Long-term Use Of NSAIDs Research Articles

Oxycodone/Ibuprofen Combination Tablet

Oxycodone/ibuprofen 5 mg/400 mg (Combunox) is an oral fixed-dose combination tablet with analgesic, anti-inflammatory and antipyretic properties. It is approved in the US for the short-term (up to 7 days) management of acute, moderate-to-severe pain and is the first and only fixed-dose combination containing ibuprofen and oxycodone. A single dose of oxycodone/ibuprofen 5 mg/400 mg provided better analgesia than low-dose oxycodone or ibuprofen administered alone in most trials and appears to be more effective than a single dose of some other fixed-dose combination analgesics. It is generally well tolerated after single or multiple doses and short-term use is not expected to produce any of the serious adverse effects typically associated with the long-term use of opioids or NSAIDs. Thus, oxycodone/ibuprofen 5 mg/400mg is an effective, convenient treatment option for the short-term management of acute, moderate-to-severe pain.

Long-term use of NSAID reduces the risk of oral cancer

1004 Background: Oral cancer is a tobacco-related cancer, with high morbidity and mortality. Although there is evidence of a possible protective effect of aspirin on oesophageal cancer, only scattered data exist on its role on cancer of the oral cavity or larynx. Methods: We performed a population-based nested case-control study by combining data from the Norwegian Institute of Public Health and the Norwegian Cancer Registry. Among persons accrued to the health survey in the period 1975–1990, 3275 persons at high risk for oral cancer, as judged by their tobacco habits, were identified through the databases of a population based national health survey, and the occurrence of carcinomas in this group was assessed through cross-linking with the database of the Norwegian cancer Registry. Additional information regarding smoking habits, medication, age, sex and comorbidity was entered in the database of the Norwegian Institute of Public Health. Results: Among the 3275 persons identified to be at risk of oral cancer, 496 were identified with a squamous cell carcinoma of the oral cavity. 496 matches controls were identified among the other 2779 person identified to be at risk of oral cancer. The hazard ration for developing oral cancer was. Among the 992 person included in the analysis (496 person from the case group and 496 person from the matched control group), 690 did not have a history of long-term NSAID use, while 302 did. The hazard ratio for developing oral cancer was 0.53 among the person who used NSAIDs. This cancer protective effect was time dependent, with hazard ratios of 0.61, 0.55, and 0.42 in person who had used NSAIDs for 6 to 12 months, 1 to 5 years, and more than 5 years, respectively. Conclusions: The long-term use of NSAIDs seems to have a protective effect on the incidence of squamous cell carcinomas of the oral cavity. Author Disclosure Employment or Leadership Consultant or Advisory Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Pfizer Pfizer Pfizer

NSAIDs and enantiomers of flurbiprofen target gamma-secretase and lower Abeta 42 in vivo.

Epidemiologic studies demonstrate that long-term use of NSAIDs is associated with a reduced risk for the development of Alzheimer disease (AD). In this study, 20 commonly used NSAIDs, dapsone, and enantiomers of flurbiprofen were analyzed for their ability to lower the level of the 42-amino-acid form of amyloid beta protein (Abeta42) in a human H4 cell line. Thirteen of the NSAIDs and the enantiomers of flurbiprofen were then tested in acute dosing studies in amyloid beta protein precursor (APP) transgenic mice, and plasma and brain levels of Abeta and the drug were evaluated. These studies show that (a). eight FDA-approved NSAIDs lower Abeta42 in vivo, (b). the ability of an NSAID to lower Abeta42 levels in cell culture is highly predicative of its in vivo activity, (c). in vivo Abeta42 lowering in mice occurs at drug levels achievable in humans, and (d). there is a significant correlation between Abeta42 lowering and levels of ibuprofen. Importantly, flurbiprofen and its enantiomers selectively lower Abeta42 levels in broken cell gamma-secretase assays, indicating that these compounds directly target the gamma-secretase complex that generates Abeta from APP. Of the compounds tested, meclofenamic acid, racemic flurbiprofen, and the purified R and S enantiomers of flurbiprofen lowered Abeta42 levels to the greatest extent. Because R-flurbiprofen reduces Abeta42 levels by targeting gamma-secretase and has reduced side effects related to inhibition of cyclooxygenase (COX), it is an excellent candidate for clinical testing as an Abeta42 lowering agent.

Long-term NSAID use, especially with non-aspirin agents, reduces the risk of low cognitive function in elderly women,

Long-term NSAID use, especially with non-aspirin agents, reduces the risk of low cognitive function in elderly women,

Esomeprazole improves quality of life in patients with upper GI symptoms associated with long-term NSAID therapy

Purpose: Upper gastrointestinal (G1) symptoms such as abdominal pain and heartburn occur in up to 40% of NSAID users, which significantly impacts on their health-related quality of life (HRQL). This muhicenter, double-blind study compared the effects of esomeprazole and placebo on HRQL in a non-ulcer population with upper Gl symptoms associated with continuous NSAID use. Methods: 608 patients with upper Gi symptoms of at least moderate seventy associated with continuous daily NSAID treatment were randomized to receive esomeprazole 20 mg (n = i95) or 40 mg (n = 206), or placebo (n = 207), once daily for up to 4 weeks. Patients were excluded if they had gastric or duodenal ulcers, were Helicobacter pylori-positive or had erosive esophagitis. HRQL assessments were made at baseline and the last study visit using the Quality of Life in Reflux and Dyspepsia (QOLRAD) instrument, the Gastrointestinal Symptom Rating Scale (GSRS) and the Short Form-36 (SF-36). Results: On the SF-36, the study population scored significantly lower on all dimensions than reference populations of healthy individuals or patients with GERD, and on the dimensions of mental health, role emotional and general health compared with a reference population of patients with arthritis. Esomeprazole significantly improved HRQL on the QOLRAD (increased scores) and GSRS dimensions (decreased scores) a priori specified (Table 1). In addition, both doses of esomeprazole produced greater improvements compared with placebo in the vitality and physical/social functioning QOLRAD dimensions and the diarrhea and constipation GSRS dimensions. Conclusion: Treatment with esomeprazole 40 mg or 20 mg equally improves important aspects of HRQL in patients with upper G[ symptoms associated with long-term NSAID use. Data from the SF-36 confirm that in such patients, in addition to the impact of ~fie underlying condition requiring NSAID therapy, NSAID-induced upper GI symptoms contribute to further worsening of HRQL

Review: Misoprostol, double-dose H2-receptor antagonists, and proton-pump inhibitors reduce GI ulcers in long-term NSAID use

Review: Misoprostol, double-dose H₂-receptor antagonists, and proton-pump inhibitors reduce GI ulcers in long-term NSAID use

Underestimated adverse effects of non-steroidal anti-inflammatory drugs on the distal intestine

NSAID-induced adverse effects are diagnosed less frequently in the distal intestine than in the gastroduodenal area. During long-term NSAID use, however, the development of life-threatening ulcerations, perforations or fibrotic stenoses must be expected from the middle segment of the small intestine to the rectum. Although the clinical symptoms are not specific, together with careful examination, endoscopy, contrast x-ray studies, or computed tomography they can provide orientation, at least with regard to stenotic processes. Diarrhea, weight loss, anorexia, irregular bowel movements, obstruction symptoms, ocoult blood loss, hypoalbuminemia, and iron deficiency may be regarded as possible signs of gastrointestinal adverse effects associated with long-term NSAID therapy. Except in the case of NSAID suppository abuse, no risk indicators are known. The pathogenesis of NSAID-induced adverse effects in the lower gastrointestinal tract has not been elucidated. As the potential of nonselective NSAIDs to cause adverse effects in distal segments of the small intestine cannot be reliably reduced by prophylactic measures in the upper gastrointestinal tract such as comedication with prostaglandin analogs or proton pump inhibitors, the indication for the use of conventional NSAIDs, in any case, must be considered with caution.

Long-term NSAID use does not prevent gallstone disease

Long-term NSAID use does not prevent gallstone disease

ACUTE HEMORRHAGIC GASTRITIS

Acute hemorrhagic gastritis is an important cause of upper gastrointestinal bleeding, accounting for approximately one fourth of UGI bleeding in endoscopic studies. Most patients with hemorrhagic gastritis have underlying predisposing conditions, such as alcohol abuse, portal hypertension, short- or long-term NSAID use, and physiologic stress associated with hospitalization in an ICU for severe life-threatening disease or trauma. The key to management is prevention; however, once established, hemorrhagic gastritis is treated with both supportive measures and measures directed toward healing the mucosal damage. In general, therapy is the same as that for classic peptic ulcer disease. These patients present a challenge, however, because of their underlying diseases and because of the potential for diffuse mucosal bleeding, the latter making the use of endoscopic therapy more difficult. Surgery is an option of last resort for the patient who continues to bleed despite aggressive medical and endoscopic therapy. Future investigations will focus on pharmacologic therapy to enhance mucosal defense mechanisms, therapy that will likely attain increasing importance in the years to come.