Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Genetic markers in people of African ancestry and tables comparing Africans and Europeans are compiled to illustrate the blood differences. The existence of the African genetic characters, R0 (cDe), D-u and Ee (e-s, ce-s) in an Rh-Hr system are discussed. The high incidence of R0 (81.9%) in Africans is evident. Studies of ABO and the sickle cell trait in East Africa reveal the African tribes responsible for the original populating of Africa. The pygmoids of Uganda and Zaire, the Nilotes of West Nile, and the Bantu of Uganda are possibly responsible. Subgroups of A antigen in Africans and Europeans are compared, and their differences are outlined. These antigens appear to be different in the two races, and a reliable method for grouping A1 and A2 in Africans is described. For convenience, A2, Aint., Abantu, and other subgroups of A in Africans are renamed "non-A1." Attention to these subgroups on African paternity studies is emphasized. African problems in MNSs, Duffy, P, Lewis, and Sutter are presented. Immunoglobulines, Rh(D) immunization, enzyme autoantibodies, and a technique to detect them are discussed and described in detail. Studies on tropical splenomegaly syndrome show that it is an immune complex disease. Fluctuation titers of ABO iso-antibodies are observed to vary more strikingly in Africans than in Europeans. This is offered as a possible explanation of the high incidence of ABO hemolytic disease of the newborn in Africans.
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PMID:Characteristics of African blood. 80 20

MRL/1 mice, reported by Murphy and Roths, are lupus mice in which monogenic mutation has occurred. They are characterized by the expression of massive lymphoadenopathy, splenomegaly, arthritis and glomerulonephritis. These specific characters are attributable to the proliferation of abnormal T cells governed by an autosomal recessive gene, which is called a lymphoproliferative (lpr) gene. In this study, the author has studied the pathology of various organs in MRL/1 mice in relation to their ages. Investigated the pathogenesis of spontaneous submaxillaritis in MRL/1 mice and mechanism of its occurrence. Based on the immunological abnormalities in MRL/1 mice studied thus far, the mechanism of onset of submaxillaritis is believed to be as follows; (1) expression of the lpr gene leads to proliferation of T cells accompanied by focal lymphocyte infiltration in the submandibular gland; (2) the helper T function of these proliferating T cells induces polyclonal B cell activation (PBA); (2) PBA leads to the formation of numerous autoantibodies and anti-gp70 antibody whose antigen is the glycoprotein of endogenous retrovirus, resulting in the massive formation of immune complexes; (4) the immune complexes are deposited on the vascular wall, resulting in activation of the complement system; (5) infiltration of neutrophils and macrophages is induced; and (6) the lysosomal enzymes, released from these cells, effects as a cytotoxic mediator and damages the vascular wall. In brief, submaxillaritis accompanied by granulomatous vasculitis can be regarded as a Type III allergic response caused by immunological abnormalities which are genetically determined by the lpr gene; it is thought to be a subtype of immune complex disease.
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PMID:[Immunohistochemical study of the submaxillaritis in MRL/1 mouse (lymphoproliferation and autoimmunity)]. 253 61

An 8-year-old boy developed anaphylaxis after receiving his maintenance dose of immunotherapy and proceeded to display the signs and symptoms of serum sickness. These consisted of fever, arthralgia, arthritis, urticaria followed by a hemorrhagic palpable rash, edema, lymphadenopathy, splenomegaly, abdominal pain, proteinuria, and neurologic manifestations consistent with vascular compromise of the posterior cerebral circulation. A skin biopsy specimen revealed perivascular infiltrates of lymphocytes and few polymorphonuclear neutrophils. The timing of events in this patient suggests that immunotherapy initiated a chain of events beginning with anaphylaxis and leading to serum sickness. It is hypothesized that the enhanced vascular permeability that accompanied the anaphylaxis allowed immune complexes that may have preexisted in the circulation to deposit in the blood vessels of the patient. These complexes may or may not have been related to the immunotherapy itself. Because antihistamines are known to prevent the induction of serum sickness, early and aggressive treatment of anaphylaxis during immunotherapy may prevent the occurrence of immune complex disease.
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PMID:Serum sickness triggered by anaphylaxis: a complication of immunotherapy. 405 55