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Community acquired pneumonia (CAP) remains an important cause of substantial morbidity and mortality in inhospital patients. We conducted a retrospective study of all patients hospitalised at our hospital with the diagnosis of bacterial pneumonia according to ICD-10 within one year. Of 360 identified charts, 335 met the requirements and were reviewed regarding risk factors, diagnosis, treatment, and overall mortality. The typical patient hospitalised with pneumonia was elderly (mean 68 years), male (60%), and suffered from comorbidities or predisposing factors (96.4%). A total of 72.8% of pneumonias were localized in the inferior lobes, and 21.1% had bilateral infiltrates. Etiologic agents were searched for in 297/335 patients (87.5%) and were found positive in 33.4%: of 169 blood cultures 9.5% were positive, of 150 sputum cultures taken 46.6% were positive, of 17 serologies taken 58.8% were positive, and of 9 pleural effusions analysed 22.2% were positive. Encapsulated bacteria were the most common found bacterial etiologies, namely Streptococcus pneumoniae (S. pneumoniae) in 30.9% of patients with known bacterial etiology, Haemophilus in 24.7%, and Klebsiella in 12.4%. Methicillin-resistant S. aureus was not found. The three most commonly used antibiotics were amoxicillin/clavulanic acid used in 77.3% of patients, clarithromycin (41.2%), and ceftriaxone (16.6%). Mean duration of treatment was 12.1 days. 245/335 (73.1%) patients had a favourable outcome, 16.7% (56/335) of patients had a protracted illness with delayed resolution (i.e. prolonged hospital stay, need for intensive care, intubation or several of these complications). Overall mortality in our unit was 8.6%.
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An unlicensed injectable medicine sold as adrenal cortex extract (ACE*) and distributed in the alternative medicine community led to the largest outbreak of Mycobacterium abscessus infections reported in the United States. Records from the implicated distributor from January 1, 1995, to August 18, 1996, were used to identify purchasers; purchasers and public health alerts were used to identify patients. Purchasers and patients were interviewed, and available medical records were reviewed. Vials of ACE* were tested for mycobacterial contamination, and the product was recalled by the U.S. Food and Drug Administration. ACE* had been distributed to 148 purchasers in 30 states; 87 persons with postinjection abscesses attributable to the product were identified. Patient and vial cultures contained M. abscessus identical by enzymatic and molecular typing methods. Unusual infectious agents and alternative health practices should be considered in the diagnosis of infections that do not respond to routine treatment.
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A 41-year-old woman was referred for severely obstructed pulmonary disease 4 years after she stopped smoking. Treatment for chronic obstructive pulmonary disease (COPD) had no effect and lung function worsened in the following years. The clinical, radiological and pathological characteristics led us to the diagnosis of diffuse panbronchiolitis. She was treated with clarithromycin. After 1 year, major improvement was seen in clinical, radiological and spirometric features. Diffuse panbronchiolitis is a rare obstructive disorder that is usually seen in people of Japanese descent. Patients respond well to treatment with low-dose macrolide treatment.
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In this study we have evaluated the reliability of a fluorescence-based method used for rapid identification of irreversible CYP inhibitors (mechanism-based inhibitors). This was accomplished by comparing the time-dependence pattern of IC50 values from fluorometric kinetic measurements. For irreversible CYP inhibitors, IC50 values decreased as incubation proceeded. This was due to progressive inactivation of corresponding enzymes by reactive metabolites generated during the incubation. This change pattern was confirmed using a number of known irreversible CYP inhibitors, including furafylline, midazolam, erythromycin, clarithromycin, oleandomycin, 17alpha-ethynylestradiol and verapamil. The pattern was different in reversible inhibition, depending upon the compounds tested in the fluorometric kinetic assay. For some compounds, such as clotrimazole, IC50 values remained relatively stable, whereas other compounds, such as miconazole, terfenadine and ketoconazole showed a significant increase with incubation time. Monitoring tested compounds by LC-MS/MS during the incubation confirmed that increases of IC50 were probably caused by the loss of inhibitors, resulting from either metabolic degradation, or non-specific binding to microsomal proteins.
Plasma ghrelin concentrations, gastric ghrelin expression, and body weight were determined in a total of 134 consecutive individuals before and 12 weeks after successful H. pylori eradication. Gastric ghrelin expression was evaluated by determining mRNA expression levels and the number of ghrelin-producing cells in gastric mucosa biopsy specimens by real-time reverse transcriptase-polymerase chain reaction and immunohistochemistry, respectively.
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We propose using O-desmethylvenlafaxine/venlafaxine for CYP2D6 phenotyping, and O-desmethylvenlafaxine/venlafaxine with venlafaxine + O-desmethylvenlafaxine for predicting venlafaxine treatment outcomes in future prospective studies.
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LB cultures [4 x 10(8)-4 x 10(9) CFU ml(-1)) either were prepared in milk at their native pH, 3.8-5.0, or were adjusted to pH 6.4-7.7. At low and neutralized pH, LB strains inhibited the growth by 40-86.7% and 16.7-66.7% of H. pylori strains, respectively. LB activity was strain-dependent. At low and neutralized pH, one and five H. pylori strains, respectively, were not inhibited by any LB strain. LB2 and LB3, taken together, were active against most metronidazole and clarithromycin resistant strains.
Nine gastroenterologic units included patients with unsuccessful eradication of H. pylori in a preceding randomized trial. Previous treatment was either omeprazole (O) 20 mg, C 250 mg, and M 500 mg [O.C.M] or RBC 400 mg, tetracycline (T) 1,000 mg, and M 500 mg [RBC x T x M]; all drugs were given twice daily for 7 days.
Treatment with 0.3% gatifloxacin or the triple combination of 0.3% gatifloxacin, topical fortified amikacin sulfate (50 mg/mL), and clarithromycin (10 mg/mL) reduced the number of mycobacterial organisms more significantly than the controls that were treated with a topical balanced salt solution (both P<.001). Therapy with 0.3% gatifloxacin was more effective than 0.3% ciprofloxacin alone (P<.001) and demonstrated synergy by enhancing the efficacy of the combination of fortified amikacin (50 mg/mL) and clarithromycin (10 mg/mL) (P<.001). Neither 0.3% ciprofloxacin nor the combination of fortified amikacin (50 mg/mL) and clarithromycin (10 mg/mL) demonstrated a significant difference in activity against mycobacteria compared with the topical balanced salt solution.