Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019214 (hepatosplenomegaly)
 4,408 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients with chronic neutrophilic leukemia, a rare myeloproliferative syndrome, are reported with a review of the literature. The major features of the 34 collected cases (including the two patients reported here) were persistent leukocytosis simulating a leukemoid reaction, hepatosplenomegaly, hyperuricemia, increased vitamin B12 blood level, increased leukocyte alkaline phosphatase and absence of the Philadelphia chromosome. Infection was the leading cause of death. Concomitant multiple myeloma was found in eight patients.
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PMID:[Chronic neutrophilic leukemia: apropos of 2 cases and review of the literature]. 208 13

Infection of BALB/c mice with the RLV-A virus typically results in an erythropoietic dysplasia characterized by hepatosplenomegaly, erythroblastosis, erythroblastemia and severe anemia without reticulocytosis. Mice hypertransfused weekly with 75%-packed red cells for 42 days prior to RLV-A infection and viral potency controls manifested this typical RLV-A response. Mice that were hypertransfused prior to and following RLV-A infection never developed the "typical" RLV-A pathogenesis. Instead, a transplantable myeloid leukemia was established. Although the reason for altered pathogenesis remains uncertain, it seems plausible that continued hypertransfusion, presumably after establishment of an altered granulopoietic microenvironment, resulted in a completely different viral expression and development of the transplantable myeloid leukemia.
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PMID:Sustained hypertransfusion and induction of a transplantable myeloid leukemia in RLV-A-infected BALB/c mice. 273 54

Infection of BALB/c mice with the RLV-A virus normally induces an erythropoietic dysplasia characterized by hepatosplenomegaly, erythroblastosis, erythroblastemia and severe anemia without reticulocytosis. Time to death varies between 20-30 weeks. Mice were inoculated with RLV-A after being hypertransfused with 75% packed red cells for 42 days which has been shown to eliminate erythropoiesis and modify the microenvironment to favor granulopoiesis. Following RLV-A inoculation, one group did not receive further transfusion (short-term) and another group continued with hypertransfusion weekly (long-term). The pathogenesis of RLV-A in the short-term group paralleled the characteristic RLV-A response. In the long-term group however, the characteristic RLV-A response was never observed. Instead, a granulocytic leukemia was developed. Continued hypertransfusion presumably after establishment of an altered microenvironment resulted in a completely different viral pathogenesis and the development of a transplantable myeloid leukemia.
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PMID:Effect of sustained hypertransfusion on Rauscher leukemia virus-variant A (RLV-A) infection in BALB/c mice. 322 6

A review of the literature about angio-immunoblastic lymphadenopathy since 1972 Flandrin's first description, attempts to define the main clinical, biological characteristics and clinical course of this disease. Clinically adenopathy, fever, weight loss, often hepatosplenomegaly of the appear as being constant. Hemolytic anemia and polyclonal hyperglobulinemia are the most common biological signs of this immunological disorder. In despite of spontaneous remissions, prognosis is severe. Infections complications are common and often fatal. Transformation in immunoblastic sarcoma is possible.
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PMID:[Angio-immunoblastic lymphadenopathy (author's transl)]. 624 2

Infection with both urinary and intestinal schistosomiasis is prevalent with patchy distribution in Taiz Province, southwest Yemen Arab Republic. Schistosoma haematobium with a prevalence as high as 90% was found in the western, southern, and northern parts of the province. Among school children the overall prevalence was 37%. Infection rates did not differ significantly among various age and sex groups. Three species of Bulinus--B. beccarii, B. truncatus, and B. wrighti--have been found in the province, B. beccarii having the widest distribution and highest density. S. mansoni was found in most parts of the province. A 100% prevalence was found in some schools. The overall prevalence was 64% among school children and 68% among inhabitants of villages surveyed. Highest prevalence was found in the age group 10-20 years. Hepatosplenomegaly was prevalent among children in highly endemic areas. Biomphalaria pfeifferi, the intermediate host of S. mansoni, was found in most valleys.
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PMID:Studies on schistosomiasis in Taiz Province, Yemen Arab Republic. 662 57

Malaria manifested during the first few months of life may be result of acquisition during pregnancy, at the time of delivery, or by mosquito bite after birth. Both congenital and perinatal malaria are acquired by the transmission of parasitized maternal erythrocytes across the placenta. An infant is described whose mother was diagnosed to have malaria at six months of gestation. The infant developed intermittent fever at 5 weeks of age and presented with anemia and hepatosplenomegaly at 3 months of age at which time Plasmodium falciparum parasites were found on examination of thick smears of the infant's blood. IgG and IgM antimalarial antibodies were detected in maternal blood, but only IgG antibodies were found in the infant's blood at delivery and at the time of diagnosis. These transplacentally transmitted antibodies may afford transient protection for the infant and thus delay the onset of clinical manifestations. Due to the absence of an exoerythrocytic life cycle in congenitally acquired malaria, chloroquine is the drug of choice for treatment. Infections with chloroquine-resistant strains require multiple drug therapy.
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PMID:Congenital malaria due to Plasmodium falciparum. 700 57

The host-parasite relationship in human visceral leishmaniasis remains poorly understood. In the present study, pathophysiological and immunological changes were examined in BALB/c mice infected with Leishmania donovani. These animals developed chronic infection with massive hepatosplenomegaly and hypergammaglobulinemia. In contrast to mice inoculated with 0.8 X 10(6) or 4 X 10(6) amastigotes, mice infected with 20 X 10(6) amastigotes failed to reduce liver parasite loads during 2 to 8 weeks of observation. At 8 weeks, liver size was increased by 26, 63, and 94%, respectively, in groups infected with 0.8 X 10(6), 4 X 10(6), or 20 X 10(6) amastigotes. Serum immunoglobulin G and M levels at 8 weeks in animals with the heaviest infection were increased by 53 and 80%, respectively, compared with controls. Specific antileishmanial antibodies were detected in the absence of antigen-specific delayed-type hypersensitivity or in vitro lymphocyte responses. Infection did not suppress the in vivo responses of mice to the non-parasite-related antigens sperm whale myoglobin or pneumococcal polysaccharide. Splenic mononuclear cell responses to phytohemagglutinin were suppressed as early as 2 weeks, and by 8 weeks, mice infected with 0.8 X 10(6), 4 X 10(6), or 20 X 10(6) amastigotes had phytohemagglutinin responses which were, respectively, 27.7, 13.9, and 15.8% of controls. Decreased phytohemagglutinin responses could not be related to reductions in splenic T cells; however, splenic B cells and macrophages were increased at 8 weeks of infection. The course of L. donovani infection and disease in BALB/c mice resembles events occurring in humans and should prove useful in defining mechanisms of immune alterations in visceral leishmaniasis.
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PMID:Host-parasite relationship in murine leishmaniasis: pathophysiological and immunological changes. 715 67

Infection with the protozoan Leishmania donovani can cause serious visceral disease or subclinical infection in humans. To better understand the pathogenesis of this dichotomy, we have investigated the host cellular immune response to cutaneous or visceral infection in a murine model. Mice infected in the skin developed no detectable visceral parasitism, whereas intravenous inoculation resulted in hepatosplenomegaly and an increasing visceral parasite burden. Spleen cells from mice with locally controlled cutaneous infection showed strong parasite-specific proliferative and gamma interferon (IFN-gamma) responses, but spleen cells from systemically infected mice were unresponsive to parasite antigens. The in situ expression of IFN-gamma, interleukin-4 (IL-4), IL-10, IL-12, and inducible nitric oxide synthase (iNOS) mRNAs was determined in the spleen, draining lymph node (LN), and cutaneous site of inoculation. There was considerably greater expression of IFN-gamma and IL-12 p40 mRNAs in the LN draining a locally controlled cutaneous infection than in the spleen following systemic infection. Similarly, there was a high level of IFN-gamma production by LN cells following subcutaneous infection but no IFN-gamma production by spleen cells following systemic infection. Splenic IL-4 expression was transiently increased early after systemic infection, but splenic IL-10 transcripts increased throughout the course of visceral infection. IL-4 and IL-10 mRNAs were also increased in the LN following cutaneous infection. iNOS mRNA was detected earlier in the LN draining a cutaneous site of infection compared to the spleen following systemic challenge. Thus, locally controlled cutaneous infection was associated with antigen-specific spleen cell responsiveness and markedly increased levels of IFN-gamma, IL-12, and iNOS mRNA in the draining LN. Progressive splenic parasitism was associated with an early IL-4 response, markedly increased IL-10 but minimal IL-12 expression, and delayed expression of iNOS.
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PMID:Regional differences in the cellular immune response to experimental cutaneous or visceral infection with Leishmania donovani. 942 34

Bone marrow hemophagocytosis may occur as an incidental finding, or it may be a manifestation of a systemic and potentially lethal disorder. When systemic, the proliferation is termed hemophagocytic lymphohistiocytosis (HLH), a clinicopathologic entity characterized by a widespread proliferation of benign hemophagocytic histiocytes, fever, pancytopenia, deranged liver function, and frequently coagulopathy and hepatosplenomegaly. A variety of infectious agents, including Epstein-Barr virus (EBV), cytomegalovirus (CMV), human herpesvirus 6 (HHV6), and parvovirus B19 (PVB19), have been associated with HLH, but the relative frequency of each using one technique has not been evaluated. In addition, infectious causes of incidental bone marrow hemophagocytosis, not occurring in the setting of HLH, have not been evaluated. Review of bone marrow reports from bone marrow examinations done between December 1986 and June 1997 showed that 20 children aged 2 months to 15 years had bone marrow examinations that indicated hemophagocytosis. Archival materials from 19 patients were successfully retrieved, and DNA was extracted from archived unstained coverslips with subsequent polymerase chain reaction for EBV, CMV, HHV6, and PVB19 genomic DNA. DNA extracted from 16 bone marrow specimens of age-matched children was used as negative controls. Eleven of the 19 patients fulfilled the clinical and pathological criteria for HLH; the remaining eight patients had isolated hemophagocytosis without a systemic presentation. Viral DNA was detected in 8 of 11 patients with HLH but in none of eight patients with isolated hemophagocytosis. EBV was present in five of the bone marrows, followed in frequency by HHV6, CMV, and PVB19. Infection with more than one agent was present in three patients. Only one control patient was positive for HHV6 DNA; the remaining control patients were negative for all viruses. Viral infection, detected by PCR analysis of bone marrow, is a common finding in patients with HLH but not in patients with isolated bone marrow hemophagocytosis. This technique may provide another marker to aid in the diagnosis of HLH and suggests a different cause of hemophagocytosis occurring in patients with and without HLH.
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PMID:Polymerase chain reaction amplification of archival material for Epstein-Barr virus, cytomegalovirus, human herpesvirus 6, and parvovirus B19 in children with bone marrow hemophagocytosis. 978 44

Infection with cytomegalovirus (CMV) in infants can be congenital or perinatal. Infected infants may be asymptomatic or present with pneumonia, rash, hepatosplenomegaly, or encephalitis.1 In the presence of an immunodeficiency, severe and sometimes fatal disease may occur. To our knowledge, CMV has not been identified previously as a cause of intractable diarrhea of infancy. We report the case of a 5-week-old immunocompetent infant with intractable diarrhea attributable to CMV-induced enterocolitis. Recognition of this infection and initiation of ganciclovir therapy was associated with a rapid improvement and resolution of the diarrhea.
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PMID:Intractable diarrhea from cytomegalovirus enterocolitis in an immunocompetent infant. 991 90


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