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)

A Graffi murine leukemia was utilized as a model system to investigate the effect of chemoimmunostimulation therapy. Subcutaneous inoculation of approximately 1.0 times 10(6) tumor cells resulted in a rapidly growing tumor at the site of inoculation and subsequent development of splenomegaly and lymphoadenopathy. All animals succumbed to the leukemia within 24 to 30 days. Treatment of diseased animals with two courses of cytoxan over a 2-week period resulted in a remission period of approximately 16 to 18 days before relapse and eventual death of approximately 70% of the drug-treated animals. A significant number of long-term survivors (50 to 83%) was obtained in groups of animals that received combined drug plus BCG or C. parvum therapy. In contrast, the administration of MER (a methanol-extracted residue of BCG) to animals in a drug-induced remission period was no more effective than drug alone. The protective effect afforded by BCG and C. parvum was dependent on the time interval between drug therapy and the administration of the immunostimulators. Treatment of leukemic animals with BCG, C. parvum, or MER alone proved ineffective as all mice died at approximately the same time as untreated control animals. No leukemic cells were observed in any of the histologically examined tissues taken from long-term survivors. The implication of these results for cancer therapy is discussed.
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PMID:Histological and combined chemoimmunostimulation therapy studies against a murine leukemia. 17 Feb 12

An infant was vaccinated at the age of 3 days with BCG vaccine. At the age of 3 years 10 months he developed an infection by Salmonella typhimurium. The infection persisted with recurrent episodes of fever, peri-nephritic abscess, abscesses of lymph nodes, hepatomegaly, splenomegaly and paravertebral and retro-peritoneal abscesses, from which Salmonella were isolated. At the age of 6 years and 2 months later. At post-mortem examination there were widespread histiocytic nodules in many organs, from which Mycobacterium bovis BCG were cultured. One previous case has been reported from Czechoslovakia. The mother of that child was the sister of the father of the child reported here. It was not possible to investigate the possibility of abnormalities of humoral or cellular immunity in the family.
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PMID:Fatal generalized BCG histiocytosis. 32 38

We have studied immunologic reactivity to leukemia-associated antigens in patients with chronic myelocytic leukemia (CML) treated with chemotherapy and adjunctive immunotherapy. All patients were immunologically competent as measured by skin test reactivity to dinitrochlorobenzene. Immunotherapy consisted of allogeneic irradiated leukemic myeloblasts injected intradermally, with BCG vaccine (Research Foundation, Chicago, Ill.) given by multiple puncture at the same site. 10(9) cells plus BCG were given weekly for 4 wk, and 10(8) cells plus BCG were given at monthly intervals thereafter. Eight patients judged clinically to be in the stable phase of their disease developed circulating antibody against the immunizing blast cells demonstrable by cytotoxicity and immunofluorescence assays. The antibody also showed reactivity against a panel of myeloblasts (12 paients) but not against the corresponding remission lymphocytes (five patients) or normal lymphocytes (20 donors). In two cases the antibody showed reactivity against the patient's own leukemic blasts. Seven of these eight patients have maintained a steady clinical course ranging from 20 to 40 mo, while one entered the blastic phase and died. Six patients were judged to be in the aggressive phase of CML because of progressive leukocytosis and splenomegaly or increasing myeloblastosis; five died an average of 16 mo after diagnosis. Humoral antibodies were not detected in these patients after repeated courses of BCG and allogeneic leukemic cells. We conclude that specific active immunotherapy of patients with CML can abet the production of humoral antibody against blast cell antigens and that this response may be impaired during the aggressive phase of the disease.
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PMID:Antibody responses to leukemia-associated antigens during immunotherapy of chronic myelocytic leukemia. 106 Apr 71

In a 3-year-old girl, who was admitted to our hospital with marked splenomegaly, a swollen abdomen and progressive loss of weight, the difficulty in establishing the correct diagnosis, namely a very rare generalized infection with Mycobacterium avium (serum type III), and the lengthy course of the disease are demonstrated. Norcardiosis, sarcoidosis and BCG-granulomatosis were excluded. From the spleen, lymphatic nodes, gastric juice, stools and urine of the child, who had not been vaccinated with BCG vaccine, masses of acid-fast bacilli were isolated. The generalisation of the disease was promoted by an immunological deficiency. At autopsy an atrophic thymus was discovered. The extensive clinical and immunological investigations pointed to a partial deficiency of the cell-mediated immune systeme. The patient died 8 months after admission.
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PMID:[Generalized mycobacterium avium infection in an infant (author's transl)]. 123 56

Eighty cases of miliary tuberculosis admitted to our hospital between January 1981 and December 1984 were reviewed. The age of the patients ranged from 3 months to 12 years, with an average of 2 years 2 months (26.5 months). Nine cases (11.25%) died during hospitalization due to the severe condition at the time of admission. Only 8 patients (10%) were in good nutritional condition. Seventy-two patients (90%) had been visiting the primary health care clinic for several times since 2-3 months but were never diagnosed as suffering from tuberculosis. Fever or recurrent fever were found in 78 cases (97.5%), anorexia in 65 cases (81.3%), chronic and/or recurrent cough in 72 cases (90%) and malaise in 43 (53.8%). Forty-one (51.3%) denied the presence of a close contact with source of infection. Hepatomegaly was found in 44 cases (55%), 19 (23.8%) of which were associated with splenomegaly. Choroidal tubercle was found in 4 cases; 1 case with coxitis, 1 with brain tuberculoma, 1 with ascites, 1 with endobronchitis and 1 with hepatitis. Forty-three (53.8%) were tuberculin negatives, 24 of which become positives after treatment. Fourteen cases had BCG scar. History of measles was found in 21 cases. Children with longterm and recurrent fever, anorexia, decrease of body weight and recurrent cough should be suspected of having TB thus enabling to get an early diagnosis.
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PMID:Miliary tuberculosis in children. A clinical review. 207 67

Factor Ei, besides exerting toxic reactions, is amphipathic, antigenic, chemotaxinogenic, causes blastic transformation, adjuvant effect, hypersensitivity (MIF, skin test), activates the RES (splenomegaly), increases the macrophage production, prevents listerial infection in mice, mycobacterial infection in guinea pigs and enhances the effect of BCG experimental tuberculosis and neoplasia in mice (Sa 180).
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PMID:The immunological properties of listerial complex Ei. 251 79

Unvaccinated mice were treated with T-2 toxin either 6 days before or 1 day after exposure to aerosols of virulent Mycobacterium tuberculosis. Mice were also treated with T-2 toxin 6 days before vaccination with Mycobacterium bovis (BCG). There was a T-2 toxin mediated increase in the number of viable vaccine organisms recovered from the spleens of toxin-treated mice at 3 weeks after vaccination, and splenomegaly at post-vaccine weeks 3 through 5. At the seventh week after vaccination, toxin-treated vaccinated, toxin-treated non-vaccinated, vaccinated, and untreated mice were exposed to aerosols of viable M tuberculosis. The number of viable mycobacteria in the lungs was determined at weeks 3, 5, 7, and 9 after pulmonary infection. The number of viable tubercle bacilli recovered from the lungs of vaccinated mice was significantly lower than from unvaccinated mice. However, T-2 toxin-treatment did not alter the vaccine efficacy.
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PMID:Influence of T-2 toxin on BCG vaccine efficacy against murine pulmonary tuberculosis. 274 6

Intraperitoneal administration of Corynebacterium parvum to BALB/c, C57Bl/6 or C3H/HeJ mice lead to the induction of elevated levels of neutral proteinase activity (125I-caseinolytic activity) similar to those observed previously in animals bearing the BCL1 leukemia or the B16-F10 melanoma. Enhanced activity reached a peak at 7-14 days postinjection of the C. parvum and then gradually returned to normal levels by 20-25 days postinjection. Increased plasma proteinase activity could be induced by C. parvum whole cells or the pyridine extract residue of C. parvum but not by BCG or the pyridine extract of C. parvum. BCG did not interfere with the induction of elevated levels of activity by C. parvum. Splenectomized animals responded the same as normal mice indicating that the splenomegaly accompanying the onset of increased plasma proteinase activity was not responsible for the changes. Administration of C. parvum via a subcutaneous site rather than intraperitoneally failed to induce systemic changes in proteinase activity while still inducing splenomegaly. Treatment of animals with C. parvum before or after transplantation of the BCL1 leukemia or the B16-F10 melanoma failed to alter the course of the disease or enhance the increased proteinase activity of plasma over that observed in plasma from animals bearing tumors alone. These observations support the hypothesis that the induction of disturbances in plasma proteinase activity in tumor-bearing animals is due to alterations in host systems and that C. parvum, in contrast to BCG, contains components which can mimic the effect of some tumors on host systems.
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PMID:Corynebacterium parvum, but not BCG, induces elevations in plasma proteinase activity similar to those observed in tumor-bearing mice. 329 43

A 3 month-old infant vaccinated with BCG at birth presented with granulomatous hepatitis with BCG isolated in the liver. Splenomegaly, infiltrates in both pulmonary apices and hilar adenopathies were simultaneously present. No immune deficiency could be found. Complete recovery followed specific polychemotherapy. Parenchymal calcifications appeared in the liver, spleen, lungs and mesenteric ganglia.
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PMID:[Generalized BCG infection, with a favorable outcome, in a 3-month-old immunocompetent infant]. 354 34

Nude athymic (nu/nu) mice on a BALB/c background and their heterozygous euthymic litter mates (nu/+) were infected with either 10(8) or 10(6) Mycobacterium lepraemurium organisms intravenously or in the left hind footpad (LHF). After LHF infection with 10(8) M. lepraemurium organisms, nu/+ mice slowly developed a response that consisted of LHF swelling and local resistance to Listeria monocytogenes. The lower inoculum induced a proportionately lower response in nu/+ mice, but the nu/nu mice developed neither LHF swelling nor resistance to L. monocytogenes in response to either dose of M. lepraemurium. Counts of M. lepraemurium in the LHF revealed no difference between the nu/+ mice and nu/nu mice. After intravenous infection the nu/+ mice developed splenomegaly, but did not otherwise differ from nu/nu mice with respect to resistance to intravenous challenge with L. monocytogenes or growth of M. lepraemurium in the spleen. In light of the poor responsiveness of nu/+ mice in this experiment, they were then compared with CB6 and B6D2 mice, which are genetically susceptible and resistant to M. lepraemurium, respectively. These mice were infected with either 10(8) or 10(6) M. lepraemurium cells or 10(6) Mycobacterium bovis BCG cells in the LHF. Once again the nu/+ mice responded poorly to M. lepraemurium, the CB6 mice responded very strongly, and the B6D2 mice gave an intermediate response with respect to LHF swelling and resistance to L. monocytogenes. However, M. lepraemurium grew to higher numbers in the LHF of nu/+ and CB6 mice than in B6D2 mice, revealing, in CB6 mice, a dissociation between resistance to L. monocytogenes and M. lepraemurium. All three mouse strains responded strongly to M. bovis BCG, but there was a suggestion that nu/+ mice might be more susceptible to this agent than the other two strains. I concluded that the failure of nu/+ mice to restrict the growth of M. lepraemurium more than nu/nu mice was due to the intrinsic genetic susceptibility of both types of mice. In effect, the nu/+ mice behaved like nu/nu mice, as if they too were deficient in T lymphocytes that were responsive to M. lepraemurium.
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PMID:Mycobacterium lepraemurium infection of nude athymic (nu/nu) mice. 389 23


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