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

Pneumocystis carinii (P.c.) pneumonia was induced in 40 rats by a prolonged corticosteroid treatment (group 1); 40 healthy rats of equal weight constituted the control group (group 2); 9 rats received the same corticosteroid treatment as group 1, together with trimethoprim-sulfamethoxazole (TMP-SFZ) in order to prevent P.c. multiplication (group 3). We could distinguish the respiratory effects induced by corticosteroids from those caused by P.c. pneumonia (group 3 vs group 1). For six weeks the blood leukocyte count, the weight of the spleen and the thymus and the pulmonary status were monitored. Blood gases and acid-base status were measured in conscious rats. There was no pulmonary oedema. The infected P.c. rats had a low PaCO2 and a slight disturbance of blood oxygenation, exemplified by A-aDO2 of 30 mmHg, compared with 17.5 mmHg in control rats and 17 mmHg in TMP-SFZ treated rats. P.c. infected rats had a lymphocyte depletion induced by corticosteroids. They did not exhibit respiratory distress. P.c. pneumonia alone in rats did not cause frank hypoxemia.
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PMID:Respiratory and pulmonary alterations in experimental Pneumocystis carinii pneumonia in rats. 391 91

The efficacy and safety of intravenous trimethoprim-sulfamethoxazole (TMP-SMZ) were evaluated in 22 adults with serious infections caused by gram-negative bacteria. These infections included pneumonia, meningitis, pyelonephritis, deep-seated abscesses, and endocarditis. Of the 19 patients who could be evaluated, 12 (63%) were cured, and four (21%) showed definite improvement; three patients (16%) failed to respond to treatment. The only serious side effect occurred in a patient who had an acute reaction after his first dose. Mild adverse reactions were relatively common: three patients (13.6%) developed skin rashes, in one case with bronchospasm and eosinophilia. Mild transient decline of renal function was observed in five patients (22.7%) and decline of hepatic function in seven patients (31.8%); these abnormalities were not necessarily attributable to the drug. Although side effects were more common than previous reports indicate, intravenous TMP-SMZ was effective in the treatment of life-threatening infections unresponsive to other antibiotics.
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PMID:Clinical evaluation of intravenous trimethoprim-sulfamethoxazole for serious infections. 698 Nov 59

Trimethoprim-sulfamethoxazole (TMP-SMZ) is effective in both the treatment and the prevention of Pneumocystis carinii pneumonitis. After initial evaluation in an animal model, TMP-SMZ was shown to be as clinically effective as pentamidine isethionate for the treatment of pneumonitis in children with cancer and to have minimal adverse effects. Treatment with TMP-SMZ (20 mg of TMP and 100 mg of SMZ per kg of body weight per day) was successful in three-fourths of patients tested. Administered prophylactically, TMP-SMZ (5.0 mg of TMP and 25 mg of SMZ per kg of body weight per day) prevented P. carinii infection in high-risk immunocompromised patients. Studies of the unstructured delivery of prophylactic TMP-SMZ have demonstrated the regimen to be feasible and effective, with a favorable benefit-risk ratio for a large number of children with cancer.
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PMID:Trimethoprim-sulfamethoxazole therapy for Pneumocystis carinii pneumonitis in children. 698 Nov 76

The use of trimethoprim-sulfamethoxazole (TMP-SMZ) for the treatment of pneumonia due to Pneumocystis carinii has not been as rigorously assessed in studies of adults as in pediatric studies that have included patients randomly assigned to receive either pentamidine or TMP-SMZ. Nonetheless, it was shown that 80% of adults with histologically proved pneumocystis pneumonia who were treated with TMP-SMZ intravenously for at least four days or orally for at least nine days (total daily dose, 10-20 mg/kg) responded clinically and radiologically. Recipients of organ transplants and patients with lymphomas or lymphatic leukemia predominated in these studies. The median time to improvement was four days. TMP-SMZ therapy was continued for up to six days before a change to pentamidine was considered. Clinical failures of treatment were associated with delayed diagnosis and initiation of treatment, poor absorption of the orally administered drug, and concomitant life-threatening infections. Thus, a regimen involving initial intravenous therapy with doses of 15-20 mg/kg per day, with subsequent reduction of dosage or change to oral medication if improvement is rapid, was developed. With large initial intravenous doses, the monitoring of drug levels in the serum may not be necessary. Historical comparisons show that treatment of pneumocystis pneumonia with TMP-SMZ is associated with a better response rate and fewer side effects than is treatment with pentamidine.
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PMID:Trimethoprim-sulfamethoxazole in the treatment of adults with pneumonia due to Pneumocystis carinii. 698 Nov 77

A total of 120 episodes of infection in 113 cancer patients were treated with intravenous trimethoprim-sulfamethoxazole (TMP-SMX) alone (92 episodes) or with TMP-SMX plus continuous infusion tobramycin (28 episodes). The overall response rates were 47% and 75%, respectively. The majority of episodes had failed to respond to prior antibiotics. Pneumonia was the most common infection, and Klebsiella pneumoniae was the most common pathogen. TMP-SMX plus tobramycin cured 86% of episodes of septicemia and 76% of episodes of pneumonia, whereas TMP-SMX alone cured 20% and 42%, respectively. The initial neutrophil count did not appear critical in determining the outcome of infection. It was the change in the neutrophil count during the infection that appeared important. The outcome of infection was less favorable where abnormal renal and/or hepatic functions were documented. The sensitivity of the organism in vitro to TMP-SMX and/or tobramycin correlated well with the in vivo response. Intravenous TMP-SMX was well tolerated with a 4% incidence of reversible toxicity. A 15% incidence of renal toxicity was attributable to tobramycin. Intravenous TMP-SMX appears to be useful antimicrobial regimen for the therapy of infections caused by susceptible organisms in cancer patients.
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PMID:Intravenous trimethoprim-sulfamethoxazole alone or combined with tobramycin for infections in cancer patients. 736 47

Pneumocystis carinii pneumonia remains one of the most common opportunistic infections in patients with acquired immune deficiency syndrome (AIDS). Treatment with either intravenous pentamidine or trimethoprim-sulfamethoxazole (TMP-SMX) is frequently complicated by serious adverse reactions. This study was a prospective, blinded comparison of 600 mg/d of pentamidine as an aerosol versus 15 mg/kg/d of trimethoprim plus 75 mg/kg/d of sulfamethoxazole for patients with mild or moderately severe P. carinii pneumonia (alveolar arterial oxygen difference of less than 55 mm Hg). Of 367 participants who were randomized to receive study therapies, 287 had proven and 16 had presumed Pneumocystis pneumonia. There were 29 deaths within 35 d of study initiation: 12 in the aerosolized pentamidine group and 17 in the TMP-SMX groups (log rank p = 0.28). The difference in mortality was 3.4% (95% CI = -3.5, 10.8%). Ninety-four patients treated with aerosolized pentamidine had to have their study therapy changed because of lack of efficacy, compared with 22 patients treated with TMP-SMX (p = 0.002). In addition PaO2 improved faster in patients treated with TMP-SMX. However, aerosolized pentamidine was discontinued less often than TMP-SMX because of toxicity (9.4 versus 40% p < 0.001). Rash (0.6 versus 14.9%), nausea and vomiting (1.7 versus 12.2%), and abnormalities of liver function tests (1.7 versus 12.2%) were the most common adverse effects necessitating treatment discontinuation. During 6-mo. follow-up there was no difference in mortality.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pentamidine aerosol versus trimethoprim-sulfamethoxazole for Pneumocystis carinii in acquired immune deficiency syndrome. 769 33

Trimethoprim-sulfamethoxazole (TMP-SMZ) is the drug of choice as prophylaxis for Pneumocystis carinii pneumonia in patients with AIDS. However, adverse reactions ascribed to TMP-SMZ are common in such patients. We previously described a rapid method of oral TMP-SMZ desensitization in patients with AIDS and varying degrees of intolerance to the drug. To assess the feasibility, safety, and long-term clinical utility of our desensitization protocol, we retrospectively studied 22 consecutive patients who underwent desensitization. Prior to the procedure each of the study subjects had exhibited moderate to severe reactions to TMP-SMZ. Desensitization was successfully completed in 19 (86%) of the patients. The three patients for whom desensitization failed experienced chills and/or vomiting that resolved promptly with symptomatic therapy. One of the 19 patients was unavailable for long-term follow-up. Of the remaining 18 patients, three discontinued taking TMP-SMZ within 2 weeks of desensitization because of macular rash and fever. The other 15 (71%) of the evaluable patients tolerated both desensitization and subsequent prophylaxis and took TMP-SMZ for a mean of 14 months (in some cases, for as long as 41 months). None had P. carinii pneumonia while receiving TMP-SMZ. These results indicate that most patients who are presumed to be TMP-SMZ-intolerant can be rapidly desensitized with oral TMP-SMZ and subsequently receive the drug for protracted periods as effective prophylaxis for P. carinii pneumonia.
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PMID:Rapid oral desensitization to trimethoprim-sulfamethoxazole (TMP-SMZ): use in prophylaxis for Pneumocystis carinii pneumonia in patients with AIDS who were previously intolerant to TMP-SMZ. 779 84

We retrospectively studied all courses of treatment with trimethoprim-sulfamethoxazole (TMP-SMZ) alone and with adjuvant corticosteroids for AIDS-associated Pneumocystis carinii pneumonia. The corticosteroids were administered for 8-21 days (mean, 14 days) because of hypoxemia. We evaluated the influence of corticosteroids on the incidence of cutaneous adverse reactions to TMP-SMZ and on the course of AIDS during 3 months of follow-up. Of 38 patients treated with TMP-SMZ alone, 18 (47%) developed cutaneous side effects, whereas three (13%) of the 23 patients who received adjuvant corticosteroid therapy experienced such effects (P = .014). Of the 21 reactive patients, 14 were treated throughout the duration of hypersensitivity. Therapy was interrupted for seven patients (18%) treated with TMP-SMZ alone and for none of those who were given adjuvant corticosteroid therapy (P = .23). During follow-up, the incidence of mucocutaneous herpes simplex virus infection was higher among patients who received adjuvant corticosteroids than among those treated with TMP-SMZ alone (P = .005). Adjuvant corticosteroids thus reduce the incidence of adverse cutaneous reactions to TMP-SMZ in patients with AIDS who are treated for hypoxemic P. carinii pneumonia.
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PMID:Effect of corticosteroids on the incidence of adverse cutaneous reactions to trimethoprim-sulfamethoxazole during treatment of AIDS-associated Pneumocystis carinii pneumonia. 801 11

Trimetrexate is a powerful inhibitor of the dihydrofolate reductase of Pneumocystis carinii. AIDS patients (n = 215) with moderate to severe P. carinii pneumonia were enrolled in a double-blind study of trimetrexate plus leucovorin versus trimethoprim-sulfamethoxazole (TMP-SMZ) for 21 days. By study day 10, study therapy failed because of lack of efficacy in 16% of patients assigned to TMP-SMZ and 27% assigned to trimetrexate (P = .064), and the PAO2-PaO2 improved significantly faster with TMP-SMZ. By study day 21, failure rates were 20% with TMP-SMZ and 38% with trimetrexate (P = .008), with respective mortality rates of 12% and 20% (P = .088). By study day 49, the difference in mortality (16% vs. 31%) was significant (P = .028). The cumulative incidence of serious and treatment-terminating adverse events including hematologic toxicities was less with trimetrexate (P < .001). Thus, trimetrexate plus leucovorin was effective, albeit inferior to TMP-SMZ, for moderately severe P. carinii pneumonia but was better tolerated than TMP-SMZ.
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PMID:Trimetrexate with leucovorin versus trimethoprim-sulfamethoxazole for moderate to severe episodes of Pneumocystis carinii pneumonia in patients with AIDS: a prospective, controlled multicenter investigation of the AIDS Clinical Trials Group Protocol 029/031. 801 93

We used an immunosuppressed rat model to test the hypothesis that normal mechanisms regulating surfactant phosphatidylcholine synthesis and secretion in alveolar type II cells are aberrant in Pneumocystis carinii pneumonia. Animal groups included: group 1, healthy controls; group 2, immunosuppressed, without pneumocystosis; group 3, immunosuppressed with pneumocystosis; group 4, immunosuppressed with well-established pneumocystosis treated with trimethoprim-sulfamethoxazole (TMP-SMX). Type II cells were isolated from rats in each group and compared for [3H]choline incorporation into phospholipid and response of the type II cells to secretagogues. Incorporation of [3H]choline into phospholipid subclasses exhibited significant differences. Incorporation into phosphatidylcholine fell from 89.3 +/- 2.2% of total incorporation in group 1 control rats to 79.6 +/- 3.1% in group 3 rats with P. carinii pneumonia, while incorporation into sphingomyelin rose from 5.6 +/- 1.2% in group 1 animals to 15.2 +/- 2.7% in group 3 rats. Incorporation of [3H]choline into phospholipid subclasses in cells from group 2 and group 4 animals was not different from incorporation for group 1 animals. Type II cells from group 1 and group 2 (immunosuppressed control) rats responded appropriately to the secretagogues ATP, TPA, and terbutaline with a marked increase in surfactant phosphatidylcholine secretion; the effect of ATP was also blocked by the lectin, concanavalin A. In contrast, type II cells from group 3 rats failed to respond to the secretagogues with a significant increase in phospholipid secretion. Although treatment of group 4 rats with TMP-SMX markedly reduced the P. carinii organism burden, type II cells from these animals also responded poorly to the secretagogues. The depressed type II cell function described here provides a mechanism for the observed decrease in surfactant phospholipids from bronchoalveolar lavage fluid of experimental animals and patients with P. carinii pneumonia. The data also suggest this defect may become irreversible with advanced disease.
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PMID:Regulation of surfactant phosphatidylcholine secretion from alveolar type II cells during Pneumocystis carinii pneumonia in the rat. 825 31


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