Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The sudden onset of plasma cell leukemia with IgG-lambda-paraproteinaemia is reported in a 59-year-old patient. In the year before clinical manifestation of the disease the patient was examined and treated for a duodenal ulcer and a head injury on three separate occasions in different wards of the hospital without detection of any sign of disease of the haemopoetic system. The clinical features and course of the disease resembled those of acute leukaemia, the maximum percentage of plasma cells in the peripheral blood being 72 and in the bone marrow 98. Osteolytic bone lesions were not observed and there was no renal insufficiency. Therapy with mephelan-prednisolone and cyclophosphamide-prednisolone was not successful in influencing the fatal outcome of the disease.
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PMID:[Acute primary plasma cell leukemia (author's transl)]. 40 52

Reports on 102 patients suffering from IgD-myeloma are reviewed and analyzed. Patients with IgD-myeloma are younger than patients with myeloma producing IgG or IgA myeloma proteins. Males are affected by this disease 3 times as often as females and 11 times as often as female patients in the group producing kappa light chain type of IgD myeloma protein. Hyperproteinaemia and extreme spikes of the monoclonal immunoglobulin occur less often. Approximately 90% of the patients have a lambda light chain myeloma protein and almost all patients excrete Bence-Jones protein. Renal insufficiency, amyloidosis, and plasma-cell leukemia are found more frequently than in other types of multiple myeloma. IgD-multiple myeloma carries a poorer prognosis, possibly related to the frequent finding of renal insufficiency.
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PMID:[IgD-multiple myeloma. Review of 102 cases reported in the literature (author's transl)]. 81 Apr 9

Patients suffering from malignant disease will probably develop some metabolic abnormality of electrolytes. Hypernatremia is defined as an elevation of serum natrium over 150 mEq/l and caused by decrease of water intake, low level of ADH secretion and impaired response of kidney to ADH. Hyponatremia below 135 mEq/l of serum natrium is caused by SI-DAH, sick cell syndrome and increased loss of natrium from the kidney. On the other hand, hyperkalemia is defined as an elevation of serum kalium over 5.0 mEq/l and caused by acute tumor cell lysis syndrome, adrenal and renal insufficiency. Hypokalemia is caused by kalium loss from kidney and hypersecretion of mineral corticoid. Hypercalcemia is found in the high frequency among patients with malignant disease. Hypercalcemia is defined as an elevation of serum calcium over 11.0 mg/dl, although the most important aspect is the level of ionized calcium. The excess calcium causes defective urinary concentration with polydipsia, nausea and vomiting leading to volume depletion. At serum calcium levels about 13.8 mg/dl, there may be rapid deterioration or renal function, dehydration, coma and cardiac arrhythmias. Hypercalcemia is rarely the first manifestation of cancer. There are three principle pathogenic causes of malignant hypercalcemia, 1) hypercalcemia is a feature of several hematological cancers, including Burkitt's lymphoma, T cell leukemia, but most commonly with myeloma. The hypercalcemia in these myeloma patients is due to the secretion of an osteoclast activator, a lymphokine by the myeloma cells. 2) all patients with bony metastases have biochemical evidence of increased bone resorption. However, not all patients with bony metastases develop hypercalcemia. Probably the hypercalcemia is due partially to increased renal tubular reabsorption of calcium, mediated by a humoral factor, with activity similar to that of parathormone. 3) hypercalcemia in the patients without bony metastases is due to increased bone resorption caused by the ectopic secretion by the tumor. Mildly symptomatic patients will benefit from modest salt loading. They are dehydrated and replacement of the extracellular fluid is the first line of treatment. This may require 4-10 l normal saline/24 h. In addition, frusemide will increase calcium excretion. Calcitonin may be given subcutaneously or intravenously to refuse the mobilisation of calcium from bone. Glucocorticoids are unhelpful, but will prolong the effect of calcitonin. A diphosphonate is also useful.
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PMID:[Palliative therapy in cancer. 4. Palliation of the symptoms from a malignant tumor. (2)]. 169 56

Until recently long-term renal toxicity has not been considered a major late complication of bone marrow transplantation (BMT). Late renal dysfunction has been described in a pediatric population status post-BMT which was attributable to the radiation in the preparatory regimen. A thorough review of adults with this type of late renal dysfunction has not previously been described. Fourteen of 103 evaluable adult patients undergoing allogeneic (96) or autologous (7) bone marrow transplantation, predominantly for leukemia and lymphomas, at the Medical College of Wisconsin (Milwaukee, WI) have had a syndrome of renal insufficiency characterized by increased serum creatinine, decreased glomerular filtration rate, anemia, and hypertension. This syndrome developed at a median of 9 months (range, 4.5 to 26 months) posttransplantation in the absence of specific identifiable causes. The cumulative probability of having this renal dysfunction is 20% at 1 year. Renal biopsies performed on seven of these cases showed the endothelium widely separated from the basement membrane, extreme thickening of the glomerular basement membrane, and microthrombi. Previous chemotherapy, antibiotics, and antifungals as well as cyclosporin may add to and possibly potentiate a primary chemoradiation marrow transplant renal injury, but this clinical syndrome is most analogous to clinical and experimental models of radiation nephritis. This late marrow transplant-associated nephritis should be recognized as a potentially limiting factor in the use of some intensive chemoradiation conditioning regimens used for BMT. Some selective attenuation of the radiation to the kidneys may decrease the incidence of this renal dysfunction.
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PMID:Late renal dysfunction in adult survivors of bone marrow transplantation. 202 44

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

We report a case of nosocomial fatal varicella infection in a 13-year-old boy with acute lymphoblastic leukemia complicated with staphylococcal scalded skin syndrome. His underlying leukemia, immunosuppressive drugs, disseminated varicella, S. aureus colonization, and acute renal insufficiency were all contributing factors that were pathogenetically linked in the development of his generalized SSSS.
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PMID:Concomitant disseminated varicella and generalized staphylococcal scalded skin syndrome in a leukemic patient. 228 Feb 6

Within two years we have had the opportunity of observing seven leukemic children who were referred to our Pediatric Nephrology Unit for delayed renal failure following bone marrow transplantation (BMT). These children (3 to 12 years old), six with acute lymphoblastic leukemia (ALL) and one with acute non-lymphoblastic leukemia (ANLL), underwent BMT (4 autologous BMT, 3 allogeneic BMT) after the first remission in two, and after the second remission in five. Preparative regimen for BMT included cyclosphosphamide in three, cyclosphosphamide, vepeside and cytosine A in four, and a total body irradiation in a single dose of 10 grays (1000 R) in all of them. Three children were treated immediately after grafting with low dose cyclosporine for four to six months. Five to 10 months after BMT, four patients developed a hemolytic uremic syndrome with severe hypertension. The remaining three were found to have isolated renal insufficiency several months post-BMT. In the seven patients, renal biopsy showed a uniform pattern of severe glomerular involvement characterized by extensive lesions of mesangiolysis associated with severe arteriolonecrosis. A repeat biopsy performed one year later, in two patients showed severe scarring of the renal parenchyma with minor lesions of mesangiolysis. The similarity of the pathologic features observed suggests that the same mechanism might have been operative in the seven patients. It is very likely that the nephropathy is related to total body irradiation enhanced by chemotherapy. We conclude that current treatments of high risk leukemia might become a new cause of chronic renal failure. Further investigations are needed to know the exact incidence of this complication.
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PMID:Delayed renal failure with extensive mesangiolysis following bone marrow transplantation. 267 66

Cytoreduction for hyperleukocytosis before the initiation of primary therapy may reduce morbidity and mortality from blast cell lysis in children with acute lymphoblastic leukemia (ALL) and from leukostasis in children with acute nonlymphoblastic leukemia (ANLL) or chronic myelogenous leukemia (CML). The clinical features of 35 children (23 with ALL, 5 with ANLL, and 7 with CML) who underwent cytoreduction before the institution of definitive therapy were studied. Twelve children had exchange transfusions and 23 underwent leukaphereses. The cytoreductive procedures were equally effective in removing peripheral leukocytes (median decrease, 60%) and produced no complications. Ten children required additional cytoreduction because of further leukocyte increase before chemotherapy became effective. Three children with ALL who had renal insufficiency and metabolic derangement prior to leukapheresis subsequently required additional therapeutic measures. Three children with respiratory symptoms attributable to leukostasis improved after cytoreduction, and there were no episodes of intracerebral hemorrhage. These observations demonstrate the safety and efficiency of exchange transfusion and leukapheresis, and provide support for the role of cytoreduction in the early management of cases of hyperleukostasis and leukemia in children.
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PMID:Cytoreductive procedures in the early management in cases of leukemia and hyperleukocytosis in children. 347 80

We have observed five patients with smoldering adult T-cell leukemia (ATL) who had skin lesions as premonitory symptoms. The illness developed slowly, but flared up after several years. Skin lesions appeared in the form of erythema, papules, or nodules. Infiltration of the skin by ATL cells was slight, and the proportion of ATL cells in the peripheral blood was 0%-2%. The serum lactate dehydrogenase (LDH) value was within normal range and was not associated with hypercalcemia; lymphadenopathy, hepatosplenomegaly, and bone marrow infiltration were very slight. In most cases, hypergammaglobulinemia was seen, and in one case, monoclonal hypergammaglobulinemia was observed. All five patients had lived in an area in which ATL was endemic, and their anti-ATLA antibodies were positive; none had ever received a blood transfusion. One patient developed typical ATL after more than 13 yr of illness and died of renal insufficiency. Another patient developed typical ATL after 5 yr of illness and died of cryptococcus meningitis. Based on clinical and pathologic differences, we believe that these cases should be distinguished from typical ATL cases for the purposes of prognosis and treatment.
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PMID:A proposal for smoldering adult T-cell leukemia: a clinicopathologic study of five cases. 622 22

In 71 adult acute myelogenous leukaemia (AML) cases, the relationship between well-known prognostic features and complete remission (CR) rate and survival was studied. These features were: (i) bone marrow karyotype classified NN, AN, AA according to Sakurai & Sandberg (5); (ii) patients' age; (iii) clinical 'negative prognostic features' (NPF): previous history of preleukaemia, septicaemia or pneumonia, hyperleucocytosis, associated pathology (diabetes, obesity, renal insufficiency etc.). 59 years of age was found to be a frontier between 2 homogeneous groups having quite different prognosis. The NN/AN/AA classification had good prognostic value (CR rate and survival) in patients under 59 years, but not in older patients. In those patients over 59, a significant difference in CR rate and survival appeared between cases with NPF and those without. For each feature having an established relationship to survival, a panel of prognostic points was determined as follows: age over 59 (1 point), AA karyotype in patients under 59 (2 points), NPF in patients over 59 (1 point). Using this stage classification, it was possible to classify every case into 1 of 3 groups (i.e.: 0 points, 1 point, 2 points). The life-table analysis of these 3 groups showed very significant differences. The median survival times were 18.5 months, 5.2 months and 1.3 month, for the 0-point group (26 cases), the 1-point group (19 cases) and the 2-point group (26 cases), respectively.
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PMID:A stage classification for prognosis in adult acute myelogenous leukaemia based upon patients' age, bone marrow karyotype and clinical features. 658 30


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