28 research outputs found
Synthesis of Some Novel Benzoxazolinonylcarboxamides as Potential Anti-Inflammatory Agents
Regional Expression and Role of Cyclooxygenase-2 Following Experimental Traumatic Brain Injury
Transcriptional regulation of endothelial constitutive PGHS-1 expression by phorbol ester
Selective DNA-Binding Activity of Interleukin-10-Stimulated STAT Molecules in Human Monocytes
PowerPoint Slides for: Use of Phosphorus Binders among Non-Dialysis Chronic Kidney Disease Patients and Mortality Outcomes
<p><b><i>Background:</i></b> Whether the benefits of phosphorus binders
extend to those without end stage renal disease is uncertain. Among a
large diverse non-dialysis chronic kidney disease (CKD) population with
hyperphosphatemia, we sought to evaluate phosphorus binder use and
compare mortality risk between patients prescribed and not prescribed
binders. <b><i>Methods:</i></b> A retrospective cohort study within an
integrated health system (January 1, 1998 - December 31, 2012) among CKD
patients (age ≥18) was performed. Non-dialysis CKD patients with 2
separate estimated glomerular filtrate rate (eGFR) <30 mL/min/1.73 m<sup>2</sup>
and serum phosphorus ≥5.0 mg/dL within 180 days of eGFR were included.
Multivariable cox proportional hazards and inverse probability of
treatment-weighted models were used to estimate mortality hazard ratios
(HRs) for patients who received phosphorus binders compared to no
binders. <b><i>Results:</i></b> Among 10,165 study patients, 2,733
subjects (27%) received phosphorus binders. Compared to the
no-phosphorus-binder group, the binder group had mortality HRs (95% CI)
of 0.86 (0.79-0.94) and 0.86 (0.80-0.93) using traditional multivariable
and inverse probability of treatment-weighted models respectively.
Sensitivity analyses removing patients who were prescribed binders
>180 days after index date revealed no difference in mortality
between those with binders and with no binders. <b><i>Conclusion:</i></b>
Our findings from a real-world clinical environment revealed that 27%
of hyperphosphatemic non-dialysis CKD patients were prescribed binders.
They also had lower risk of mortality compared to those not prescribed
phosphorus binders. However, the lower mortality risk was not observed
when we accounted for immortal time bias. Whether phosphorus binder use
in CKD improves survival remains to be determined.</p
Supplementary Material for: Use of Phosphorus Binders among Non-Dialysis Chronic Kidney Disease Patients and Mortality Outcomes
<p><b><i>Background:</i></b> Whether the benefits of phosphorus binders
extend to those without end stage renal disease is uncertain. Among a
large diverse non-dialysis chronic kidney disease (CKD) population with
hyperphosphatemia, we sought to evaluate phosphorus binder use and
compare mortality risk between patients prescribed and not prescribed
binders. <b><i>Methods:</i></b> A retrospective cohort study within an
integrated health system (January 1, 1998 - December 31, 2012) among CKD
patients (age ≥18) was performed. Non-dialysis CKD patients with 2
separate estimated glomerular filtrate rate (eGFR) <30 mL/min/1.73 m<sup>2</sup>
and serum phosphorus ≥5.0 mg/dL within 180 days of eGFR were included.
Multivariable cox proportional hazards and inverse probability of
treatment-weighted models were used to estimate mortality hazard ratios
(HRs) for patients who received phosphorus binders compared to no
binders. <b><i>Results:</i></b> Among 10,165 study patients, 2,733
subjects (27%) received phosphorus binders. Compared to the
no-phosphorus-binder group, the binder group had mortality HRs (95% CI)
of 0.86 (0.79-0.94) and 0.86 (0.80-0.93) using traditional multivariable
and inverse probability of treatment-weighted models respectively.
Sensitivity analyses removing patients who were prescribed binders
>180 days after index date revealed no difference in mortality
between those with binders and with no binders. <b><i>Conclusion:</i></b>
Our findings from a real-world clinical environment revealed that 27%
of hyperphosphatemic non-dialysis CKD patients were prescribed binders.
They also had lower risk of mortality compared to those not prescribed
phosphorus binders. However, the lower mortality risk was not observed
when we accounted for immortal time bias. Whether phosphorus binder use
in CKD improves survival remains to be determined.</p
The production of interleukin-1β from human fetal membranes is not obligatory for increased prostaglandin output
Bacterial endotoxin increased the expression of mRNA (maximal after 4 hr) for interleukin-1β (IL-1β) and the release of mature protein from intact human fetal membranes. In contrast, the change in expression of mRNA for type 2 cyclo-oxygenase (COX-2) was biphasic, with peaks after 0·5–1 hr and after 8 hr of culture. An antibody to IL-1β was without effect after 4 hr of culture, inhibited endotoxin-stimulated prostaglandin E2 (PGE2) production after 8 hr of culture, and caused a parallel decrease in the expression of mRNA for COX-2. We conclude that endotoxin induced the expression of COX-2 through IL-1β-independent and IL-1β-dependent mechanisms, and these differences are time dependent. Corticotrophin-releasing hormone (CRH) or platelet-activating factor (PAF) also increased the expression of mRNA for IL-1β and the release of IL-1β from some, but not all, fetal membranes. The antibody to IL-1β did not affect CRH-stimulated or PAF-stimulated PGE2 production or COX-2 expression. We conclude that CRH and PAF can induce the expression of IL-1β, but this is not obligatory for increased PGE2 release, and the effect of these stimuli on COX-2 expression is a direct, IL-1β-independent effect