Therapeutic Drug Monitoring of Prednisolone After Lung Transplantation

Morton, J.; Williamson, S; Kear, Laurie M.; McWhinney, Brett; Potter, Julia M.; Glanville, Allan R.

doi:10.1016/j.healun.2005.11.460

Cited by 25 publications

(24 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Synthetic glucocorticoids such as prednisolone and dexamethasone are commonly used in clinical practice both in therapeutic and in diagnostic settings [11]. The measurement of cortisol, cortisone and synthetic glucocorticoids in plasma and urine are potentially useful in the investigation and management of both over and under production of cortisol such as in cases of Cushing syndrome and Addison disease.…”

Section: Abbreviationsmentioning

confidence: 99%

Measurement of cortisol, cortisone, prednisolone, dexamethasone and 11-deoxycortisol with ultra high performance liquid chromatography–tandem mass spectrometry: Application for plasma, plasma ultrafiltrate, urine and saliva in a routine laboratory

McWhinney

Briscoe

Ungerer

et al. 2010

Journal of Chromatography B

View full text Add to dashboard Cite

Section: Abbreviationsmentioning

confidence: 99%

Measurement of cortisol, cortisone, prednisolone, dexamethasone and 11-deoxycortisol with ultra high performance liquid chromatography–tandem mass spectrometry: Application for plasma, plasma ultrafiltrate, urine and saliva in a routine laboratory

McWhinney

Briscoe

Ungerer

et al. 2010

Journal of Chromatography B

View full text Add to dashboard Cite

“…The analyses evaluated drug exposures in relation to treatment response since starting MPA and drugrelated adverse events. [7][8][9][10][11][12][13][14][15][16][17][18][19] was observed in patients with lowest tertile exposure to both total MPA and prednisolone as compared with patients with middle and higher tertile exposure (17% vs. 74%, P = 0.023). …”

mentioning

confidence: 91%

“…However, substantial between-subject variability in total prednisolone pharmacokinetics has been observed in childhood-onset systemic lupus erythematosus (SLE) [9] and transplant recipients [10][11][12]. Based on limited data, there is a possible relationship between total prednisolone exposure and SLE disease activity as well as the occurrence of some drug-related side effects [9].…”

Section: Introductionmentioning

confidence: 99%

Exposure–effect relationship of mycophenolic acid and prednisolone in adult patients with lupus nephritis

Rahman

Tett

Gafor

et al. 2015

Brit J Clinical Pharma

View full text Add to dashboard Cite

AIMSThe aim was to examine relationships between total and unbound mycophenolic acid (MPA) and prednisolone exposure and clinical outcomes in patients with lupus nephritis. METHODSSix blood samples were drawn pre-and at 1, 2, 4, 6 and 8 h post-dose and total and unbound MPA and prednisolone pre-dose (C 0 ), maximum concentration (C max ) and area under the concentration-time curve (AUC) were determined using non-compartmental analysis in 25 patients. The analyses evaluated drug exposures in relation to treatment response since starting MPA and drugrelated adverse events. [7][8][9][10][11][12][13][14][15][16][17][18][19] was observed in patients with lowest tertile exposure to both total MPA and prednisolone as compared with patients with middle and higher tertile exposure (17% vs. 74%, P = 0.023). RESULTS Dose CONCLUSIONSThis study suggests a potential role for therapeutic drug monitoring in individualizing immunosuppressant therapy in patients with lupus nephritis.

show abstract

“…Prednisolone is an anti-inflammatory and immunosuppressive drug widely used for treatment of bronchial asthma, chronic obstructive pulmonary disease, autoimmune disease, and leukemia (2,6,17,23,28). Prednisolone is also routinely used postoperatively in patients with IPAH who have undergone lung transplantation (24,42). The use of immunosuppressants to treat pulmonary hypertension has shown promising beneficial effects in some patients (4,19).…”

mentioning

confidence: 99%

Prednisolone inhibits PDGF-induced nuclear translocation of NF-κB in human pulmonary artery smooth muscle cells

Ogawa¹,

Firth²,

Yao³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

inhibits PDGF-induced nuclear translocation of NF-B in human pulmonary artery smooth muscle cells. Am J Physiol Lung Cell Mol Physiol 295: L648 -L657, 2008. First published August 15, 2008 doi:10.1152/ajplung.90245.2008.-Pulmonary vascular remodeling, a major cause for the elevated pulmonary vascular resistance in patients with pulmonary arterial hypertension (PAH), is partially due to increased proliferation of pulmonary arterial smooth muscle cells (PASMC) in the media, resulting in vascular wall thickening. Plateletderived growth factor (PDGF) is a potent mitogen that may be involved in the progression of PAH. Blockade of PDGF receptors has been demonstrated to have therapeutic potential for patients with severe pulmonary hypertension. Prednisolone is an immunosuppressant shown to have anti-inflammatory and antiproliferative effects on PASMC. This study was designed to investigate whether PDGF and prednisolone affect human PASMC proliferation by regulating the nuclear translocation of NF-B (a transcription factor composed of 2 subunits, p50 and p65). Treatment of human PASMC with PDGF (10 ng/ml) significantly increased nuclear translocation of p50 and p65 subunits. Inhibition of NF-B activation or nuclear translocation of p50/p65 significantly attenuated PDGF-induced PASMC proliferation (determined by [ 3 H]thymidine incorporation). In the presence of prednisolone (200 M), the PDGF-induced nuclear translocation of p50 and p65 subunits was markedly inhibited (P Ͻ 0.05 vs. the cells treated with PDGF alone). These results indicate that PDGF-induced nuclear translocation of NF-B may play an important role in stimulating PASMC proliferation (and/or enhancing PASMC survival), whereas prednisolone may exert anti-inflammatory and antiproliferative effects on PASMC by inhibiting NF-B nuclear translocation. proliferation; pulmonary arterial hypertension; immunosuppressant; therapy PULMONARY VASCULAR REMODELING is a major contributor to the elevated pulmonary vascular resistance in patients with pulmonary arterial hypertension. Increased growth factors (e.g., PDGF) and enhanced inflammatory responses (characterized with cytokines and chemokines that can stimulate or activate NF-B) have recently been demonstrated to be important causes for the development of pulmonary vascular remodeling in patients with idiopathic pulmonary arterial hypertension (IPAH) and chronic thromboembolic pulmonary hypertension (26,29). Prednisolone is an anti-inflammatory and immunosuppressive drug widely used for treatment of bronchial asthma, chronic obstructive pulmonary disease, autoimmune disease, and leukemia (2,6,17,23,28). Prednisolone is also routinely used postoperatively in patients with IPAH who have undergone lung transplantation (24, 42). The use of immunosuppressants to treat pulmonary hypertension has shown promising beneficial effects in some patients (4,19). In addition to its immunosuppressive effects, prednisolone has been shown to inhibit PDGF-stimulated proliferation of pulmonary artery smooth muscle cells (PASMC) from p...

show abstract

Therapeutic Drug Monitoring of Prednisolone After Lung Transplantation

Cited by 25 publications

References 38 publications

Measurement of cortisol, cortisone, prednisolone, dexamethasone and 11-deoxycortisol with ultra high performance liquid chromatography–tandem mass spectrometry: Application for plasma, plasma ultrafiltrate, urine and saliva in a routine laboratory

Measurement of cortisol, cortisone, prednisolone, dexamethasone and 11-deoxycortisol with ultra high performance liquid chromatography–tandem mass spectrometry: Application for plasma, plasma ultrafiltrate, urine and saliva in a routine laboratory

Exposure–effect relationship of mycophenolic acid and prednisolone in adult patients with lupus nephritis

Prednisolone inhibits PDGF-induced nuclear translocation of NF-κB in human pulmonary artery smooth muscle cells

Contact Info

Product

Resources

About