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)

The spleen cells transfer from mice CBA at the 25th day of the carcinogenesis latent period induced by adenovirus SA7(S8) to newborn syngeneic animals caused the graft versus host reaction in them. There was splenomegaly and progressive decrease in weight of the recipients' thymus. Analogous alterations of lymphoid organs were noted in the animals infected during the neonatal period by oncogenic adenovirus SA7(C8). Results showed that adenoviral carcinogenesis had some manifestations of autoimmune disease.
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PMID:[Mechanisms of changes in the mass of the organs central to immunity during adenovirus carcinogenesis]. 2 79

The clinical and pathologic findings in 24 patients with "angio-immunoblastic lymphadenopathy with dysproteinemia" (AILD) are presented. The patients' ages ranged from 44 to 80 years, with a median age of 68 years. The disease has an acute onset. In many respects, the clinical presentation is suggestive of malignant lymphoma. Generalized lymphadenopathy was always present. Hepatomegaly was found in 20 patients, splenomegaly in 17, constitutional symptoms in 20 and skin rashes in nine. Twenty patients had anemia, with positive Coombs' test in eight of 14 tested. Polyclonal hypergammaglobulinemia was found in 17 of 22 patients. Two patterns of evolution were recognizable: (1) long survival (24 to 67 months) without treatment or after the administration of intensive combination chemotherapy; and (2) rapid progression (one to 19 months) regardless of the treatment given. Sixteen patients died; postmortem examination in 10 cases showed the cause of death to be attributable to severe infection in eight patients, to renal disease in one and to cardiovascular disease in one. No evidence of malignant lymphoma was seen in any of these autopsies. Histologically, the disease is systemic, with specific lesions in the lymph nodes. The spleen, liver, bone marrow, skin and lung are also involved, but the changes are less characteristic than in the lymph nodes. In the patients in whom sequential biopsies were performed, a trend toward restoration of the nodal architecture was observed. AILD is a clinical-pathologic entity in a spectrum of yet to be defined immune reactions. The clinical, laboratory and pathologic manifestations of AILD are consistent with an autoimmune disorder, in which a deficiency of the T-cell regulatory functions probably predisposes to an abnormal proliferative and autoaggressive reaction of the B-cell system. Surgical staging procedures do not appear to be indicated. Intensive cytotoxic treatment may be hazardous in some patients, precipitating their death, but long survival after such therapy has been observed in others. Supportive therapy and small doses of steroids appear to be a safer therapeutic approach.
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PMID:Angio-immunoblastic lymphadenopathy. Diagnosis and clinical course. 119 Feb 54

Chronic energy intake restriction (CEIR) prolonged the median life span and inhibited autoimmunity and development of autoimmune disease in BXSB mice, as has been established for mice of several other autoimmune-prone, short-lived strains. Whether imposed just after weaning or delayed until manifestations of disease had appeared, CEIR inhibited or reversed development of autoimmunity and immune complex-based renal disease in male BXSB mice. CEIR also prevented the formation of anti-DNA antibodies and prevented the increase in circulating immune complex levels that is typically observed in male mice of this strain. Moreover, CEIR inhibited development of splenomegaly and prevented the normal age-associated decline of a number of immunological functions, including interleukin 2 production, cell-mediated cytotoxic responses, and mixed lymphocyte reactivity. The observed improvement in cell-mediated immune responses was attributed largely to the capacity of CEIR to inhibit development of the splenomegaly that occurs concomitant with expansion of a non-T, non-B lymphoid cell population. These findings emphasize that CEIR, even when imposed relatively late in life in BXSB mice, can influence expression of autoimmunities and autoimmune diseases of different genetic origins and presumed pathogenetic bases.
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PMID:The effects of dietary restriction on immune function and development of autoimmune disease in BXSB mice. 134 65

Chronic energy (calorie) intake restriction (CEIR) prolonged life, inhibited autoimmune disease, and influenced immunologic and hematologic parameters in NZB mice. Abnormalities in numbers and proportions of T and B cells populations were corrected. Deficient responses to phytomitogens, mixed lymphocyte reactions, formation of plaque-forming cells to sheep red blood cells in vitro, production of cytotoxic T lymphocytes after in vitro stimulation, and interleukin 2 production were also corrected. CEIR prevented the extreme splenomegaly that normally occurs with age in NZB mice. This influence was associated with reduction of a greatly expanded non-T, non-B lymphoid cell population. Calorie restriction also prevented in NZB mice the rapid decrease in total numbers of colony-forming B cells in bone marrow that is also characteristic of mice of this strain. The influences of CEIR on immune parameters and hematopoiesis were generally less marked in non-autoimmune-prone DBA/2 mice than in autoimmune-prone NZB mice. CEIR has been shown to produce profound influences on several strains of autoimmune-prone mice (NZB x NZW)F1, MRL/lpr, BXSB, and NZB herein). In each of these strains, the pathogenesis and manifestations of autoimmune disease are dissimilar. Therefore, it seems likely that calorie restriction acts on an as yet elusive mechanism that operates to foster development of the diseases associated with aging common to each of these autoimmune strains as well as autoimmune-resistant mice and rats. Further investigation of the molecular and cellular bases of the benefits of CEIR seems urgent.
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PMID:Effects of calorie restriction on immunologic functions and development of autoimmune disease in NZB mice. 140 33

We have previously reported that non-T, non-B 'null' cells increase with age in New Zealand Black (NZB) mice resulting in splenomegaly. Using a panel of monoclonal antibodies recognizing lineage-specific cell surface antigens we demonstrate four distinct subsets within this null cell compartment: (1) undifferentiated; (2) T lineage with undetectable Thy-1.2; (3) myeloid/erythroid; and (4) a pre-B/plasma cell type. All four subsets also occur in non-autoimmune mice. The frequency of these populations are similar in the young mice of all the strains examined, although the total number of null cells is higher in NZB. The elevation of null cells in young NZB mice is controlled by a single dominant gene in the genetic cross with New Zealand White (NZW) mice and does not appear closely related to the subsequent development of autoimmune disease. The proportion of myeloid/erythroid null cells increases with age in NZB as splenomegaly develops.
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PMID:Murine splenic null cell compartment contains distinct haemopoietic subpopulations: enlargement of a myeloid and an undifferentiated subset with the development of splenomegaly in New Zealand black mice. 157 92

The toxic oil syndrome is characterized by IgE elevation and eosinophilia, as well as scleroderma-like skin manifestations and other symptoms of autoimmune disease. Fatty acid anilides, found in large amounts in adulterated cooking oil, were suspected to be the etiologic agent in this disease. The capacity of oleic acid anilide to induce features of autoimmunity in vivo was investigated. B10.S mice were continuously treated i.p. with oleic acid anilide for 6 wk by using osmotic pumps. A significant increase in IgE and IgM serum levels was observed after 1 to 3 wk; subsequently five of six mice developed IgG1 levels 3.5- to 10-fold higher than the controls. Anilide-treated mice developed splenomegaly with a 2.1- and a 3.5-fold increase in IgM- and IgG-bearing splenocytes, respectively, and a 5.6- and 29-fold elevation in functional IgM- and IgG-secreting cells, respectively. Increased serum levels of predominantly IgM antibodies to histone, denatured DNA, and DNP as well as rheumatoid factor were detected. In vivo expression in the spleen of 10 cytokine genes was also examined, and mRNA encoding IL-1 beta and IL-6 were significantly elevated in splenocytes of anilide-treated mice. The enhanced Ig production suggests that anilide induced a cytokine-mediated polyclonal activation of B cells. Elicitation of IgM antibodies to denatured forms of autoantigens indicates that anilide treatment partially broke autoimmune tolerance in these mice. Anilide-treated mice may be a useful animal model for further exploring the mechanism and pathogenesis of systemic autoimmunity in the toxic oil syndrome.
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PMID:Isotype-restricted hyperimmunity in a murine model of the toxic oil syndrome. 158 38

Autoimmune neutropenia is thought to be an uncommon disorder in adults. Over a 2-year period, however, autoimmune neutropenia was diagnosed in seven adults in a county with a population of approximately 105,000 people. The median age of the patients was 52 years old (range of 22 to 81 years), and five of the seven patients were women. All seven patients had at least one other symptom of autoimmune disease. Three patients had splenomegaly, three patients had positive direct antiglobulin tests, and two patients had immune thrombocytopenia. Antibodies reacting to neutrophils were detected by either granulocyte agglutination (GA) or granulocyte immunofluorescence (GIF) testing in five of the seven patients. Antibodies in four patients reacted with an 80 kd neutrophil membrane glycoprotein, and antibodies from two people reacted with a 60 kd membrane glycoprotein. Three patients were given treatment with splenectomy, which resulted in only transient improvement in the neutrophil counts. Serious infections occurred in only three patients over the 2 years of observation. In summary, autoimmune neutropenia in adults may occur more often than appreciated. Most cases of autoimmune neutropenia in adults appear to be associated with other autoimmune phenomena.
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PMID:Autoimmune neutropenia in Sheboygan County, Wisconsin. 159 17

MRL/MpJ-lpr/lpr mice spontaneously develop a lupus-like autoimmune disorder characterized by massive proliferation of T cells and rapidly fatal immune complex glomerulonephritis. We evaluated the therapeutic effect of 5-azacytidine (5AC), a cytidine analogue known as an inhibitor of DNA methylation, in MRL/MpJ-lpr/lpr mice. Intraperitoneal injection of 5AC (50 micrograms, twice a week) starting from 6 weeks of age retarded the development of lymphadenopathy and autoimmune syndrome. Its beneficial effects included: (a) increased life-span, (b) diminution of lymphadenopathy and splenomegaly, (c) reduction in circulating levels of autoantibodies such as anti-DNA and rheumatoid factors, and (d) suppression of lupus glomerulonephritis. However, similar treatment in BALB/c mice did not affect the development of IgG anti-human IgG antibody responses. These results suggest that the protective effect of 5AC is related to the inhibition of the lpr gene-induced T cell proliferation, thereby suppressing the autoimmunity-accelerating effect mediated by the lpr gene.
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PMID:5-Azacytidine inhibits the lpr gene-induced lymphadenopathy and acceleration of lupus-like syndrome in MRL/MpJ-lpr/lpr mice. 169 37

The effects of SM-8849 on the development of autoimmune disease in MRL/Mp-1pr/1pr mice were examined. SM-8849 improved survival as well as renal disease, restored the deficits in splenic cell responsiveness to stimulation by mitogens or conventional antigens, and prevented lymphadenopathy and splenomegaly coincident with a decrease in the number of Thy-1+/Lyt-2-/L3T4- cells. SM-8849 also suppressed the production of the B-cell differentiation factor, possibly with a resulting preferential reduction of autoantibodies. In addition, SM-8849 depressed the production of hydrogen peroxide from macrophages. These results suggest that the administration of SM-8849 to a subject with autoimmune diseases can induce immunological improvements with possible clinical effectiveness.
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PMID:Alteration in progression of murine autoimmune disease by treatment with a novel immunomodulator, SM-8849. 178 57

Ultrasonography was used to evaluate spleen size in patients with various clinical conditions including those of the liver, blood, collagen, or autoimmune disease. To express spleen size, a spleen index (SI), the product of the transverse diameter and its perpendicular diameter measured on the maximum cross-sectional image of the spleen, was used. SI correlated well with the volumes of resected spleens. Splenomegaly was present in high percentages of patients with liver, blood, collagen, and autoimmune disease, even though a majority of these spleens were not large enough to palpate. By grading the SI, characteristic distributions of SI were obtained for patients with different types of diseases. Obtaining and grading the SI by the use of ultrasound appears to be a significant supplemental aid for evaluating spleen size, especially in patients whose spleens are not palpable.
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PMID:Sonographic assessment and grading of spleen size. 184 75


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