Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002878 (hemolytic anemia)
 7,530 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The leucocyte alkaline phosphatase (LAP) score of peripheral blood neutrophils was examined in 20 patients with multiple myeloma and compared with the score in 18 patients with monoclonal gammopathy of undetermined significance (MGUS). The mean (95% confidence limit) LAP score in those with multiple myeloma was 186 (169-218) compared with 92 (64-120) in the MGUS group. In the multiple myeloma group all but one patient had a high LAP score, irrespective of disease. No cause for raised LAP, such as infection, was present in any of the patients with multiple myeloma. In the MGUS group six patients had a raised LAP score; in two of them another cause for such a rise was present (autoimmune haemolytic anaemia and primary thrombocythaemia). In neither group did the LAP score correlate with duration of the disease, bone marrow plasma cell count, paraprotein concentration, haemoglobin, total white cell or neutrophil count. It is concluded that a normal LAP count in patients with paraproteinaemia suggests a benign condition, but a raised count does not indicate a malignant condition.
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PMID:Use of leucocyte alkaline phosphatase (LAP) score in differentiating malignant from benign paraproteinaemias. 171 23

A transplantable mononuclear cell leukemia (MCL) was established from spontaneous MCL in an F344 rat. In this work, we paid special attention to a nodular tumor, named MCL-YSK, developed at the subcutaneous transplant site. MCL-YSK was serially passaged in subcutaneous tissue of syngeneic rats up to the 19th generation. Transplants from MCL-YSK grew into nodules 3 cm in diameter and 11.3 g in weight 9 weeks after subcutaneous implantation. Neoplastic cells forming the nodules had azurophilic cytoplasmic granules, which ultrastructurally appeared to be lysosomes. The cells reacted positively for acid phosphatase and nonspecific esterase, but not for alkaline phosphatase, alpha-1 antitrypsin and lysozyme, nor reacted with anti-rat monocyte/macrophage monoclonal antibody and anti-rat CD-8 monoclonal antibody. They possessed Fc-receptor. Leukemic cells first appeared in the peripheral blood 6 weeks after transplantation when subcutaneous nodules reached an average diameter of one cm. Subsequently, leukemic changes progressed in recipients as MCL-YSK grew larger. The recipients died during the period from 8 to 12 weeks after transplantation, showing anemia, depression, splenohepatomegaly and lymph node enlargement. Diffuse or focal proliferation of sprinkled tumor cells was present in many organs. Hematologic changes suggestive of hemolytic anemia, elevated plasma enzymes and decreased drug-metabolizing enzymes, indicative of hepatic malfunction, were seen in transplant recipients. MCL-YSK was easily transplanted into athymic nude mice. The transplanted mice showed leukemic changes similar to those observed in rats with transplanted MCL-YSK.
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PMID:Transplantable mononuclear cell leukemia in F344 rat with particular reference to nodular tumor developing at the transplant site. 183 99

Congenital erythropoietic porphyria (CEP) is a rare disorder of heme biosynthesis that results in the production of large quantities of photoactive porphyrins. The clinical syndrome is dominated by extreme photosensitivity with mutilation of light exposed extremities and hemolytic anemia. Bone disease has been occasionally noted, but is not well characterised. We describe a man with CEP who developed bone pain and spinal crush fractures at the age of 22. Skeletal radiographs revealed features typical of other severe hemolytic anemias, but in addition there was loss of the terminal phalanges of the hand as a result of photomutilation. Spinal bone density (assessed by DPA) was reduced and at the hip bone density was at the lower limit of normal. The metacarpal cortical bone density was 2.9 standard deviations below normal. Biochemical and histological studies accelerated bone turnover. Although the serum 250H vitamin D concentration was very low (because of light avoidance) there was no evidence that the bone disease was a consequence of this. Treatment for one year with clodronate and a high transfusion regime was associated with small reductions in serum alkaline phosphatase and urine hydroxyproline excretion, but there was no improvement in bone mineral density. We conclude that CEP has a distinctive osteodystrophy comprising osteolysis of light-exposed extremities and a high turnover type of osteoporosis. Privational vitamin D deficiency may also occur. The effect upon bone of the new therapies for CEP should be considered.
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PMID:The osteodystrophy of congenital erythropoietic porphyria. 206 45

Acute zinc toxicosis from the ingestion of pennies was diagnosed in a dog with Heinz body hemolytic anemia (PCV = 14%), leukocytosis (51,000 cells/ml) with a left shift (3,060 band neutrophils; 37,740 segmented neutrophils) and monocytosis (4,080 cells/ml), azotemia (BUN = 60 mg/dl), bilirubinemia (total bilirubin = 5.3 mg/dl), hypokalemia (3.0 mEq/L), high serum alkaline phosphatase activity (691 U/L), high total plasma solids (8.1 g/dl), hemoglobinuria, and proteinuria. Despite aggressive medical treatment, renal failure ensued, and the dog died of cardiac arrest. The clinical signs, clinical course, and laboratory findings in this dog were similar to what has been reported in other cases of acute zinc toxicosis in dogs, with the exception of a history of generalized seizures and the findings of Heinz bodies. Although a causative relationship between plasma zinc values and Heinz body formation cannot be proven, their association suggests that oxidative damage to erythrocyte hemoglobin and cell membrane proteins may be involved in the pathogenesis of zinc-induced hemolysis.
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PMID:Heinz body hemolytic anemia associated with high plasma zinc concentration in a dog. 226 50

Both erythrocytes and leukocytes from a patient with erythrocyte pyrimidine 5'-nucleotidase (P5N) deficiency were shown to contain increased amounts of pyrimidine nucleotides. These findings suggested that the leukocytes were also deficient for P5N. Measurement of the P5N activity in lysates from lymphocytes or granulocytes, in the presence of inhibitors for non-specific 5'-nucleotidase or alkaline phosphatase, indeed showed a deficiency for P5N in lymphocytes and granulocytes of the patient with erythrocyte P5N deficiency. However, the P5N deficiency in the leukocytes did not cause clinical disturbances in addition to the weak haemolytic anaemia.
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PMID:Deficiency of pyrimidine 5'-nucleotidase in human leukocytes. 255 46

Low values for serum alkaline phosphatase activity were observed early in the course of two patients with Wilson's disease presenting with the combination of severe liver disease and Coombs' negative acute hemolytic anemia. A review of other cases of Wilson's disease revealed that 11 of 12 patients presenting with hemolytic anemia had values for serum alkaline phosphatase less than their respective sex- and age-adjusted mean values; in eight, serum alkaline phosphatase activity was less than the lower value for the normal range of the test. Low values for serum alkaline phosphatase were much less common in Wilson's disease patients with more chronic forms of presentation. Copper added in high concentration to serum in vitro did not have an important effect on serum alkaline phosphatase activity. The mechanism responsible for the decrease in serum alkaline phosphatase activity in patients is uncertain.
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PMID:Low serum alkaline phosphatase activity in Wilson's disease. 375 40

Large numbers of eccentrocytes (erythrocytes with hemoglobin contracted to one side of the cell) were seen on a stained blood smear from a Dachshund with compensated hemolytic anemia. The 7-kg dog had been given 325 mg of acetaminophen orally once daily for 6 weeks by the client, because the dog exhibited signs attributed to abdominal pain. More than half of the erythrocytes contained small Heinz bodies visualized after methyl violet staining. The methemoglobin content was 6.4% (normal less than 2%) when measured 16 hours after the last acetaminophen tablet was given. High serum alanin transaminase and alkaline phosphatase activities and hyperbilirubinuria were measured. All abnormal laboratory findings were attributable to acetaminophen-induced oxidative damage to erythrocytes and hepatocytes.
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PMID:Hematologic abnormalities associated with chronic acetaminophen administration in a dog. 379 79

A 52 yr old Caucasian female (F. E.) had hemolytic anemia, a leukemoid reaction, and fatal sepsis due to Escherichia coli. Her leukocytes ingested bacteria normally but did not kill catalase positive Staphylococcus aureus, Escherichia coli, and Serratia marcescens. An H(2)O(2)-producing bacterium, Streptococcus faecalis, was killed normally. Granule myeloperoxidase, acid and alkaline phosphatase, and beta glucuronidase activities were normal, and these enzymes shifted normally to the phagocyte vacuole (light and electron microscopy). Intravacuolar reduction of nitroblue tetrazolium did not occur. Moreover, only minimal quantities of H(2)O(2) were generated, and the hexose monophosphate shunt (HMPS) was not stimulated during phagocytosis. These observations suggested the diagnosis of chronic granulomatous disease. However, in contrast to control and chronic granulomatous disease leukocytes, glucose-6-phosphate dehydrogenase activity was completely absent in F. E. leukocytes whereas NADH oxidase and NADPH oxidase activities were both normal. Unlike chronic granulomatous disease, methylene blue did not stimulate the hexose monophosphate shunt in F. E. cells. Thus, F. E. and chronic granulomatous disease leukocytes appear to share certain metabolic and bactericidal defects, but the metabolic basis of the abnormality differs. Chronic granulomatous disease cells lack oxidase activity which produces H(2)O(2); F. E. cells had normal levels of oxidase activity but failed to produce NADPH due to complete glucose-6-phosphate dehydrogenase deficiency. These data indicate that a complete absence of leukocyte glucose-6-phosphate dehydrogenase with defective hexose monophosphate shunt activity is associated with low H(2)O(2) production and inadequate bactericidal activity, and further suggest an important role for NADPH in the production of H(2)O(2) in human granulocytes.
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PMID:Complete deficiency of leukocyte glucose-6-phosphate dehydrogenase with defective bactericidal activity. 440 Dec 71

Paroxysmal nocturnal hemoglobinuria is characterized by chronic hemolytic anemia, leukopenia, and thrombocytopenia. The increased hemolysis and hemoglobinuria associated with sleep have been observed so frequently that these features have been incorporated into the syndrome's name. Infections, especially of the respiratory and urinary system, can cause hemolytic episodes. Patients with paroxysmal nocturnal hemoglobinuria have increased susceptibility to infections. Some PNH patients are leukopenic, but many are not. It has been reported that leukocyte alkaline phosphatase of granulocytes in patients with PNH is low. As Hartmann and Kohlhouse point out, "The principles of treating infection in PNH seem no different than the therapy of infections in any group. "If major surgery is indicated, preparation should include saline-washed red cells, which would increase the patient's number of circulating normal red blood cells, if necessary. The prognosis is variable. A small percentage of patients with PNH develop leukemia. However, in at least half of all patients, the number of complement sensitive cells decreases, and many of these patients live a fairly normal life.
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PMID:Paroxysmal nocturnal hemoglobinuria: report of case with odontogenic infection. 693 60

Hematologic, serum chemical, and histopathologic studies were performed on 17 aged Fischer 344 rats with mononuclear leukemia. Twelve of the rats had leukemic hemograms, while five had nonleukemic or marginally abnormal differential leukocyte counts. Hematologic findings revealed that all rats were profoundly anemic. Serum chemistry studies confirmed the occurrence of icterus observed clinically, a finding consistent with hemolytic anemia. Alanine aminotransferase and serum alkaline phosphatase values were elevated.
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PMID:Hematologic and serum chemical characteristics of mononuclear leukemia in Fischer 344 rats. 709 30


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