar findings. Apparently, procainamide occasionally may induce a reversible, reticulocytopenic, Coombs' positive anemia that is not associated with laboratory evidence of acute hemolysis.
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PMID:Reticulocytopenic, coombs' positive anemia induced by procainamide. 685 67

Effects of dietary iron deficiency on lactate metabolism were studied in weanling female rats. Following an iron-deficient diet for 5 weeks, mean hemoglobin concentration was lowered to 6.4 g/dl relative to 12.2 in the control group. Mean plasma iron levels were 58 and 162 micrograms/dl, respectively. Significantly elevated resting lactate levels were observed in whole blood and plasma from iron-deficient anemic (relative to control) rats. Total activity of lactate dehydrogenase (LDH) was elevated in soleus and gastrocnemius muscles in response to iron deficiency from 269 +/- 51 to 364 +/- 60 (Mean +/- SD) and from 265 +/- 65 to 372 +/- 61 IU . 10(-3) . g-1, respectively. The LDH activity in heart was lowered from 700 +/- 61 to 593 +/- 45 IU . 10(-3) . g-1. The M3H and M2H2 isozymes in soleus were increased from 12.7 +/- 2.8 to 20.4 +/- 5.8% and from 19.4 +/- 6.1 to 28.2 +/- 3.6%, respectively. Similar increase was observed in M2H2 and MH3 in gastrocnemius from 9.8 +/- 0.9 to 14.8 +/- 2.0% and from 17.4 +/- 2.0 to 20.5 +/- 2.3%, respectively. The H4 isozyme was significantly reduced in soleus, gastrocnemius, and plantaris muscles from 27.7 +/- 4.7 to 12.4 +/- 4.4, from 15.8 +/- 1.9 to 7.2 +/- 2.9, and from 10.5 +/- 2.9 to 3.9 +/- 2.1%, respectively. It was suggested that iron-deficiency anemia induces an elevation of lactate production following an increase in total LDH activity and change in LDH isozyme patterns.
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PMID:Adaptations of lactate metabolism in iron-deficient rats. 686 1

Dapsone has been used in various dermatological disorders and in leprosy. One of the main side effects of dapsone therapy is anemia, mostly hemolytic. We aimed at finding the effect of dapsone therapy on serum haptoglobin levels which could be an indirect evidence for intravascular hemolysis, supported by secondary investigations such as liver functions (serum lactic dehydrogenase, alkaline phosphatase, bilirubin), blood hemoglobin levels, urinary excretion of urobilinogen, and erythrocytes. As in other infectious conditions, haptoglobins were raised in untreated lepromatous cases, compared to controls (p less than 0.05). Dapsone treatment of 100 mg daily for 14 days brought down the haptoglobin level significantly as compared to the untreated cases and the controls (p less than 0.05). An elevated alkaline phosphatase and lactate dehydrogenase indicate some liver dysfunction following dapsone therapy. A significant drop in blood hemoglobin level and a concomitant increase in serum bilirubin, urinary excretion of urobilinogen, and a significant fall in the serum hemoglobin binding capacity (haptoglobin level) following treatment with dapsone are quite suggestive of mild intravascular hemolysis.
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PMID:Dapsone induced hypohaptoglobinemia in lepromatous leprosy patients. 719 20

Hemolytic or blood loss anemia was induce in six ponies and red blood cell concentrations of creatine, glucose-6-phosphate dehydrogenase (G-6-PD), lactate dehydrogenase (LDH), and aspartate transaminase (AST) were measured during the ensuing regenerative period. Creatine and G-6-PD levels correlated well and increased concentration of either was good indication of increased erythrogenesis. Erythrocyte LDH levels were of value in assessing the response to hemolytic anemia but not to blood loss anemia. The difference may be, at least in part, the result of differing degrees of regenerative effort seen in the two experimental groups. Red cell AST concentrations fluctuated markedly and were of no value in assessing the anemia in either group.
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PMID:Biochemical changes in equine erythrocytes during experimental regenerative anemia. 726 89

A rare isozyme of serum creatine kinase (CK) migrating cathodic to CK-MM on electrophoresis was found in a 30-year-old male with stomach cancer complicated by disseminated intravascular coagulation leading to massive upper gastrointestinal bleeding and marked anemia. Serum CK activity rose to a maximum of 374 U/l without detectable CK-MB isoenzyme. The patient was also characterized by a marked increase in serum lactate dehydrogenase (all isozymes elevated) and by preferential leakage of mitochondrial aspartate aminotransferase and glutamate dehydrogenase, indicating the presence of extensive tissue damage involving mitochondria. Skeletal muscle mitochondria were considered the most likely source of the additional CK isozyme.
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PMID:Cathodic isozyme of serum creatine kinase in a case of stomach cancer complicated by disseminated intravascular coagulation. 744 49


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