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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kidney disease was studied patho-histologically, electron microscopically and immunologically in Wistar rats ranging in age from 2 weeks to 24 months. Glomerular lesions characterized by adhesion of podocyte foot processes were first detected at 3 months of age. The kidney lesions became more pronounced with age, as manifested by an increase of mesangial matrix, basement membrane thickening, crescent formation and hyalinization of glomeruli, and tubular degeneration. Evidence for the deposition of immune complexes in the kidney was obtained by immunofluorescence and electron microscopy, as well as by immuno-electrophoretic analysis of kidney elutions. Tests with antiserum reagent against Moloney leukemia virus antigen revealed its presence in some but not all glomeruli. The presence of other viruses in Moloney leukemia virus negative glomeruli was not ruled out. Serum autoantibody against an array of rat tissues could not be detected. Therefore, it would appear that autoimmune mechanism may not be the primary underlying cause of pathogenesis of the disease. Accordingly, the disease could be referred to as chronic immune complex glomerulonephropathy with nephrotic syndrome, but sources of the antigens in the complex were mostly unknown, althougn virus could be one portion of them. The possibility that diet antigens may also be present in the complex seems unlikely because attempts to demonstrate serum antibodies against diet pellet in old rats were unsuccessful.
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PMID:Characterization of age-associated kidney disease in Wistar rats. 12 95

The nephrotic syndrome complicating malignancy in the absence of renal vein thrombosis, amyloid or neoplastic infiltration of the kidney is an unusual occurrence. A case of diffuse, well differentiated, lymphocytic lymphoma and lipoid nephrosis documented by light microscopy, electron microscopy and immunofluorescent studies is reported. A review of the literature revealed 76 case reports in which the nephrotic syndrome was associated with neoplasia. The most frequently associated neoplasms are Hodgkin's disease, various carcinomas, nonHodgkin's lymphoma and leukemia in descending order. The most frequent renal lesion in patients with the nephrotic syndrome associated with various carcinomas is membranous glomerulonephritis (81 per cent) as opposed to patients with lymphomas or leukemias who have predominantly lipoid nephrosis (60 per cent). The evidence is reviewed suggesting that the lesions in membranous nephropathy are immunologically mediated by tumor or viral antigen-antibody complexes and in lipoid nephrosis perhaps by a defect in t-lymphocyte function.
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PMID:The nephrotic syndrome associated with neoplasia: an unusual paraneoplastic syndrome. Report of a case and review of the literature. 18 Aug 1

A study of 3451 cholesterol determinations in different diseases was carried out. The mean cholesterol levels for male and female adults and children with different diseases were compared with values for their healthy counterparts. Sickle cell anemia, leukemia, liver cirrhosis, hepatosplenomegaly, tuberculosis, and diabetic, nutritional, ataxic, and tropical neuropathies in male and female adults were associated with reduced cholesterol level while in children malnutrition and anemia were the main causes of low cholesterol levels. Obesity and hypertension caused an elevated level but the mean values were within the range for adult Nigerians in the high income group. Only nephrotic syndrome in both adult and children was associated with a markedly increased cholesterol level in Nigerians of low income status.
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PMID:Serum cholesterol and diseases in Nigerians. 50 76

A boy, aged 14, suffered since his 5th year from nephrotic syndrome. During the first 7 years he had been treated with adrenocorticosteroids, but his condition hardly improved. Then a cyclophosphamide treatment was started with a total dosis of 5 g in 50 days. The nephrotic syndrome had disappeared, but relapsed 3 years afterwards, this time accompanied by chronic myelogenous leukaemia. The possibility of the onset of chronic myelogenous leukaemia in connection with the immunosuppressive therapy (adrenocorticosteroids and cyclophosphamide) is discussed.
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PMID:[Chronic myelogenous leukaemia as a possible consequence of immunosuppressive treatment of nephrotic syndrome (author's transl)]. 105 34

The authors present a 4-year-old girl with nephrotic syndrome who developed actue lymphoblastic leukaemia 5 months after the start of a combined treatment of alternate day prednisone and daily cyclophosphamide during 3 months. The nephrotic syndrome was due to focal segmental glomerulosclerosis. The occurrence of leukaemia might be related to the preceeding treatment with cyclophosphamide.
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PMID:Acute lymphoblastic leukaemia after treatment of nephrotic syndrome with immunosuppressive drugs. 106 23

Erythrocyte 2,3-diphosphoglycerate (2,3-DPG) concentrations in 10 patients with acute lymphoblastic leukemia rose 21.3%(P smaller than 0.02) after 3 weeks of prednisone and vincristine therapy, and returned to pretreatment level 2 weeks after therapy had been discontinued. The mean 2,3-DPG level of three patients on vincristine alone did not vary significantly from the control level of the leukemia patients on prednisone and vincristine. No significant change in serum inorganic phosphate level was observed. The mean erythrocyte 2,3-DPG concentration of 17 nephrotic syndrome patients being treated with chronic prednisone therapy was 14.0% higher than a control group of 20 nephrotic syndrome patients not being treated with prednisone (P small than 0.01). A significant positive correlation was observed between the dose of prednisone and 2,3-DPG level.
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PMID:Pharmacologic manipulation of human erythrocyte 2,3-diphosphoglycerate levels by prednisone administration. 109 Aug 92

Testicular function was examined by means of HCG-stimulation tests in 6 prepubertal or pubertal patients with leukemia or malignant tumours during cytostatic therapy and in 5 patients with nephrotic syndrome after discontinuation of treatment. The results of urinary testosterone assays suggest no damaging effect of cyclophosphamide on Leydig cell function.
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PMID:Testicular endocrine function and cyclophosphamide in prepubertal and pubertal patients. 118 97

In this report the association of autoimmunity and autoimmune syndromes with lymphoproliferative disorders (LPD) is described in 15 patients. Non-Hodgkin's lymphoma (NHL) developed in 10 patients, Hodgkin's disease (HD) in 3 and chronic lymphocytic leukemia (CLL) in two. In most instances clinical and laboratory phenomena preceded the development/diagnosis of these disorders. Manifestations ranged from the presence of autoantibodies in the serum to the presence of both ill defined or incomplete autoimmune syndromes including cold urticaria, Raynaud's phenomenon, cold agglutinin disease, thyroiditis, nephrotic syndrome and vasculitis to typical systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and even one of scleroderma. It is suggested that in some patients (in)complete clinical manifestations of autoimmunity may precede the development of lymphoid neoplasias. The link between autoimmunity and lymphoproliferative disorders is briefly discussed.
Leukemia 1992 Nov
PMID:Autoimmunity and auto-immune syndromes associated with and preceding the development of lymphoproliferative disorders. 143 18

A leukaemic phase is uncommon in large cell lymphoma, particularly at presentation of the disease, and very few cases have been reported since immunological markers became available. We have studied 24 cases presenting over a period of 15 years. 16 were B-lineage and eight T-lineage. In five patients the large cell lymphoma represented a transformation of a preceding low grade, small cell lymphoproliferative disease. Three other patients with T-lineage large cell lymphoma presented with skin infiltration (two cases) or lymphoma-associated nephrotic syndrome (one case) 3-9 months before leukaemia occurred. The other 16 patients (12 B-lineage and four T-lineage) presented with de novo large cell leukaemia/lymphoma. With the exception of skin infiltration, clinical features did not differ between T and B-lineage cases. Prognosis was generally poor although a minority of patients lived 1-2 years. Median survival was 7 months. In the B-cell lymphomas immunological markers were those expected but among the T-cell cases there were many unusual immunophenotypes with frequent failure to express markers which are usually positive in peripheral T cells. Without the availability of immunological markers diagnosis would have been difficult, with acute myeloid leukaemia being the most important differential diagnosis. T-lineage and B-lineage cases could not be distinguished on cytological features. In the majority of cases the cells were very pleomorphic with nuclear lobulation, prominent nucleoli and marked cytoplasmic basophilia being commonly observed. Marked nuclear lobulation was not confined to T-lineage cases but was seen also in seven of 12 cases of de novo B-lineage leukaemia/lymphoma; it was readily apparent in histological sections and on ultrastructural examination.
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PMID:Leukaemia as a manifestation of large cell lymphoma. 201 54

Humoral immunity involves molecules in solution in biological fluids including effectors of non specific immunity (e.g. complement, cytokines) and specific immunity (antibodies) as well. Acquired humoral immunodeficiences are often multifactorial in origin and associated with defects of cell-mediated immunity. The most common etiologies are those of iatrogenic immunodeficiencies: surgery (especially splenectomy), radiotherapy, chemotherapy of leukemia and cancer, immunosuppressive treatments in organ transplanted patients. Protein-caloric malnutrition also induces cellular and humoral immunodeficiencies. Among other causes, three types of diseases may induce defective antibody production: 1/B cell neoplasias (e.g. multiple myeloma, chronic lymphocytic leukemia...) 2/renal diseases (nephrotic syndrome, renal insufficiency) and 3/various infectious diseases, including AIDS. Some principles of prevention and treatment of secondary humoral immunodeficiencies are given.
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PMID:[Secondary deficiencies of humoral immunity]. 204 15


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