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 hematopoietic disregulation in adult mice induced by the malignant histiocytosis sarcoma virus (MHSV) and the Harvey murine sarcoma virus (Ha-MuSV), which both possess c-Ha-ras-related oncogenic sequences, was investigated. Spleen focus formation induced by MHSV and Ha-MuSV was not restricted by the Fv-2 resistance locus in congenic DDD and C57BL/6 mice, unlike leukemogenesis induced by Friend virus, Rauscher virus, and the myeloproliferative sarcoma virus (MPSV). C57BL/6 mice were much more resistant to MHSV and Ha-MuSV-induced spleen focus formation than DDD mice regardless of their Fv-2 state. Infection of DDD mice with MHSV caused a systemic histiocytic neoplasia, best described as murine malignant histiocytosis. Transformed histiocytic cells proliferated excessively in the bone marrow, spleen, and lymph nodes and, in the final stages of the disease, in all major parenchymal organs. The Ha-MuSV caused a strikingly different benign histiocytic tumor in DDD mice and, unlike MHSV, did not induce a rapid, progressive splenomegaly in C57BL/6 mice. Infection of DDD mice with MHSV induced a rapid and synchronized depletion of early and late erythroid precursor cell pools. In MHSV-infected C57BL/6 mice comparable changes were observed with dissimilar kinetics. Macrophage colony-forming cells of MHSV-infected mice were increased in number and proliferated independently of stimulating growth factors. The disease induced by MHSV in mice can thus serve as a model for malignant histiocytosis in humans.
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PMID:Murine retrovirus-induced malignant histiocytosis, an experimental model for the disease in humans. 282 12

Infection of 10-day-old chickens with an avian osteopetrosis virus resulted in a severe regenerative aplastic crisis. Hematopoietic and lymphopoietic tissues of chickens infected with myeloblastosis-associated virus (of subgroup B, inducing osteopetrosis, MAV-2(O] were analyzed for integrated and unintegrated viral DNA sequences, cell population shifts, weight changes, and morphological alterations. By 6 days postinfection (p.i.), DNA from bone marrow cells and peripheral blood leukocytes (PBL) contained between 0.50 and 0.70 copies of viral DNA per haploid genome. Erythrocytes and splenic leukocytes contained less than 0.10 copies/haploid genome. Granulocytes and precursor mesomyelocytes were absent from bone marrow, but numbers of erythrocytes, erythroblasts, and reticulocytes were normal. By 9 days p.i., bone marrow was severely hypoplastic and both granulopoietic and erythropoietic colonies were depleted. By 12 days p.i., erythrocytes and granulocytes were maximally depressed in peripheral blood and the amount of integrated virus in bone marrow and PBL decreased to less than 0.20 copies/haploid genome. In contrast, erythrocytes contained integrated viral DNA of up to 0.30 copies/haploid genome, indicating infection of erythrocyte precursors. At 18 days p.i., viral DNA was detected only in erythrocytes. Unintegrated viral DNA was not detected in any organs. Anemia was accompanied by splenomegaly and erythrophagocytosis. Viral DNA was never detected in thymus or bursa. Differential counting and flow cytometry of cells from bursa, thymus, and spleen, and of blood lymphocytes did not detect significant population shifts. These results suggest that MAV-2(O) infection of immunocompetent chickens occurs primarily in myelopoietic tissues, and tissues are selectively infected.
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PMID:Analysis of hematopoietic and lymphopoietic tissue during a regenerative aplastic crisis induced by avian retrovirus MAV-2(O). 283 18

The prevalence of antibodies against HTLV-III and -I was studied among populations of 6 distinctly different regions of Kenya, an equatorial African country in which AIDS has rarely been observed. Overall, 21% of subjects had ELISA reactions suggesting the presence of antibody against HTLV-III. The frequency of HTLV-III antibodies was highest among the Turkana people (50%) and lowest among the Masai (8%). Prevalence increased with age but was not related to sex. The pattern of ELISA-detected antibody against HTLV-I was similar. The specificity of these antibodies was supported by Western blot analysis of a subset of sera with high and low ELISA ratios, in which 66% and 73% of those with ELISA ratios considered positive (= greater than 5.0 in this study) also had a profile of bands consistent with HTLV-III and HTLV-I respectively. The antibodies detected were not cross-reactive between HTLV-III and HTLV-I on Western blot analysis. In a series of subjects with various parasitic and infectious diseases, patients with idiopathic splenomegaly and with schistosomiasis had a high proportion of antibodies against both HTLV-III and HTLV-I. This survey shows that reactivity in the ELISA HTLV-III and HTLV-I assays are common among Kenyans but vary considerably by region.
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PMID:Regional variation in prevalence of antibody against human T-lymphotropic virus types I and III in Kenya, East Africa. 298 91

Early reports suggested that hemophiliacs with factor IX deficiency (Christmas Disease) may be at less risk for developing the acquired immunodeficiency syndrome (AIDS) than patients with classic hemophilia. We evaluated 12 factor IX deficient patients for clinical and immunologic abnormalities related to infection with the human immunodeficiency virus (HIV). Antibody to HIV was not detected in these patients prior to 1982. By 1985, 66 percent (eight of 12) patients were seropositive. All three concentrates available commercially before 1985 were associated with seropositivity. Furthermore, seropositive hemophiliacs had received on average significantly more factor IX concentrate than seronegative hemophiliacs (27,825 +/- 17,976 (S.D.) versus 1,250 +/- 1,500 factor units/year, (p less than 0.02). Half of the seropositive individuals had generalized lymphadenopathy with splenomegaly. Two seropositive patients have developed AIDS, one with cryptococcal meningitis and another with a large cell immunoblastic lymphoma. Infection with HIV has occurred with high frequency in hemophiliacs who received unmodified factor IX concentrates.
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PMID:The spectrum of human immunodeficiency virus infection in patients with factor IX deficiency (Christmas disease) 303 83

Liver biopsy specimens previously taken from 16 haemophilic patients with chronic non-A, non-B hepatitis were reviewed. The degree of fibrosis correlated with serum procollagen III peptide (sPIIIP) concentrations, measured both at the time of biopsy and 4.25 years later. Two patients with extremely high sPIIIP concentrations had collateral veins on computed tomography, suggesting portal hypertension. Twenty eight of 47 patients (60%) had splenomegaly on computed tomography, and of 28 patients in whom intravenous contrast medium was used, seven (25%) had collateral oesophageal veins. Serum procollagen III peptide estimations and computed tomography, both non-invasive investigations, indicated that hepatic fibrosis and portal hypertension had developed in a proportion of haemophilic patients with non-A, non-B hepatitis. Infection with the human immunodeficiency virus (HIV) may modify the course of this presumably cytopathic virus infection of the liver.
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PMID:Non-invasive investigation of liver disease in haemophilic patients. 314 33

Cellular changes in the spleens of mice infected with Sarcocystis muris have been studied. Immunofluorescent staining for B and T cells and alpha-naphthyl acetate esterase (ANAE) staining for macrophages combined with histological studies revealed marked changes in the populations and distributions of all three cell types. Infection was accompanied by a marked splenomegaly, attributable mainly to widespread hyperplasia of the white pulp. Following infection there was an increase in the relative proportions of B cells (i.e. surface immunoglobulin+) and ANAE+ cells and a decrease in the proportion of T cells (i.e. Thy 1.2+). There was also a progressive accumulation of immunoglobulin-containing cells in the periarteriolar lymphocytic sheaths. Splenomegaly was most pronounced 20 days after infection. At this time there were 9.3 times as many B cells, 3.7 times as many T cells and 16.6 times as many ANAE+ cells as in uninfected mice.
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PMID:Cellular changes in the spleens of mice infected with Sarcocystis muris. 314 39

Microbiological features, diagnostic investigations, treatment, and complication rate in 53 cases of infective endocarditis were reviewed in this study. Infection occurred both on prosthetic (47%) and native valves (38%), while in 15% of the cases no prior valvular disease was known. Streptococcal (38%) and staphylococcal (30%) infections were predominant. In 17% of the cases apparent negative blood cultures were obtained. The most frequent portal of entry was dental infection or manipulation (45%), however in 28% of the patients etiology remained obscure. Major clinical signs and symptoms included heart murmurs (96%), fever (91%), dyspnoea (32%), and splenomegaly (30%). Echocardiography revealed vegetations in 78%, aortic and mitral valve being nearly equally affected. All patients were medically treated and 53% received antibiotics prior to blood cultures. Associations of ampicillin or penicillin with an aminoglycoside (43%) and penicillinase-resistant antibiotics (30%) were most frequently administered. In 28% of the patients, it was necessary to insert a prosthetic (aortic or mitral) valve. During follow-up, heart failure (28%), embolization (11%), and infections (11%) were the major complications.
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PMID:A six years review on 53 cases of infective endocarditis: clinical, microbiological and therapeutical features. 325 78

Soluble glucan, a beta-1,3-linked glucopyranose biological response modifier, is effective in the therapy of experimental neoplasia, infectious diseases and immune suppression. Currently, soluble glucan is undergoing phase I clinical trials. The present study describes the pre-clinical safety evaluation of soluble glucan in mice, rats, guinea pigs and rabbits. ICR/HSD mice and Harlan Sprague-Dawley rats received a single i.v. injection of soluble glucan in doses ranging from 40 to 1000 mg/kg. Soluble glucan administration did not induce mortality, appearance or behavioral changes in mice or rats. In subsequent studies, mice and guinea pigs were injected i.p. with glucan (250 mg/kg) for 7 consecutive days. ICR/HSD mice gained weight at the same rate as the saline-treated controls. In contrast, guinea pigs receiving i.p. injections of soluble glucan showed a significant (P less than 0.05) 10-13% decrease in weight gain over the 7 day period. No other toxicologic, behavioral or appearance changes were noted. To examine chronic toxicity, soluble glucan was administered twice weekly for a period of 30 or 60 days to ICR/HSD mice in the dose of 40, 200 or 1000 mg/kg. No deaths were observed in any group. Chronic glucan administration did not alter body weight, liver, lung or kidney weight. However, a significant splenomegaly was observed in both the 30 and 60 day study. Histopathologic examination showed no tissue alterations at 40 or 200 mg/kg. However, at 1000 mg/kg a mononuclear infiltrate was observed in the liver. Pyrogenicity testing, employing New Zealand white rabbits, revealed that parenteral glucan administration (5 mg/kg) did not significantly alter body temperature. These data indicate that the systemic administration of soluble glucan, over a wide dose range, does not induce mortality or significant toxicity, an important consideration in preparing soluble glucan for parenteral administration to human populations.
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PMID:Pre-clinical safety evaluation of soluble glucan. 326 94

Infection with Listeria monocytogenes stimulates T cell proliferation and T cell-derived lymphokine production. The release of lymphokines, in turn, "activates" macrophages, enhancing their bactericidal capacity. Because prior studies suggest that I-A+ accessory cells play a critical role in this pathway, we assessed the effects of an anti-I-A antibody on the murine host resistance to listerial infection. To this end, we infused Listeria into control C57BL/6 mice (I-Ab haplotype) and mice of the same strain which had been pretreated 18 hr earlier with D3137 (a monoclonal IgG2a anti-I-Ab,d antibody). Preliminary studies demonstrated that this antibody can markedly inhibit antigen-induced proliferation of Listeria-dependent T cells in vitro and (at a dose of 1 mg/animal) can markedly reduce I-A expression on splenocytes in vivo. Even though D3137 pretreatment prevented the splenomegaly normally observed after Listeria infusion into mice, it protected animals infused with otherwise lethal concentrations of Listeria. Because antibody-treated animals had sevenfold fewer organisms in their spleens 18 hr after infection and 1000-fold fewer organisms than control animals 3 days after infection, improved survival resulted from an antibody-induced increase in the bactericidal capacity of the MPS. Protection was not noted when C1.18.4 (an IgG2a myeloma protein without known antibody activity) was infused into C57BL/6 mice or when D3137 was infused in B10.BR (I-Ak) mice. D3137 also protected (B10 X B10.BR)F1 mice (which are hybrids bearing I-Ab and I-Ak), suggesting that complete blockade of antigen presentation is not a prerequisite for its protective action. Further studies into the mechanism for these effects may provide new insights into the pathophysiology of MPS activation in response to immunologic challenge.
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PMID:The effects of an anti-I-Ab antibody on murine host resistance to Listeria monocytogenes. 349 82

Acquired immunodeficiency syndrome (AIDS) is a lethal infectious disease that has reached epidemic proportions in urban centers of the United States. Intraabdominal opportunistic infections and malignancies are common features of this syndrome. A prodromal phase or possibly milder form of infection is known as the AIDS-related complex. Abdominal computed tomography (CT) in patients with AIDS-related complex often demonstrates a triad of mild retroperitoneal and mesenteric adenopathy, splenomegaly, and perirectal inflammation. Lymph node enlargement greater than 1.5 cm is unusual in the AIDS-related complex and should prompt CT-guided biopsy. Abdominal adenopathy (greater than 1.5 cm) in AIDS, in our experience, is most commonly related to non-Hodgkin lymphoma, Kaposi sarcoma, or infection with Mycobacterium avium-intracellulare. In most instances, CT-guided biopsy with appropriate staining technique can readily distinguish these entities. However, the subtyping of non-Hodgkin lymphoma by fine-needle aspiration biopsy alone remains controversial. Unusual features of abdominal malignancies are common in AIDS. These include a purely lymphadenopathic form of AIDS-related Kaposi sarcoma and a predilection for extranodal sites of lymphoma in AIDS. In general, patients with AIDS-related lymphoma present with advanced stages of disease with highly malignant histologic subtypes. Abdominal CT may be useful clinically for diagnosing intraabdominal complications of AIDS.
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PMID:Abdominal CT in acquired immunodeficiency syndrome. 351 46


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