Pilot study of continuous infusion cefepime in adult patients with cystic fibrosis

HIV RNA load below the detection threshold. At this point, the median (Q1–Q3) change in the CD4+ cell count was 44 (–47 to 139) cells/mm 3. Other relevant characteristics of the population studied are shown in Table 1. Three patients (3%) had suffered a severe liver event: one individual (1%) developed grade 3 HT and two (2%) suffered from liver decompensation. The density of incidence of grade 3–4 HT was 1.1 per 100 person-years (95% CI = 0.06–6.9) and that of any severe liver event was 3.3 per 100 person-years (95% CI = 0.9–10). Among HCV-or HBV-coinfected patients, one (2.4%) presented with grade 3 HT and two (4.9%) developed hepatic decompensation. Thus, the density of incidence of grade 3–4 HT among coinfected individuals was 2.5 per 100 person-years (95% CI = 0.1–15.1) and that of any severe liver event was 7.6 per 100 person-years (95% CI = 2.01–21.9) in this population. Ten individuals (10%) had a grade 4 increase in the plasma level of total bilirubin (TB), i.e. a plasma TB value ‡5 mg/dL. A grade 4 increase in TB was observed in five patients (12.2%) coinfected with HBV or HCV. Atazanavir was stopped in one patient (1%) due to hyperbilirubinaemia. HCV seropositivity and a low baseline CD4+ cell count were associated with the development of severe liver events (Table 1). There was no significant difference in the CD4+ cell gain at month 6 between patients who developed grade 3– 4 HT or hepatic decompensation and those who did not [median (Q1–Q3) = 60 (37–146) cells/mm 3 versus 41 (–48 to 136) (P = 0.6), respectively]. The relationship between other parameters and the emergence of these events is shown in Table 1. The above results show that severe adverse liver events are uncommon in patients receiving antiretroviral combinations including atazanavir. In particular, grade 3–4 HT is seen less frequently than has been reported in patients taking other PIs and non-nucleoside reverse transcriptase inhibitors in both cohort studies and clinical trials. 1,2 In this regard, in our study most patients were treatment-experienced, showed undetectable HIV viral load and had high CD4+ cell counts. Perhaps, if a higher number of naive patients, with more severe immunosuppression, had been included, more increases in aminotransferases due to immune reconstitution would have been observed. Thus, the rate of HT would have been higher. In agreement with that, the emergence of HT or hepatic decompensation was …