Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypercalcemia is a rare metabolic disorder in course of B cell lymphoma. The mechanism of hypercalcemia in patients with malignancy may include the increased extrarenal production of vitamin D from tumoral cells or neighboring macrophages, i-PTH or PTHrP from tumoral cells. In this case we reported a 34 years old caucasian woman with acute renal failure and hypercalcemia as onset of splenic lymphoma in absence of abnormal levels of serum vitamin D and PTHrP. Because of dramatic recovery of renal function and hypercalcemia after splenectomy, we can speculate that main mechanism of hypercalcemia is related to vitamin D production from neighboring lymphoma macrophages.
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PMID:Acute renal failure and hypercalcemia as onset in splenic lymphoma. 2178 May 56

Gaucher disease is a multisystemic metabolic disorder due to a genetic deficiency of the lysosomal enzyme glucocerebrosidase, which leads to the accumulation within the lysosomes of macrophages of its natural substrate, glucosylceramide and its deacylated product glucosylsphingosine. The most prevalent form of the disease is the so-called non-neuronopathic form (type 1) characterized by anemia, thrombocytopenia, enlargement of liver and/or spleen, skeletal abnormalities. Etiology of anemia and thrombocytopenia may be multifactorial and not necessarily predicted by the degree of splenomegaly. Bleeding diathesis may not always be related to absolute platelet count but may be influenced by abnormal platelet function or coagulation factor deficiencies. A significant increased risk of severe hematological co-morbidities, including multiple myeloma and B-cell lymphoma, has been reported. Accumulation of glucosylceramide and glucosylsphingosyne in macrophages and the resulting chronic inflammation with the secretion of cytokines leading to polyclonal and monoclonal B cell proliferation up to multiple myeloma, as a continuum clonal expansion, is a key pathophysiological mechanism. Enzyme replacement therapy has been shown to be effective in reducing glucosylceramide storage burden and the deleterious effects caused by its accumulation, including hematological manifestations.
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PMID:Hematological manifestations and complications of Gaucher disease. 2656 53