Suppurative mediastinitis after heart transplantation: early diagnosis with CT-guided needle aspiration.
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Biomedical subjects
Publications and source records attributed to J M Cisneros.
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A multiinstitutional study of 307 heart transplant recipients was carried out to determine the clinical, radiographic, and prognostic characteristics, the incidence, and the etiology of pneumonias in the first year after transplantation. There were 21.1 cases of pneumonia per 100 heart transplantations. Seventy-five percent of the cases occurred in the first trimester. Eighty-two causal agents were identified, of which 60% were opportunistic, 25% were nosocomial, and 15% were community-acquired. The most frequent isolates were cytomegalovirus (20), Aspergillus species (13), and Pneumocystis carinii (11). Hemoptysis occurred more frequently in aspergillus pneumonias than in other pneumonias (54% vs. 6%, respectively; P < .05); aspergillus pneumonia was the only type of pneumonia during which cavitated nodules were noted on thoracic radiographs. The overall mortality rate was 30.8%; the independent factors of a poor prognosis were aspergillus infection (relative risk [RR], 7.4; 95% confidence interval [CI], 5.8-9.1) and bilateral pulmonary infiltrates (RR, 10; 95% CI, 8.5-11.4).
A prospective, multicenter study was carried out over a period of 10 months. All patients with clinically significant bacteremia caused by Enterococcus spp. were included. The epidemiological, microbiological, clinical, and prognostic features and the relationship of these features to the presence of high-level resistance to gentamicin (HLRG) were studied. Ninety-three patients with enterococcal bacteremia were included, and 31 of these cases were caused by HLRG (33%). The multivariate analysis selected chronic renal failure, intensive care unit stay, previous use of antimicrobial agents, and Enterococcus faecalis species as the independent risk factors that influenced the development of HLRG. The strains with HLRG showed lower levels of susceptibility to penicillin and ciprofloxacin. Clinical features (except for chronic renal failure) were similar in both groups of patients. HLRG did not influence the prognosis for patients with enterococcal bacteremia in terms of either the crude mortality rate (29% for patients with bacteremia caused by enterococci with HLRG and 28% for patients not infected with strains with HLRG) or the hospital stay after the acquisition of enterococcal bacteremia. Hemodynamic compromise, inappropriate antimicrobial therapy, and mechanical ventilation were revealed in the multivariate analysis to be the independent risk factors for mortality. Prolonged hospitalization was associated with the nosocomial acquisition of bacteremia and polymicrobial infections.
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Sulphasalazine is the drug most widely used in intestinal inflammatory disease given its efficacy and low cost. Nonetheless, its administration is not lacking adverse effects. Two cases of severe hypersensitivity are herein described. Moreover, the diagnostic difficulties observed and their implication in the management of the underlying disease are discussed.
The number of nosocomial infections caused by Acinetobacter baumannii has increased in recent years. During a 12-month study, there were 1.8 episodes of A. Baumannii bacteremia per 1,000 adults admitted to a hospital in Seville, Spain. Seventy-nine patients were included in the study. A. baumannii bacteremia occurred after a mean (+/- SD) hospitalization of 18 +/- 20 days. In all cases the infections were acquired nosocomially; 71% wee acquired in intensive care units. Ampicillin/ sulbactam was found to be the most active agent against A. baumannii. The common source of the bacteremia was the respiratory tract (32 cases [71%]). Twenty patients (25%) had septic shock, and 24 (30%) had disseminated intravascular coagulation (DIC). Treatment with imipenem or ampicillin/sulbactam was most effective (cure rates, 87.5% and 83%, respectively). The deaths of 27 patients (34%) were related to A baumannii bacteremia. The presence of DIC (odds ratio [OR] = 116.4; P < .0001) and inappropriate antimicrobial treatment (OR = 15.2; P < .01) were independently associated with mortality. We conclude that most A. baumannii isolates are multiresistant and that nosocomial A. baumannii bacteremia may cause severe clinical disease that is associated with a high mortality.
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Pharmacokinetic parameters of zidovudine (ZDV) were not altered in 16 patients receiving concomitant therapy with ZDV and trimethoprim-sulfamethoxazole by oral administration. ZDV areas under the concentration-time curves were (means +/- standard deviations) 1.80 +/- 0.70 and 1.69 +/- 0.64 micrograms.h/ml in the absence and presence of trimethoprim-sulfamethoxazole, respectively. ZDV clearances were 1.57 +/- 0.61 and 1.74 +/- 0.66 liters/h/kg, respectively.
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BACKGROUND: The aim of this study was to know the pharmacokinetics of zidovudine (ZDV) in steady state in patients with infection by the human immunodeficiency virus (HIV) in whom the risk factor was intravenous drug use. METHODS: The study was carried out in 8 patients in stage IV of the Centers for Disease Control (CDC) with no acute intercurrent process, with normal liver and renal function, orally receiving 250 mg of ZDV every 6 hours. Blood samples were taken between 30 and 360 minutes from the last doses taken during fasting. Plasma concentrations of ZDV and glucuronide zidovudine (G-ZDV) were determined by radioimmunoassay with the data being adapted to a monocompartmental pharmacokinetic model. RESULTS: The maximum concentration (Cmax) of ZDV was 0.81 +/- 0.38 microgram/ml demonstrating high interindividual variability with values between 0.35 microgram/ml and 1.45 microgram/ml. The mean Cmax of G-ZDV was 1.44 +/- 0.64 microgram/ml. The mean t1/2 of ZDV and G-ZDV was 1.63 +/- 0.75 hours and 1.12 +/- 0.32 hours, respectively, with values oscillating between 0.99 and 3.14 h in the case of ZDV. The area below the curve concentration/time (AUC) of ZDV was 1.43 +/- 0.34 microgram-h/ml and in the case of G-ZDV the AUC was 2.73 +/- 0.91 microgram-h/ml. Total body clearance (Clb) of ZDV was 2.11 +/- 0.64 l/kg/h and the volume of distribution (Vd) of ZDV was 5.6 +/- 1.73 l/kg. CONCLUSIONS: The results of this study demonstrate that there is a marked interindividual variability in the pharmacokinetics of zidovudine suggesting the need for adapting dosage to patients weight and monitoring plasma concentration.
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OBJECTIVE: To study the pharmacokinetics of zidovudine (ZDV) and its glucoronide metabolite (G-ZDV) in a patient with end-stage renal disease in haemodialysis. DESIGN: Pharmacokinetics study performed during and between haemodialysis sessions. METHODS: The patient was treated with oral ZDV (100 mg every 8 h). Concentrations of ZDV and G-ZDV were measured by radioimmunoassay. A monocompartmental model was used to calculate pharmacokinetic parameters. RESULTS: The peak plasma concentrations of ZDV and G-ZDV after drug administration between haemodialysis sessions were 0.57 and 10.01 micrograms/ml, respectively. The half-lives of ZDV and G-ZDV rose to 3.2 and 14.2 h, respectively. The total body clearance for ZDV in the period between haemodialysis sessions (0.44 l/kg/h) was 66% lower than normal values. The ZDV half-life was normalized by haemodialysis, the total body clearance of ZDV increased (1.12 l/kg/h) and the G-ZDV half-life shortened (5.9-7.9 h). Neither G-ZDV accumulation nor derived ZDV toxicity occurred. CONCLUSIONS: Our data suggest that ZDV is safe and an efficient drug when administered at a dosage of 100 mg three times daily in patients with end-stage renal disease in haemodialysis sessions, and that ZDV and G-ZDV are cleared by haemodialysis.
BACKGROUND: Adenosine deaminase (ADA) is an essential enzyme for the differentiation and proliferation of T lymphocytes and the monocyte-macrophage system. The basic immunitary response of brucellosis is cellular. To this end, ADA activity was evaluated in brucellosis. METHODS: Serum ADA activity was assessed by a colorimetric method in 67 patients with brucellosis, before therapy and at 1, 3 and 6 months of follow up. RESULTS: Serum ADA activity in brucellosis was higher than that in 52 healthy controls, both in those with the acute febrile noncomplicated form (48 patients) and in those with focal symptoms from one organ (19 patients) (p less than 0.0001 and p less than 0.001). There were no differences between both groups of brucellosis. There was a negative correlation between the duration of the disease and ADA activity. After therapy there was a rapid decrease of ADA values, more marked in patients with noncomplicated brucellosis. During the follow up, only one patient had a new increase in ADA activity, coincident with a clinical and bacteriological relapse, and previous to the increase of IgG anti-Brucella titers. CONCLUSIONS: The results indicate that adenosine deaminase activity is increased during the active stage of brucellosis. It can be considered as a biochemical follow up marker of the disease and, probably, as a marker of relapses.
The effectiveness of treating human brucellosis caused by Brucella melitensis with a 6-week course of doxcycline plus streptomycin for 2 of those weeks was analyzed by a multicenter prospective study of 139 patients. Subjects with central nervous system involvement, endocarditis, or spondylitis were excluded from the study. All but 5 of the 139 patients completed the full treatment schedule and became afebrile in the first week of therapy. Four patients suffered relapses during the follow-up period. Of the five patients who did not complete the treatment, two left because of adverse secondary effects (1.4%), another two left for noncomplicance with the treatment (1.4%), and the remaining patient was considered a therapeutic failure because his symptoms persisted after the first week of therapy (0.7%). We concluded that the combination of doxycycline and streptomycin is an effective treatment for the types of brucellosis included in our study.
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