Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myeloproliferative disease of childhood is frequently associated with chromosomal anomalies, usually of the C group. Clinical features are similar to those of the juvenile type of chronic myeloid leukemia. A child with this disease is described. Marked myeloid proliferation, anemia, thrombocytopenia and hepatosplenomegaly were present; leukocyte alkaline phosphatase and fetal hemoglobin were moderately elevated. Chromosome analysis of bone marrow cells revealed a mosaicism 47,XX,+21/46,XX. Down's syndrome was ruled out by the child's normal phenotype and dermatoglyphic analysis. The cytogenetic finding is probably evidence for the clonal origin of the trisomy 21 cell line.
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PMID:Myeloproliferative disease of childhood associated with a trisomy 21 clone. 11 7

Three siblings with a lifelong history of a bleeding disorder and thrombocytopenia died from a myeloproliferative disease. In 2, the terminal event resembled juvenile chronic myelogenous leukemia, and in the third, the diagnosis was acute monocytic leukemia. A family study revealed that the mother and 5 other siblings had a variety of hematologic abnormalities. These included chronic thrombocytopenia, abnormal platelet function, elevated concentrations of HgbF or serum vitamin B12, and low leukocyte alkaline phosphatase (LAP) scores either singly or in combination. At the time of study, none had evidence of malignancy. Members of this family have a myeloproliferative disorder that has the potential for terminating in nonlymphocytic leukemia, a combination of events which appears not to have been reported previously.
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PMID:A fatal myeloproliferative syndrome in a family with thrombocytopenia and platelet dysfunction. 27 71

Fifty consecutive patients with blastic chronic myelogenous leukemia were evaluated clinically, morphologically, biochemically, and therapeutically. Forty-five patients had a preceding stable phase (38 Ph'+, 7 Ph'-); five patients presented with de novo Ph+ blast crisis. The most frequent clinical signs of impending blast crisis were weakness, fatigue, increasing splenomegaly, anemia, thrombocytopenia, marrow fibrosis, and a rising neutrophil alkaline phosphatase. Fever (unrelated to infection), skin infiltration, lymphadenopathy, hepatomegaly, thrombocytosis, and basophilia were much less common. The development of aneuploidy occurred in less than one-half of the total group. Myeloblastic morphology at blastic transformation was most frequent with occasional lymphoblastic, promyelocytic, and undifferentiated cases seen. Terminal deoxynucleotidyl transferase was present in one-third of the patients, but had no clear-cut relationship to the morphology. Response to treatment was generally disappointing (two complete and 15 partial remissions in 45 treated patients).
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PMID:Blastic transformation in chronic myelogenous leukemia: experience with 50 patients. 27 33

Four patients with malignant histiocytosis are described. Major clinical signs were fever, lymphadenopathy, hepatomegaly and splenomegaly. Laboratory studies showed leukopenia, thrombocytopenia, low leukocyte alkaline phosphatase (LAP) score, normal erythrocyte sedimentation rate (ESR) and elevated serum triglycerides. There was evidence of bone marrow involvement in all four cases. Typical changes were seen in the histological study.
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PMID:Malignant histiocytosis. A clinical and morphological study of four cases. 67 3

Forty-seven male Macaca mulatta, 3 to 4 kg weight, were inoculated intravenously or subcutaneously with various doses of yolk sac-grown Rickettsia rickettsii. Thirty-four macaques became febrile and exhibited signs of infection ranging from transient illness with a few days of fever to severe illness with subsequent death. The rash appeared more frequently in the macaques inoculated subcutaneously. Febrile macaques that survived had leukocytosis, with concomitant neutrophilia. Febrile macaques that died had, in addition, marked terminal leukopenia and thrombocytopenia. Packed cell volume of all febrile macaques decreased. In almost all of the febrile macaques, there were increased serum urea nitrogen, glutamic-oxaloacetic transaminase, and lactate dehydrogenase and decreased total serum protein and amylase concentrations. A few febrile macaques had increased bilirubin values and decreased sodium, chloride, phosphorus, and alkaline phosphatase concentrations. Changes did not occur in serum glucose, potassium, calcium, and glutamic-pyruvic transaminase values. The experimental form of Rocky Mountain spotted fever in the macaque provides a subhuman primate model for studying the pathophysiology of this disease.
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PMID:Changes in blood serum constituents and hematologic values in Macaca mulatta with Rocky Mountain spotted fever. 82 Feb 24

Although anemia has not been widely appreciated as a complication of primary hyperparathyroidism, 5.1% of the individuals with this disorder seen at the Massachusetts General Hospital since 1962 had a normochromic, normocytic anemia that could not be related to blood loss,a deficiency state, or uremia. The anemic group had more advanced bone disease and higher levels of serum calcium, alkaline phosphatase, and parathyroid hormone than the nonanemic group. Results of bone marrow biopsies performed in five patients showed variable degrees of myelofibrosis. However, none of the patients had hepatosplenomegaly, a myelophthisic peripheral blood smear, leukopenia, or thrombocytopenia. Removal of the abnormal parathyroid glands led to improvement or correction of the anemia.
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PMID:Anemia in primary hyperparathyroidism. 85 57

Beagle dogs inoculated with the agent of Rocky Mountain spotted fever, Rickettsia rickettsii, developed a clinical syndrome that extended from febrile exanthema to death and appeared to be dose related. Infected dogs were anorectic and lethargic and developed cutaneous lesions characteristic of Rocky Mountain spotted fever, including petechia, ecchymosis, edema, and necrosis. Hematologic changes after inoculation included anemia, leukopenia proceeding to leukocytosis, and thrombocytopenia. Changes in blood chemistry values included increases in serum alkaline phosphatase and cholesterol, and hyponatremia and hypochloremia. The prominent histopathologic change was necrotizing vasculitis. The canine disease is comparable with human Rocky Mountain spotted fever on a clinical, hematologic, biochemical, and pathologic basis, and may provide a model system for this disease in man. The results suggest the dog may be involved in the epidemiology of R rickettsii infections.
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PMID:Studies on the pathogenesis of Rickettsia rickettsii in the dog: clinical and clinicopathologic changes of experimental infection. 87 82

Thirty five patients with psoriasis (plaque type 26, guttate 3, pustular 4, and erythrodermic 2) were treated with oral mycophenolic acid for a period ranging from 52 to 104 weeks. The average follow-up was 89 weeks, and the dose schedule ranged from 2,400 to 7,200 mg daily. Excellent response was noted in 20 patients, good in 13 patients, and poor in 2. The most common clinical side effects were in the gastrointestinal tract, namely, diarrhea, nausea, abdominal cramps, and soft stools. A high incidence of herpes simplex, herpes zoster, and a flu-like syndrome was noted. Laboratory abnormalities consisted of mild blood hemoglobin reduction, one case of leukopenia (3,9000 WBCs per cubic millimeter), two cases with thrombocytopenia and mild elevation of alkaline phosphatase. Mycophenolic acid appears as a promising drug for the treatment of severe psoriasis.
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PMID:Mycophenolic acid in the treatment of psoriasis: long-term administration. 87 14

The juvenile type of chronic myelogenous leukemia (CML) is characterized by hemorrhagic diathesis, hepatosplenomegaly, generalized enlargement of lymph nodes, reduced erythro- and thrombopoiesis, leukemic infiltration of bone marrow, and decreased activity of leukocyte alkaline phosphatase. The disorder differs from the adult type by the early manifestation of anemia and thrombocytopenia, the minor degree of leucocytosis, the failure to demonstrate the Philadelphia chromosome, and the presence of fetal markers in the patients' erythrocytes. The persistence of fetal markers in erythrocytes and the clinical manifestation in infancy and early childhood suggest that the disease is congenital in origin. The occurrence of CML of the juvenile type in an 8-year-old boy, which is reported in this paper, favors a postnatal acquisition of the disorder. The significance of hematological and cytogenetic findings and new aspects of nosological classification are discussed.
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PMID:[The "juvenile" type of chronic myelogenous leukemia (author's transl)]. 105 23

Treatment with flucytosine of 20 patients with fungal infections gave favorable results in four patients with crytococcal infections, two of four patients with disseminated candidiasis, eight of ten patients with urinary tract infections due to Candida albicans and Torulopsis glabrata, and tow of three patients with miscellaneous infections due to Calbicans. Two patients with crytococcal meningitis and altered host resistance and one patient with an aorto femoral graft infection due to C albicans were treated with flucytosine and smphotericin B. The infection was eradicated in one of the patients with meningitis, and cultures from an infected arterial graft became negative. Adverse side effects of flucytosine included mild leukopenia and thrombocytopenia, a transient increase in alkaline phosphatase and glutamic oxaloacetic transaminase, and nausea and diarrhea.
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PMID:Treatment of fungal infections with flucytosine. 109 40


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