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)

Infectious mononucleosis is an acute viral illness associated with a high incidence of splenomegaly, although the incidence of splenic rupture is low. When rupture occurs, the mortality has been significant, presumably, because a history of trauma is not present. The spleen may be vulnerable to injury due to the histopathologic changes that occur as a result of this illness. Essentially all patients with spontaneous rupture related to infectious mononucleosis have epigastric or upper abdominal pain. The diagnosis of splenic rupture may be confirmed in a variety of ways. In those patients who are hemodynamically stable, CT scan, ultrasound, or radionuclide scan may aid in establishing the diagnosis. Selective splenic angiography is very accurate but has been largely abandoned because of the invasive nature of the study. Peritoneal lavage is efficacious in establishing the diagnosis in hemodynamically unstable patients. The treatment of choice, at this time, is splenectomy. Current interest in splenic salvage has resulted in reports of nonoperative therapy in stable patients and splenorrhaphy in one instance. Due to the extent of the histologic changes in the spleen, caution is urged in electing the conservative approach to this clinical situation.
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PMID:Splenic rupture and infectious mononucleosis. 269 60

Antitumor antibiotic streptonigrin (STN-COOH) is a potent inhibitor of avian myeloblastosis virus (AMV) and human immunodeficiency virus reverse transcriptases. The carboxyl group at 2'-position of STN-COOH was modified to give esters, hydrazide, amides and amino acid derivatives for biological studies. Against AMV reverse transcriptase, the hydrazide, amides and amino acid derivatives showed inhibitory activity, which compared favorably to that of STN-COOH, with the ID50 values ranging 2-8 micrograms/ml. In contrast, the esters lacked this activity except for those having a dimethylamino group in the substituent. Splenomegaly caused by Friend leukemia virus infection was significantly inhibited by STN-COOH and STN-COO(CH2)3N(CH3)2, but not STN-CONH(CH2)3N(CH3)2. Doxorubicin-resistant murine lymphoblastoma L5178Y cells showed collateral sensitivity to both STN-COOH and STN-COO(CH2)3N(CH3)2 not only in vitro but also in vivo.
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PMID:Biological properties of streptonigrin derivatives. III. In vitro and in vivo antiviral and antitumor activities. 273 55

Nineteen children who presented with fever, hepato-splenomegaly, bone marrow and/or hepatic failure, and biopsy evidence of histiocytic proliferations were evaluated for lymphocyte dysfunction and evidence of prior viral infection. Seventeen of the children had erythrophagocytosis consistent with the previously described virus-associated hemophagocytosis syndrome (VAHS) or Familial erythrophagocytic lymphohistiocytosis (FEL). The other two had benign histiocytic proliferations in the central nervous system (CNS) with liver and bone marrow dysfunction. There were two sibling pairs and six patients with known disorders of immune deficiency. The remaining nine cases appeared to be sporadic and idiopathic. Epstein-Barr Virus (EBV) was identified in patients by serologic or DNA hybridization studies (15), EBV and cytomegalovirus (CMV) (1), adenovirus plus EBV and CMV (1), or adenovirus and EBV (1). Herpes zoster was associated with reactivation of symptoms in one patient. Immunologic impairment was evidenced by lymphopenia in 10 of 19 patients. More extensive evaluations could be done at diagnosis on only some of the children because the histiocytic proliferative syndrome was not recognized or because there were insufficient numbers of lymphocytes in samples obtained. For those who could be evaluated, the following immune deficiencies were found: decreased lymphocyte proliferation to mitogens (4 of 9), absent or markedly decreased natural killer function (5 of 5), and decreased cytotoxic lymphocyte reactivity to allogenic EBV-infected target cells (3 of 3). A new finding reported here is a higher than expected prevalence of HLA types A30, B8, and A1/B8 among the patients tested.
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PMID:Virus-associated histiocytic proliferations in children. Frequent association with Epstein-Barr virus and congenital or acquired immunodeficiencies. 284 31

The Celebes black macaque (Macaca nigra) colony at the Oregon Regional Primate Research Center has a high incidence of an immunodeficiency syndrome characterized by recurrent diarrhea and the development of retroperitoneal fibromatosis (RF). We have examined the relationship of type D viral infection to the immunodeficiency syndrome by surveying the colony for viral infection and for mitogen reactivity. Type D virus-positive monkeys (28% of the colony) have a higher prevalence of diarrhea, splenomegaly, lymphadenopathy and weight loss than do virus-negative monkeys, and RF has been found to occur only in virus-positive animals. Comparison of the concanavalin A (con-A) and phytohemagglutinin reactivities of the virus-positive and -negative populations has revealed no significant difference. However, within the virus-positive population, those with RF have reduced con-A reactivity and there are both high and low mitogen responders in the groups lacking RF. Thirty-two percent of the virus-positive monkeys are free of clinical symptoms, 40% have clinical symptoms but no RF, and 27% have clinical symptoms and RF. Five of the six monkeys with RF are older than the RF-free monkeys but monkeys are susceptible to type D retrovirus infection regardless of age or sex. The progressive nature of this immunodeficiency syndrome, its broad age range, and the probability that the etiological agent is also a type D retrovirus and the similarity of RF to Kaposi's sarcoma make this a potentially useful model for human AIDS.
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PMID:Relationship of mitogen reactivity to type D retrovirus infection in Celebes black macaques (Macaca nigra). 301 9

Eighty-five patients with chronic splenomegaly and proven oesophageal varices were studied at Kenyatta National Hospital, Nairobi. The major defined groups were hepatosplenic schistosomiasis (24%), cirrhosis (20%) and portal vein occlusion (11%). Hyper-reactive malarial splenomegaly (tropical splenomegaly syndrome) was considered as the cause of oesophageal varices in only one patient. In 26% of cases liver biopsy was non-diagnostic and the extrahepatic portal vein was demonstrated radiologically to be patent. Such patients were thought to be suffering from idiopathic portal hypertension, not previously described elsewhere in Africa. Hepatitis B surface antigen was detected in 12% of controls and in 58% of patients with cirrhosis (p less than 0.001). Some serological marker of previous hepatitis B virus infection was present in 92% of patients with cirrhosis and in 79% of controls. Kamba patients from Machakos and Kitui Districts were significantly more prevalent than expected among these 85 cases of portal hypertension.
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PMID:Chronic splenomegaly in Nairobi, Kenya. II. Portal hypertension. 312 51

Liver biopsy specimens previously taken from 16 haemophilic patients with chronic non-A, non-B hepatitis were reviewed. The degree of fibrosis correlated with serum procollagen III peptide (sPIIIP) concentrations, measured both at the time of biopsy and 4.25 years later. Two patients with extremely high sPIIIP concentrations had collateral veins on computed tomography, suggesting portal hypertension. Twenty eight of 47 patients (60%) had splenomegaly on computed tomography, and of 28 patients in whom intravenous contrast medium was used, seven (25%) had collateral oesophageal veins. Serum procollagen III peptide estimations and computed tomography, both non-invasive investigations, indicated that hepatic fibrosis and portal hypertension had developed in a proportion of haemophilic patients with non-A, non-B hepatitis. Infection with the human immunodeficiency virus (HIV) may modify the course of this presumably cytopathic virus infection of the liver.
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PMID:Non-invasive investigation of liver disease in haemophilic patients. 314 33

Diagnosis of malignant histiocytosis (MH) often resembles the solving of an intricate puzzle consisting of clinical symptoms such as lymphadenopathy, splenomegaly, fatigue, fever, and rapid progression, and hematopathological findings such as the presence of atypical histiocytes, especially in blood and bone marrow smears. The lack of one or more of these criteria may greatly impede diagnosis, as in the case of a 45-year-old male with an unusual hematopathological manifestation of MH. The major clinical findings included panhemocytopenia, splenomegaly, and signs of liver dysfunction with severe jaundice. During life, a definite diagnosis could not be established. Histological and cytological evaluation of the spleen following splenectomy revealed a marked increase in histiocytes/macrophages with pronounced hemophagocytosis. These findings were interpreted as a (benign) hemophagocytic syndrome, possibly related to a viral infection. Extensive serological investigations, however, furnished no evidence of a so-called virus- or infection-associated hemophagocytic syndrome. The patient died 5 months after the onset of disease with symptoms of progressive liver failure. Meticulous histological examination of bone marrow revealed a few patchy tumorous infiltrates consisting of dense pleomorphic histiocytes. Thus, a diagnosis of MH was established. This case of MH was unusual with particular regard to its pronounced hemophagocytosis, slight cytological atypia of the histiocytes, and absence of infiltration of lymph nodes.
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PMID:Hemophagocytic syndrome. Differential diagnostic aspects in a case of well-differentiated malignant histiocytosis. 336 52

Gross and microscopic lesions associated with Bolivan hemorrhagic fever virus infection in the rhesus monkey were studied in 10 animals which died following inoculation. Gross lesions included skin rash, lymphadenopathy, splenomegaly, meningeal edema, hydropericardium and enlarged friable livers. Hemorrhagic manifestations of the infection were not consistently observed, but hemorrhages were present in the skin, heart, brain and nares in some monkeys. Histopathologic lesions were fairly consistent. Hepatic necrosis with the presence of acidophilic hyaline bodies, necrotizing enteritis, epithelial necrosis and adrenal cortical necrosis were present in all monkeys. Those monkeys which died after the seventeenth day of infection had nonsupurative meningoencephalitis; lymphoid necrosis was present in 3 monkeys that died after day 18. Other microscopic lesions included myocardial degeneration, lymphoid and reticuloendothelial cell hyperplasia and lymphoid depletion. Most of the histopathologic lesions described in human autopsy material were reproduced; however, the necrosis in the skin and oral mucosa, mucosa of the gastrointestinal tract and the adrenal cortex have not been described in man. Despite these apparent discrepancies the results of this investigation indicate that the rhesus monkey is a good experimental model for the study of Bolivian hemorrhagic fever infection.
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PMID:Pathology of Bolivian hemorrhagic fever in the rhesus monkey. 420 35

Lead acetate was administered continuously in the drinking water to CD-1 male mice beginning at 4 weeks of age. An LD(10-20) of the lytic viruses or 300 plaque-forming units of RLV was inoculated intrapertioneally at 6 weeks of age. Lead increased the response of the mice to all classes of viruses against which it was tested: an RNA picornavirus-encephalomyocarditis (EMCV), a DNA herpesvirus-pseudoribies, an RNA leukemia-virus-Rauscher leukemia (RLV), an RNA arbovirus B-St. Louis encephalitis, and an RNA arbovirus A-western encephalitis. Most studies were performed between lead and EMCV. Increases in EMCV mortality in lead treated mice over controls ranged from 2x at a lead level of 0.004M to 7x (100% mortality) at a 0.1M lead level. Splenomegaly with spleens 800 to 1100 mg in weight containing high titers of RLV occurred in lead (0.03M)-treated mice 3 and 6 weeks after RLV inoculation; spleens or RLV controls were normal in weight (200 mg) and were free of virus. Lead did not reduce the protective effect of mouse interferon (IF) against the lethal action of EMCV, but it did repress the EMCV antiviral effect of poly I/poly C (PIC) and of Newcastle disease virus (NDV) against EMCV mortality. These data indicate several new facts concerning adverse effects lead may have on an animal: (1) lead aggravates viral disease, most likely in part, through reduced IF synthesis; (2) lead represses the anti-EMCV protective effects of both PIC and of NDV, which, in other reports, were shown to induce IF in radioresistant macrophages (PIC) or in radiosensitive lymphocytes (NDV); (3) lead may then be said to repress IF induction in two kinds of cells; (4) however, lead does not inhibit IF action.
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PMID:Lead aggravates viral disease and represses the antiviral activity of interferon inducers. 436 44

Hb Altdorf alpha 2 beta 2 135 Ala leads to Pro is an unstable variant occurring near Lecce in Italy. The abnormal hemoglobin does not separate from Hb A in the electrophoresis. In vitro a marked Heinz body formation is produced with phenylhydrazin. In heterozygous individuals an almost compensated hemolysis and a slight splenomegaly are found. Hemolysis can be aggravated by exogenous factors. A rather severe hemolysis was induced by a viral infection in a 3 years old girl.
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PMID:[Clinicohematologic effects of hemoglobin Altdorf (alpha 2 beta 2 135 Ala replaced by Pro)]. 616 32


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