Mo2054 Role of Autophagy in Nonsteroidal Antiinflammatory Drug-Induced Small Intestine Damage in Rats

2012 ◽  
Vol 142 (5) ◽  
pp. S-729-S-730
Author(s):  
Ken Narabayashi ◽  
Yuko Ito ◽  
Yuichi Kojima ◽  
Yukiko Yoda ◽  
Toshihiko Okada ◽  
...  
Keyword(s):  
Small Intestine ◽  
Antiinflammatory Drug ◽  
Nonsteroidal Antiinflammatory Drug ◽  
Drug Induced

Nonsteroidal Antiinflammatory Drug-Induced Renal Dysfunction Related to Inhibition of Renal Prostaglandins

1987 ◽  
Vol 21 (12) ◽  
pp. 954-960 ◽  
Author(s):  
Richard G. D'Angio
Keyword(s):  
Renal Dysfunction ◽  
Antiinflammatory Drug ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Nonsteroidal Antiinflammatory Drug ◽  
Antiinflammatory Drugs ◽  
Drug Induced ◽  
Frequent Use ◽  
The Face ◽  
Patients At Risk

This article reviews the role of prostaglandins (PG) in maintaining renal function in the face of vasoconstrictive substances and decreased renal blood flow. Inhibition of the synthesis of renal PG by nonsteroidal antiinflammatory drugs (NSAID) may lead to the development of hemodynamically induced renal dysfunction in patients with a decreased effective plasma volume or chronic renal insufficiency. The importance of stimulation of renal PG activity to the action of diuretics and a pharmacodynamic mechanism for NSAID-induced diuretic resistance are presented. Evidence for the relative selectivity of sulindac in inhibiting systemic PG without inhibiting renal PG is also reviewed. Inhibition of renal PG synthesis has been postulated to be a contributing factor for other forms of NSAID-induced renal dysfunction (interstitial nephritis, analgesic-associated nephropathy). The relationship between renal PG inhibition by NSAID and these syndromes is briefly discussed. Considering the frequent use of NSAID, it is important that practitioners are aware of the mechanisms whereby patients may develop NSAID-induced renal dysfunction and that they are able to identify patients at risk.

Treatment of nonsteroidal antiinflammatory drug-induced gastric ulcers with misoprostol

1992 ◽  
Vol 37 (12) ◽  
pp. 1820-1824 ◽  
Author(s):  
Richard Jaszewski ◽  
David Y. Graham ◽  
Scott C. Stromatt
Keyword(s):  
Antiinflammatory Drug ◽  
Nonsteroidal Antiinflammatory Drug ◽  
Gastric Ulcers ◽  
Drug Induced

Effect of Antiulcer Drugs for Treatment of Nonsteroidal Antiinflammatory Drug-Induced Ulcers

2001 ◽  
pp. 215-218 ◽  
Author(s):  
Yuji Mizokami ◽  
Takahisa Shiraishi ◽  
Toshiya Otsubo ◽  
Yoshiyuki Kariya ◽  
Hiroshi Nakamura ◽  
...  
Keyword(s):  
Antiinflammatory Drug ◽  
Nonsteroidal Antiinflammatory Drug ◽  
Drug Induced ◽  
Antiulcer Drugs

scholarly journals Glucagon-like peptide 2 decreases mortality and reduces the severity of indomethacin-induced murine enteritis

1999 ◽  
Vol 277 (5) ◽  
pp. E937-E947 ◽  
Author(s):  
Robin P. Boushey ◽  
Bernardo Yusta ◽  
Daniel J. Drucker
Keyword(s):  
Biological Effects ◽  
Antiinflammatory Drug ◽  
Nonsteroidal Antiinflammatory Drug ◽  
Myeloperoxidase Activity ◽  
Drug Induced ◽  
Mucosal Epithelium ◽  
Crypt Cell Proliferation ◽  
Glucagon Like Peptide ◽  
Complementary Actions

Glucagon-like peptides (GLPs) are secreted from enteroendocrine cells in the gastrointestinal tract. GLP-1 actions regulate blood glucose, whereas GLP-2 exerts trophic effects on intestinal mucosal epithelium. Although GLP-1 actions are preserved in diseases such as diabetes, GLP-2 action has not been extensively studied in the setting of intestinal disease. We have now evaluated the biological effects of a human GLP-2 analog in the setting of experimental murine nonsteroidal antiinflammatory drug-induced enteritis. Human (h)[Gly2]GLP-2 significantly improved survival whether administered before, concomitant with, or after indomethacin. h[Gly2]GLP-2-treated mice exhibited reduced histological evidence of disease activity, fewer intestinal ulcerations, and decreased myeloperoxidase activity in the small bowel ( P < 0.05, h[Gly2]GLP-2- vs. saline-treated controls). h[Gly2]GLP-2 significantly reduced cytokine induction, bacteremia, and the percentage of positive splenic and hepatic bacterial cultures ( P < 0.05). h[Gly2]GLP-2 enhanced epithelial proliferation ( P < 0.05 for increased crypt cell proliferation in h[Gly2]GLP-2- vs. saline-treated mice after indomethacin) and reduced apoptosis in the crypt compartment ( P < 0.02). These observations demonstrate that a human GLP-2 analog exerts multiple complementary actions that serve to preserve the integrity of the mucosal epithelium in experimental gastrointestinal injury in vivo.

Nonsteroidal Antiinflammatory Drug-Induced Pseudoporphyria: A Case Series

2002 ◽  
Vol 6 (4) ◽  
pp. 320-326 ◽  
Author(s):  
Jeffrey R. LaDuca ◽  
Peter H. Bouman ◽  
Anthony A. Gaspari
Keyword(s):  
Case Series ◽  
Antiinflammatory Drug ◽  
Nonsteroidal Antiinflammatory Drug ◽  
Drug Induced

Nonsteroidal antiinflammatory drug-induced colonic stricture

1995 ◽  
Vol 40 (2) ◽  
pp. 315-319 ◽  
Author(s):  
Michael H. E. Robinson ◽  
Timothy Wheatley ◽  
Ian H. Leach
Keyword(s):  
Antiinflammatory Drug ◽  
Nonsteroidal Antiinflammatory Drug ◽  
Colonic Stricture ◽  
Drug Induced
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