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)

Treating MRL/1pr mice, which spontaneously develop systemic lupus erythematosus and rheumatoid arthritis, with 15-DOS resulted in a decrease in the amount of autoantibodies and inhibited proteinuria of the developing glomerulonephritis with an improved survival rate of these autoimmune mice. 15-DOS treatment also lowered the percentage of animals with swollen lymph nodes and inhibited the development of splenomegaly. In the established disease 15-DOS returned urine-protein values and renal function (serum urea and creatinine) to normal levels. Circulating rheumatoid factor and autoantibodies to double-stranded DNA were reduced and the increase in paw volume (signs of a polyarthritis) was inhibited.
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PMID:15-Deoxyspergualin (15-DOS) has a curative effect on the development of SLE-like autoimmune disease in MRL/1 mice. 179 21

33 children (22 girls) with brucellosis seen between 1972-1988 were studied retrospectively. All but 1 were Bedouins. The mean age at diagnosis was 9.8 years (range: 17 months-17 years). Duration of illness prior to diagnosis was less than 1 week in 13 (39%), 1-4 weeks in 8 (24%) and 1-3 months in 10 (30%). In 2 cases the symptoms lasted 6 and 8 months, respectively, before diagnosis. Presenting symptoms included fever (85%), articular involvement (65%), hepatomegaly (45%) and splenomegaly (33%). Less common manifestations were anorexia (30%) and weight loss (15%) cases. Meningoencephalitis developed in 2 patients and uveitis and glomerulonephritis in 1 each. Diagnosis was based on positive agglutination titers (greater than 160), which were found in all. Brucella melitensis was isolated in blood cultures in 8 of the 33. 18 were treated with tetracycline and 9 with tetracycline and streptomycin, all of whom responded well. 3 of the 6 treated with trimethoprimsulphamethoxazole were only cured when therapy was changed to tetracycline in 2 and tetracycline plus streptomycin in 1. All patients recovered without sequelae. We conclude that brucellosis due to Brucella melitensis is endemic among the Bedouin of the Negev. An increased incidence of brucellosis among hospitalized children has been noted in the past 2 years, indicating the need for diagnostic awareness.
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PMID:[Childhood brucellosis in the Negev]. 228 18

An allergic disease may develop in any organ or system. The respective etiological factors include foreign proteins, infectious agents such as various microbes, viruses, moulds, parasites, chemical compounds often in the form of drugs usually designated as haptens, polysaccharides, benign and malignant neoplasms. Of the factors operating in the causal pathogenesis of such diseases the most important one is an exaggerated formation of antibodies, which appears to be uncontrolled and occurring irrespective of the demands of the organism. The essential morphological features in allergic inflammation are rather variegated, their diagnostic value differing in a wide range but being never absolute. The above features include eosinophilic leucocytes, allergic arteritis and phlebitis, fibrinoid necrotic glomerulonephritis, histiocytic granulomatous inflammation or histiocytic granuloma. Granulomatous capsulitis and trabeculitis affecting the spleen and lymph nodes are believed to be of major diagnostic significance. The immunofluorescent and immunoperoxidase methods and electron microscopy are important diagnostic tools. It has been generally acknowledged that many drugs operate as antigens. They may cause death of the respective patient, but allergic manifestations may subside after withdrawal of such drugs. On occasion they operate as a trigger mechanism with the allergy progressing even after treatment had been interrupted. Therefore they have been receiving extreme attention. Our collection of cases a case of giant-cell myocarditis following sulfamethoxypyridazine, anaphylactic shock has been reported to occur after intravenous administration of novocaine, and generalized cutaneous vasculitis developed in the same patient during the subsequent phase. A similar cutaneous finding was reported to have developed after penicillin injection, granulomatous inflammation developed owing to sulfonamide treatment. Allergic tumour-like lymphadenitis developed after administration of anti-anthracic serum; an anticonvulsive syndrome developed after hydantoinate administration. The latter consisted of generalized exanthema, hepatomegaly, splenomegaly and generalized lymphadenopathy. The lymph nodes showed tumour-like lymphadenitis mimicking lymphogranuloma or reticulosis. Allergic diseases appear as either isolated organ lesions or systemic diseases. Thus, isolated and systemic polyarteritis nodosa, isolated nasal, pulmonary or systemic Wegener's granulomatosis have been recognized. Temporal arteritis has been recognized as a localized form of systemic giant-cell arteritis. The haemolytic-uraemic syndrome appears to be a milder variety of thrombotic thrombocytopenic purpura. Allergic diseases or manifestations occasionally affect two or more organs or systems.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pathology of allergic diseases. 248 27

The association between glomerular disease and hepatosplenic schistosomiasis is well documented in reports from South America. During the present hospital investigation in Sudan, 58 patients admitted for intercurrent complications of advanced hepatosplenic schistosomiasis were studied. The patients, median age 35 years, had no concurrent Schistosoma haematobium infection. Diagnostic criteria included an enlarged spleen (n = 58), at least 1 episode of hematemesis (n = 55) and/or melena (n = 36), endoscopical demonstration of gastroesophageal varices (29/29 studied), ultrasonographical imaging of hepatic periportal fibrosis (18/18 studied), and intraoperative liver biopsy with characteristic histological findings (11/16 biopsied). Serum creatinine, urea, electrolytes, cholesterol, total protein, and electrophoresis were within normal limits. Median urinary protein/creatinine ratio was 0.06 and thereby not significantly different from European reference values. Only 1 patient had proteinuria of 1.7 g/l. Minimal hematuria was found in 5 patients. Ten kidney biopsies were taken intraoperatively during a portal decompression procedure (Hassab operation). Light, immunofluorescence, and electron microscopy produced no evidence of glomerulonephritis. These findings indicate that S. mansoni induced nephrotic syndrome may be less frequent in Sudan than in South America. Renal involvement due to S. mansoni infection may therefore encompass geographical variances.
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PMID:Renal function and morphology in Sudanese patients with advanced hepatosplenic schistosomiasis and portal hypertension. 249 2

Nailfold capillary microscopy was used to study the microcirculation patterns in 26 adult patients with infective endocarditis. Abnormal patterns were found in 13 patients (50%). Enlargement of capillary loops was never observed. Significant correlations were found between the number of capillary abnormalities and both systemic involvement (cutaneous vasculitis, arthritis, splenomegaly and/or glomerulonephritis) and immunological disturbances (circulating immune complexes, rheumatoid factor and/or hypocomplementemia) (p = 0.02 and 0.003, respectively). Capillary abnormalities were significantly reduced in 14 patients studied 4 to 48 months after endocarditis was cured. However, due to the lack of specificity, nailfold capillary microscopy cannot be regarded as a useful tool for the diagnosis of infective endocarditis. Connective tissue disorders are not the sole diagnosis to be considered in patients with abnormal nailfold capillary microcirculation patterns.
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PMID:[Cutaneous microcirculation in infectious endocarditis]. 253 85

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

Autoimmune MRL/Mp-lpr/lpr (MRL/l) mice were treated with the immunostimulating anti-cancer drug OK-432 (a streptococcal preparation), a potent inducer of tumour necrosis factor. Treatment was initiated at 8 weeks of age, before the onset of the autoimmune disease. OK-432 prevented the development of immune complex-mediated glomerulonephritis in a dose-dependent manner, and prolonged the life in this strain of mice. At 36 weeks of age, the incidence of proteinuria was 90% in the controls, 60% in the 0.5-KE(1 KE = 0.1 mg) treatment group, and 33% in the 2.0-KE group. The 50% survival time was 23 weeks for the controls; 32 weeks for the 0.5-KE group; and greater than 36 weeks for the 2.0-KE group. Immune complex deposition in glomeruli was significantly reduced in the treated groups. The IgM class of serum autoantibody levels was significantly increased by OK-432 treatment but the IgG class was almost unchanged. Furthermore, lymphadenopathy and splenomegaly were not suppressed. The results indicate that OK-432 may be useful in the treatment of autoimmune disease in humans.
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PMID:Autoimmune kidney disease in MRL/Mp-lpr/lpr mice inhibited by OK-432, a streptococcal preparation. 280 13

C57BL/6 (B6) and female BXSB mice were infected with 10 cercariae of Schistosoma mansoni per head in order to examine whether chronic parasite infection induced glomerulonephritis (GN) with polyclonal B-cell activation. Six months after the infection, mice were sacrificed and various immunological and histopathological examinations were performed. The following results were obtained. (1) Severe GN was induced in parasite-infected female BXSB mice. The renal changes were similar to those of male BXSB mice which spontaneously develop lupus-like GN. No substantial renal changes were observed in infected B6 mice. (2) Massive IgG and C3 deposits were found in capillary loops and also at the mesangial area of infected BXSB mice. No significant IC deposits were found in the kidney of infected B6 mice. (3) A high level of IC was detected in sera of some parasite-infected female BXSB mice, though no significant difference in the level of IC was found between infected and control mice. (4) Numbers of spleen IgG-producing cells were significantly increased in infected B6 mice. Infected female BXSB mice with splenomegaly showed higher numbers of IgGPC than uninfected mice, but there was no difference between the groups. These results suggest that genetic backgrounds played an important role in the development of lupus-like GN following the chronic infection of parasite-causing polyclonal B-cell activation.
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PMID:Schistosoma mansoni: induction of severe glomerulonephritis in female BXSB mice following chronic infection. 312 32

We established chronic graft vs host disease in (BALB/c x A/J) F1 mice with the injection of lymphoid cells from the parental A/J strain. These animals developed glomerulonephritis, forefoot edema, alopecia, splenomegaly, and lymphadenopathy to various degrees, and all developed antinuclear antibodies. To determine whether these antibodies were directed against the small nuclear ribonucleoprotein (snRNP) particles that are characteristic targets for autoimmune responses in human rheumatic diseases, sera were studied in the 32P immunoprecipitation and immunoblotting assays. Among 20 mice, antibodies to snRNP developed in 10. These antibodies usually reached maximal levels about 4 wk after induction of graft vs host disease and generally fell thereafter. However, two mice developed antibodies to snRNP between the 10th and 20th wk of follow-up. Sera from six mice strongly recognized the U1 snRNP and an additional serum strongly bound both the U1 and U3 particles. Several sera contained lower levels of antibodies specific for the U3 and possibly pre-U2 snRNP particles. In immunoblots, sera that immunoprecipitated the U1 snRNP bound epitopes located on its 70,000 Da, A, B'/B, and/or C polypeptides. Sera that immunoprecipitated the U3 snRNP recognized a 34,000-Da polypeptide. These polypeptides are known to bear the autoantigenic epitopes that are recognized by human sera containing anti-U1 RNP and anti-U3 RNP autoantibodies. We conclude that chronic graft vs host disease in mice provides a model for the study of the autoimmune responses that characterize human diseases such as mixed connective tissue disease, scleroderma, and SLE.
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PMID:Murine graft vs host disease. A model for study of mechanisms that generate autoantibodies to ribonucleoproteins. 337 98

Autoimmune MRL/1 mice were treated with a recently developed substance with immunomodulating properties, LS-2616. Treatment was initiated at the age of 8 weeks, before the onset of clinically apparent disease, and at 16 weeks of age, after development of established lupus disease. Beneficial therapeutic effects were obtained, even when LS-2616 was administered at the lowest dose tested (1 mg/mouse/week) to 16-week-old mice. The effects of LS-2616 on longevity, as well as on development of lymphadenopathy, splenomegaly, glomerulonephritis, and vasculitis, were pronounced and were comparable with those of cyclophosphamide. The results obtained suggest a potential role for LS-2616 in the treatment of autoimmune disease in humans.
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PMID:Successful treatment of autoimmunity in MRL/1 mice with LS-2616, a new immunomodulator. 377 45


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