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)

Spleen size, stomatocytosis, macrothrombocytopenia, haemoglobin level, white cell count, and abdominal pain episodes were assessed in a coded study of healthy Mediterranean immigrants to Australia. Spleen size was estimated from a length measurement, L, on a standardized plain abdominal radiograph and expressed both as spleen weight and as a spleen length index, L/square root BSA; the platelet count and size parameters were determined electronically and the presence of stomatocytes was evaluated in stained blood films. In relation to 16 Northern European control women 12 of 25 Mediterranean women had radiographic splenomegaly, 10 had macrothrombocytopenia, 9 had stomatocytosis, but none had episodes of abdominal pain. The median spleen weights of the two groups were estimated as 157 and 247 g with ranges from percentile 2.3 to 97.7 of 75 to 328 and 112 to 669 g. Within the Mediterranean group splenomegaly correlated with macrothrombocytopenia (P less than 0.001) but not with stomatocytosis, haemoglobin values or white cell counts. Thus, mild splenomegaly may be expected in Mediterranean macrothrombocytopenia, Mediterranean stomatocytosis appears unrelated, and all of these apparently benign anomalies may be incidental findings in patients from the Italian and Balkan peninsulas.
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PMID:Splenomegaly, macrothombocytopenia and stomatocytosis in healthy Mediterranean subjects (splenomegaly in Mediterranean macrothrombocytopenia). 115 55

The evaluation of spleen length from routine x-ray films of the left epigastrium of 97 healthy patients suggested a close correlation to the height of the 12th thoracic and the first three lumbar vertebral bodies. The normal ratio of spleen length to the vertebral height Th 12- L 3 is 0,82 +/- 0,09, two standard deviations are represented by ratios from 0,64 to 1,0. Spleen length over vertebral height Th 12 -L 3 indicates pathologic enlargment of the spleen. 54 patients with diseases which may cause splenomegaly showed spleen lengths mostly over the heights Th 12 - L 3.
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PMID:[The individual limit of normal spleen size in routine x-ray film (author's transl)]. 127 1

Three patients infected with human immunodeficiency virus (HIV) presented with pseudotumoral splenomegaly, CD8 lymphocytosis (3.5-5.1 x 10(9)/l), and hypergammaglobulinaemia. Spleen and bone marrow showed diffuse CD8 lymphocyte and plasma-cell infiltration. Amplification of the T-cell-receptor gamma chain gene did not reveal any clonal T-cell population. Phenotypic analysis showed a predominance of CD8/CD57 suppressor T cells with expression of activation markers (DR and CD38). No cytotoxic T lymphocytes specific for HIV could be detected. The three patients shared the HLA haplotype A1, B8, DR3. The association with this haplotype suggests a genetically determined host immune response to HIV.
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PMID:CD8 lymphocytosis and pseudotumoral splenomegaly in HIV infection. 136 50

Spleen cell graft versus host (GvH) reactivity was determined in male and female, either virgin or breeder, C57BL mice from 3 to 24 months of age. The GvH reaction was assessed by a local popliteal lymph node assay and by a splenomegaly test for a systemic reaction. Although the GvH reactivity declines progressively with age in both sexes the virgin female response was greater than that of males throughout the period of 6-18 months of age. Two-year-old mice of both sexes were practically unable to mount a GvH reaction. No differences were evident in aging female reactivity after one or two syngeneic pregnancies. On the other hand, 3 or more consecutive pregnancies resulted in enhanced GvH reactivity of 12-24-month-old females, which responded comparably to young virgin mice. This long-lasting immunopotentiating effect of multiparity was similar after 3-4 and 8-9 pregnancies. The possible role of developing foetuses on the maintenance of high GvH reactivity in breeder females is suggested.
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PMID:The effect of age, sex and breeding on graft versus host reactivity of spleen cells from C57BL mice. 140 87

Irradiated C57BL/6(B6) mice, when they were injected with spleen cells of C57BL/6J-lpr/lpr(B6-lpr) mice, developed splenomegaly at 2 weeks post-transfer, but afterward displaced by GVH-like disease. At 2 weeks the enlarged spleen in the chimeric mice, designated as [B6-lpr----B6] chimera, contained about 70% of the total cell population as CD8-positive T cells. Spleen cells from [B6-lpr----B6] chimeras were unresponsive to Con A and LPS stimulation and suppressed the mitogenic response of B6, B6-lpr, and C3H spleen cells to Con A. However, they had no cytotoxic activity towards Con A blasts of B6 and B6-lpr spleen cells. The suppressor activity found in the [B6-lpr----B6] spleen cells was removed by pretreatment of them with anti-Thy-1.2 or anti-CD8(Lyt2.2) plus complement. The present experiment showed that enormous proliferation of CD8-positive suppressor T cells was induced in the [B6-lpr----B6] chimeras. These cells were probably responsible for the GVH-like lymphoid atrophy observed in these [B6-lpr----B6] chimeras.
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PMID:Analysis of the mechanism of graft-versus-host-like disease in B6 mice with transferred B6-lpr spleen cells. 171 58

The three non-allelic gld, lpr and mev mutations in the mouse all lead to profound immunodeficiency besides a splenomegaly and a generalized autoimmunity. Spleen cells from young B6 gld, B6 lpr and B6 mev mice all display a decreased proliferative response to the T-cell mitogen concanavalin A (ConA), but the nature of the deficiency seems very different. No restoration of proliferation could be obtained by adding exogenous recombinant rIL2 to ConA-treated mev spleen cells, this lack of IL2-responsiveness suggesting a lack of (functional) IL2-receptors. In young mice of both gld and lpr strains, a B6 wild-type level of proliferation could be reached by rIl2 addition to ConA-treated spleen cells, this normal responsiveness to exogenous IL2 suggesting a normal expression of IL2-receptors. The endogenous IL2 production by ConA-treated spleen cells decreased very much with ageing in both B6 gld and B6 lpr mice. Yet, IL2 production in young mice revealed an earlier deficiency of the B6 lpr mice: the young B6 gld IL2 levels reached about 60% of age-matched B6 wild cell levels, but the B6 lpr levels reached 14% only. Finally the addition of exogenous rIL2 to ConA-pretreated cells from old B6 gld and B6 lpr mice, while enhancing the proliferative responses, could not restore the B6 wild-type levels. This suggests that, with ageing, the expression of functional IL2-receptors may become as abnormal in these gld and lpr mutants as it is from birth in the mev mutant mice.
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PMID:Different nature of the proliferation defects of GLD, LPR and MEV C57BL/6 mouse lymphoid cells. 175 26

Ehrlichia risticii propagated in a murine macrophage cell line were freed from the host cell by hypotonic lysis of the infected cells. The cell-free ehrlichiae were inactivated with beta-propiolactone and combined or not combined with polymyxin-B. The vaccines were administered to mice with Quil-A (saponin) as an adjuvant twice at 2 to 3 week intervals and the mice were challenged with live E. risticii 2 to 3 weeks after the last vaccination. With or without the addition of polymyxin-B, the vaccine preparations protected mice from developing clinical signs and gross pathologic changes such as thymic atrophy, splenomegaly, and increase in whole intestinal weight. Mice vaccinated with or without polymyxin-B developed high titer IgG antibody against E. risticii before and after the challenge with live E. risticii. Spleen lymphocyte proliferative response assay at 11 days post challenge revealed that with polymyxin-B a higher lymphocyte proliferation occurred as compared with that of the mice which received polymyxin-B-free vaccine. Spleen lymphocytes of the placebo (polymyxin-B and Quil-A) pretreated/challenged mice showed no proliferative activity. Western blot analysis revealed that vaccinated mice reacted mainly with 110, 57 and 33 kDa antigen bands before and after challenge. The placebo (polymyxin-B and Quil-A)/challenged mice showed a very weak response to ehrlichial antigens at day 10 to 11 post challenge. Comparison with inactivated Renografin-purified E. risticii or 0.25% SDS-insoluble fraction of E. risticii with the inactivated host cell-free vaccine revealed no increased protection. These results indicate that inactivated host cell-free E. risticii can protect mice from murine Potomac horse fever. The presence of polymyxin-B appeared to be not harmful but rather beneficial for lymphocyte proliferation response upon challenge with live E. risticii.
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PMID:Protection against murine potomac horse fever by an inactivated Ehrlichia risticii vaccine. 188 7

Forty-two with hepatosplenic patients treated with praziquantel and followed up for 5 years. One half of the patients received a single 30 mg/kg dose and the other half, two doses of 25 mg/kg given 4 hrs apart. According to Hoffman and Kato-Katz stool exams, an 83.3% cure rate, was observed after twelve months. Stool egg counts in cases of incomplete cure were greatly reduced. Liver function, as assessed by serum levels of aspartate aminotransferase, alanine aminotransferase, gamma glutamyltransferase and alkaline phosphatase activities as well as albumin and gamma globulin showed marked improvement after one year. Hepatomegaly was reduced in 81.0% of patients and splenomegaly in 78.8%. Spleen regression was complete in 15.1% of the total, and in 18.5% of those with compensated hepatosplenic disease. As a result of these observations, the authors recommend early treatment with anti-schistosomal medication, either oxamniquine or praziquantel, to halt progression of disease and reduce splenomegaly.
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PMID:Reduction of morbidity in hepatosplenic schistosomiasis mansoni after treatment with praziquantel: a long term study. 212 17

Thirty seven patients with sarcoidosis were examined using ultrasound (US) to determine the size of the spleen. A Spleen Index (SI) was employed to evaluate splenomegaly and the SI was calculated using long (a) and short (b) dimensions on the sectional splenotomogram (SI = a x b). In 21 (57%) of these patients the spleen was judged ultrasonographically to be enlarged (SI 30), but in only 3 was it palpable. The clinical records of patients with and without splenomegaly detected by US were compared. There were no differences between patients with or without splenomegaly in hematologic findings (peripheral blood and bone marrow) or blood chemistry; furthermore no patients with hypersplenism were seen. In immunological parameters, the serum immunosuppressive acid protein level was significantly (p less than 0.05) higher in patients with splenomegaly than in those without splenomegaly; however, there were no differences in serum angiotenins converting enzyme activity, serum lysozyme level, PPD skin test or bronchoalveolar lavage fluid analysis. The patients with splenomegaly had significantly higher evidence of increased uptake of 67-Gallium in lung fields and positive lung infiltrates in chest X-ray than those without splenomegaly (p less than 0.01, p less than 0.05). These data suggest that ultrasound is a promising diagnostic tool for the assessment of the size of the spleen and is useful to detect disease activity and extent of disease in sarcoidosis. Patients with sarcoidosis who had splenomegaly had more disseminated disease, especially pulmonary parenchymal disease, than did those without splenomegaly.
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PMID:[Ultrasonographic analysis of splenomegaly in patients with sarcoidosis]. 221 17

We previously reported that streptococcal preparation (OK-432), which is a TNF inducer, inhibits insulitis and development of autoimmune diabetes in nonobese diabetic (NOD) mice and Bio-Breeding (BB) rats, as animal models of insulin-dependent diabetes mellitus. We have recently shown that recombinant human (h)TNF-alpha also suppresses development of diabetes in NOD mice. In this study we have extended our observation on TNF to BB rats in order to see whether TNF generally inhibits autoimmune diabetes. A total of 5 x 10(4) U of rhTNF-alpha was administered i.p., twice a week to male and female BB rats from 4 to 27 wk of age. The cumulative incidence of diabetes by 27 wk of age in nontreated rats was 36.4% (8/22), whereas that in hTNF-alpha-treated rats was 0% (0/21) (p less than 0.001). The hTNF-alpha-treated rats did not lose body weight and maintained normal blood glucose concentrations. Immunologic and histologic examinations were performed at the end of the experiment. Spleen cell cytotoxicities for NK-sensitive YAC-1 and rat insulinoma (RINm5F) cells in hTNF-alpha-treated rats significantly decreased in comparison with nontreated and nondiabetic BB rats. Intensity of insulitis was also inhibited in hTNF-alpha-treated rats. Interestingly, a huge hepatomegaly and splenomegaly was found in two of the 21 hTNF-alpha-treated rats. The latter consisted of W3/13dull+ and W3/25dull+ cells, which did not exhibit cytotoxicity for either YAC-1 or RINm5F cells. These results indicate that the chronic and systemic administration of TNF has a regulatory role in autoimmune diabetes in BB rats as well as in NOD mice, and that these animals may have a defect in TNF-mediated immunoregulation.
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PMID:Inhibition of type 1 diabetes in BB rats with recombinant human tumor necrosis factor-alpha. 238 63


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