Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.16.2 (PCP)
 3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anti-tumor necrosis factor-alpha therapy, infliximab, has become an established effective therapy for Crohn's disease and rheumatoid arthritis. However, infliximab has been associated with various opportunistic pathogens such as tuberculosis, histoplasmosis, listeriosis, aspergillosis, and Pneumocystis jiroveci (carinii) pneumonia. We reviewed the FDA Adverse Event Reporting System for cases of Pneumocystis associated with infliximab use from January 1998 through December 2003. The database revealed 84 cases of PCP following infliximab therapy. Concomitant immunosuppressive medications included methotrexate, prednisone, azathioprine, 6-mercaptopurine, and cyclosporine. Mean time between infliximab infusion and onset of symptoms of pneumonia, when reported, was 21 days (+/-18 days; n=40). Twenty-three of the 84 (27%) patients died. The use of infliximab is associated with PCP infection. Further, the mortality rate for Pneumocystis following the use of infliximab is significant. The potential for severe disease, mortality, and often subtle presentation of these infections warrant close follow-up and careful monitoring after therapy.
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PMID:Pneumocystis jiroveci (carinii) pneumonia after infliximab therapy: a review of 84 cases. 1820 May 15

Our objective was to describe the risk factors for the development of bronchiectasis in HIV-1 infected children. This study was a retrospective, case controlled study based upon medical record review of HIV-1 infected children receiving primary care at a single large, urban medical center in Miami, Florida. Cases (HIV-1 infected children who developed bronchiectasis while being cared for between January 1982 and September 2000) were matched 1:3 (birth +/- 24 months) with controls (HIV-1 infected children without bronchiectasis). Variables analyzed including number of episodes of pneumonia (including Pneumocystis jiroveci pneumonitis [PCP], lymphoid interstitial pneumonitis (LIP), and CDC category of immunosuppression) were noted in both cases and controls until the age at which the cases developed bronchiectasis. Of the 749 patients whose charts were reviewed, 43 met the case definition for bronchiectasis and 19 met the eligibility criteria for this study. Fifty-seven controls were randomly selected from the patients without bronchiectasis. Cases were more likely to have experienced recurrent pneumonia than the controls; 17 (89.5%) versus 5 children (8.8%) respectively (P-value <or=0.001) as well as a greater mean number of episodes of pneumonia 8.2 (range, 4-13) versus 1.45 (range, 0-9) respectively (CI = (5.58,7.82); P-value <or=0.001). Cases were more likely to have progressed to CDC immunological category 3 than the controls; 19 (100%) versus 32 (56%) children respectively (P-value <0.001). LIP occurred more frequently in the cases than in the controls; 14/19 (73.6%) versus 19/57 (33.3%), respectively (P-value = 0.005). HIV-1 infected children with a history of recurrent pneumonia, profound immuno-suppression (CDC immunologic category 3), and LIP appear to have a higher risk of developing bronchiectasis.
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PMID:Risk factors for the development of bronchiectasis in HIV-infected children. 1772 16

Pneumocystis jiroveci (formerly carinii) pneumonia (PCP) is a serious opportunistic infection in children and adolescents with cancer. It was the most common cause of death among children receiving chemotherapy prior to the inclusion of PCP prophylaxis as part of standard care for children with leukemia. The incidence of PCP has decreased significantly since initiation of prophylaxis; however, breakthrough cases continue to occur. Hematologic malignancies, brain tumors necessitating prolonged corticosteroid therapy, hematopoietic stem cell transplantation, prolonged neutropenia, and lymphopenia are the most important risk factors for PCP in children not infected with HIV. Of children with leukemia, 15-20% may develop PCP in the absence of prophylaxis. Infection with P. jiroveci occurs early in life in most individuals. However, clinically apparent disease occurs almost exclusively in immunocompromised persons. Dyspnea, cough, hypoxia, and fever are the most common presenting symptoms of PCP. Chest radiography and high-resolution CT scans of the chest demonstrate a characteristic ground-glass pattern. Induced sputum analysis and bronchoalveolar lavage are the diagnostic procedures of choice. Gomori's methenamine-silver stain, Geimsa or Wright's stain, and monoclonal immunofluorescent antibody stains are most commonly used to make a diagnosis. However, identification of P. jiroveci DNA using polymerase chain reaction assays in bronchoalveolar lavage fluid is more sensitive. Trimethoprim-sulfamethoxazole (TMP-SMZ; cotrimoxazole) is the recommended drug for the treatment of PCP. Patients who are intolerant of TMP-SMZ or who have not responded to treatment after 5-7 days of therapy with TMP-SMZ should be treated with pentamidine. A short course of corticosteroids is recommended for moderate to severe cases of PCP within the first 72 hours after diagnosis. Mutations in the dihydropteroate synthetase gene may confer resistance to TMP-SMZ; however, the clinical relevance of these mutations is not well established. TMP-SMZ is the most commonly used agent for prophylaxis. Myelosuppression is the most important adverse effect of TMP-SMZ and the most frequent cause for choosing alternative prophylactic agents in children undergoing chemotherapy. Alternative agents for chemoprophylaxis include dapsone, aerosolized pentamidine, and atovaquone. Alternative prophylactic agents must be used in patients developing myelosuppression secondary to TMP-SMZ or dapsone.
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PMID:Management of Pneumocystis jiroveci pneumonia in children receiving chemotherapy. 1792 2

In recent years, clusters of Pneumocystis jirovecii (formerly Pneumocystis carinii) pneumonia (PCP) among immunocompromised individuals have been reported. Mostly, the source of infections was suspected to be within the clinical settings when transplant recipients and PCP patients shared hospital facilities. We report on a cluster of 16 renal transplant recipients positive for P. jirovecii. None of them received anti-Pneumocystis prophylaxis prior to P. jirovecii detection. Epidemiological studies revealed that 15 of them had received kidney transplants at a German university hospital and attended the same inpatient and outpatient clinic from January through September 2006. Multilocus sequence typing (MLST) was performed on the following genes: ITS1, beta-tub, 26S, and mt26S. P. jirovecii DNA was available from 14 patients and showed identical MLST types among these renal transplant recipients. Surprisingly, one patient who was treated at a different nephrological center and reported no personal contact with patients from the renal transplantation cluster harbored an identical P. jirovecii MLST type. Three HIV-positive patients and one bone-marrow-transplanted hematologic malignancy patient--treated at different medical centers--were used as controls, and different MLST types were revealed. Interestingly, in three of the four previously described regions, new alleles were detected, and one new polymorphism was observed in the mt26S region. The epidemiological data and the genotyping results strongly suggest a nosocomial patient-to-patient transmission of P. jirovecii as the predominant transmission route. Therefore, strict segregation and isolation of P. jirovecii-positive/suspected patients in clinical settings seems warranted.
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PMID:Molecular evidence of nosocomial Pneumocystis jirovecii transmission among 16 patients after kidney transplantation. 1821 17

Chronic obstructive pulmonary disease (COPD) results in significant morbidity and mortality. Smoking has long been recognized as the primary risk factor for development of COPD, but factors determining the severity or pattern of disease in smokers are largely unknown. Recent interest has focused on the potential role of infectious agents and the associated host response in accelerating progression of airway obstruction or in perpetuating its progression following discontinuation of tobacco exposure. Pneumocystis jirovecii is a fungal pathogen that causes pneumonia in immunocompromised individuals. Recent evidence has linked this organism with COPD. Using sensitive molecular techniques, low levels of Pneumocystis have been detected in the respiratory tract of certain individuals and termed colonization. Several findings support the theory that colonization with Pneumocystis is involved in the "vicious circle" hypothesis of COPD in which colonization with organisms perpetuates an inflammatory and lung remodeling response. Pneumocystis colonization is more prevalent in smokers and in those with severe COPD. The presence of Pneumocystis in the lungs, even at low levels, produces inflammatory changes similar to those seen in COPD, with increases in numbers of neutrophils and CD8(+) lymphocytes. HIV-infected subjects who have had PCP develop permanent airway obstruction, and HIV-infected patients have a high prevalence of both emphysema and Pneumocystis colonization. In addition, a non-human primate model of colonization shows development of airway obstruction and radiographic emphysema. Additional studies are needed to confirm the role of Pneumocystis in the pathogenesis of COPD, given that this agent might be a treatable co-factor in disease progression.
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PMID:Pneumocystis: a novel pathogen in chronic obstructive pulmonary disease? 1825 74

Pneumocystis jivorecii (formerly known as carinii) pneumonia (PCP) is potentially a life-threatening opportunistic infection after organ transplantation, occurring most frequently in the first 12 months, where the incidence rate is several-fold higher than in later years. PCP typically presents with fever, cough, dyspnoea and hypoxia. In organ transplant recipients, the onset of symptoms is generally more fulminant compared to patients infected with the human immunodeficiency virus. We present a patient who developed PCP five years after a renal transplantation. His presentation was characterised by atypical symptoms and an indolent onset. Previous acute vascular rejection, ongoing maintenance prednisolone usage, cytomegalovirus seropositivity and past tuberculous infection may have predisposed this patient to PCP.
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PMID:Late-onset and atypical presentation of Pneumocystis carinii pneumonia in a renal transplant recipient. 1875 1

Rituximab enhances treatment efficacy of B-lineage lymphoma by targeting CD20+ B-cells. Such target therapies may compromise the immune system and render patients susceptible to opportunistic infections. We report 2 cases of lymphoma complicated with Pneumocystis jiroveci (previously known as P. carinii) pneumonia (PCP) while being treated with rituximab-containing chemotherapy regimens. In both cases, PCP developed during the neutropenic period. With timely diagnosis and proper management, both were treated successfully. We searched the literature and found that such opportunistic infection occurred only infrequently in lymphoma patients, and it has not been reported in the large-scale clinical trials of rituximab. Such cases demonstrate the importance of taking PCP into diagnostic consideration in lymphoma patients receiving similar therapies.
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PMID:Pneumocystis jiroveci pneumonia in patients with non-Hodgkin's lymphoma receiving chemotherapy containing rituximab. 1901 57

Pneumocystis carini (PCP) has been recognized as a cause of pneumonia in immuocompromised patients, most notably in AIDS patients, but also in those receiving immunosuppressive therapy for a variety of other conditions, including malignancy, having an organ transplant, connective tissue diseases, and vasculitic syndromes. In non-HIV PCP patients, presentations may be more dramatic than in HIV-related PCP and the mortality may be higher, thus emphasizing the need to identify and provide prophylaxis for those at highest risk for PCP. The incidence of PCP varies in different rheumatic disorders, with the highest rated noted in Wegener's granulomatosis and the lowest noted in rheumatoid arthritis. Prophylactic regimens should be used in patients with Wegener's granulomatosis taking cyclophosphamide and daily corticosteroids and in other rheumatic disease patients who are treated with this regimen, such as in PAN, microscopic polyarteritis, or severe systemic lupus erythematosus. Prophylaxis should be strongly considered in patients taking prolonged, high doses of daily corticosteroids (>40mg/day for > 3 months) with a second immunosuppressive agent other than cyclophosphamide, such as methotrexate, for example, as in PM/DM and in alternative regimens for Wegener's granulomatosis. Emerging data suggest the utility of CD4 counts as a method to distinguish those at highest risk for PCP to selectively apply prophylactic therapy. TMP-SMX is the usual first choice for prohpylaxis.
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PMID:Pneumocystis carinii pneumonia prophylaxis in patients with rheumatic diseases undergoing immunosuppressive therapy: prealence and associated features. 1907 57

Pneumocystis jirovecii is an opportunistic pathogen causing life-threatening pneumonia in immunosuppressed patients. The number of non-HIV immunosuppressed patients at risk for Pneumocystis pneumonia is rapidly growing. In contrast to HIV patients, there are no guidelines for Pneumocystis prophylaxis in other immunocompromised hosts. A detailed analysis of current literature data allowed us hereby to define the type of immunocompromised patients for whom evidence suggests a benefit for PCP prophylaxis.
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PMID:[Pneumocystis pneumonia in patients with immunosuppression other than HIV infection]. 1912 97

Deep mycosis (aspergillus pneumonia (AsP)) and carinii pneumonitis (PCP) are complications of immunosuppressive treatment for antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). The objective was to clarify the clinical significance of plasma titer of antibody against beta-glucans (anti-BG antibody) as a predictor of complications such as AsP or PCP and the prognosis of patients. Enzyme-linked immunosorbent assay was used to measure the plasma titer of antibodies against beta-glucans (BG) from Candida albicans in 22 healthy subjects and 52 patients with various stages of AAV. The mean plasma titer of the anti-BG antibody was 2,677 +/- 1,686 U in healthy subjects, 691 +/- 522 U in patients with untreated active vasculitis (n = 14), and 547 +/- 416 U in patients soon after immunosuppressive treatment (n = 24). Healthy subjects had significantly higher antibody titers than the other two groups (P < 0.05). Repeated measurements over the clinical course of AAV revealed an increase during remission to 1,180 +/- 130 U (n = 11), while there was a significant rapid decrease to 369 +/- 441 U (P < 0.01) concomitantly with elevation in plasma C-reactive protein and BG levels in patients with AAV that had AsP or PCP infection. Antifungal therapy resulted in a rapid rise of anti-BG antibody titer. Experiments in mice suggested that the anti-BG antibody neutralizes BG. Rapid decrease of the anti-BG antibody titer may be a useful indicator for diagnosis of the presence of AsP or PCP and for estimating the prognosis of patients with these opportunistic infections during immunosuppressive treatment of AAV.
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PMID:Rapid decrease of anti-beta-glucan antibody as an indicator for early diagnosis of carinii pneumonitis and deep mycotic infections following immunosuppressive therapy in antineutrophil cytoplasmic antibody-associated vasculitis. 1919 Sep 77


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