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)

C57BL/6Kh mice were infected with a single i.p. injection of 1 x 10(5) FFU of LP-BM5 MuLV. The development and progress of the virus-induced lymphoproliferative disease was followed for 12 weeks after infection. As anticipated, progressive splenomegaly and lymphadenopathy, as well as almost total abrogation of immune responsiveness ensued. In contrast to previous reports, there was a dramatic increase in the frequency of CD4+ cells in spleens among which over 20% expressed V beta 5 TCR, as compared with fewer than 3% in spleens of normal mice. Spleen cells from infected mice retained their in vitro ability to proliferate upon stimulation with IL-2 and anti-CD3, but were unable to respond when stimulated with phorbol ester and either a low dose of IL-2 or calcium ionophore (ionomycin). A similar pattern of in vitro proliferative responses was obtained when normal spleen cells were treated with K252a compound, a known inhibitor of protein kinase C activity. Together with the observations that viral infection impaired down-regulation of the phorbol-induced kinase activity and that the kinase inhibitor only marginally enhanced suppression of virus-infected cells proliferation, this finding suggests that disturbances of protein kinase C activity may underly the pathological effects seen after viral infection. However, since no apparent quantitative and qualitative changes in protein kinase C itself and its translocation were observed, it is more likely that the virus may interfere with either the substrate or product of kinase activity.
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PMID:Acquired immunodeficiency in murine lymphoproliferative disease: considerations on pathogenesis. 808 52

Portal hypertension in the presence of chronic hepatitis is generally thought to develop during the progression of the chronic hepatitis to cirrhosis. Before the establishment of assays for diagnosing hepatitis C virus infection, such a case of portal hypertension without liver cirrhosis could be misdiagnosed as idiopathic portal hypertension. It had not fully determined whether portal hypertension might precede the onset of cirrhosis in type C chronic hepatitis. This report presents two cases of women with chronic hepatitis C who developed severe thrombocytopenia; each showed splenomegaly and hypersplenism due to portal hypertension. Angiographic study and histological analysis were conducted to determine the cause of the portal hypertension. Histological evaluation showed an intrahepatic presinusoidal block pattern and fibrotic changes in the periportal area, but no evidence of liver cirrhosis or of other incidental complications such as idiopathic portal hypertension. Both of these patients exhibited normal platelet counts after splenectomy. Thus, type C chronic hepatitis can lead to portal hypertension, as demonstrated in these two patients.
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PMID:Type C chronic hepatitis associated with thrombocytopenia in two patients. 815 75

Murine AIDS (MAIDS) is a disease that shows many similarities to human HIV infection. The etiological agent of MAIDS is a defective murine leukemia virus that seems to be able to induce disease in the absence of viral replication. This animal model has been useful in stimulating the search of answers to questions and the formation of new hypotheses related to human AIDS. The monovalent cation lithium can influence a number of immunohematopoietic cell types and cellular processes where proliferation and differentiation occur. We describe here the result of in vivo studies investigating the effect of lithium treatment on MAIDS-infected mice. Viral control and lithium-treated animals were monitored for survival and development of MAIDS pathology. MAIDS animals treated with lithium demonstrated a marked reduction in their development of lymphadenopathy and splenomegaly. Both MAIDS control and lithium-treated virus-infected mice developed evidence of lymphoma; however, the involvement was much more massive both at the gross and microscopic levels in the MAIDS control compared with the lithium-treated mice. These data suggest that lithium may be effective in modulating murine immunodeficiency virus infection and raise important questions related to the potential role lithium may play in the pathophysiological processes associated with retroviral infections.
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PMID:Effect of lithium in murine immunodeficiency virus infected animals. 821 44

A 16-year old woman with LGL leukemia developed peripheral neuropathy. She showed virus-associated hemophagocytic syndrome (VAHS)-like signs including high fever, liver dysfunction, huge splenomegaly, hepatomegaly and pancytopenia. The presence of chronic active EB virus infection was proved by marked high titers for IgG and IgA antibodies to the Epstein-Barr viral capsid and early antigens and low titers of antibody to Epstein-Barr nuclear antigens. She showed dysesthesia and paresthesia of bilateral lower extremities with marked swelling and tenderness, and later developed muscular weakness and atrophy with areflexia of lower extremities. Findings of the central nervous system dysfunction were not observed except for the acceleration of jaw jerk. Pleocytosis and increased protein levels in the cerebrospinal fluid were found. Pulse therapy of methyl-prednisolone and high dose intravenous immunoglobulin therapy (20 g/day for 3 days) were effective for neurological findings. The increased neopterin in the cerebrospinal fluid suggested that peripheral neuropathy was caused by activated macrophages.
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PMID:[Peripheral neuropathy in large granular lymphocytic leukemia]. 821 4

Infection with Rauscher leukaemia virus (RLV) causes erythroleukaemia, anaemia, viraemia, and splenomegaly, features which develop very quickly in mice of strains susceptible to RLV but more slowly or not at all in strains resistant to RLV. We compared the effects of bone marrow transplantation (BMT) of donor cells obtained from a mouse strain resistant to the virus with the effects of BMT of donor cells obtained from strains susceptible to the virus, in recipient virus-susceptible mice which had previously been inoculated with RLV. Our results indicated that bone marrow transplantation from a marrow-resistant donor, but not from a susceptible donor, delayed the expression of leukaemia and delayed death, although such treatment did not appear to inhibit viral infection in susceptible recipients.
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PMID:Bone marrow transplantation therapy using resistant donors for retrovirus-induced leukaemia in mice. 828 97

We report on a tourist returning from Thailand, who presented with classical dengue fever. While in Thailand a 36-year-old Swiss female laboratory assistant suddenly developed fever, devastating headache, retro-ocular pain, myalgia and arthralgia, photophobia, nausea and diarrhea. In addition she suffered from epistaxis, urogenital and skin bleeding, and a morbilliform exanthema. After her return to Switzerland we noted lymphadenopathy and splenomegaly, enanthema and laboratory findings of mild hepatitis, thrombocytopenia and leukopenia. The diagnosis of dengue virus infection was verified serologically. Apart from a long lasting convalescent asthenia we observed restitutio ad integrum within days under symptomatic therapy. Epidemiological clinical and diagnostic aspects of dengue virus infection are discussed.
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PMID:[Imported dengue fever following a stay in the tropics]. 842 57

The clinical, biochemical and histological features of 102 consecutively referred patients with chronic hepatitis C virus infection were analysed. Demographic, epidemiological, biochemical, haematological and histological details were catalogued for each patient. The mean follow-up was 49 +/- 6 months. Liver biopsies were obtained from 92 patients; a second biopsy was obtained from 35 patients. The average known duration of infection was 8.6 +/- 0.7 years. The most common risk factors that could be identified were past blood transfusion, surgery or intravenous drug abuse. Twenty-four of the 27 patients (85%) with past blood transfusion had received blood in countries outside of northern Europe. In contrast, 12 of the 16 former drug users were northern European. Patients were frequently diagnosed incidentally; one-quarter had no symptoms of liver disease and were generally asymptomatic or had presented with non-specific complaints and were found to have abnormal serum aminotransferase levels after routine screening. The mean serum aminotransferase levels were not significantly different in those presenting with fatigue compared to those diagnosed incidentally. The most common physical sign in these patients was a palpable liver, which was present in 52%. The mean serum albumin concentration in patients older than 40 years was significantly lower than that in younger patients. Splenomegaly and endoscopic evidence of varices was also more common in older patients. Cirrhosis was present in 37% of patients at presentation: 20% showed progression on rebiopsy, and 5% developed cirrhosis within 4 years of initial presentation. Of those treated, 27% showed histological improvement. Histological severity did not correlate with duration of disease, but did correlate with age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical, biochemical and histological features in 102 patients with chronic hepatitis C virus infection. 846 87

Atraumatic splenic ruptures in the course of infectious diseases are rare but have been reported. Various germs of viruses can be at the origin of such rupture. The more often quoted viral disease is infectious mononucleosis. The more frequently involved bacteria are Streptococcus non pneumoniae, Pseudomonas, staphylococci and Clostridium. Rupture mechanism is not clearly elucidated; it can be connected with sepsis diffusion at spleen level via haematogenic way and consequently splenomegaly. Splenic rupture following septicaemia does not always entail major splenomegaly nor abscess formation but the attack of the splenic tissue itself is sometimes sufficient to bring about the rupture. The present case of atraumatic splenic rupture on spleen sepsis, no abscess, starting from a pulmonar infection with Streptococcus pneumoniae is, to our knowledge, the first case reported in literature.
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PMID:Atraumatic splenic rupture in the course of a pneumonia with Streptococcus pneumoniae. Case report and literature review. 847 Apr 45

Human ehrlichiosis is a zoonotic disease, caused by a rickettsia that infects leukocytes. It was described for the first time in the United States of America in 1986. More than 300 cases have been reported in that country. One case has been reported in Portugal, two in France and one more in a tourist coming from Mali (Africa). In Venezuela, a tropical country, where ehrlichiosis is endemic in dogs and horses, the first case of human ehrlichiosis is reported in a seventeen month old girl. She initially had symptoms compatible with a viral illness. Then she developed a rash, acute respiratory failure, hepato-splenomegaly, neurologic abnormalities, renal failure and hematologic alterations including pancytopenia and disseminated intravascular coagulation (DIC). Different diagnoses were given before it was concluded that it was a case of ehrlichiosis. She was treated with tetracycline and very soon recovered. The initial diagnosis was made using buffy coat blood smears stained with Diff Quick Stain. Indirect Immunofluorescence (IFA) test was used to detect antibodies against Ehrlichia chaffeensis (1:126) but not to other rickettsias. Also the presence of platelets with ehrlichia bodies similar to E. platys from dogs, it was demonstrated, in peripheral blood from the child. The presence of these bodies in human platelets has not been previously reported. In this case, it could not be proved that the disease was transmitted by a tick bite. The presence of ehrlichia bodies in platelets from the girl's peripheral blood is also described.
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PMID:[Human ehrlichiosis: report of the 1st case in Venezuela]. 892 30

Virus-associated hemophagocytic syndrome (VAHS) is associated with a systemic viral infection and is mainly observed in immunosuppressed adult patients. This rare disease is characterized by symptoms which include a high fever, pancytopenia, and splenomegaly and sometimes results in a fatal outcome. However, thus far, little has been reported on VAHS in general surgical patients. We herein report this rare complication which occurred in a patient with hepatocellular carcinoma, as well as chronic hepatitis C, after a hepatic resection. A 66-year-old man with chronic hepatitis C and recurrent hepatocellular carcinoma underwent a repeat hepatic resection without any blood transfusions. In the early postoperative period, he recovered uneventfully. However, he suddenly began to suffer from a high fever (38.4 degrees C) and severe pancytopenia 8 days after surgery. Activated macrophages, which phagocytosed erythrocytes, were identified by a cytological study of the bone marrow. The patient was therefore treated with methylprednisolone pulse therapy 13 days after surgery. On the day following the initial administration of methylprednisolone, his clinical condition drastically improved. Fortunately, with methylprednisolone therapy, our patient recovered from acute, severe pancytopenia. In general surgery, it is often difficult for surgeons to use steroids due to their negative side effects. However, when symptoms such as fever, general fatigue and pancytopenia are observed, even in posthepatectomy patients with hepatocellular carcinoma and hepatitis, a bone marrow aspiration should be performed as soon as possible, and when VAHS is suspected, steroid pulse therapy should be the first treatment of choice. This rare but sometimes fatal complication should thus be taken into consideration in the postoperative management of hepatectomized patients with chronic hepatitis C.
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PMID:Virus-associated hemophagocytic syndrome after hepatic resection: a case report. 949 16


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