Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Africa, the "dark continent" and the source of such wonderful tales as King Solomon's Mines and Jock of the Bushveld, has an equally enthralling story to tell about malignant disease in general and the lymphomas in particular as they occur among its varied people. It is uncertain how far back in history contact existed with the rest of the world, primarily in the form of slave trading and colonization by, among others, the Portuguese and the British. Until recent times, however, Africa's secrets have remained largely undisturbed. Fragments of medical information are recorded in the diaries of those early, intrepid explorers, such as Albert Cook, Henry Stanley, David Livingstone, and Albert Schweitzer. However, it is only in recent years that the great natural experiments that have for so long been underestimated, and very much less understood, belatedly started to attract attention. Examples are the systematic studies by Denis Burkitt, who through perseverance unraveled the lymphoma that now bears his name, and the thought-provoking description of the immunoproliferative small intestinal disease carried out by the Cape Town group, with both illustrating the axiom that "the study of man is man." Despite such occasional outstanding achievements, there is still considerable paucity of data pertaining to the various lymphoreticular malignancies, so that only limited conclusions are possible. Certainly, lymphoma in Africa differs from that elsewhere in the world. In part, this may reflect a background of immunologic disturbance attributable to parasitic infestation, viral infection, rampant malnutrition, and the impact of a wide variety of vectors, such as mosquitoes, in disease transmission. Striking differences exist in the distribution of these tumors as the incidence and pattern are followed from the equator to the milder climates in the south. This confirmed phenomenon gives rise to the tantalizing suggestion that, to some significant extent, the changes reflect the influence of geography. Thus, there may be associated alterations in the fauna and flora that determine the presence of intermediary hosts that have an impact on the eventual expression of the malignant clone. Many questions remain unanswered. For example, how can the lower incidence of Hodgkin's disease and the predominance of high-grade malignancies in the tropics and subtropics be explained? To what extent does the lymphocytic and plasmacytic hyperplasia, ascribed to intense antigenic stimulus in Burkitt's lymphoma and myeloma--perhaps even other lymphomas, such as IPSID--predispose the host to a mutational event that leads to the emergence of each distinctive neoplasm?(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The malignant lymphomas in Africa. 193 63

An 8-yr-old nonallergic girl with non-Hodgkin's lymphoma had markedly elevated serum IgE at presentation (greater than 10,000 IU/ml), negative skin tests to a battery of 24 common allergens, and no evidence of parasitic infestation. Serum levels of IgG, IgA, and IgM were normal. Remission after cytotoxic chemotherapy was accompanied by a marked reduction in serum IgE levels (to less than 200 IU/ml) with no change in the level of serum IgG, IgM, or IgA. Recurrence of the lymphoma 7 mo after remission was accompanied by an isotype specific rise in serum IgE (to 3,850 IU/ml). Isoelectric focusing revealed that the IgE was polyclonal. Phenotypic analysis of the lymphoma obtained during relapse revealed all (greater than 98%) cells to be T3+, T4+, and T8+. Incubation of lymphoma cells with human myeloma IgE followed by immunosorbent purified fluorescein tagged goat anti-human IgE (anti-IgE PS-adsorbed over IgE ADZ) stained 25% of the cells. In contrast, less than 1% of the cells were stained after incubation with human IgG followed by fluorescein conjugated goat anti-human IgE. Supernatants from lymphoma cells (5 X 10(6)/ml, 48 h) enhanced IgE production in B cells derived from four patients with allergic rhinitis (mean +/- SD picograms per milliliter of net IgE 930 +/- 320 in unstimulated cultures versus 2,450 +/- 650 in cultures stimulated with lymphoma supernatants; P less than 0.01) but did not induce IgE synthesis in B cells from two normal subjects that synthesized no IgE spontaneously. Lymphoma supernatants failed to enhance IgG synthesis by B cells of both allergic and nonallergic subjects. These results indicate that a T cell lymphoma comprised of cells bearing Fc receptors for IgE with a phenotype characteristic of immature T cells (i.e., T3+, T4+, T8+) exhibited IgE specific helper function. This lymphoma may represent the monoclonal expansion of a subpopulation of IgE specific helper T cells.
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PMID:A human T cell lymphoma secreting an immunoglobulin E specific helper factor. 315 54

In the treatment of osteoporosis, M. Kahler and bone metastases from prostate and breast cancer bisphosphonates play a major role. Not all patients respond well to bisphosphonate treatment. Since a few years adverse effects of these drugs have been reported. A new drug, denosumab, a fully human monoclonal antibody to RANKL, has recently been developed. This case reports a 74-year-old male patient with a medical history of diabetes mellitus, angina pectoris, coronary bypasses, hypertension, and prostate cancer with multiple metastases to lymph nodes, bone and lungs. The prostate cancer was treated according to the protocol. But he was never treated with bisphosphonates. Instead he was included in a phase III randomized double blind multicenter trial, testing the efficacy of denosumab compared to zoledronic acid in the treatment of bone metastases of hormone resistant prostate cancer. Only 7 months after start of denosumab infectious symptoms developed, followed by infestation of the mandible. Despite surgical treatment fistula and exposed bone remained. This case illustrates that use of denosumab can lead to a type of osteonecrosis resembling bisphosphonate related osteonecrosis of the jaws.
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PMID:Denosumab osteonecrosis of the mandible: a new entity? A case report. 2326 7

We report the case of a 59-year-old Afro-Caribbean woman who presented with symptoms of anorexia, lethargy, abdominal distension and vomiting on the background of newly diagnosed multiple myeloma, treated with one cycle of cyclophosphamide-thalidomide-dexamethasone chemotherapy 20 days previously. A diagnosis of subacute bowel obstruction was made; however, the aetiology of the obstruction remained elusive. Common electrolyte abnormalities were excluded and a midline laparotomy revealed minimal intra-abdominal adhesions. Histological examination of a small bowel mesentery biopsy showed inflammatory cell infiltrate composed of lymphocytes, eosinophils and occasional plasma cells with a foreign body giant cell reaction suggestive of worm infection. A postoperative stool sample revealed heavy infestation with the rhabditiform larvae of Strongyloides stercoralis. The patient recovered following ivermectin treatment. In the absence of other causality, we attribute the subacute bowel obstruction to S stercoralis hyperinfection, triggered by immunosuppression secondary to chemotherapy and multiple myeloma.
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PMID:Strongyloides stercoralis hyperinfection presenting as subacute small bowel obstruction following immunosuppressive chemotherapy for multiple myeloma. 2446 40