scholarly journals The efficacy of a sumatriptan and naproxen combination pill in a patient with chronic migraines who discontinued triptan therapy in the past due to a self-reported poor response to sumatriptan monotherapy

Author(s):  
Ethan M. Cohen

A clinical decision report using: Mathew NT, Landy S, Stark S, et al. Fixed-dose sumatriptan and naproxen in poor responders to triptans with a short half-life. Headache. 2009;49(7):971-982. https://doi.org/10.1111/j.1526-4610.2009.01458.x for a patient with chronic migraines who had self-reported poor response to sumatriptan monotherapy.

2009 ◽  
Vol 49 (7) ◽  
pp. 971-982 ◽  
Author(s):  
Ninan T. Mathew ◽  
Stephen Landy ◽  
Stuart Stark ◽  
Gretchen E. Tietjen ◽  
Frederick J. Derosier ◽  
...  

1977 ◽  
Vol 16 (04) ◽  
pp. 157-162 ◽  
Author(s):  
C. Schümichen ◽  
B. Mackenbrock ◽  
G. Hoffmann

SummaryThe bone-seeking 99mTc-Sn-pyrophosphate compound (compound A) was diluted both in vitro and in vivo and proved to be unstable both in vitro and in vivo. However, stability was much better in vivo than in vitro and thus the in vitro stability of compound A after dilution in various mediums could be followed up by a consecutive evaluation of the in vivo distribution in the rat. After dilution in neutral normal saline compound A is metastable and after a short half-life it is transformed into the other 99mTc-Sn-pyrophosphate compound A is metastable and after a short half-life in bone but in the kidneys. After dilution in normal saline of low pH and in buffering solutions the stability of compound A is increased. In human plasma compound A is relatively stable but not in plasma water. When compound B is formed in a buffering solution, uptake in the kidneys and excretion in urine is lowered and blood concentration increased.It is assumed that the association of protons to compound A will increase its stability at low concentrations while that to compound B will lead to a strong protein bond in plasma. It is concluded that compound A will not be stable in vivo because of a lack of stability in the extravascular space, and that the protein bond in plasma will be a measure of its in vivo stability.


2021 ◽  
Vol 14 ◽  
pp. 175628482098819
Author(s):  
Klaudia Farkas ◽  
Daniella Pigniczki ◽  
Mariann Rutka ◽  
Kata Judit Szántó ◽  
Tamás Resál ◽  
...  

The coronavirus disease 2019 (COVID-19) outbreak emerged in December 2019 in China and rapidly spread worldwide. Inflammatory bowel disease (IBD) patients are likely to be more susceptible to viral infections, and this is significantly influenced by the type of therapy they receive. Thus, issues specifically concerning the medical treatment of IBD patients were shortly addressed at the beginning of the pandemic. However, recently available data on the occurrence and outcome of SARS-CoV-2 infection in IBD patients does not address the concerns raised at the beginning of the pandemic. Growing evidence and the rapid changes happening over the past few weeks have helped elucidate the current situation, contribute to our understanding of the disease, and many previously raised questions could now be answered. We hereby summarise available evidence regarding viral infections and IBD, focusing on SARS-CoV infections, and we provide practical recommendations related to patient management during the COVID-19 pandemic era.


Mitochondrion ◽  
2015 ◽  
Vol 21 ◽  
pp. 27-32 ◽  
Author(s):  
Yang Xu ◽  
Ashim Malhotra ◽  
Steven M. Claypool ◽  
Mindong Ren ◽  
Michael Schlame

1998 ◽  
Vol 84 (2) ◽  
pp. 435-441 ◽  
Author(s):  
Christophe Adrie ◽  
Fumito Ichinose ◽  
Alexandra Holzmann ◽  
Larry Keefer ◽  
William E. Hurford ◽  
...  

Adrie, Christophe, Fumito Ichinose, Alexandra Holzmann, Larry Keefer, William E. Hurford, and Warren M. Zapol. Pulmonary vasodilation by nitric oxide gas and prodrug aerosols in acute pulmonary hypertension. J. Appl. Physiol. 84(2): 435–441, 1998.—Sodium 1-( N, N-diethylamino)diazen-1-ium-1,2-diolate {DEA/NO; Et2N[N(O)NO]Na} is a compound that spontaneously generates nitric oxide (NO). Because of its short half-life (2.1 min), we hypothesized that inhaling DEA/NO aerosol would selectively dilate the pulmonary circulation without decreasing systemic arterial pressure. We compared the pulmonary selectivity of this new NO donor with two other reference drugs: inhaled NO and inhaled sodium nitroprusside (SNP). In seven awake sheep with pulmonary hypertension induced by the infusion of U-46619, we compared the hemodynamic effects of DEA/NO with those of incremental doses of inhaled NO gas. In seven additional awake sheep, we examined the hemodynamic effects of incremental doses of inhaled nitroprusside (i.e., SNP). Inhaled NO gas selectively dilated the pulmonary vasculature. Inhaled DEA/NO produced nonselective vasodilation; both systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) were reduced. Inhaled SNP selectively dilated the pulmonary circulation at low concentrations (≤10−2 M), inducing a decrease of PVR of up to 42% without any significant decrease of SVR (−5%), but nonselectively dilated the systemic circulation at larger doses (>10−2 M). In conclusion, despite its short half-life, DEA/NO is not a selective pulmonary vasodilator compared with inhaled NO. Inhaled SNP appears to be selective to the pulmonary circulation at low doses but not at higher levels.


2008 ◽  
Vol 24 (2) ◽  
pp. 89-98 ◽  
Author(s):  
V. F. Gopka ◽  
A. V. Yushchenko ◽  
V. A. Yushchenko ◽  
I. V. Panov ◽  
Ch. Kim

2015 ◽  
Vol 31 (8) ◽  
pp. 1074.e7 ◽  
Author(s):  
Francesco Santoro ◽  
Riccardo Ieva ◽  
Matteo Di Biase ◽  
Natale Daniele Brunetti

1987 ◽  
Vol 25 (26) ◽  
pp. 103.1-103

A letter to the Lancet (S S Adams, 21 Nov 1987, 1204–5) points out that when the CSM adverse reactions data for the 11 NSAIDs cited in our table are ranked in descending order of toxicity, nearly all those with a long plasma elimination half-life of about 10 hours or more (for the drug + active metabolites) come at the top of the list. The other compounds have a short half-life, 4 hours or less. The table below shows the relevant CSM data rearranged in rank order, and the approximate half-lives of the drugs. Half-lives vary widely between patients and tend to be longer in the elderly. Toxicity is obviously not determined by slow elimination alone, but prolonged high concentrations of a drug in the tissues are likely to exacerbate any toxic effects. Short-acting drugs may allow some recovery between doses from the potentially damaging inhibition of prostaglandin synthesis at vulnerable sites, such as the gut and kidney. NSAIDs with a short half-life should therefore be preferred unless a somewhat longer action is needed to alleviate morning stiffness. Sustained-release forms of NSAIDs with an otherwise short half-life should also be used cautiously.


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