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Query: UMLS:C0032285 (pneumonia)
54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemolytic-uremic syndrome (HUS) is an uncommon complication of pneumococcal infection. Highly suggesting findings in a patient with Streptococcus pneumoniae infection are: microangyopatic hemolytic anemia, thrombocytopenia and acute renal failure. We report a 41 years old woman, admitted to the hospital due to a severe pneumonia, that required the surgical drainage of an empyema. On admission, a drop in packed red cell volume from 41 to 25%, the presence of schistocytes in the blood smear, an elevation of LDH to 1,700 IU/L, a fall in haptoglobin to 5.8 mg/dL and a thrombocytopenia of 72,000 per mm3 were detected. These alterations coincided with an oliguric acute renal failure. She was treated with hemodialysis and the hemolytic syndrome was managed with plasmapheresis. She was discharged 35 days after admission and in the follow up, after 2.5 months, her serum creatinine is 1.2 mg/dL and her packed red cell volume is 41%.
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PMID:[Hemolytic-uremic syndrome and Streptococcus pneumoniae]. 1219 92

Legionella pneumophyla is the agent responsible of Legionnaire's disease. It appears as a severe pneumonia and often requires admission in Intensive Care Unit. In literature, renal failure is reported to occur in 15 percent of Legionnaire disease and this event induce a mortality over 50% of these cases. The authors describe a case of Legionnaire's pneumonia with respiratory failure, rhabdomyolysis and acute renal failure. Patient was a female, 61 yrs old, admitted to our hospital because of fever (38 degrees-38.5 degrees C), severe respiratory failure (pH = 7.49, PaCO2 = 23.1 mmHg, PaO2 = 56.7 mmHg), oliguria (< 200 ml/24 h); chest x-rays and computed tomography (TC) showed a pneumonia at right lower lobe. Among other things, in blood analysis was noted the following values: BUN = 47 mg/dl, creatinine = 2.1 mg/dl, Na+ = 133 mmol/L, Cl- = 97 mmol/L, Ca+ = 7.2 mg/dl, K+ = 5.8 mmol/L, AST = 213 U/L, ALT = 45 U/L, LDH = 1817 U/L, CPK = 16738 U/L, CPK-MB = 229 U/L, myoglobin > 4300 ng/ml., leucocyte count = 17,500/mmc (N = 92%, L = 3%, M = 5%), positive anti Legionella IgG and IgM (IgG > 1:64, IgM > 1:96), evidence of Legionella soluble antigen in the urine analysis. Therapy with clarytromicyne (500 mg b.i.d i.v.) and rifampicin (600 mg/die i.v.) was begun; computed tomography showed after six days an improvement of pulmonary lesion but, in the following days, health status and blood analysis got worse. Patient went on antibiotics and underwent haemotherapy (Hb: 8 gr/dl), haemodialysis because of acute renal failure but healthy status worse furthermore and she died on 18th days after admission. This case point out rhabdomyolysis with acute renal failure is suggestive for Legionnaire's disease and is associated with high rate of mortality.
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PMID:[Legionnaire's pneumonia with rhabdomyolysis and acute renal failure. A case report]. 1294 1

Infectious processes cause the majority part of all clinically relevant pleural effusions which frequently complicate the course of pneumonia. The assessment of an inflammatory effusion requires a careful history, physical examination, imaging techniques and clinical workup. The presence of polymorphonuclear leukocytes, high LDH-activity (> 200 U/L) and protein level (> 3 g/dL) in a pleural effusion indicates acute inflammation. An effusion is usually called empyema, when large numbers of neutrophils form thick, turbid exudates within preexisting body cavities. A thoracic empyema may occur as a result of primary or secondary pleural pathologies and in most cases involves infection with bacteria, frequently provided by progressing pneumonia. There are several therapeutic options for treatment of parapneumonic effusions and of thoracic empyemata, respectively. Optimal therapeutic management and antimicrobial medication to the infected pleural space depend in part on the stage of the empyema at presentation. Treatment can vary from a conservative medical approach in uncomplicated or small parapneumonic effusions to invasive surgical interventions in fibroprulent or organizational stages of empyema. Empyemata usually progress from a parapneumonic exudative stage (stage I), when the fluid is still sterile, with low leukocyte counts, low LDH, physiological pH, and normal glucose, to the fibropurulent [figures: see text] stage (stage II) with high leukocyte counts, high LDH activity, low pH, and low glucose, and finally to the organizational stage (stage III), in which fibroblasts convert fibrin strands into inelastic membranes. Pleural peels and pockets may compartmentalize the viscous empyematous fluid and can cause serious restrictive ventilatory impairment. Each patient must be individually evaluated to determine the nature of the exudate and the stage of the pleural space infection. Due to its high mortality rate (5%) a thoracic empyema requires prompt treatment. Diagnostic thoracentesis and withdrawal of liquid for the microbiological, cytological and biochemical analysis is urgently recommended in all cases to assess severity of the disease and the likelihood of a complicated or uncomplicated course, and to select the most appropriate treatment option.
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PMID:[From pneumonic infiltration to parapneumonic effusion--from effusion to pleural empyema: internal medicine aspects of parapneumonic effusion development and pleural empyema]. 1367 57

A 77-year-old man was referred to our hospital because of elevated LDH and leukoblastosis in the peripheral blood in June 2002. Physical examination revealed neither hepatosplenomegaly nor superficial lymphadenopathy. A bone marrow film showed dysmegakaryocytopoiesis with many micromegakaryocytes and MPO-positive blasts appearing in 20-30% of NCC. A diagnosis of MDS (RAEB-t) was made. Blastic cells were positive for CD13, 33, 34 and HLA-DR. Karyotypic analysis at diagnosis revealed 46XY, inv(3) (q21q26), t(9;22) (q34; q11) and minor-BCR/ABL chimeric m-RNA was detected by RT-PCR. Mild chemotherapy (low dose Ara-C etc) was given but the disease progressed to the AML stage with thrombocytosis in August. In September imatinib was given because of Ph positivity, but the effect was transient. In October massive leukocytosis with myeloblastosis was uncontrollable. In December 2002 the patient died of pneumonia, after a total course of 7.5 months. This rare case with Ph chromosome and 3q21q26 syndrome showed a poor prognosis as previously reported.
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PMID:[3q21q26 syndrome with minor-BCR/ABL type Ph chromosome]. 1497 33

The prevalence of Pneumocystis carinii pneumonia (PCP), its clinical and radiological features and the outcome in 121 children aged 2-60 months presenting with severe pneumonia over a 2-month period at Mulago Hospital, Kampala are described. Children presenting with severe pneumonia had sputum induction using 3% hypertonic saline. The sputum was stained using PCP monoclonal antibodies and viewed with fluorescent microscopy. Twenty children with confirmed PCP were compared with 101 without PCP. The prevalence of PCP was 16.5%, and 12 (60%) were < 6 months of age. Eighteen (42%) of 43 children infected with HIV had PCP and two of 78 not infected with HIV. The outcome in children with PCP was poor with a case fatality rate of 40% compared with 20% in those without HIV. Radiological findings were non-specific. Clinical features associated with PCP included: HIV-positive infants with a small head circumference, AIDS, a clear chest on auscultation and elevated LDH levels. PCP occurs in one in six children < 5 years with severe pneumonia in Mulago Hospital. In developing countries where investigations for PCP are not routinely available, infants suspected of PCP should be treated as an emergency.
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PMID:Pneumocystis carinii in children with severe pneumonia at Mulago Hospital, Uganda. 1547 72

In 1996 36-year-old man was admitted into our hospital because of polyarthralgia, skin eruptions followed by multiple cutaneous ulcers, dry cough and elevation of C-reactive protein level. The finding of skin biopsy from left elbow was vasculitis. Chest CT showed linear interstitial shadow at bilateral dorsalis lungs. Transbronchial lung biopsy (TBLB) revealed marked infiltration of inflammatory cells in the bronchial walls and peripheral alveoli. In addition, eosinophils were not in branchoalveolar lavage (BAL) fluid. Moreover, video-assisted thoracic surgery (VATS) revealed organizing fibroblastic polyp and bronchiolitis obliterans at terminal bronchiole. We diagnosed his pneumonia as bronchiolitis obliterans organizing pneumonia (BOOP). Administration of oral prednisolone (40 mg/day) was begun and he experienced diminished BOOP and other clinical manifestations. Three years later he developed dry cough, dyspnea and digital ulcers again. Arterial blood gas analysis revealed marked hypoxemia and laboratory studies showed LDH (377 IU/ml) and CRP (8.27 mg/dl) levels were elevated. Chest CT pointed out an exacerbation of BOOP. Treatment with intravenous pulses methylprednisolone and oral prednisolone (60 mg/day) resulted in marked improvement of the clinical manifestations. We describe a rare case of vasculitis associated with BOOP.
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PMID:[A case of vasculitis syndrome associated with bronchiolitis obliterans organizing pneumonia (BOOP)]. 1567 96

Enteric gram-negative bacilli, such as Escherichia coli are the most common cause of nosocomial pneumonia. In this study a wild-type extraintestinal pathogenic strain of E. coli (ExPEC)(CP9) and isogenic derivatives deficient in hemolysin (Hly) and cytotoxic necrotizing factor (CNF) were assessed in vitro and in a rat model of gram-negative pneumonia to test the hypothesis that these virulence factors induce neutrophil apoptosis and/or necrosis/lysis. As ascertained by in vitro caspase-3/7 and LDH activities and neutrophil morphology, Hly mediated neutrophil apoptosis at lower E. coli titers (1 x 10(5-6) cfu) and necrosis/lysis at higher titers (> or =1 x 10(7) cfu). Data suggest that CNF promotes apoptosis but not necrosis or lysis. We also demonstrate that annexin V/7-amino-actinomycin D staining was an unreliable assessment of apoptosis using live E. coli. The use of caspase-3/7 and LDH activities and neutrophil morphology supported the notion that necrosis, not apoptosis, was the primary mechanism by which neutrophils were affected in our in vivo gram-negative pneumonia model using live E. coli. In addition, in vivo studies demonstrated that Hly mediates lung injury. Neutrophil necrosis was not observed when animals were challenged with purified lipopolysaccharide, demonstrating the importance of using live bacteria. These findings establish that Hly contributes to ExPEC virulence by mediating neutrophil toxicity, with necrosis/lysis being the dominant effect of Hly on neutrophils in vivo and by lung injury. Whether Hly-mediated lung injury is due to neutrophil necrosis, a direct effect of Hly, or both is unclear.
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PMID:E. coli virulence factor hemolysin induces neutrophil apoptosis and necrosis/lysis in vitro and necrosis/lysis and lung injury in a rat pneumonia model. 1580 36

Streptococcus pneumoniae is the major pathogen of community-acquired pneumonia and a common cause of otitis, meningitis and sepsis. During pneumococci infection accompanied with bacterial invasion and hematogenous spreading, the endothelium is directly targeted by pneumococci and their virulence factors. Therefore, we tested the hypothesis that pneumococci induced endothelial apoptosis. Unencapsulated R6x pneumococci strongly induced apoptosis of human endothelial cells both from lung microvasculature and umbilical vein, whereas an encapsulated strain D39 mainly led to necrotic cell death. Deletion of the gene coding for pneumolysin reduced pneumococci-induced apoptosis in HUVEC. Furthermore, N-acetyl-L-cysteine, an antioxidant thiol, significantly reduced apoptosis caused by R6x, and LDH release induced by D39, pointing to a role for reactive oxygen species in the pathogenesis. Apoptotic cells showed increased cleavage and activity of caspases 6 and 9 but only late activation of caspase 3. Programmed cell death could be strongly reduced by pan-caspase inhibitor zVAD. Reduced levels of Bcl2 and cytosolic increase of apoptosis-inducing factor in pneumococci-infected cells implicated involvement of mitochondrial death pathways. Caspase activation and apoptosis were abolished by cAMP elevation. Moreover, p38 mitogen-activated protein kinase and c-Jun NH(2)-terminal kinase were activated in pneumococci-infected cells and inhibitors of both kinases strongly reduced pneumococci-induced caspase activation and apoptosis. Hence, kinase- and caspase-dependence of pneumococci-induced endothelial apoptosis may bear relevance to novel therapeutic approaches to pneumococci-related disease.
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PMID:Streptococcus pneumoniae R6x induced p38 MAPK and JNK-mediated caspase-dependent apoptosis in human endothelial cells. 1611 18

Detection of urinary antigen by a rapid immunochromatographic membrane test (Binax NOW) was widely accepted as a powerful tool for diagnosis of Streptococcus pneumoniae pneumonia. This is a qualitative kit, so the value of quantitative analysis of urinary antigen, especially correlation of antigen titers and severity of diseases, remained to be determined. We examined semi-quantitative antigen titer in urines collected from urinary antigen-proven S. pneumoniae pneumonia on admission, and analyzed the kinetics of antigen titer and its relation to severity of diseases. After serial 2-fold dilution of urine, the highest dilution for positive results was determined, and this was designated as maximum dilution factor (MDF). MDFs varied from 1 to 4096 in 29 patients examined (mean MDF, 317.8). Importantly, severe cases of S. pneumoniae pneumonia were higher values of MDFs (mean MDF: 760.5) than those of non-severe cases (mean MDF: 5.4). The patients with high MDFs (> or = 64) demonstrated higher values of LDH, CRP and lower values of WBC and PaO2 compared to those of low MDFs group (< or = 32). There was no clear correlation between CRP values and antigen titers, and conversely the majority of severe cases showed relatively weak CRP responses, despite high levels of bacterial antigen. Kinetic analysis of urinary and serum antigen titers in 4 cases of S. pneumoniae pneumonia exhibited consistently higher values of antigen titers in urine than those in serum. The half lives of urinary and serum antigen titers were calculated to be 1.0-3.4 and 1.1-2.3 weeks, respectively. These data suggest that quantitative analysis of urinary antigen may be a useful indicator for severity of disease and course of S. pneumoniae pneumonia. Our results demonstrate an application for S. pneumoniae antigen titer determination in urine and serum, which may be crucial not only for diagnostic measures, but also may provide a better understanding of the pathogenesis of S. pneumoniae infection.
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PMID:Semi-quantitative analysis of Streptococcus pneumoniae urinary antigen: kinetics of antigen titers and severity of diseases. 1757 39

Children with sequelae of perinatal hypoxic-ischemic encephalopathy (HIE) occasionally suffer from cytokine-related disease. We investigated 12 children with perinatal HIE sequelae, who died in childhood, concerning (1) the incidence of cytokine-related disease as the cause of death, and (2) the characteristics of the cytokine-related disease. Six (50%) of the 12 patients died from cytokine-related disease:two had virus-associated hemophagocytic syndrome (VAHS) ; one had acute encephalopathy;one had systemic inflammatory response syndrome (SIRS); and two had severe pneumonia/acute respiratory distress syndrome (ARDS). These six patients presented with increased liver transaminase, LDH, and CK, and decreased platelet count and albumin. This study shows the high incidence of cytokine-related disease as the cause of death in children with perinatal HIE sequelae. Further investigation is needed to clarify the pathogenesis of this disease.
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PMID:[High incidence of fatal cytokine-related disease among children with sequelae of perinatal hypoxic-ischemic encephalopathy]. 1709 63


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