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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Idiopathic dyspepsia refers to pain and/or discomfort perceived in the epigastrium that is not secondary to organic, systemic, or metabolic diseases. Symptoms may overlap with those of gastroesophageal reflux disease and irritable bowel syndrome. Gastrointestinal motor disorders, hypersensitivity to mechanical or chemical stimuli, and psychosocial factors can act individually or in concert to induce the symptoms of dyspepsia. Accordingly, there is no single therapy, and treatment must be individualized. Eradication of Helicobacter pylori infection rarely achieves symptom improvement. Treatment of idiopathic dyspepsia should begin by reassuring the patient about the benign nature of the syndrome and educating them on the knowledge that has been achieved in recent years regarding potential causes of the syndrome. Both prokinetic and antisecretory drugs have been reported to improve dyspeptic symptoms, but results are not completely convincing. Although well-designed studies demonstrate superiority of proton pump inhibitors over placebo, it should be noted that patients with nonerosive gastroesophageal reflux disease were invariably included; when these patients are excluded, the benefit of antisecretory medications is questionable. We suggest that patients with idiopathic dyspepsia be initially treated according to the predominant symptom. Those with epigastric pain/burning should receive a trial with standard doses of proton pump inhibitors for 4 to 8 weeks, whereas prokinetic patients should be prescribed at recommended doses for similar periods of time to patients with nonpainful dyspeptic symptoms such as posprandial fullness, early satiety, nausea, or vomiting. Nonresponders may benefit from combination therapies or short trials with higher doses of drugs. Visceral analgesics and antidepressants can also be prescribed alone or in combinations with other therapeutic strategies. Recent studies demonstrate utility for psychologic therapy and hypnotherapy, although truly controlled studies are difficult in this area. Herbal medicines deserve further evaluation.
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PMID:Idiopathic Dyspepsia. 1576 39

Functional chest pain is a common, yet poorly understood entity. The focus of this review is to explore the evolving research and clinical approaches with a particular emphasis on the sensory or afferent neuronal dysfunction of the esophagus as a key player in the manifestation of this pain syndrome. Although once regarded as a psychologic or esophageal motility disorder, recent advances have shown that many of these patients have visceral hyperalgesia. Whether visceral hypersensitivity is a central or peripheral perturbation of the gut-brain axis remains debatable. Response to empirical therapy with high-dose proton pump inhibitors, upper endoscopy, or prolonged recording of esophageal pH may identify gastroesophageal reflux disease as a source of chest pain. Esophageal balloon distension study can serve as a useful test for identifying hypersensitivity. Newer techniques, including functional magnetic resonance imaging, magnetoencephalogram, and cortical evoked potentials, are being investigated. High doses of proton pump inhibitors and low doses of tricyclic antidepressants or trazadone remain the mainstay of therapy, although several new approaches including theophylline have been shown to be beneficial.
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PMID:Functional chest pain: nociception and visceral hyperalgesia. 1579 86

Chronic pain in the elderly is frequently a result of arthritic disorders, particularly osteoarthritis. The cyclo-oxygenase (COX)-2 inhibitors are as effective as standard NSAIDs for the relief of pain and for improving function in elderly patients with osteoarthritis and rheumatoid arthritis. COX-2 inhibitors increase the risk of serious gastroduodenal adverse reactions but there is evidence that they carry a lower risk for these adverse effects than standard NSAIDs, except when there is concurrent aspirin use. Since gastroduodenal disorders are the most frequently reported serious adverse effects of NSAIDs and these disorders occur more frequently in the elderly, COX-2 inhibitors offer an alternative to standard NSAIDs in this age group. However, they are not appropriate for many patients with cardiovascular and renal disease. The adverse reaction profile of the COX-2 inhibitors has confirmed the role of the COX-2 enzyme in renal function, salt and water homeostasis and the vascular endothelium. Thus, like standard NSAIDs, COX-2 inhibitors can cause renal failure, hypertension and exacerbation of cardiac failure. Of note is that these disorders are dose related. Thus, there are good reasons to avoid high doses of COX-2 inhibitors in the elderly. Clinical trials indicate that daily doses of rofecoxib 12.5 mg, celecoxib 100-200 mg, valdecoxib 10mg and etoricoxib 60 mg are the minimum effective doses of these agents. Data from the New Zealand Intensive Medicines Monitoring Programme indicate that celecoxib 200 mg/day and rofecoxib 25 mg/day are/were the most commonly prescribed doses and that 6% of patients had taken rofecoxib 50 mg/day for longer than recommended. Recent research indicates that COX-2 inhibitors have a thrombotic potential, especially in high doses and when use is prolonged, and this further limits the extent to which they can be used in the elderly. Important interactions with COX-2 inhibitors in the elderly include those with warfarin, which can result in loss of control of anticoagulation, and those with ACE inhibitors, angiotensin II type 1 receptor antagonists and diuretics, which can result in loss of control of blood pressure and cardiac failure and, in hypovolaemic conditions, renal failure. The clinical significance of an interaction between celecoxib and aspirin to reduce the antiplatelet effect of the latter drug is unknown. Preliminary information from spontaneous reporting systems indicates that there may be differences in the risk of cardiac failure and hypertension between standard NSAIDs and COX-2 inhibitors and between rofecoxib and celecoxib. More formal studies using equivalent doses are needed to test this observation. Use of COX-2 inhibitors may be considered in the elderly to reduce the risk of gastroduodenal complications associated with standard NSAIDs but only when consideration has first been given to use of less toxic medicines as alternatives or supplements, the appropriate dose of the COX-2 inhibitor or standard NSAID, the presence and possible impact of co-morbidities, and the implications of taking COX-2 inhibitors with any concomitant medications. Equally important is regular monitoring of the patient taking a COX-2 inhibitor for efficacy and adverse effects, and ensuring that the patient has a continuing need to keep taking the drug. Close attention also needs to be paid to intercurrent illnesses and new prescriptions that may reduce the safety of the COX-2 inhibitor. A standard NSAID plus a proton pump inhibitor may be equally effective as a COX-2 inhibitor in reducing the risk of gastroduodenal toxicity and if used the same prescribing advice applies. Current knowledge concerning the thrombotic potential of COX-2 inhibitors suggests that this combination, if tolerated, may be preferable to a COX-2 inhibitor, particularly where prolonged use is required. This knowledge also indicates that for patients with or at high risk of ischaemic heart disease or stroke, COX-2 inhibitors are contraindicated.
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PMID:Cyclo-oxygenase-2 inhibitors: when should they be used in the elderly? 1581 52

Non-steroidal anti-inflammatory drugs (NSAIDs) are indicated for treatment of rheumatoid arthritis and osteoarthritis, but often induce gastric adverse experiences (AE), including gastric ulcers and complications. Inhibitors of proton pump and H(2) antagonists are very effective for duodenal ulcer; meanwhile, cytoprotective drugs are more effective for gastric ulcer. D-002 is a mixture of higher aliphatic alcohols obtained from beeswax, wherein triacontanol is the most abundant. D-002 induces anti-ulcer effects through a cytoprotective mechanism, being more effective in protecting against ethanol- and NSAID-induced ulcers. The present double-blind, placebo-controlled clinical study was undertaken to investigate the effects of D-002 on gastric symptoms associated to piroxicam use on patients suffering osteoarthritis. Fifty-nine patients, all taking piroxicam, 20 mg/day, were randomized to placebo or D-002 (40 or 100 mg/day) for 14 days. The primary efficacy variable was the reduction on the frequency of patients with gastric AE compared with placebo. Pain evolution was investigated to discard any influence on D-002 on the analgesic effect of piroxicam. The frequency of patients treated with D-002, 40 and 100 mg/day, reporting acidity [0 of 18 (0%) and 1 of 21 (4.8%), respectively] was lower (P < .05) than in placebo [6 of 20 (30%)]. Also, the frequency of patients treated with 100 mg/day reporting some gastric AE [5 of 21 (23.8%)] was lower (P < .05) than in placebo [13 of 20 (65.0%)]. The analgesic effect of piroxicam was unaffected with D-002. Treatment was well tolerated. Two patients discontinued from the study because of gastrointestinal AE: one in the placebo group and the other treated with D-002, 40 mg/day. Other three patients discontinued because of other AE: mildly uncontrolled hypertension (one in the placebo group, one treated with D-002, 40 mg/day) and headache (one treated with D-200, 100 mg/day). It is concluded that D-002 could be useful for controlling gastric AE of patients treated with NSAIDs, although further studies with a larger sample size and longer follow-up are needed for definitive conclusions.
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PMID:Effects of D-002, a product isolated from beeswax, on gastric symptoms of patients with osteoarthritis treated with piroxicam: a pilot study. 1585 12

Pantoprazole is the third proton pump inhibitor (PPI) to be launched for the treatment of acid-peptic diseases. Like other drugs in this class, pantoprazole causes long-lasting inhibition of acid secretion by inactivating the parietal cell H+/K+-ATPase. Compared with H2 antagonists, pantoprazole results in faster pain relief, more rapid ulcer healing, healing of resistant ulcers and far greater efficacy in oesophageal reflux disease. The three PPIs currently available display almost identical efficacy in the treatment of acid-peptic diseases and when included as part of Helicobacter pylori eradication regimes. However, pantoprazole shows improvements in selectivity and pharmacokinetic properties compared with omeprazole and lansoprazole. The bioavailability of pantoprazole is considerably higher than omeprazole, remains constant upon repeated dosing, and is unaffected by food. Significantly, pantoprazole does not influence hepatic cytochrome P450 activity and does not therefore interact with co-administered drugs. This is in contrast to omeprazole, which inhibits P450, and lansoprazole, which appears to weakly induce multiple metabolic pathways. Although pantoprazole is entering an antisecretory market dominated by omeprazole and ranitidine, it has a number of potential advantages. In this respect it is worth recalling that enhanced specificity and the absence of drug interactions were decisive factors in determining market share in the H2 antagonist era. Pantoprazole may therefore achieve significant market penetration, particularly at the expense of lansoprazole and the H2 blockers.
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PMID:Pantoprazole: a new and more specific proton pump inhibitor. 1598 51

Functional heartburn (FH) is a common disorder that accounts for 30% to 50% of the patients with nonerosive reflux disease. FH is composed from a heterogeneous group of patients. They primarily include the hypersensitive and the nonacid sensitive esophagus. The mechanisms responsible for pain, clinical characteristics, and the optimal therapeutic approach of FH remain to be fully elucidated. Symptom response rate to potent antireflux treatment is significantly lower in FH patients as compared with any other gastroesophageal reflux disease (GERD) group, suggesting that in proton pump inhibitor (PPI) non-responders mechanisms other than acid reflux are likely the cause of symptoms. Patients with FH should be approached therapeutically as patients with GERD and should initially receive antireflux medications. Due to the need for profound acid suppression in this group of patients, PPIs should be considered relatively early in their care. Failure to respond to standard dosage of PPI is common and will require doubling the dose. If patients continue to report heartburn symptoms while receiving PPI twice daily, adding or switching to pain modulators/visceral analgesics is an appropriate therapeutic approach. Data about the usage of other therapeutic modalities in FH such as antireflux surgery, endoscopic treatment for GERD, and psychotherapy are still unavailable. Emerging treatment will likely include novel pain modulators and more effective antireflux medications.
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PMID:Functional heartburn. 1600 29

The close anatomical relations of the heart and oesophagus, and the similarity of symptoms attributable to disorders of either organ, often lead to diagnostic difficulty in patients with chest pain. A definitive diagnosis of non-cardiac chest pain attributable to oesophageal reflux or spasm is hampered, both by the need for prolonged ambulatory monitoring of pH, manometry, and endoscopy, and by the common occurrence of asymptomatic reflux and spasm, and the corresponding difficulty in linking an episode of reflux or spasm with an episode of pain. Moreover, some patients with non-cardiac chest pain and normal tests of oesophageal structure and function have centrally mediated hypersensitivity, both within and without the oesophagus. Rather than proceed with investigations, in the absence of symptoms to suggest structural disease of the oesophagus, it would be reasonable to attempt symptomatic treatment with a proton pump inhibitor or an antidepressant.
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PMID:The heart and the oesophagus: intimate relations. 1608 43

Recommendations for treatment with NSAIDs that take into account the latest study results must note that both the duration of treatment and the NSAID dose must be kept as small as possible. Elevated gastrointestinal risk is the rationale for the use of selective COX-2 inhibitors in place of conventional NSAIDs, or, where indicated, co-medication with a proton pump inhibitor. A manifest cardiovascular risk is aggravated by the use of coxibs, but probably also by the administration of traditional NSAIDs. Cardioprotective medication in the form of low-dose acetyl salicylic acid can probably reduce the cardiovascular risk, but at the same time increases the gastrointestinal risk. In such cases, proton pump inhibitors can offer some relief. However, the latter have no effect on the situation in the lower gastrointestinal tract. In patients with an elevated cardiovascular risk, the use of coxibs, and probably also NSAIDs for the treatment of pain, is problematical. The decision on what treatment to apply should be made on the basis of a benefit/risk assessment, and consideration should be given to alternative therapeutic strategies.
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PMID:[Recommendations for treatment with nonsteroidal anti-inflammatory drugs]. 1612 92

Nonsteroidal anti-inflammatory drugs (NSAIDs), including both traditional nonselective NSAIDs and the selective cyclo-oxygenase (COX)-2 inhibitors, are among the most widely used medications in the USA. Traditional NSAIDs, although effective at relieving pain and inflammation, are associated with a significant increase in the risk for gastrointestinal adverse events. Throughout the 1990s these events were estimated to result in approximately 100,000 hospitalizations and 16,500 deaths each year nationally. Recent studies have indicated that the risk for serious NSAID gastropathy has declined substantially during the past decade as a result of a number of factors, including lower doses of NSAIDs, the use of gastroprotective agents such as proton pump inhibitors and misoprostol, and the introduction of the selective COX-2 inhibitors. One therapeutic approach that may reduce the risk for gastrointestinal side effects associated with traditional NSAIDs while retaining their efficacy is the inclusion of co-therapy with a proton pump inhibitor; these agents inhibit acid secretion and have been demonstrated to promote ulcer healing in patients with NSAID-related gastric ulcers. Alternatively, COX-2 selective agents have been used to treat patients at high risk for such events. Both nonselective and selective COX-2 inhibitors have now been shown to be associated with an increased risk for cardiovascular events. These studies, together with the outcomes of the recent US Food and Drug Administration decision to require 'black box' warnings regarding potential cardiovascular risks associated with NSAIDs, suggest that the use of COX-2 inhibitors as the sole strategy for gastroprotection in patients with arthritis and other pain syndromes must be reconsidered, particularly among those at risk for cardiovascular events.
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PMID:Current state of therapy for pain and inflammation. 1616 76

Conventional 'nonselective' nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used for the treatment of pain and inflammation; however, the potential gastrointestinal risks associated with their use can be a cause for concern. In response to the adverse effects that can accompany nonselective NSAID use, selective cyclo-oxygenase (COX)-2 inhibitors were developed to target the COX-2 isoenzyme, thus providing anti-inflammatory and analgesic benefits while theoretically sparing the gastroprotective activity of the COX-1 isoenzyme. Data from large-scale clinical trials have confirmed that the COX-2 inhibitors are associated with substantial reductions in gastrointestinal risk in the majority of patients who do not receive aspirin. However, some or all of the gastrointestinal benefit of COX-2 inhibitors may be lost in patients who receive low, cardioprotective doses of aspirin, and recent evidence suggests that some of these agents, at some doses, may be associated with an increased risk for cardiovascular adverse events compared with no therapy. The risks and benefits of conventional NSAIDs and of COX-2 inhibitors must be weighed carefully; in clinical practice many patients who might benefit from NSAID or COX-2 therapy are likely to be elderly and at relatively high risk for gastrointestinal and cardiovascular adverse events. These patients are also more likely to be taking low-dose aspirin for cardiovascular prophylaxis and over-the-counter NSAIDs for pain. Identifying therapies that provide relief from arthritis related symptoms, confer optimum cardioprotection, and preserve the gastrointestinal mucosa is complex. Factors to consider include the interference of certain NSAIDs with the antiplatelet effects of aspirin, differences in the adverse gastrointestinal event rates among nonselective NSAIDs and selective COX-2 inhibitors, emerging data regarding the relative risks for cardiovascular events associated with these drugs, and the feasibility and cost of co-therapy with proton pump inhibitors.
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PMID:Cardiovascular and gastrointestinal effects of COX-2 inhibitors and NSAIDs: achieving a balance. 1616 77


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