UMLS:C0038002 - FACTA Search

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 single i.p. injection of 2.5 times 10-8 killed B. pertussis cells protected 23 out of a group of 24 NMRI mice (95.8%) against the subsequent intracerebral infection, whilst 13 out of 24 mice (54.2%) survived the intracerebral challenge with virulent B. pertussis cells after prior oral administration of 2.5 times 10-11 killed B. pertussis cells, as demonstrated by the mouse protection test. Similar treatment with non-specific substances, such as egg white and saline, did not result in any increase of resistance. Systemic anaphylactic hypersensitivity to bovine serum albumin could also be achieved, when either both the protein antigen and the B. pertussis vaccine were given by the oral route or when the B. pertussis vaccine was injected intraperitoneally into mice which had received the soluble protein antigen by the oral route. Such effects were not produced at all in the reverse situation, when the B. pertussis vaccine was orally administered in mice, which were given the soluble protein antigen by the intraperitoneal route. After oral inoculation of 6 times 10-11 killed B. pertussis cells neither splenomegaly nor blood lymphocytosis became detectable. It is still unknown, in which manner the orally administered B. pertussis vaccine effects protection against the intracerebral infection with virulent bacteria as well as susceptibility for systemic anaphylaxis. The data presented do not favor the view that those effects are due to the phenomenon of persorption.
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PMID:Studies on the immunizing capacity of orally administered particulate antigens. I. The efficiency of killed Bordetella pertussis cells. 16 35

A novel compound, LY83583 (6-anilino-5,8-quinolinedione), was found to lower basal levels of cyclic GMP (cGMP) in fragments of guinea-pig lung incubated in vitro. The lowering of cGMP was dose-related reaching a maximum of 72% at 5 X 10(-5) M. Basal levels of cyclic AMP (cAMP) were not lowered by LY83583. cGMP concentrations were also reduced in guinea-pig heart and cerebellum after incubation with LY83583. However, the drug did not alter the levels of this cyclic nucleotide in spleen. Exposure of lung fragments from sensitized guinea pigs to ovalbumin resulted in a marked increase in cGMP and cAMP. LY83583 prevented completely the accumulation of cGMP and attenuated the rise in cAMP. Similar results were obtained in rat cerebellum stimulated with kainic acid. The compound also blocked ovalbumin-induced release of slow reacting substance of anaphylaxis (leukotrienes) from guinea-pig lung. Subcutaneous administration of LY83583 to guinea pigs did not affect cGMP concentrations in vivo in lung, but the total amount of cGMP in spleen was reduced dramatically. This was accompanied by a marked splenomegaly. LY83585 did not inhibit lung guanylate cyclase. In fact, activity was increased in a cell-free preparation from guinea-pig lung. The mechanism by which LY83583 reduced concentrations of cGMP is presently unknown. Nevertheless, our studies suggest that LY83583 will be a valuable pharmacological tool to help elucidate the role of cGMP in biological events.
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PMID:LY83583: an agent that lowers intracellular levels of cyclic guanosine 3',5'-monophosphate. 285 87

An 8-year-old boy developed anaphylaxis after receiving his maintenance dose of immunotherapy and proceeded to display the signs and symptoms of serum sickness. These consisted of fever, arthralgia, arthritis, urticaria followed by a hemorrhagic palpable rash, edema, lymphadenopathy, splenomegaly, abdominal pain, proteinuria, and neurologic manifestations consistent with vascular compromise of the posterior cerebral circulation. A skin biopsy specimen revealed perivascular infiltrates of lymphocytes and few polymorphonuclear neutrophils. The timing of events in this patient suggests that immunotherapy initiated a chain of events beginning with anaphylaxis and leading to serum sickness. It is hypothesized that the enhanced vascular permeability that accompanied the anaphylaxis allowed immune complexes that may have preexisted in the circulation to deposit in the blood vessels of the patient. These complexes may or may not have been related to the immunotherapy itself. Because antihistamines are known to prevent the induction of serum sickness, early and aggressive treatment of anaphylaxis during immunotherapy may prevent the occurrence of immune complex disease.
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PMID:Serum sickness triggered by anaphylaxis: a complication of immunotherapy. 405 55

Mast cells participate in pathophysiological processes that range from antimicrobial defense to anaphylaxis and inflammatory arthritis. Much of the groundwork for the understanding of mast cells was established in mice that lacked mast cells through defects in either stem cell factor or its receptor, Kit. Among available strains, C57BL/6-Kit(W-sh) (W(sh)) mice are experimentally advantageous because of their background strain and fertility. However, the genetic inversion responsible for the W(sh) phenotype remains poorly defined, and its effects beyond the mast cell have been incompletely characterized. We report that W(sh) animals exhibit splenomegaly with expanded myeloid and megakaryocyte populations. Hematopoietic abnormalities extend to the bone marrow and are reflected by neutrophilia and thrombocytosis. In contrast, mast cell-deficient WBB6F1-Kit(W)/Kit(W-v) (W/W(v)) mice display mild neutropenia, but no changes in circulating platelet numbers. To help define the basis for the W(sh) phenotype, a "DNA walking" strategy was used to identify the precise location of the 3' breakpoint, which was found to reside 67.5 kb upstream of Kit. The 5' breakpoint disrupts corin, a cardiac protease responsible for the activation of atrial natriuretic peptide. Consistent with this result, transcription of full-length corin is ablated and W(sh) mice develop symptoms of cardiomegaly. Studies performed using mast cell-deficient strains must consider the capacity of associated abnormalities to either expose or compensate for the missing mast cell lineage.
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PMID:Genetic inversion in mast cell-deficient (Wsh) mice interrupts corin and manifests as hematopoietic and cardiac aberrancy. 1898 2

Hidatid cysts of the spleen are a rare occurrence, the spleen being the third most common organ for the development of Echinococcus Granulosus. Splenic hydatid cysts are commonly part of multi-organ hydatid disease. Diagnosis is often established when investigating a splenomegaly or by chance during an unrelated consult. It can also be diagnosed after rupture, be it following trauma (the most common occurrence)or spontaneous. Splenic hydatid cyst rupture requires immediate action and is a life-threatening condition. It results, most often, in splenectomy. We present the case of a patient with multi-organ hydatid disease that presented with a ruptured splenic cyst and developed anaphylaxis. The case was resolved by splenectomy and recovered well.
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PMID:Spontaneous rupture of a splenic hydatid cyst with anaphylaxis in a patient with multi-organ hydatid disease. 2495 47

Systemic mastocytosis (SM) is a rare chronic myeloproliferative neoplasm with only limited epidemiologic data published so far. We aimed to analyze the clinical and molecular diagnostic features, and the prognosis and cumulative incidence of SM cases in a cohort of south-eastern Hungarian patients of 13 year follow up. In the period 2001-2013, 35 consecutive SM cases were diagnosed in our regional centre. Immunophenotype, KIT D816V mutation frequency and clinical characteristics, and the prognosis impact of clinical subtypes were tested and compared with published data. Indolent SM (ISM) was diagnosed in 14 patients, SM with an associated clonal hematologic non-mast cell lineage disease (SM-AHNMD) in 15 patients and aggressive SM (ASM) in 6 patients. The KIT D816V mutation was found in 11/14 (78%) of the ISM cases, in 12/15 (80%) of the SM-AHNMD cases and in 5/6 (83%) of the ASM cases. The life expectancy of ISM patients was better, whereas the SM-AHNMD and ASM groups exhibited a reduced median survival. The cumulative incidence for 13 year of the SM was 0.27/10,000. We detected lower 13 year cumulative SM incidence than of published epidemiologic data due to in our analyses involved only those patients who had bone marrow biopsy and histopathologically confirmed SM. This clinical overview clearly showed that the clinical characteristics differ between ISM (UP, anaphylaxis and osteoporosis) and SM-AHNMD/ASM (cytopenia, eosinophilia and splenomegaly).
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PMID:Clinical and Molecular Diagnostic Evaluation of Systemic Mastocytosis in the South-Eastern Hungarian Population Between 2001-2013--A Single Centre Experience. 2654 82

Mast cell-deficient mice are widely used to identify and quantify contributions of mast cells to diverse biological responses in vivo, including allergic inflammation. However, despite the fact that scores of genes have been identified as modifiers of allergic inflammation, most mast cell-deficient models have been available only on a single genetic background. We transferred the Kit^W-sh allele onto the BALB/c background to generate BALB/c mast cell-deficient mice (BALB/c-Kit^W-sh/W-sh). BALB/c-Kit^W-sh/W-sh mice have dramatically reduced mast cell numbers (0-2% of wild type) in all tissues examined, as well as subtle hematologic differences from the corresponding wild type mice, including splenomegaly with evidence of increased splenic hematopoiesis. We examined in BALB/c-Kit^W-sh/W-sh mice models of allergic inflammation that are substantially diminished in C57BL/6-Kit^W-sh/W-sh mast cell-deficient mice. In a model of acute allergic inflammation, i.e., IgE-dependent passive cutaneous anaphylaxis, both ear swelling and leukocyte infiltration were largely or entirely absent in BALB/c-Kit^W-sh/W-sh mice. In contrast, in two different models of allergic airway inflammation, airway hyperresponsiveness, lung inflammation, and airway remodeling developed robustly in mast cell-deficient BALB/c-Kit^W-sh/W-sh mice. These results support the conclusion that the importance of mast cell contributions in various models of allergic inflammation may be at least partially determined by genetic background.
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PMID:Development of multiple features of antigen-induced asthma pathology in a new strain of mast cell deficient BALB/c-Kit^W-sh/W-sh mice. 3185 99