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)

Prosthetic valve endocarditis may be considered present when two fo the following criteria are met: (1) two or more blood cultures are positive with the same organism in the absence of extracardiac infections, (2) evidence of bacterial endocarditis by histology or cultures is obtained from surgical or autopsy specimens, and/or (3) a clinical picture compatible with endocarditis (fever, new or changing regurgitant murmur, splenomegaly, hematuria, or evidence of peripheral emboli) is present. The overall incidence of PVE ranges from 0.98 to 4.4 per cent. Early and late PVE (that is endocarditis developing less than 60 and 60 or more days following valve implantation, respectively) accounts for 18 to 36 per cent and 64 to 82 per cent of infections, respectively. The overall mortality is 53 per cent and is higher in patients with early versus late PVE. Coagulase-negative staphylococci are responsible for a higher percentage of early (43 per cent) than late (28 per cent) infections. Streptococci are more common in late (27 per cent) than in early (3 per cent) PVE, while diphtheroids are most common in early PVE. The diagnosis of PVE may be difficult to establish, especially in patients with postoperative bacteremias who have other potential sources of extracardiac infections. Antimicrobial therapy is generally based on the susceptibility of the offending pathogen. With respect to the use of synergistic combinations, results are controversial, and most available data are derived from patients with native-valve endocarditis. Surgery remains an important aspect of treatment, and the mortality among patients who undergo early surgical intervention, particularly if their illness is complicated, is less than in those who are treated only with antibiotics. Indications for surgery include: (1) moderate-severe refractory congestive heart failure, (2) persistent bacteremia or fungemia, (3) multiple emboli, (4) myocardial abscesses, (5) relapsing PVE, and possibly (6) patients with clinical evidence of PVE and negative blood cultures and persistent fever despite 1 week or more of appropriate antibiotics. Pacemaker infections occur in less than 6 per cent of patients who undergo pacemaker insertion. These infections generally result from wound contamination at the time of surgery, and 75 per cent of infections are due to staphylococci. Staphylococcus aureus causes most infections occurring within 2 weeks after surgery, while S. epidermidis causes most later infections. The need to remove infected pacemakers is controversial.
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PMID:Infections of prosthetic heart valves and cardiac pacemakers. 266 79

A 37-year-old woman with clinically occult, abscessed uterine myomas presented with fever, anemia, splenomegaly, and viridans streptococcal bacteremia. An initial diagnosis of endocarditis was made, but fever persisted despite appropriate antibiotics. Pelvic pain evolved and laparotomy revealed an infected myoma. Streptococcus milleri was isolated from both the blood and the uterine abscess. Infected uterine myomata may be clinically silent despite producing sustained bacteremia. The occurrence of suppurating myomas and the significance of S milleri isolates are briefly reviewed.
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PMID:Streptococcus milleri pyomyoma simulating infective endocarditis. 373 76

We prospectively studied 40 patients with prosthetic heart valves and community-acquired febrile illness. The mean age of the group studied was 35.2 +/- 12.8 years, and the mean length of time that the prosthetic valve had been in place was 53.4 +/- 43.7 months. There was a high incidence (37.5%) of infectious endocarditis in the patients studied, with a total mortality of 15% in the group. The presence of a new regurgitant murmur, skin or retinal lesions, splenomegaly, vegetations shown on echocardiograms, and persistent bacteremia was associated with infectious endocarditis (P less than .05). The patients with mechanical Starr-Edwards valves had a significantly higher incidence (P less than .001) of infectious endocarditis than those with other types of prosthetic valves implanted in our hospital. Complete evaluation is mandatory in febrile patients with prosthetic heart valves because of the high risk of prosthetic valve endocarditis as the cause of the fever.
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PMID:Community-acquired febrile illness in patients with prosthetic heart valves. 407 Nov 69

Myelomonocytic myeloproliferative disease in a horse was diagnosed on the basis of hematologic, enzymatic, and histopathologic findings. It was characterized clinically by depression, weight loss splenomegaly, lymphadenopathy, coagulopathy, and bacteremia. Hematologic findings included severe refractory anemia, thrombocytopenia, monocytosis, and pleomorphic leukocytes, with a left shift of the myeloid series. The serum lysozyme concentration was 14.5 microgram/ml (normal, less than 5 microgram/ml). The bone marrow contained many immature cells of the myeloid series and had a myeloid-to-erythroid ratio of 30.5 to 1. The horse died after brief hospitalization. Necropsy revealed generalized lymphadenopathy and hemorrhages throughout the body. Histopathologically, primitive cells were seen in several tissues. Cells that proliferated in the bone marrow were primarily myeloblastic, with some additional erythropoietic cells. Myeloblastic cells with evidence of normal erythropoiesis were seen in numerous lymph nodes and in the spleen, whereas primarily normal erythropoietic cells proliferated in the adrenal glands. Myeloid blast-type cells predominated in the lungs, myocardium, liver, and kidneys.
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PMID:Myelomonocytic myeloproliferative diseases in a horse. 705 85

We conducted a retrospective study to characterize the clinical course, microbiologic spectrum, and risk factors for endocarditis and for associated mortality in a large series of patients with documented pacemaker endocarditis. Using a computerized search through the medical records of 10 major hospitals in Israel from 1982 to 1992, and carefully reviewing the charts, we identified 44 patients with pacemaker endocarditis. The cases were categorized as definite (n = 25), probable (n = 12), or possible (n = 7) infective endocarditis based on strict case definition. Fever and chills were the most common symptoms. Increased ESR, leukocytosis, microscopic hematuria, and anemia were the most common laboratory findings. A relatively high proportion of the patients were diabetic. The most common source of endocarditis was infection acquired by the placement procedure or infection of the pacemaker pouch. Demographic, clinical, and laboratory features were similar to those of endocarditis patients of a similar age range without pacemakers, although the frequency of fever and chills was higher in our patients than in those patients and splenomegaly, vascular embolic phenomena, and new or changing murmurs were rare in our patients. The major pathogens were Staphylococcus aureus and Staphylococcus epidermidis, similar to other series of pacemaker-associated bacteremia and similar to the microbiologic findings of early prosthetic-valve endocarditis. However, this microbiologic profile is different from that of native-valve endocarditis. Although the present series did not show a statistically significant advantage to electrode removal over conservative treatment, when analyzed together with pooled data from other studies, it suggests that the surgical approach is preferable.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pacemaker endocarditis. Report of 44 cases and review of the literature. 798 81

A 67-year-old man presented with a high fever and a generalized rash. His extended hospital stay was characterized by fever with repeated staphylococcal bacteremia and the appearance of axillary lymphadenopathy and splenomegaly. Skin lesions became hyperpigmented, dry, and atrophic with areas of exfoliation and uclers. Examination of skin and lymph node biopsy specimens showed findings consistent with mycosis fungoides. The patient unexpectedly recovered on discontinuation of captopril. A positive macrophage inhibiting factor response for both captopril and enalapril indicated that the non-sulfhydryl moiety was the antigenic stimulant for the lesion resembling mycosis fungoides.
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PMID:Generalized pustular eruption associated with converting enzyme inhibitor therapy. 856 12

Three dogs became lethargic and had poor appetites within 2 months after anticonvulsant treatment was initiated to control seizures. Dogs were neutropenic, thrombocytopenic, and anemic and had splenomegaly. Sensitivity to phenobarbital and related anticonvulsants may induce life-threatening leukopenia, thrombocytopenia, and anemia in dogs. Phenobarbital-induced neutropenia in these 3 dogs may have posed a risk for developing bacteremia. It is important for clinicians to be aware of adverse effects so that adequate precautions can be taken. A baseline hemogram should always be obtained before starting anticonvulsant treatment, and periodic hemograms should be obtained to monitor animals. Furthermore, client education should include instructions on recognizing signs of bacteremia, thrombocytopenia, and anemia.
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PMID:Neutropenia and thrombocytopenia in three dogs treated with anticonvulsants. 952 40

Our laboratory has previously shown that after immunization with a strain of Salmonella typhimurium, SL3235, made avirulent by a blockage in the pathway of aromatic synthesis, murine splenocytes were profoundly suppressed in their capacity to mount an in vitro antibody plaque-forming cell (PFC) response to sheep erythrocytes. Evidence indicated that suppression was mediated by nitric oxide (NO), since the in vitro addition of NG-monomethyl-L-arginine blocked suppression. The present studies examined the effect of blocking NO production on Salmonella-induced immunosuppression by in vivo administration of aminoguanidine hemisulfate (AG). AG was administered to C3HeB/FeJ mice in their drinking water (2.5% solution) for 7 days prior to intraperitoneal inoculation with SL3235. AG treatment inhibited the increase in nitrate and nitrite levels in plasma and nitrite levels in the spleen seen in immunized mice. Importantly, AG treatment completely blocked suppression of the splenic PFC response and markedly attenuated the suppression of the response to concanavalin A in immunized mice, providing further evidence that Salmonella-induced immunosuppression is mediated by NO. AG treatment also alleviated the majority of the splenomegaly associated with SL3235 inoculation, which correlated with a blockage of influx of neutrophils and macrophages into spleens, as assessed by flow cytometry. AG treatment unexpectedly resulted in 90% mortality in mice injected with the highly attenuated vaccine strain of Salmonella, SL3235. Increased mortality in AG-treated mice correlated with inability to clear organisms from the spleen by day 15 postinoculation and with persistent bacteremia, compared with control mice. Collectively, these in vivo results underscore the dual biological consequences of NO production following Salmonella infection, with NO being necessary for host defense, but also having the potentially adverse effect of immunosuppression. A unifying hypothesis to explain how these seemingly paradoxical effects could both result from NO production is presented.
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PMID:In vivo blockage of nitric oxide with aminoguanidine inhibits immunosuppression induced by an attenuated strain of Salmonella typhimurium, potentiates Salmonella infection, and inhibits macrophage and polymorphonuclear leukocyte influx into the spleen. 991 5

Hepatic IVC disease (HVD), a disease caused by complete obstruction or stenosis of inferior vena cava (IVC) near cava-atrial junction is endemic in Nepal. It is a chronic disease characterized by upper abdominal pain, hepatomegaly, splenomegaly and dilated superficial veins in the body trunk. Ascites commonly, with high protein content is a feature of acute and subacute stages and during acute exacerbation of the chronic disease. We assessed the occurrence of bacterial peritonitis among patients of HVD with ascites. One hundred and sixty seven consecutive patients with ascites, which included 91 patients with HVD were examined for the presence of bacterial peritonitis. The ascitic fluids were examined for total and differential WBC count. The fluid and the blood were cultured for aerobic microorganisms by bedside inoculation in blood culture bottles. HVD is a common cause of non-cirrhotic high protein content ascites in Nepal. It was uniquely associated with high incidence of bacteremia (61%) and high incidence of mono-bacterial peritonitis (67%) from Gram-negative enteric bacteria (58.5%) and Staphylococcus aureus (42.5%). Ascites and bacterial peritonitis generally occurred almost simultaneously in these patients. It is postulated that when bacteremia occurred the defective portion of IVC near the cava-atrial junction become infected resulting in hepatic venous outflow obstruction and formation of ascites with high protein content. And spread of infection from the infected IVC to the peritoneum resulted in bacterial peritonitis.
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PMID:Bacterial peritonitis in hepatic inferior vena cava disease: a hypothesis to explain the cause of infection in high protein ascites. 1224 91

We report on a 58-year-old male diagnosed as having primary myelofibrosis with thrombocytopenia, who died of fatal septic shock and rhabdomyolysis after platelet concentrates (PCs) transfusion. The initial diagnosis of primary myelofibrosis was established by splenomegaly, leukoerythroblastosis and bone marrow fibrosis. PCs were transfused because of thrombocytopenia with marked bleeding tendency. Soon after the PCs transfusion in March 2000, he had attacks of chest pain, back pain and myalgia, then went into shock and died of unknown causes. PCs were suspected as being the cause of death, because Streptococcus pneumoniae was found in the culture of PCs in the WBC-reduction in-line filter and fresh frozen plasma from the same donor preserved in the Japan Red Cross Center. Rhabdomyolysis, neutrophil infiltration and phagocytosed bacteria were found from the autopsy materials, which were identified by DNA analysis as the same species found in the PCs. PCs are kept at room temperature because platelet function is lost in the cold. When PCs are contaminated with bacteria, marked multiplication induces fatal bacteremia. This is a rare report in Japan of fatal septic shock caused by PCs with bacterial contamination. We must pay strict attention to bacterial contamination in blood components.
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PMID:[Fatal septic shock and rhabdomyolysis following transfusion of platelet concentrates contaminated with Streptococcus pneumoniae]. 1288 16


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