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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although many cross-sectional studies and a small number of randomized controlled trials have addressed the relationship between schistosomiasis and anemia, the conflicting results make the magnitude of the relationship unclear. In fact, only one randomized controlled trial that treated solely for schistosomiasis has demonstrated an impact of praziquantel on hemoglobin concentration. The potential mechanisms underlying a relationship between schistosomiasis and anemia are also unclear. In this article, we discuss four possible mechanisms that might mediate this relationship, based on animal and human models, including extra-corporeal loss of iron, splenomegaly leading to red blood cell sequestration, autoimmune hemolysis and anemia of inflammation.
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PMID:Human schistosomiasis and anemia: the relationship and potential mechanisms. 1596 25

Hemolymphangiomatosis is an extremely rare entity that has never been described in the diffuse form. Its main pathologic feature is proliferation of lymphatic and vascular cells inducing interstitial and hematic lakes and then splenomegaly. We report a complete imaging study, including magnetic resonance (MR) imaging, after administration of a superparamagnetic contrast agent. Ultrasonography (US), basal MR imaging, and late computed tomography (CT) contrastographic features are quite similar to those of other diffuse benign vascular neoplasms, without real hemangioma-like enhancement during the vascular phase. Its late contrastographic pattern could be considered specific if CT and iron oxide-enhanced MR imaging are applied as complementary diagnostic tools, however.
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PMID:Hemolymphangiomatosis of the spleen: imaging features. 1627 60

Iron homeostasis is one of the most critical functions in living systems. Too little iron can lead to anemia and tissue-specific disorders, such as splenomegaly. Excessive systemic iron is characteristic of hemochromatosis and is implicated in the brain in Parkinson's disease. With the exception of some single gene diseases like hemochromatosis, we know little about genetic-based, individual differences in iron-related parameters and their impact on biology. To model genetic control of iron homeostasis, we measured liver, spleen, and plasma iron concentrations, hematocrit and hemoglobin, transferrin saturation, and total iron-binding capacity in several BXD/Ty recombinant inbred mouse strains derived from C57BL/6 and DBA/2 progenitors. At 120 days of age, the animals were killed for iron analysis. All measures showed genetic-based variability consistent with polygenic influence. Analysis of principal components of the seven measures revealed three factors that we named availability, transport, and storage. Quantitative trait loci (QTL) analysis revealed one suggestive QTL on chromosome 5 for availability, two suggestive QTL (one on chromosome 1 and the other on chromosome 7) for transport, and one weak QTL on chromosome 2 for storage. The results show that iron homeostasis is a complex trait and is influenced by multiple genes.
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PMID:Systems genetic analysis of peripheral iron parameters in the mouse. 1747 78

Abdominal tuberculosis (TB) is infrequent in the Western world. This disease occurs more commonly among at-risk populations, mainly among older patients and patients with HIV infection. Abdominal TB usually manifests as intestinal TB, peritoneal TB, and mediastinal lymphadenitis. Gastric TB is a rare manifestation of abdominal TB. We present the case of an 80-year-old man, who had been diagnosed with anemia 2 years previously without establishing the etiology. Treatment consisted of oral iron administration without improvement. Symptoms included epigastralgia, nausea and vomiting, as well as asthenia, anorexia and weight loss (approximately 20 kg in 2 years). A computed tomography scan showed mediastinal and mesenteric adenopathy, ascites, splenomegaly, and thickening of the gastric wall. Diagnosis was made by endoscopic biopsy of the affected areas in the antral region, the result being granulomatous chronic gastritis suggestive of tubercular origin.
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PMID:[Gastric tuberculosis. Review apropos of a case]. 1766 16

Anemia is a common complication in malarial infection, although the consequences are more pronounced with Plasmodium falciparum malaria (Ghosh, Indian J Hematol Blood Tranfus 21(53):128-130, 2003). Anemia in this infection is caused by a variety of pathophysiologic mechanisms, and in areas where malaria infection is endemic, co-morbidities like other parasitic infestations, iron, folate and Vitamin B12 deficiency, deficiency of other nutrients, and anemia, which is aggravated by anti-malarial drugs both through immune and non-immune mechanisms, are important considerations. In different endemic areas, beta-thalassemia, alpha-thalassemia, Hb S, Hb E, G6PD deficiency, or ovalocytosis in different proportions interact with this infection. Finally, aberrant immune response to repeated or chronic falciparum malarial infection may produce tropical splenomegaly syndrome, a proportion of which show clonal proliferation of B lymphocytes. Cooperation between chronic malarial infection and infection with E-B virus infection in producing Burkitt's lymphoma is well known. In this review, the fascinating and multifaceted pathophysiolgoy of malarial anemia has been discussed.
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PMID:Pathogenesis of anemia in malaria: a concise review. 1787 26

The essentiality of zinc for humans was recognized only 40 years ago. Zinc deficiency was suspected to occur in Iranian patients with growth retardation, hypogonadism in males, hepato-splenomegaly, rough and dry skin, geophagia and severe iron deficiency anemia. Later we documented zinc deficiency in similar patients in Egypt. The diet of these patients consisted of mainly cereal proteins which contained high phytate and this led to decreased availability of iron and zinc. These patients had severe immune dysfunctions, inasmuch as they died of intercurrent infections by the time they were 25 years of age. In our studies in experimental human model of zinc deficiency, we documented decreased serum testosterone level, oligospermia, severe immune dysfunctions mainly affecting T helper cells, decreased serum thymulin activity hyperammonemia, neuro-sensory disorders and decreased lean body mass. The basic mechanisms of zinc action on immune cells have been reviewed in this paper. Our studies showed that the activation of many zinc dependent enzymes and transcription factors were affected adversely due to zinc deficiency. The gene expression and production of Th1 cytokines were affected adversely due to zinc deficiency. Zinc is also an antioxidant and has anti-inflammatory actions. We have reported decreased plasma zinc, increased plasma oxidative stress markers and increased generation of inflammatory cytokines in the elderly subjects which were corrected by zinc supplementation. In cell culture studies, we have observed that zinc induces A20 which inhibits NF-kappaB activation resulting in decreased generation of inflammatory cytokines.
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PMID:Clinical, immunological, anti-inflammatory and antioxidant roles of zinc. 1805 90

In gram-negative bacteria, iron acquisition proteins are commonly regulated by Fur (ferric uptake regulator), which binds iron-regulated promoters (the Fur box). We hypothesized that Coxiella burnetii requires iron and employs an iron-regulatory system and used various approaches to define a Fur regulon. Cloned C. burnetii fur complemented an Escherichia coli fur deletion mutant. A ferrous iron transporter gene (CBU1766), a putative iron binding protein-encoding gene (CBU0970), and a cation efflux pump gene (CBU1362) were identified by genome annotation and using a Fur titration assay. Bioinformatically predicted Fur box-containing promoters were tested for transcriptional control by iron. Five genes demonstrated at least a twofold induction with minimal iron. Putatively regulated genes were evaluated in a two-plasmid regulator/promoter heterologous expression system. These data suggested a very limited Fur-regulated system in C. burnetii. In an in vitro tissue culture model, a significant increase in bacterial growth was observed with infected cells treated with deferoxamine in comparison to growth under iron-replete conditions. In an iron-overloaded animal model in vivo, the level of bacterial growth detected in the iron-injected animals was significantly decreased in comparison to growth in control animals. In a low-iron-diet animal model, a significant increase in splenomegaly was observed, but no significant change in bacterial growth was identified. The small number of predicted iron acquisition systems, few Fur-regulated genes, and enhanced replication under a decreased iron level predict a requirement of a low level of iron for survival, perhaps to avoid creation of additional reactive oxygen radicals.
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PMID:Limited role for iron regulation in Coxiella burnetii pathogenesis. 1831 81

Phenylhydrazine (PHZ) oxidation resulting in free iron release followed by free radical generation has increased frequency of cancer. This study aims towards the dose-dependent response of PHZ and the role of melatonin in comparison with vitamin E following PHZ-induced toxicity within the lymphoid tissue (spleen) of Indian tropical seasonal breeder, Funambulus pennanti, during reproductively active phase. An increase in the damages in terms of lipid peroxidation (LPO), apoptosis percentage, and splenomegaly was observed following different doses of PHZ treatment, i.e., 0.025, 0.5, and 1 mg/100 g body weight (b.wt.), where dose of 1 mg/100 g b.wt. showed more significant damages. Both melatonin (0.5 mg/100 g b.wt.) and vitamin E (1 mg/100 g b.wt.) administration ameliorated oxidative damages of 1 mg/100 g b.wt. PHZ-treated group. Melatonin altered PHZ-induced responses significantly to a greater degree than vitamin E as evidenced by LPO status, SOD activity, and ABTS radical cation scavenging activity of antioxidants. Thus, melatonin might be able to restrict carcinogenic property of PHZ-induced oxidative stress by protecting macromolecules of the cell from harmful effects of PHZ and instead preserving cell viability.
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PMID:Comparative effect of melatonin and vitamin E on phenylhydrazine-induced toxicity in the spleen of Funambulus pennanti. 1844 75

Gardos channel, the erythrocyte Ca(2+)-activated K(+) channel (K(Ca)3.1), is considered a major regulator of red blood cell (RBC) volume by mediating efflux of potassium and thus cell dehydration and shrinkage. However, the functional importance of K(Ca)3.1 in RBC in vivo is incompletely understood. Here, we used K(Ca)3.1(-/-)-mice to investigate the consequences of K(Ca)3.1 deficiency for RBC indices, functions, and sequestration. RBCs of K(Ca)3.1(-/-)-mice of all ages were mildly macrocytic but their biconcave appearance being preserved. RBC number, total hemoglobin, and hematocrit were unchanged in the adult K(Ca)3.1(-/-)-mice and increased in the premature K(Ca)3.1(-/-)-mice. Filterability, Ca(2+)-dependent volume decrease and osmotic tolerance of RBCs lacking K(Ca)3.1 were noticeably reduced when compared to RBC of wild-type littermates. Deformability to increasing shear stress was unchanged. Strikingly, K(Ca)3.1(-/-)-mice developed progressive splenomegaly which was considerable ( approximately 200% of controls) in the >6-month-old mice and was paralleled by increased iron deposition in the aged mice presumably as a consequence of enhanced RBC sequestration. Daily injections of the K(Ca)3.1-blocker TRAM-34 (120 mg/kg) also produced mild splenomegaly in wild-type mice. We conclude that genetic deficit of erythroid K(Ca)3.1 causes mild RBC macrocytosis, presumably leading to reduced filterability, and impairs volume regulation. These RBC defects result in mild but progressive splenomegaly.
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PMID:Disruption of the Gardos channel (KCa3.1) in mice causes subtle erythrocyte macrocytosis and progressive splenomegaly. 1903 56

Natural resistance-associated macrophage protein 1 (Nramp1) is a divalent metal transporter expressed exclusively in phagocytic cells. We hypothesized that macrophage Nramp1 may participate in the recycling of iron acquired from phagocytosed senescent erythrocytes. To evaluate the role of Nramp1 in vivo, the iron parameters of WT and KO mice were analyzed after acute and chronic induction of hemolytic anemia. We found that untreated KO mice exhibited greater serum transferrin saturation and splenic iron content with higher duodenal ferroportin (Fpn) and divalent metal transporter 1 (DMT1) expression. Furthermore, hepatocyte iron content and hepcidin mRNA levels were dramatically lower in KO mice, indicating that hepcidin levels can be regulated by low-hepatocyte iron stores despite increased transferrin saturation. After acute treatment with the hemolytic agent phenylhydrazine (Phz), KO mice experienced a significant decrease in transferrin saturation and hematocrit, whereas WT mice were relatively unaffected. After a month-long Phz regimen, KO mice retained markedly increased quantities of iron within the liver and spleen and exhibited more pronounced splenomegaly and reticulocytosis than WT mice. After injection of (59)Fe-labeled heat-damaged reticulocytes, KO animals accumulated erythrophagocytosed (59)Fe within their liver and spleen, whereas WT animals efficiently recycled phagocytosed (59)Fe to the marrow and erythrocytes. These data imply that without Nramp1, iron accumulates within the liver and spleen during erythrophagocytosis and hemolytic anemia, supporting our hypothesis that Nramp1 promotes efficient hemoglobin iron recycling in macrophages. Our observations suggest that mutations in Nramp1 could result in a novel form of human hereditary iron overload.
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PMID:Nramp1 promotes efficient macrophage recycling of iron following erythrophagocytosis in vivo. 1932 19


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