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)

Autoimmune (NZB X NZW) F1 female hybrid mice were treated with LS-2616, a recently developed substance with immunomodulating properties. Treatment was initiated at the age of 4 months (i.e. at the early stage of the disease) as well as at 7 months of age (i.e. after the development of established lupus-like disease). Control groups treated with cyclophosphamide and physiological saline were also studied. Beneficial therapeutic effects were obtained regardless of when the treatment was initiated and the dose of LS-2616 administered (1 and 8 mg/mouse/week). The effects of LS-2616 on longevity, splenomegaly and glomerulonephritis were pronounced and sometimes comparable to those of cyclophosphamide (1.8 mg/mouse/week). The results obtained suggest that LS-2616 may be useful in the treatment of autoimmune disease in man.
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PMID:Effects of LS-2616 administration upon the autoimmune disease of (NZB x NZW) F1 hybrid mice. 380 79

In the past 10 years we have examined 20 children with inflammatory liver disease associated with high serum titers of anti-liver-kidney microsome antibody (anti-LKM). The first hepatic symptoms were progressive fatigue and jaundice, the fortuitous finding of hepatomegaly or splenomegaly with raised transaminase activity, or an acute hepatitis-like illness. At the time of diagnosis, hepatomegaly was present in 18 children, splenomegaly in 16, jaundice in nine, and ascites in two. Serum alanine transferase activities were elevated in all but two, who had already received steroids. Serum total gammaglobulin values were greater than 2.0 gm/dl in 16 children, prothrombin activity less than or equal to 60% in six, and serum titer of anti-LKM between 1:100 and 1:100,000. All children but one had cirrhosis, and histologic signs of aggressivity were present in 14. In 11 children one or more extrahepatic diseases were present, including type 1 diabetes, vitiligo, glomerulonephritis, autoimmune hemolytic anemia, hypoglycemia with hyperinsulinism, autoimmune thyroiditis, chronic mucocutaneous candidiasis with hypoparathyroidism, and multiple cutaneous and visceral telangiectasias. Treatment with prednisone and azathioprine improved the liver condition in 16 of the 18 patients given treatment. In eight of them discontinuation of treatment resulted in rapid relapse; 14 are still receiving treatment and have stable hepatic function with follow-up from 8 months to 6 1/2 years. Only two are free of treatment. Four children died, two in spite of immunosuppressive therapy, one during a relapse, and one of extrahepatic disease. These results indicate that this autoimmune inflammatory liver disease may have onset early in life, with several clinical patterns; is frequently associated with certain types of extrahepatic manifestations of autoimmune origin; and is a potentially fatal disease for which immunosuppressive treatment must be started early.
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PMID:Liver disease associated with anti-liver-kidney microsome antibody in children. 395 Aug 19

One splenectomized and 6 intact coyotes (Canis latrans), and 2 coydogs were experimentally inoculated with a recent isolate of Babesia gibsoni. The disease was mild in intact animals, was fatal in the splenectomized coyote, and was characterized by a regenerative hemolytic anemia with the PCV decreasing to 16% in intact animals and to 6% in the splenectomized coyote. Peak parasitemia ranged from 3% to 21% of erythrocytes infected and was inversely correlated to PCV. Serum lactate dehydrogenase, bilirubin, and globulin concentrations were increased in all infected animals. Three weeks after inoculation, specific antibody titers increased to 1:65,536 and remained elevated in the chronically infected animals. The splenectomized coyote had progressive weakness until death, 24 days after inoculation. Intact animals had splenomegaly and anorexia at the height of infection. The splenectomized coyote had generalized edema, omental petechiae, renal and hepatic degeneration, membrano-proliferative glomerulonephritis and congestion, extramedullary hematopoiesis, lymphoid hyperplasia, and severe hemosiderosis in an accessory spleen. The only consistent change in the intact animals was splenomegaly.
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PMID:Experimental babesiosis in coyotes and coydogs. 397 Apr 35

Nonspecific immunity (NSI) was manifested in rats injected intravenously with killed Corynebacterium parvum and challenged with Trypanosoma lewisi, Plasmodium chabaudi, or Babesia rodhaini. The NSI became evident some 5 days after infection as a suppressed parasitemia, a more rapid recovery from patent infection and as enhanced survival among rats infected with B. rodhaini. The C. parvum injections produced anemia and thrombocytopenia with splenomegaly and signs of glomerulonephritis in rats. The signs became evident about 5 days after injection and were accompanied by reduced titers of lytic complement, elevated titers of antibody against fibrinogen products (Anti-F), antibody against soluble serum antigen of malaria and babesiosis (ABSA), and antibody against the third component of fixed complement or immunoconglutinin (IK). These were the autoantibodies associated with anemia and reduced parasitemia of infection-induced NSI. In as much as immunoconglutination of blood cells or parasites coated with complement fixing immune complexes was implicated as a functional mechanism in infection-induced NSI, it is possible that these same factors might function in C. parvum induced NSI.
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PMID:Anemia and thrombocytopenia from Corynebacterium parvum-stimulated resistance against malaria, trypanosomiasis, and babesiosis. 635 27

A new spontaneous autosomal recessive mutation has recently occurred at the motheaten (me) locus on Chromosome 6 in strain C57BL/6J mice. Homozygotes for the new allele, designated "viable motheaten" (mev), have a mean life span of 61 +/- 2.4 days, compared with only 22 +/- 1.3 days for C57BL/6J-me/me mice. Like the original motheaten mutation, the immediate cause of death in mev/mev mice appears to be severe pneumonitis associated with accumulations of macrophages, granulocytes, and lymphocytes in the lungs. However, because of its longer life span, progression of the disease in mev/mev mice is more amenable to investigation. Eosinophilic crystalline material in alveolar macrophages from mev/mev mice is associated with extravasation of erythrocytes into alveoli. These crystals are morphologically indistinguishable from hematoidin, which results from hemoglobin breakdown following uptake of erythrocytes by macrophages. Severe macrocytic hypochromic anemia with abnormalities in size and shape of erythrocytes develops by 7 weeks. A two-fold increase in peripheral leukocyte count and a five-fold increase in the percentage of neutrophils is seen by 10 weeks. Viable motheaten mice develop focal granulocytic skin lesions by 4 days of age, show depletion of cells from the thymus cortex by 4 weeks, and lack lymphoid follicles in the lymph nodes, spleen, and Peyer's patches. Excessive erythropoiesis and myelopoiesis in the spleen result in marked splenomegaly. Lymph nodes and spleens from mev/mev mice contain increased numbers of plasma cells by 3 weeks; and by 6 weeks, large numbers of atypical plasma cells with Russell bodies are evident. Development of glomerulonephritis by 10 weeks is characterized by granular depositis of immunoglobulin and complement within glomeruli. A twofold increase of blood urea nitrogen levels is present by 15 weeks. Sterility of male mev/mev mice is associated with Leydig cell depletion in the testes, lowered testosterone levels, and impaired spermatogenesis.
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PMID:"Viable motheaten," a new allele at the motheaten locus. I. Pathology. 638 Feb 98

Therapeutic trials with mizoribine (MZR), an imidazole nucleoside immunosuppressant, on experimental lupus nephropathy of NZB/W F1 mice resulted in the following. The MZR treatment, 20 mg per kilogram of body weight every other day, starting at 14 weeks of age, caused a significantly prolonged survival time of mice with a mean life span of 54.3 +/- 4.2 weeks, compared with the untreated controls, who had a mean survival time of 38.1 +/- 2.9 weeks (P less than 0.01). In addition, MZR suppressed the elevation of serum anti-DNA antibody titers, the spontaneous development of splenomegaly, and the histological development and progression of glomerulonephritis observed in untreated animals. Although no definite explanation is available at present to explain how MZR caused decreased anti-DNA antibody production and delay in the development of glomerulonephritis in these animals, it is suggested that it acts by directly suppressing the hyperfunctioning B cells of lupus mice. MZR may prove to be a promising immunosuppressant for the treatment of human lupus, in view of its lesser side effects such as bone marrow suppression or hepatotoxicity.
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PMID:Effect of mizoribine on lupus nephropathy of New Zealand black/white F1 hybrid mice. 647 55

BXSB male mice spontaneously develop progressive autoimmune disease characterized by high serum immunoglobulins, including anti-nuclear antibodies (ANA), enlarged spleen and lymph nodes, and diffuse proliferative glomerulonephritis. Females develop symptoms at a much slower rate. The mechanisms underlying the autoimmune disease and the nature of the Y-linked accelerating factor have not yet been elucidated. We found that the male progeny of the cross between the non-autoimmune strain CBA/Ca and BXSB (CBA/Ca X BXSB)F1 showed progressing signs of autoimmunity starting at 6 to 7 mo. In contrast, the male progeny that resulted from BXSB males crossed with immune-defective CBA/N females (Xid) were devoid of splenic B colonies, were nonresponsive to TNP-Ficoll, and were free of autoimmune disease for at least 10 mo. At 18 mo, some of the (CBA/N X BXSB)F1 mice developed weak antinuclear antibodies, but no spleen or lymph node enlargement was seen. The same mice had low anti-TNP Ficoll responses but did not produce B colonies in vitro. The role of the X chromosome in regulating expression of autoimmunity in young and old BXSB mice is discussed.
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PMID:CBA/N X-linked defect delays expression of the Y-linked accelerated autoimmune disease in BXSB mice. 660 Apr 68

Trypanosoma brucei EATRO 110 infection of the deer mice (Peromyscus maniculatus) produced moderate to marked lesions in the spleen, liver, heart, and kidney seven to ten weeks after infection. Splenic lesions consisted of marked splenomegaly, with infected spleens weighing 25.9 times control spleens. Transmission electron microscopy of the sinuses and Billroth's cords of the splenic red pulp demonstrated an increased cellularity with greater contact between cells due partly to proliferation of macrophages, transformed lymphocytes and plasma cells and partly to accelerated erythropoiesis with increases in the numbers of rubricytes and reticulocytes. Erythrocytes also were present in large numbers, and erythroclasis was accelerated. Hepatic lesions consisted of necrosis of few hepatocytes, proliferation and hypertrophy of Kupffer's cells which exhibited increased phagocytosis--particularly of erythrocytes, as well as perivascular cuffs consisting of lymphocytes, plasma cells and macrophages. Myocarditis was marked and was characterized by degeneration of myocardial fibers with decreases in mitochondrial size and myofibril contents and fragmentation of some degenerating fibers, and was accompanied by accumulation of inflammatory cells including lymphocytes, transformed lymphocytes, plasma cells, and macrophages between the myocardial fibers. Renal lesions consisted of severe glomerulonephritis characterized by deposition of electron dense material along the basement membrane and in the mesangium of the glomerular tufts, and less frequently beneath the basement membrane and visceral epithelium of the Bowman's capsule and within the peritubular vessels. Neutrophils with fewer macrophages and lymphocytes invaded the glomeruli.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathogenesis of Trypanosoma brucei infection in deer mice (Peromyscus maniculatus). Ultrastructural pathology of the spleen, liver, heart, and kidney. 673 Feb 6

An agent morphologically similar to Haemobartonella muris was isolated from the blood of rats infected with a strain of Trypanosoma lewisi kept at this Department. It caused acute hemolytic anemia, splenomegaly, glomerulonephritis, and death within 5 to 8 days in mature Sprague-Dawley rats. The disease was less severe in weanling rats which usually recovered within 3 to 4 wk. The anemia was accompanied by phagocytosis of erythrocytes by monocytes of the spleen and bone marrow, by high titers of cold-active hemagglutinin, high titers of antibody to the third component of fixed complement (immunoconglutinin), and antibody to fibrinogen/fibrin related products. Filtrates of blood from anemic rats passing a 0.20-micron filter did not produce disease or signs of infections, but filtrate from a 0.45-micron filter was infective. Attempts to grow the agent on rat embryo fibroblast cultures and in embryonated chicken eggs were successful. Tests for bacteria, mycoplasma, and spirochetes gave negative results. Blood of infected rats did not produce signs of infections when inoculated into laboratory mice, and normal rats housed in cages with acutely infected rats did not develop signs of infection or disease. Morphological similarity did not allow differentiation of the agent from H. muris. However, its virulence for mature rats differs markedly from that usually seen in H. muris infection.
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PMID:Immunoconglutinin and antibody against fibrinogen products in hemolytic anemia and nephritis resulting from infection with a Haemobartonella-like agent. 726 35

Congenital neutropenias include a heterogenous group of diseases characterized by a decrease in circulating neutrophils. In phase I/II/III studies in patients with severe congenital and cyclic neutropenia, treatment with recombinant human granulocyte colony-stimulating factor (r-metHuG-CSF) resulted in a rise in the absolute neutrophil counts (ANC) and a reduction in infections. We report the effects of long-term safety of subcutaneous r-metHuG-CSF administration in 54 patients (congenital n = 44. cyclic n = 10) treated for 4-6 years. A sustained ANC response was seen in 40/44 severe congenital neutropenia patients and 10/10 cyclic neutropenia patients. Two patients required an increase of > 25% in dose to maintain a clinical response; one patient became refractory to therapy. A significant decrease in the incidence of severe infections and the need for intravenous antibiotics was noted. Significant adverse events noted which may or may not be related to therapy included: osteopenia (n = 15), splenomegaly (n = 12), hypersplenism (n = 1), vasculitis (n = 2), glomerulonephritis (n = 1), BM fibrosis (n = 2), MDS/leukaemia (n = 3), and transient inverted chromosome 5q with excess blasts (n = 1). R-metHuG-CSF has been well tolerated in the majority of patients and resulted in a long-term improvement in their clinical status.
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PMID:Long-term safety of treatment with recombinant human granulocyte colony-stimulating factor (r-metHuG-CSF) in patients with severe congenital neutropenias. 1093 Oct 6


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