Avoidance Of Nonsteroidal Anti-inflammatory Drugs Research Articles

Peptic ulcer disease

The introduction of the Maastricht 2-2000 document provides some guidance with regard to the management of Helicobacter pylori infection in both primary and specialist practice settings, albeit primarily in the European setting. The putative role of H. pylori in gastric carcinogenesis was supported by a further study. Studies on the natural history of peptic ulcer disease (PUD) highlight the particular vulnerability of the elderly patient to PUD and its complications, and focus attention on targeted intervention in this group, particularly the avoidance of nonsteroidal antiinflammatory drugs (NSAID). Little has evolved with regard to the introduction of new NSAID, but reports indicate the potential association of cyclooxygenase-2 (COX 2)-selective agent use with an increased risk of cardiovascular events. The role of H. pylori and NSAID as risk factors for peptic ulcer disease and its complications is again explored, and both meta-analysis and clinical studies provide some evidence of their synergistic effect. The introduction of esomeprazole, the S-isomer of omeprazole, has widened the clinician's therapeutic choice; the true value of this agent remains to be determined.

Tolerance induction to rofecoxib in a patient with Bartter's syndrome

Rationale We performed a desensitization to rofecoxib in a patient with Bartter's syndrome (inherited renal defective salt reabsorption) and multiple drug intolerance syndrome. Methods A 28-year-old woman Bartter's syndrome had manifested generalized erythema and itching after taking rofecoxib (12.5 mg) and other anti-inflammatory drugs, despite a preventive antireactive therapy (loratadine 10 mg, cromolyn sodium 500 mg). Avoidance of non-steroidal anti-inflammatory drugs was recommended. Since she needed a COX II-inhibitor for Bartter's syndrome management, after a preliminary evaluation (negative prick and patch tests) we attempted a desensitization to rofecoxib, according to a new original protocol, on the basis of our encouraging previous experiences dealing with drug desensitization. Oral 8-day desensitizing treatment to rofecoxib was performed starting with an initial dose of 1 ml of a rofecoxib solution (2.5 mg/mL) diluted 1:10 5, progressively decreasing dilutions until the 6th day, when patient took 10 mL of the pure solution (25 mg); she received a cumulative dose of 37.5 mg on the 7th day and of 50 mg of rofecoxib on the 8th day. When the desensitization was completed, she went on taking 50 mg a day. Antihistamine medication (loratadine 10 mg/die) was administered during the treatment. Results The desensitization was well tolerated, without side effects, and the therapeutic daily dose (50 mg) has been rapidly reached (8 days). Conclusions In case of intolerance to rofecoxib, clinical tolerance induction, by our desensitizing protocol, can represent an useful tool.

Right dorsal colitis in the horse: minireview and reports on three cases in Ireland

Right dorsal colitis (RDC) is an ulcerative inflammatory bowel disorder of the horse that has been associated with the administration of non-steroidal anti-inflammatory drugs (NSAIDs), particularly in horses treated when dehydrated or toxaemic. The acute form of RDC may result in profuse diarrhoea, severe colic, dehydration, endotoxic shock and even death; the chronic form may be manifest by mild to moderate intermittent colic, ventral oedema and weight loss with or without diarrhoea. The most consistent laboratory findings are anaemia, hypoproteinaemia, hypoalbuminaemia and hypocalcaemia. Medical management of RDC requires avoidance of NSAIDs, of stressful experiences and of large-volume diets. Specific medications such as sucralfate and metronidazole have been used to treat RDC in the horse. The use of dietary additions such as psyllium and corn oil has been mentioned in the literature.RDC has not been reported previously in Ireland or Britain; here we report that the condition was diagnosed in three horses in Ireland on the bases of a history of phenylbutazone therapy, clinical signs, clinical pathology and ultrasonography. In two of the three horses the diagnosis was confirmed by direct inspection of the affected colon at celiotomy.

Patient's view of heart failure: from the understanding to the quality of life.

Non-pharmacological management is one of heart failure treatment cornerstones. Despite its importance several studies showed lack of clinical advising by medical staff as well as poor patient compliance to education and pharmacological treatment. Hospitalizations and symptoms of heart failure negatively influence patients' quality of life. In Slovenia there is a scarcity of non-pharmacological management and quality of life data in heart failure patients. We wanted to obtain data on heart failure patient's quality of life and their satisfaction with management of the condition in Slovenia. During 6 weeks, patients from one university and two community Slovenian hospitals were prospectively enrolled to the EuroHeart survey. We invited 415 patients (mean age 70.6+/-11.4 years, 53% men) to attend an interview 12 weeks after the discharge. Out of 415 eligible patients 25 (6%) died during follow up period and 187 (45%) attended the interview. Twenty-three percent of them were re-hospitalized. Vast majority (89%) of interviewed patients were aware of their heart condition but only 61% were satisfied with the explanation of their clinical condition given by medical staff. On average they were taking 6.3+/-2.3 drugs. General clinical advice (salt intake 65%, cholesterol or fat intake 63%) was more common than specific (daily weighing 35%, avoidance of non-steroidal anti-inflammatory drugs 17%). Patients reported high adherence as only 3% of given advice were neglected. Symptoms of heart failure were much less common at rest than during daily activity (breathlessness in 20% and 78%, fatigue in 18% and 81%, respectively). Psychological symptoms as anxiety (70%), depression (50%) and stress (48%) were common, as well as cognitive and sleep disturbances, both present in more than half of the patients. Patients with heart failure experienced restrictions in quality of life and psychological status. Non-pharmacological and pharmacological management and patient's satisfaction with medical care were below optimal. Educational strategies for medical staff and patients as well as organization of an out-patient setting in community hospitals are needed.

Peptic ulcer disease

The introduction of the "Maastricht 2-2000" document provides some guidance with regard to the management of Helicobacter pylori infection in both primary and specialist practice settings, albeit primarily in the European setting. The putative role of H. pylori in gastric carcinogenesis was supported by a further study. Studies on the natural history of peptic ulcer disease (PUD) highlight the particular vulnerability of the elderly patient to PUD and its complications, and focus attention on targeted intervention in this group, particularly the avoidance of nonsteroidal antiinflammatory drugs (NSAID). Little has evolved with regard to the introduction of new NSAID, but reports indicate the potential association of cyclooxygenase-2 (COX 2)-selective agent use with an increased risk of cardiovascular events. The role of H. pylori and NSAID as risk factors for peptic ulcer disease and its complications is again explored, and both meta-analysis and clinical studies provide some evidence of their synergistic effect. The introduction of esomeprazole, the S-isomer of omeprazole, has widened the clinician's therapeutic choice; the true value of this agent remains to be determined.

Drug-induced congenital defects: strategies to reduce the incidence.

Approximately 1% of congenital anomalies relate to pharmacological exposure and are. in theory, preventable. Prevention consists of controlled administration of drugs known to have teratogenic properties (e.g. retinoids, thalidomide). When possible, prevention could take the form of the use of alternative pharmacological therapies during the pre-conception period for certain specific pathologies, selecting the most appropriate agent for use during pregnancy [e.g. haloperidol or a tricyclic antidepressant instead of lithium; anticonvulsant drug monotherapy in place of multitherapy; propylthiouracil instead of thiamazole (methimazole)], and substitution with the most suitable therapy during pregnancy (e.g. insulin in place of oral antidiabetics; heparin in place of oral anticoagulants; alpha-methyldopa instead of ACE inhibitors). Another strategy is the administration of drugs during pregnancy taking into account the pharmacological effects in relation to the gestation period (e.g. avoidance of chemotherapy during the first trimester, avoidance of nonsteroidal anti-inflammatory drugs in the third trimester, and avoidance of high doses of benzodiazepines in the period imminent to prepartum).

Genetics of aspirin induced asthma

Aspirin induced asthma (AIA) is more common in women than in men. The first symptoms of the disease are often a viral respiratory infection which is followed by a prolonged...

Clinical features and diagnosis of aspirin induced asthma

Although for therapeutic reasons it has become convenient to consider asthma as a single disease entity, this clearly is not the case, with many variants occurring. From a clinical standpoint,...

Prevention of the gastrointestinal adverse effects of nonsteroidal anti-inflammatory drugs: the role of proton pump inhibitors.

The associations between nonsteroidal anti-inflammatory drugs (NSAIDs) and the presence and complications of gastroduodenal erosions and ulcers are well established. Evidence that acid aggravates NSAID-induced injury provides a rationale for minimising such damage by acid suppression. Other strategies discussed include avoidance of NSAIDs or minimising their dosage, selecting NSAIDs known to cause less damage, and co-prescription of various agents. Cytoprotection with misoprostol, a prostaglandin analogue, has been shown to be effective in reducing NSAID-related peptic ulcers and their complications. Unfortunately, adverse effects may limit compliance in some patients. Histamine H2 antagonists have only limited efficacy in the prevention of NSAID-induced ulcers in humans, particularly in the stomach, except at higher than standard dosages. This may relate to their relatively modest effect in elevating gastric pH, especially in comparison with proton pump inhibitors. Several studies now confirm the efficacy of proton pump inhibitors in the short and longer term prevention of NSAID-induced upper gastrointestinal injury. Placebo-controlled studies suggest reductions of over 70% in gastric and duodenal ulcer rates over 3 to 6 months. The recent ASTRONAUT (Acid Suppression Trial: Ranitidine versus Omeprazole for NSAID-Associated Ulcer Treatment) study documented the greater prophylactic efficacy of omeprazole over ranitidine at standard dosages for 6 months. The OMNIUM (Omeprazole versus Misoprostol for NSAID-Induced Ulcer Management) study showed omeprazole to be slightly more effective overall than misoprostol in preventing the upper gastrointestinal adverse effects of NSAIDs, with both substantially more effective than placebo, although misoprostol was somewhat less well tolerated. Although substantial reductions in NSAID ulceration are now achievable when co-therapy with a proton pump inhibitor is given, a few patients will still develop ulcers and their complications. Hence the judicious use of NSAIDs in the first instance cannot be overemphasised.

The role of acid in upper gastrointestinal haemorrhage due to ulcer and stress-related mucosal damage.

A peptic ulcer is a lesion in which acid and pepsin are essential components of pathogenesis. Regardless of the type of patient or the setting in which the ulcer presents, the basic pathogenetic scheme is the same. The primary event is disruption of mucosal integrity. In the presence of acid and pepsin, such disruption of integrity leads to an ulcer. While rarely sufficient by itself to cause ulceration, the presence of acid is a necessary cofactor. The causes of disruption of mucosal integrity include nonsteroidal anti-inflammatory drugs (NSAIDs), Helicobacter pylori and critical illness. With the latter, tissue ischaemia may be the primary event, leading to back-diffusion of H+ ions through increased membrane permeability. Impaired mucosal buffering then leads to intramural acidosis and cell death. Risk factors for bleeding peptic ulcer in the intensive care unit (ICU) include severe trauma, sepsis, respiratory failure, and coagulopathy. Potential roles for decreasing gastric acidity in the treatment of bleeding peptic ulcer include cessation of active bleeding, prevention of rebleeding in hospital and primary prevention of bleeding. Most published studies dealing with the first two situations suggest no benefit with antisecretory therapy. However, the optimal pH for clot and platelet function may be > or = 7.0. Can such pH levels be maintained with antisecretory agents such as the proton pump inhibitors? Are the published trials adequate to demonstrate any benefit from antisecretory agents? Primary prevention of bleeding ulcer in the outpatient setting includes avoidance of NSAIDs, use of antisecretory agents and eradication of H. pylori.(ABSTRACT TRUNCATED AT 250 WORDS)