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)

A patient presented with characteristic historical, physical, and laboratory findings of angio-immunoblastic lymphadenopathy with dysproteinemia. This newly described entity apparently represents a nonneoplastic proliferation of the B-lymphocyte system with immunoblastic transformation of many lymphocytes and excessive production of immunoglobulins. It is associated with fever, sweats, weight loss, skin rash, lymphadenopathy, splenomegaly, hepatomegaly, and characteristic histologic features of the involved lymph nodes. Noteworthy in the patient reported here are the extent and course of radiographically and clinically evident pulmonary involvement and the biopsy documentation of an interstitial pneumonia marked by histopathologic changes closely resembling those found in the lymph nodes, with immunohistologic demonstration of immunoglobulins in the alveolar walls.
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PMID:Interstitial pneumonia in angio-immunoblastic lymphadenopathy with dysproteinemia. A case report with special histopathologic studies. 79 65

Simian hemorrhagic fever (SHF) virus and a new strain of Ebola virus were isolated concurrently in recently imported cynomolgus monkeys (Macaca fascicularis) being maintained in a quarantine facility. Ebola virus had never been isolated in the U.S. previously and was presumed to be highly pathogenic for humans. A chronology of events including measures taken to address the public health concerns is presented. The clinicopathologic features of the disease were abrupt anorexia, splenomegaly, marked elevations of lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase, with less prominent elevations of blood urea nitrogen, creatinine, and other serum chemistry parameters. Histologically, fibrin deposition, hemorrhage, and necrosis of lymphoid cells and reticular mononuclear phagocytes were present in the spleens of SHF and of Ebola virus-infected animals. Intravascular fibrin thrombi and hemorrhage were also present in the renal medulla and multifocally in the gastrointestinal tract. Necrosis of lymphoid and epithelial cells was occasionally noted in the gastrointestinal tract. The histopathologic findings considered specific for Ebola virus infection include hepatocellular necrosis, necrosis of the zona glomerulosa of the adrenal cortex, and interstitial pneumonia, all of which were generally associated with the presence of 1 to 4 mu intracytoplasmic amphophilic inclusion bodies. The disease spread within rooms despite discontinuation of all direct contact with animals, and droplet or aerosol transmission was suspected. Antibody to Ebola virus developed in animal handlers but no clinical disease was noted, suggesting a less virulent strain of virus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Combined simian hemorrhagic fever and Ebola virus infection in cynomolgus monkeys. 131 46

A red-tailed hawk (Buteo jamaicensis) with signs of respiratory distress and diarrhea was captured in the Manchac Wildlife Management Area, Louisiana (USA) and died the following day. At necropsy, the carcass was emaciated and there were splenomegaly, and fibrinous pericarditis, airsacculitis, and perihepatitis. Microscopically, there were fibrinous pericarditis and airsacculitis, myocardial necrosis, necrotizing hepatitis, splenic necrosis with reticuloendothelial cell hyperplasia, interstitial pneumonia and focal pancreatic necrosis. Intracytoplasmic chlamydial inclusion bodies were noticed in macrophages in the fibrinous exudate covering air sac and pericardium, and in spleen, liver, heart, lung, and pancreas. Schizonts compatible with a Sarcocystis sp.-like protozoon were present in the walls of air capillaries in the lung. A Chlamydia sp.-like organism was isolated in embryonating chicken eggs and cell culture and identified as C. psittaci with immunofluorescent staining.
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PMID:Chlamydiosis in a red-tailed hawk (Buteo jamaicensis). 160 82

This report describes toxoplasmosis lesions in Australian marsupials. Clinical signs, necropsy findings and histopathological changes are summarized for 43 macropods, two common wombats, two koalas, six possums, 15 dasyurids, two numbats, eight bandicoots and one bilby. Animals either died suddenly without clinical signs or exhibited signs associated with respiratory, neurological or enteric disease. At necropsy, many marsupials had no visible lesions. Where present, common necropsy findings included pulmonary congestion, oedema and consolidation, adrenal enlargement and reddening, haemorrhage and ulceration of stomach and small intestine, and lymphadenomegaly and splenomegaly. Microscopically, affected lungs showed interstitial pneumonia and macrophage accumulation. Myocardial, skeletal and smooth muscle necrosis and neutrophilic inflammation were common. Organs had focal necrosis and/or fibrosis and lymphoid infiltrates. Toxoplasma gondii tissue cysts were common in muscle and nervous tissue. Free tachyzoites were commonly present in areas of necrosis. Selected sections from four macropods, two koalas, two dasyurids, one wombat and one possum stained specifically with avidin-biotin complex and anti-Toxoplasma gondii serum.
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PMID:Lesions of toxoplasmosis in Australian marsupials. 224 91

An 81-year-old woman had chills, fever, nausea, vomiting, and epigastric pain. On day 3 she had hematuria and was treated with trimethoprim-sulfamethoxazole. On day 5 she had a cough, hypotension, anemia, azotemia, and elevated hepatic enzyme levels. Her condition deteriorated with thrombocytopenia, anuria requiring dialysis, edema, and hypoalbuminemia. Treatment with chloramphenicol and doxycycline was started on day 10. By day 11, she was in hypotensive shock; on day 12 she had seizures and died. Murine typhus was diagnosed by demonstration of antibodies to Rickettsia typhi by indirect immunofluorescence. Necropsy revealed interstitial pneumonia, pulmonary edema, hyaline membranes, alveolar hemorrhages, petechiae and vasculitis in the central nervous system, interstitial myocarditis, multifocal interstitial nephritis and hemorrhages, splenomegaly, portal triaditis, and mucosal hemorrhages in urinary tract. Immunofluorescent R. typhi were demonstrated in the lungs, brain, kidneys, liver, and heart. This unusual death occurred in an elderly patient without rash who was treated too late with antirickettsial drugs.
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PMID:Histopathology and immunohistologic demonstration of the distribution of Rickettsia typhi in fatal murine typhus. 249 81

The severity of the graft-versus-host (GVH) reaction, judged by splenomegaly and immunosuppression, was augmented by murine cytomegalovirus (MCMV) infection. Profound GVH-induced immunosuppression was seen in adult unirradiated MCMV-infected F1, mice even after challenge with extremely low doses of parental spleen cells. Mice receiving MCMV+GVH challenge died from days 16-21, with interstitial pneumonia being the most prominent pathological lesion. Pulmonary disease was unrelated to levels of viral replication in the lung. These results suggest that in human marrow recipients, cytomegalovirus infection may play a primary role both in provoking or accentuating GVH disease, as well as in the development of interstitial pneumonia.
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PMID:Augmentation of graft-versus-host reaction by cytomegalovirus infection resulting in interstitial pneumonitis. 298 27

Results of HLA-identical allogeneic marrow transplantation were analyzed for 66 patients with accelerated-phase chronic myelogenous leukemia (CML). Multivariate proportional hazards regression models were used to determine disease-related and transplant-related factors associated with posttransplant mortality and relapse. The projected 5-year survival rate was estimated at 18% by the product-limit method. The major causes of death were interstitial pneumonia, infection, and relapse. Splenomegaly at initial diagnosis and longer time interval from diagnosis to transplant were associated with decreased overall survival and event-free survival. Sixteen patients have relapsed between 17 and 1,569 days (median, 486) posttransplant. The use of T-cell-depleted marrow and older age of the donor or recipient were associated with an increased probability of leukemic relapse. Ten of the 16 relapses occurred among the 15 patients who received T-cell-depleted marrow. The actuarial relapse risk 2.5 years posttransplant was 100% in patients administered T-cell-depleted marrow as compared with 25% in patients administered unmodified marrow. The data in this report emphasize the increased risks and relatively poor results that occur when marrow transplantation is deferred until after signs of acceleration appear. When compared with results for patients who received transplants during chronic phase, the poor results seen here in patients administered unmodified marrow stem primarily from increased transplant-related mortality rather than increased relapse risk. The strikingly increased relapse rate associated with the use of T-cell depletion would discourage its use for graft-v-host disease prevention in patients who receive transplants for CML.
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PMID:HLA-identical marrow transplantation during accelerated-phase chronic myelogenous leukemia: analysis of survival and remission duration. 305 33

The effects of pregnancy on primary acute and chronic persistent infection with cytomegalovirus (CMV) were examined in the guinea pig model. Pregnant guinea pigs developed a more severe acute CMV infection than did nonpregnant animals. High death rate, pronounced splenomegaly, interstitial pneumonia, and necrosis with inclusions in various tissues were observed only in pregnant animals. Acutely infected pregnant animals also differed from nonpregnant animals by the absence of tissue inflammation and by a delay in the peripheral lymphoproliferative response. During persistent infection, salivary gland virus titers were significantly higher in pregnant animals than in nonpregnant guinea pigs. These results indicate that during acute guinea pig CMV infection, virus clearance and recovery from clinical disease are altered in the pregnant host. Furthermore, enhancement of persistent chronic guinea pig CMV infection occurs in the salivary glands during pregnancy.
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PMID:Enhancement of cytomegalovirus infection during pregnancy in guinea pig. 630 8

Adult Hartley guinea pigs infected with guinea pig cytomegalovirus (CMV) develop a mononucleosis syndrome with a brief viremia, splenomegaly, lymphadenopathy, and peripheral lymphocytosis with circulating atypical lymphocytes. The present study used this experimental model to evaluate in vivo the therapeutic efficacy of acyclovir (ACV) and phosphonoformate (PFA) during CMV infection. Guinea pigs were treated with ACV or PFA from day 3 to day 7 postinoculation. The course of the mononucleosis syndrome and the spread of virus in various tissues were similar in drug- and sham-treated infected guinea pigs. Infected animals treated with ACV or PFA developed disseminated CMV disease with severe interstitial pneumonia, whereas sham-treated infected and drug-treated noninfected animals did not. In addition, mortality rates in infected animals treated with ACV were significantly higher than those in sham-treated animals. Furthermore, the normal lymphoproliferative response to CMV infection appeared to be reduced in ACV-treated as compared to sham-treated animals, with fewer peripheral lymphocytes, less lymphoid tissue in the spleen and lymph nodes, and less mononuclear inflammation around the inclusion-containing cells of the liver and salivary gland. These results show that ACV and PFA are not useful in the treatment of CMV infection in guinea pigs but instead may have harmful effects.
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PMID:Effect of acyclovir and phosphonoformate on cytomegalovirus infection in guinea pigs. 632 60

Right heart failure associated with postmortem evidence of pulmonary hypertension (cor pulmonale) was observed in nearly 1% of the young beagles of a large research colony. During the past 18 years, 176 dogs with cor pulmonale were observed. Most cases occurred between September and April of each year. Nearly equal numbers of males and females were involved, and some siblings were affected. Ninety-six percent of known affected dogs died, and 85% of the deaths occurred by 5 weeks of age. Clinically, most dogs were stunted and exhibited ascites, subcutaneous edema, hypothermia, dyspnea, cyanosis, and systolic murmur. Radiography revealed cardiomegaly, and electrocardiography revealed right axis deviation and an enlarged right atrium. Postmortem evidence of cor pulmonale included subcutaneous edema, ascites, hydrothorax, mediastinal and mesenteric edema, splenomegaly, centrolobular hepatic congestion and necrosis, right ventricular hypertrophy, interstitial pneumonia, and medial hypertrophy of pulmonary arteries and arterioles. The specific cause of the disease was not determined.
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PMID:Spontaneous cor pulmonale in laboratory beagles. 687 38


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