Tissue factor (TF) is the predominant physiological initiator of coagulation, and its regulation is a critical aspect of endothelial cell hemostatic function. This report describes the regulation of TF mRNA expression by two physiological agonists: minimally oxidized low-density lipoprotein (MM-LDL), which may modulate endothelial hemostatic function in atherosclerosis, and lipopolysaccharide (LPS), which is a mediator of septic shock. Northern blot analysis of total RNA from human endothelial cells exposed to either MM-LDL or LPS for varying times showed that TF mRNA increased sharply at 1 hour, peaked at 2 to 3 hours, and declined to basal levels by 6 to 8 hours after treatment. The half-life of TF mRNA in MM-LDL-and LPS-exposed endothelial cells was approximately 45 minutes and 40 minutes, respectively.
It is not uncommon to see amphotericin B treatment failure in patients with systemic infection caused by Candida lusitaniae. We report a patient with stage IV ovarian carcinoma and C. lusitaniae sepsis whose treatment with amphotericin B failed. The initial blood isolate was susceptible to amphotericin B in vitro; however, the MIC for a blood isolate recovered 7 weeks after treatment began showed a fourfold increase. Direct subculture of two positive blood samples obtained within a week of the patient's death showed the coexistence of two distinct colony color variants on CHROMagar Candida (CAC). One variant was susceptible to amphotericin B, and one was resistant. These results emphasize the importance of repeat amphotericin B susceptibility testing for patients with persistent C. lusitaniae infection. The presence of colony variants on CAC may signal the emergence of amphotericin B resistance in C. lusitaniae and should be investigated.Candida lusitaniae is considered an opportunistic pathogen, causing infection primarily in immunocompromised patients (1)(2)(3)(4)(5)17). Recent studies have shown that the incidence of serious infection caused by C. lusitaniae is increasing. Clinical management of systemic infection by this organism is challenging because of innate amphotericin B resistance in some isolates (3, 10, 16). Moreover, some isolates of C. lusitaniae may develop amphotericin B resistance in vivo, a finding which is supported by in vitro studies (14). Recently, Yoon et al. reported high-frequency, reversible, in vitro switching of isolates from being amphotericin B susceptible to amphotericin B resistant after exposure to the drug (18). Here we report a case of fatal systemic infection caused by C. lusitaniae with amphotericin B treatment failure. Blood cultures obtained during therapy yielded colonies with distinct differences in color on CHROMagar Candida (CAC) between amphotericin B-susceptible and amphotericin B-resistant strains. CASE REPORTA 69-year-old woman with stage IV metastatic ovarian carcinoma had fever for 5 days, respiratory distress, and metabolic acidosis despite metronidazole and imipenem therapy for 2 weeks. The culture of a central venous pressure catheter tip and three Isolator (Wampole Laboratories, Cranbury, N.J.) blood cultures drawn 2 days later were positive for C. lusitaniae. The catheter line was removed, and empiric treatment with fluconazole was started on day 1 (Table 1). The treatment was switched to amphotericin B at 35 mg (0.7 mg/kg of body weight) four times a day on day 6 and then to lipid complex amphotericin B (Abelcet) at 350 mg (7 mg/kg) four times a day on day 10 because of persistent fungemia, which was confirmed by another positive blood culture. The patient's symptoms improved, and after approximately 5 weeks of hospitalization, she was discharged on continuing treatment with lipid complex amphotericin B. Seven days after discharge, she experienced shortness of breath and was readmitted. She denied having fever, chills, or nausea. A pleural effusion prompted...
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