High blood pressure. Causes, symptoms, treatments

Susceptibilities of 540 anaerobic gram-negative bacilli to amoxicillin, amoxicillin-BRL 42715, amoxicillin-clavulanate, temafloxacin, and clindamycin.


In this 6-week double-blind, active comparator controlled, parallel-group study eligible osteoarthritis patients were randomised to receive either etoricoxib 60 mg once daily (n = 256) or diclofenac 50 mg three times daily (n = 260). The primary study endpoint was the Western Ontario McMaster osteoarthritis index (WOMAC) pain subscale. Other endpoints included were the WOMAC stiffness and physical function subscales, and the Patient's Global Assessment of Response to Therapy (PGART) questionnaire. Early efficacy was evaluated using WOMAC first question (pain walking on a flat surface) and PGART 4 h after the morning dose of each drug on days 1 and 2. Rescue medication (paracetamol) used was also recorded. The study was designed to show comparable efficacy between etoricoxib 60 mg once daily and diclofenac 50 mg three times daily with respect to the primary endpoint and was conducted outside the United States at 67 centres in 29 countries.

A total of 23 504 patients were randomized with mean treatment duration from 19.4 to 20.8 months. The thrombotic CV risk hazard ratio (HR) (etoricoxib to diclofenac) was 0.96 (95% CI 0.81, 1.15), consistent with non-inferiority of etoricoxib to diclofenac. The cumulative gastrointestinal (GI)/liver adverse events (AEs) discontinuation rate was significantly lower for etoricoxib than diclofenac in each patient cohort; HR (95% CI) of 0.46 (0.39, 0.54), 0.52 (0.42, 0.63) and 0.49 (0.39, 0.62) for the 60 mg OA, 90 mg OA and RA cohorts. The maximum average change in systolic blood pressure (BP) with etoricoxib was 3.4-3.6 mmHg (diastolic BP: 1.0-1.5 mmHg), while diclofenac produced a maximum average change of 0.9-1.9 mmHg (diastolic BP: 0.0-0.5 mmHg). Both agents resulted in similar efficacy regardless of etoricoxib dose.

We assessed 31 adults (21 women and 10 men) who reported one or more adverse reactions to NSAIDs, manifested as cutaneous, respiratory or anaphylactic symptoms. Sixteen of them reported reactions to a single NSAID (single reactors) and 15 to more than one NSAID (multiple reactors); the most frequently involved drug was acetylsalicylic acid. First, each patient underwent allergologic tests (skin and/or oral challenge tests) with culprit NSAIDs and then tolerability tests with increasing doses of etoricoxib up to 120 mg. All challenges were performed under single-blind, placebo-controlled conditions.

The discovery of the two isoenzymes of cyclooxygenase COX-1 and COX-2 and their separate functions, localization and regulation, has initiated the search for new and more selective inhibitors of prostaglandin biosynthesis. Selective COX-2 inhibitors were developed in order to improve an anti-inflammatory and analgesic specificity and potency. The role of inducible COX-2 at the peripheral site of inflammation is well known. The discovery of COX-2 in the spinal cord suggests that it is responsible for spinal prostaglandin release in nociceptive processes following a peripheral inflammatory stimulus. In the future, selective COX-2 inhibitors such as celecoxib (GD Searle & Co), rofecoxib (Merck & Co Inc) and the recently developed etoricoxib (Merck & Co Inc) may play an important role in the treatment of a wider range of pain conditions in addition to their present use as anti-inflammatory and analgesic drugs.

To compare the efficacy of oral etoricoxib and placebo combined with paracervical block for pain relief during fractional curettage

Etoricoxib 90 mg demonstrated a significantly lower risk for discontinuing treatment due to GI AEs compared with diclofenac 150 mg. Discontinuations from renovascular AEs, although less common than discontinuations from GI AEs, were significantly higher with etoricoxib.

Both drugs caused a reduction in WOMAC and VAS scores for pain and the severity of the disease. Etoricoxib demonstrated a significantly high rate of occurrence and completeness of its analgesic effect. Meloxicam showed a less pronounced decrease in joint stiffness and an insufficient analgesic effect. The incidence of side effects was similar in both groups.

We performed a systematic literature review of randomised controlled trials of NSAIDs in patients with active AS. We included trials that reported efficacy at 2-12 weeks. Efficacy outcomes were the change in pain score and change in the duration of morning stiffness. We also examined the number of adverse events. We used Bayesian network meta-analysis to compare effects directly and indirectly between drugs.

Postoperative pain is an adverse effect of periodontal surgeries and may therefore be prevented or minimized. This study was conducted to evaluate the clinical efficacy of two selective cyclooxygenase-2 inhibitors, celecoxib and etoricoxib, on pain prevention after periodontal surgery.

Etoricoxib alleviates and prevents acute pain. The hypothesis of our study was that the pre-operative use of etoricoxib would reduce the post-operative need for additional pain treatment.

We assessed the effects of equipotent analgesic doses of celecoxib, rofecoxib, valdecoxib, etoricoxib and lumiracoxib and of the NSAIDs, diclofenac and naproxen, on postpartum kidney development in mice, from postnatal day 1 (P1) to P21.