scholarly journals Oxaliplatin for Metastatic Colon Cancer in a Patient with Renal Failure

2008 ◽  
Vol 2 ◽  
pp. CMO.S412
Author(s):  
Kenji Katsumata ◽  
Tetsuo Sumi ◽  
Tatehiko Wada ◽  
Yasuharu Mori ◽  
Masayuki Hisada ◽  
...  

Objective Oxaliplatin, a key part of the standard regimen for colorectal cancer in Western countries, has become available in Japan. In a hemodialysis patient with cecal cancer, we investigated the efficacy, safety, pharmacokinetics, and dialysability of oxaliplatin. Methods A 65-year-old man who had cecal cancer was treated with oxaliplatin (40 mg/m2) and l-leucovorin(l-LV) (200 mg/m2), which were administered simultaneously over 120 min via the side and main arms of a Y-tube, respectively. Then 5-FU (400 mg/m2) was administered rapidly via the side tube, followed by 5-FU (2,000 mg/m2) over 46 hours via the main tube. The patient had chronic renal failure due to diabetic nephropathy and hemodialysis was performed 3 times a week. Blood samples were collected from the dialyzer before and after each hemodialysis session to examine platinum clearance. Results The patient received 3 courses of oxaliplatin before he died of cancer. During hemodialysis, the platinum level fell from 0.32 μg/mL to 0.15 μg/mL. Conclusion Since patients with renal failure have various associated disorders and oxaliplatin has a long half-life, it is necessary to obtain more pharmacokinetic data to investigate its accumulation and dialysability during long-term treatment. Such data will assist in treating the rapidly increasing number of hemodialysis patients with colorectal cancer.

Pharmaceutics ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 714
Author(s):  
Sung Hun Bae ◽  
Sun-Young Chang ◽  
So Hee Kim

Tofacitinib is a Jak inhibitor developed as a treatment for rheumatoid arthritis. Tofacitinib is metabolized mainly through hepatic CYP3A1/2, followed by CYP2C11. Rheumatoid arthritis tends to increase renal toxicity due to drugs used for long-term treatment. In this study, pharmacokinetic changes of tofacitinib were evaluated in rats with gentamicin (G-ARF) and cisplatin-induced acute renal failure (C-ARF). The time-averaged total body clearance (CL) of tofacitinib in G-ARF and C-ARF rats after 1-min intravenous infusion of 10 mg/kg was significantly decreased by 37.7 and 62.3%, respectively, compared to in control rats. This seems to be because the time-averaged renal clearance (CLR) was significantly lower by 69.5 and 98.6%, respectively, due to decreased creatinine clearance (CLCR). In addition, the time-averaged nonrenal clearance (CLNR) was also significantly lower by 33.2 and 57.4%, respectively, due to reduction in the hepatic CYP3A1/2 and CYP2C11 subfamily in G-ARF and C-ARF rats. After oral administration of tofacitinib (20 mg/kg) to G-ARF and C-ARF rats, both CLR and CLNR were also significantly decreased. In conclusion, an increase in area under plasma concentration-time curves from time zero to time infinity (AUC) of tofacitinib in G-ARF and C-ARF rats was due to the significantly slower elimination of tofacitinib contributed by slower hepatic metabolism and urinary excretion of the drug.


1998 ◽  
Vol 81 (s3) ◽  
pp. 53-55 ◽  
Author(s):  
M.L. Chiozza ◽  
M. Plebani ◽  
C. Scaccianoce ◽  
M. Biraghi ◽  
G. Zacchello

2015 ◽  
Vol 87 (4) ◽  
pp. 846-856 ◽  
Author(s):  
Geert J. Behets ◽  
Goce Spasovski ◽  
Lulu R. Sterling ◽  
William G. Goodman ◽  
David M. Spiegel ◽  
...  

Pteridines ◽  
1999 ◽  
Vol 10 (4) ◽  
pp. 190-196
Author(s):  
Karoline Vrecko ◽  
Manfred Walz ◽  
Erwin Tafeit ◽  
G. Reibnegger

Summary In 30 atherosclerotic patients different serum analytes and neopterin concentrations in serum and urine were determined before and after Heparin-Induced Extracorporeal LDL and Fibrinogen Precipitation therapy. Neopterin concentrations in serum of all 30 patients were increased (mean=9.18 nmol/l, SD=3.23) compared to age matched healthy people (mean=5.34 nmol/l, SD=2.70) and were significantly lowered after H.E.L.P therapy (mean=S.22 nmol/l; SD=3.22, p=0.002, t-test) . These results suggest the involvement of the cellular immune system in the occurrence of atherosclerosis. Further neopterin, the macrophagederived immune activation marker, is significantly correlated with fibrinogen (linear correlation coefficient r=0.36, p=0.05). Long-term neopterin concentrations in serum of 4 patients (three with coronary heart disease and one with Papilla edema), from the first up to the 9th, respectively 12th therapy decreased, in contrast to fibrinogen which stayed stable or even increased during long-term treatment.


Author(s):  
Luca Faes ◽  
Daniele Marinazzo ◽  
Sebastiano Stramaglia ◽  
Fabrice Jurysta ◽  
Alberto Porta ◽  
...  

This work introduces a framework to study the network formed by the autonomic component of heart rate variability (cardiac process η ) and the amplitude of the different electroencephalographic waves (brain processes δ , θ , α , σ , β ) during sleep. The framework exploits multivariate linear models to decompose the predictability of any given target process into measures of self-, causal and interaction predictability reflecting respectively the information retained in the process and related to its physiological complexity, the information transferred from the other source processes, and the information modified during the transfer according to redundant or synergistic interaction between the sources. The framework is here applied to the η , δ , θ , α , σ , β time series measured from the sleep recordings of eight severe sleep apnoea–hypopnoea syndrome (SAHS) patients studied before and after long-term treatment with continuous positive airway pressure (CPAP) therapy, and 14 healthy controls. Results show that the full and self-predictability of η , δ and θ decreased significantly in SAHS compared with controls, and were restored with CPAP for δ and θ but not for η . The causal predictability of η and δ occurred through significantly redundant source interaction during healthy sleep, which was lost in SAHS and recovered after CPAP. These results indicate that predictability analysis is a viable tool to assess the modifications of complexity and causality of the cerebral and cardiac processes induced by sleep disorders, and to monitor the restoration of the neuroautonomic control of these processes during long-term treatment.


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