Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The levels of serum gamma-glutamyl transpeptidase (GGT) and, when appropriate, alkaline phosphatase (AP) and 5'-nucleotidase (NTD) have been measured as a routine in 276 patients with malignant haematological diseases during a 26-month trial period. GGT levels add no prognostic information to the routine haematological surveillance of leukaemia. Polychemotherapy does not appear to be an inducer of liver drug-metabolising microsomal enzymes. Polycythaemia rubra vera, myelofibrosis and chronic lymphocytic leukaemia may cause little change in GGT, AP and NTD levels despite marked hepatomegaly. A raised GGT in Hodgkin's disease and non-Hodgkin lymphoma is generally associated with active and widespread disease, but not necessarily a sign of malignant tissue in the liver. The elevations of GGT in myeloma may be secondary to liver infiltration though this group merits further detailed study.
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PMID:Evaluation of the usefulness of serum gamma-glutamyl transpeptidase levels in the management of haematological neoplasia. 2 19

In 56 patients with Hodgkin's disease, the following bloodtests were carried out: erythrocyte sedimentation rate (ESR), fibrinogen, alpha2-globuline, serium iron concentrations and alkaline phosphatase activity. In some patients we additionally measured alkaline leucocyte phosphatase and serum ribonuclease activity. In our series ESR, serum iron and alpha2-globuline concentrations were the most sensitive metabolic parameters. A rise in fibrinogen concentration, alkaline phosphatase and serum ribonclease activity seems to indicate extensive disease. It is not possible, however, to discern between a state of remission and stage I by means of these parameters. ESR, serum iron and alpha2-globuline concentrations might be either elevated or normal in both instances. These parameters seem important in order to distinguish between a remission or stage I on the one hand and extensive disease in stage III and IV on the other hand. Concomitant findings of ESR above 40 mmh, elevated concentrations of fibrinogen and alpha2-globuline, as well as elevated alkaline phosphatase and serum and serum ribonuclease activity mostly indicate stage III or IV.
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PMID:[Significance of metabolic parameters in Hodgkin's disease (author's transl)]. 5 79

Monolayer and suspension cell cultures prepared from Hodgkin's disease tumors in the spleen were examined microscopically and by cytogenetics, tested for lymphocyte and monocyte cell surface properties, and assayed for enzymes by histochemical and spectrophotometric techniques. Hodgkin's disease monolayer cultures were composed of rapidly proliferating round and polygonal cells that were capable of propagation in vitro for an indefinite period of time. Abnormal aneuploid chromosomes were found in short-term Hodgkin's disease monolayers that had been passaged 16-20 times, and in established cell lines carried in culture longer than 3 yr and passaged more than 200 times. Cells fromHodgkin's disease monolayers contained lysozyme (muramidase), fluoride-resistant alpha naphthol acetate esterase, acid and alkaline phosphatase, and chymotrypsin-like activity. The monolayers did not exhibit specific cell surface markers or phagocytosis. Suspension cultures derived from Hodgkin's disease monolayers were composed of cells with aneuploid karyotypes and similar enzymes. The Hodgkin's disease suspension culture cells had surface receptors for complement and IgGFc, lacked surface or cytoplasmic immunoglobulin, and did not form Erosettes, react with an antithymocyte serum, nor exhibit phagocytosis. Normal monolayer culture cells, derived from adult spleen and human fetal spleen and thymus, were composed of spindle cells with a diploid number of chromosomes that could be carried for only a finite period of time in vitro. Normal cultured cells contained similar esterases and phosphatases, but were devoid of lysozyme and chymotrypsin-like activity. The morphologic, cytogenetic, cell surface, and enzymatic findings indicate that our Hodgkin's disease monolayer and suspension cultures are composed of cells with many properties suggesting an origin from monocytes (macrophages) rather than lymphocytes or fibroblasts. The presence of aneuploid karyotypes is consistent with a neoplastic origin and derivation from a malignant cell of Hodgkin's disease.
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PMID:Tissue culture studies in Hodgkin's disease: Morphologic, cytogenetic, cell surface, and enzymatic properties of cultures derived from splenic tumors. 6 93

The physiocochemical and immunological properties of alkaline phosphatase extracted from Hodgkin's nodes, non-Hodgkin's lymphoma nodes and leukemic leukocytes have been studied. The alkaline phosphatase from these three tumor types possesses the same biophysical and biochemical properties and immunological determinants as the placental alkaline phosphatase. However, it is more heat-labile than the placental isoenzyme. Immunological experiments indicate that, of these tumor types, Hodgkin's tumor contains the largest amounts of heat-labile Regan type of alkaline phosphatase.
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PMID:Occurrence of heat-labile Regan type of alkaline phosphatase in hematopoietic tumors. 11 39

Electron spin resonance spectroscopy has proved a useful and simple technique for the measurement of levels of caeruloplasmin and iron transferrin in whole blood from 50 patients with Hodgkin's disease. Those patients with clinically active disease show higher caeruloplasmin levels and lower iron transferrin levels than those with inactive disease. The results indicate that these tests are good indicators of the state of the disease and that serial measurement of these parameters may help in early prediction of clinical reactivity and in monitoring response to treatment. The combined information from iron transferrin and caeruloplasmin levels appears to be more predictive than that from the erythrocyte sedimentation rate and neutrophil alkaline phosphatase score.
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PMID:Electron spin resonance as a useful technique in the management of Hodgkin's disease. 19 8

Pinealectomy leads to increased formation of fibrous tissue in the abdominal cavity, increased skin pigmentation and elevated cholesterol and alkaline phosphatase levels. It also leads to reduced formation and/or action of prostaglandin (PG) E1 and thromboxane (TX) A2. PGE1 plays an important role in enhancing function of T suppressor lymphocytes which control overactive antibody-producing B lymphocytes. In primary biliary cirrhosis there are increased skin pigmentation, hepatic fibrosis, elevated cholesterol and alkaline phosphatase levels, defective T lymphocytes and hyperactive B lymphocytes. Primary biliary cirrhosis may be a pineal deficiency disease. Serotonin is important in the pineal and the serotonin antagonist methysergide may cause retroperitoneal fibrosis by interfering with pineal function. There is a good deal of other evidence which suggests that melatonin PGE1 and TXA2 are important in the regulation of fibrosis in other situations such as "collagen" diseases, lithium-induced fibrosis and cardiomyopathies. This suggests that enhancement of formation of PGE1 and TXA2 may be of value in diseases associated with excess fibrosis and defective T suppressor cell function. PGE1 levels may be raised by zinc, penicillin, penicillamine and essential fatty acids. TXA2 levels may be raised by low dose colchicine. These new approaches to treatment may prove safer and more effective than existing ones. They may be of value in disorders such as cardiomyopathy, Hodgkin's disease and other lymphomas, multiple sclerosis, Crohn's disease, atopy and other diseases in which defective T cell function is suspected.
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PMID:The pineal and regulation of fibrosis: pinealectomy as a model of primary biliary cirrhosis: roles of melatonin and prostaglandins in fibrosis and regulation of T lymphocytes. 31

Clustering of lymphocytes around Reed-Sternberg cells was noticed in single cell suspensions made from viable Hodgkin's lymphoid tissue. Cytocentrifugation of the suspension showed that clustering also occurred around a smaller cell type, thought to be the precursor of the classical Reed-Sternberg cell. Time-lapse cine films taken of the clustering showed unceasing activity on the part of the lymphocytes migrating over the surface of the central cell. Reed-Sternberg cells were reacted with anti-monocyte serum using indirect fluorescence techniques. In its mature form at least, the Reed-Sternberg cell showed no activity with the antiserum. No immunoglobulin was detected in the Reed-Sternberg cell using fluorescence techniques, but a few Reed-Sternberg cells showed diffuse cytoplasmic staining using the peroxidase-labelled antibody technique. Membrane receptor tests showed the lymphocytes surrounding the Reed-Sternberg cell to be T-cells. After proteolytic enzyme treatment to free lymphocytes from the surface, the Reed-Sternberg cell bound IgG-coated red blood cells indicating a probable Fc receptor. Cytochemistry demonstrated weak non-specific esterase activity in a small minority of Reed-Sternberg cells, and absence of acid phosphatase, alkaline phosphatase and peroxidase. A subpopulation of lymphocytes with distinctive segmentation of the nucleus was noted. These were often to be seen participating in lymphocyte rosettes around the Reed-Sternberg cell.
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PMID:Rosetting and other reactions of the Reed-Sternberg cell. 32 44

A characteristic alkaline phosphatase (orthophosphoric monoester hydrolase, alkaline pH optimum, EC 3.1.3.1) was detected in the sera of most patients with infectious mononucleosis, acute and chronic lymphatic leukaemia, non-Hodgkin's lymphoma, Burkitt's lymphoma and nasopharyngeal carcinoma. The enzyme was also present in the sera of nine out of 26 patients with cancer of the cervix. N-APase in these cases counted 30-100% of the total alkaline phosphatase activity. N-APase was absent from the sera of healthy individuals and of patients with acute and chronic granulocytic leukaemia, breast cancer, colon cancer, rheumatoid arthritis, ulcerative colitis, systemic lupus erythematosis, hepatitis and obstructive jaundice. Only three of 22 patients with Hodgkin's disease showed n-apase activity in the serum. In infectious mononucleosis the presence of N-APase activity was well correlated with the clinical course. In 13 cases studied, the clinical improvement was associated with the decrease or disappearance of N-APase activity. N-APase activity could not be detected in white cells of acute myeloid leukaemic patients, nor in the cells of myeloid blastic crisis of chronic granulocytic leukaemia. It was present in the cells of lymphoid blastic crisis of chronic granulocytic leukaemia.
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PMID:N-alkaline phosphatase: a potential disease marker for lymphoproliferative disorders. 43 2

Serum alkaline phosphatase levels in patients with Hodgkin's and non-Hodgkin's lymphoma were studied. The findings were correlated with clinical stage, particularly hepatic involvement, and histologic findings. Serum levels of other hepatic enzymes (SGOT, 5,N and gamma GT) were also measured. The usefulness of these studies for clinical staging was described, as well as speculation on the observed differences in Hodgkin's and non-Hodgkin's patients.
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PMID:Hepatic enzymes in Hodgkin's and non Hodgkin's lymphoma. 46 73

In 71 patients with lymphogranulomatosis (35 males and 36 females aged from 19 to 67 years) the hepatic function was studied prior to and during the cytostatic treatment. There were found considerable disturbances in the liver functioning and parallelism between the activity of the mentioned enzymes and the presence of intoxication, the enlarged liver size and intensity of the pathological process. During the treatment in some patients the activity of the enzymes under study was decreased or normalized. Changes in the activity of blood transminase, aldolase and alkaline phosphatase would reflect the gravity of destructive processes and disturbances in the liver function in patients with lymphogranulomatosis. The data obtained are of certain value for the treatment and prognosis of the disease.
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PMID:[Liver function in lymphogranulomatosis]. 46 63


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