ACE Inhibitor–Induced Angioedema

Much has been written about hereditary angioedema (HAE) in recent literature; however, the prevalence of angiotensin-converting enzyme inhibitor–induced angioedema (ACEiIA) far exceeds that of HAE. Similarly, multiple therapies have been developed for HAE, yet no definitive therapy is available for ACEiIA. In this article, we discuss the mechanism, prevalence, pathophysiology, and management of ACEiIA, with focus on newer therapies recently approved for HAE and how they may be effective for ACEiIA.     

Major Cardiac–Psychiatric Drug–Drug Interactions: a Systematic Review of the Consistency of Drug Databases

Cardiovascular Drugs and Therapy - Major depressive disorder (MDD) and anxiety disorders (AD) are both highly prevalent among individuals with arrhythmia, ischemic heart disease, heart failure,...     

Therapeutic Effects of Ecabet Sodium,an Antiulcer Drug,on Dextran Sodium Sulfate–Induced Ulcerative Colitis in Rats

Ecabet, an antiulcer drug, is reported to be effective in patients with ulcerative colitis. We investigated the effect of ecabet enema on ulcerative colitis in rats and some mechanisms underlying this effect. In vivo ecabet enema showed a therapeutic effect in the rat ulcerative colitis model induced by dextran sodium sulfate in the drinking water. The amount of ecabet bound to damaged mucosa was higher than that bound to normal mucosa 30 min after intrarectal administration. In vitro ecabet accelerated the restitution of epithelial cells, which was not affected by a TGF- antibody. Ecabet inhibited the leukotriene B₄ production and 5-lipoxygenase activity in human neutrophils. In conclusion, ecabet enema showed a therapeutic effect in rats with ulcerative colitis. This effect may be attributable to the high binding affinity for damaged mucosa, the acceleration of restitution, and the inhibition of leukotriene B₄ production.     

Does Helicobacter pylori Exacerbate Gastric Mucosal Injury in Users of Nonsteroidal Anti-Inflammatory Drugs? A Multicenter,Retrospective, Case-Control Study

Background/Aims

The interaction between nonsteroidal anti-inflammatory drugs (NSAIDs) and Helicobacter pylori remains controversial. We retrospectively investigated whether H. pylori infection exacerbates severe gastric mucosal injury among chronic NSAID users.

Methods

From January 2010 to December 2013, a total of 245 long-term NSAID (including low-dose aspirin) users who had undergone an esophagogastroduodenoscopy and had been evaluated for H. pylori infection were enrolled at Okayama University Hospital and Tsuyama Chuo Hospital. The degree of gastric mucosal injury was assessed according to the modified Lanza score (MLS). Severe gastric mucosal injury was defined as an MLS ≥4. Univariate and multivariate logistic regression analyses were performed.

Results

In the univariate analysis, age ≥75 years (odds ratio [OR], 2.4; 95% confidence interval [CI], 1.3 to 4.2), H. pylori-positivity (OR, 2.0; 95% CI, 1.2 to 3.5), and the concomitant use of proton pump inhibitors (PPIs) (OR, 0.48; 95% CI, 0.26 to 0.86) were significantly associated with severe gastric mucosal injury. The multivariate analysis was adjusted by age and sex and demonstrated that H. pylori-positivity (OR, 1.8; 95% CI, 1.0 to 3.3) and the concomitant use of PPIs (OR, 0.53; 95% CI, 0.28 to 0.99) significantly contributed to severe gastric mucosal injury.

Conclusions

H. pylori infection exacerbates severe gastric mucosal injury among chronic NSAID users.     

Porcine Ileitis Model Induced by TNBS–Ethanol Instillation

Nine young pigs were used to evaluate the ability of an trinitrobenzene sulfonic acid–ethanol (TNBS–EtOH) mixture, in varying combinations, to induce ileitis comparable to that caused by intraintestinal instillation in other species. The distal ileum was accessed via laparotomy in anesthetized animals and the TNBS–EtOH was instilled via hypodermic needle. In three pigs in which the instillate was not held within an ileal segment, there were no ileal lesions noted upon necropsy at two weeks after instillation. In all six pigs in which the instillate was confined to a 10-cm length of distal ileum for 10–15 min, there was definite gross and histologic evidence of severe ileitis upon necropsy at one week after instillation. The histopathology was more consistent with Th-1- than Th-2-mediated inflammation.