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

Patients with gastro-oesophageal reflux disease (GORD) who are not responding to proton pump inhibitors (PPIs) given once daily are very common. Various underlying mechanisms have been shown to contribute to the failure of PPI treatment. These include weakly acidic reflux, duodenogastro-oesophageal reflux, residual acid reflux and functional heartburn, as well as others. Diagnostic evaluation of patients with GORD who have failed PPI treatment may include an upper endoscopy, pH testing and oesophageal impedance with pH monitoring. Commonly, doubling the PPI dose or switching to another PPI will be pursued by the treating physician. Failure of such a therapeutic strategy may result in the addition of a transient lower oesophageal sphincter reducer or pain modulator. Anti-reflux surgery may be suitable for a subset of carefully studied patients.
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PMID:Management of heartburn not responding to proton pump inhibitors. 1913 23

H(2)-receptor blockers and proton pump inhibitors are now used extensively to control gastric and duodenal ulcer, inflammation and pain, but these drugs have limitations and are not always affordable. The development of novel nontoxic antiulcer drugs, including from medicinal plants, is therefore desirable, and Azadirachta indica A. Juss, commonly known as Neem, is known to have potent gastroprotective and antiulcer effects. This review deals with the pharmacological and biochemical studies carried out regarding the antiulcer activities of Neem extracts and their mechanism of action, including the inhibition of acid secretion. A comparison with ranitidine and omeprazole in some animal models has been included and clinical studies, where available, have also been incorporated, along with a safety evaluation. Neem bark extract has the potential for the development of novel medicines for the therapeutic control of gastric hyperacidity and ulcer.
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PMID:The use of neem for controlling gastric hyperacidity and ulcer. 1914 Jan 19

Functional heartburn is considered one of the most common functional esophageal disorders. The disorder is more common in young women and is associated with other functional bowel disorders and psychological co-morbidity, primarily somatization. The etiology of functional heartburn remains unknown. Most patients, however, demonstrate esophageal hypersensitivity. Functional heartburn has been identified as the main cause for proton pump inhibitor (PPI) failure in patients with heartburn. Treatment is still a challenge, and patients should be started with PPI treatment. In non-responders, escalation of the PPI dose could be attempted and, if unsuccessful, pain modulators should be prescribed.
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PMID:Functional heartburn: what it is and how to treat it. 1923 78

Proton pump inhibitor (PPI) failure is very common and may affect up to one-third of the PPI consumers. Identifying the underlying mechanisms for PPI failure in each individual patient is essential for treatment success. For residual acid reflux, increasing the PPI dose to twice daily; switching to another PPI, or adding an histamine 2 receptor antagonist could be a successful therapeutic strategy. In patients with duodenogastroesophageal reflux, weak acidic/alkaline reflux and hypersensitivity to acid reflux, therapeutic modalities that reduce transient lower esophageal sphincter relaxation or visceral pain could be entertained. Treatment of PPI failure due to delayed gastric emptying should be focused on improving gastric motor activity. Psychological management may supplement any medical or surgical approach toward PPI failure.
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PMID:Proton pump inhibitor failure--what are the therapeutic options? 1926 45

Gastroesophageal reflux (GER) is a common problem in infants but the distinction between GER and GER disease remains difficult. Clinical manifestations such as vomiting, poor weight gain, respiratory disorders, and apneas do always not correlate with the demonstration of reflux episodes. Premature infants frequently suffer from reflux but correlations with apneas are also poor. Esophagitis is a complication suggested in infants experiencing pain but reflux by itself can induce pain as well. The "gold" diagnosis test is pH recording; however, overlap between normal and abnormal indices is obvious. Impedance measurement demonstrates more reflux episodes but non-acid reflux harm is not established. GER disease is probably self-limited in most infants, although it is impossible to predict whether some of them continue to have GER in adult life. The treatment raises doubts concerning indications and efficacy. Overprescription is frequent in infants with regurgitations. Nonpharmacological treatment - small-volume thickened milk and correct positioning - should be the first-line treatment. Prokinetic drugs have not proved their efficacy. Among anti-acid drugs, proton pump inhibitors are the best choice, but their indications are not very clearly established for infants. On the other hand, considerable variations of their metabolism due to the patients' age and genetic factors can explain variations in therapeutic effects.
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PMID:[Gastroesophageal reflux in infants: myths and realities]. 1930 64

Pain medication should be based on patient's needs and risk profile. Age > 65 years, prior ulcer, co-morbidities, large daily dose, Helicobacter pylori infection, concurrent use of glucocorticoids, serotonin re-uptake inhibitors, or warfarin increase the risk of upper gastrointestinal bleeds. As a preventive strategy the use of concurrent proton pump inhibitors with non-selective NSAIDs is recommended. It is also possible to use COX-2 selective NSAIDs but they are contraindicated for persons with atherosclerotic diseases and special consideration is required for persons with risk factors of heart diseases. Paracetamol is the drug of choice for pain.
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PMID:[Update on current care guidelines. Safe use of non-steroidal anti-inflammatory drugs]. 1938 45

Gastroesophageal reflux disease (GERD) is typically heralded by the substernal burning pain of heartburn. On endoscopic examination, about one third of GERD subjects with heartburn have erosive disease, and the remainder have nonerosive reflux disease (NERD). Unlike patients with erosive disease, those with NERD (approximately 50%) often do not respond to therapy with proton pump inhibitors (PPIs), raising the question of whether they have NERD and, if they do, whether the cause of their symptoms is similar to those who respond to PPIs. Recently, biopsies established that subjects with heartburn and PPI-responsive NERD, like those with erosive esophagitis, have lesions within the esophageal epithelium known as dilated intercellular space (DIS). In this article, we discuss the physicochemical basis for DIS in acid-injured esophageal epithelium and its significance in GERD. Although DIS is not pathognomic of GERD, it is a marker of a break in the epithelial (junctional) barrier reflecting an increase in paracellular permeability.
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PMID:Dilated intercellular spaces as a marker of GERD. 1946 18

Over the past decade, there has been a significant increase in the number of children and adults with eosinophilic esophagitis (EE). This recently recognized form of chronic pan-esophagitis is characterized by dense eosinophilic infiltration of the esophageal mucosa. EE is closely associated with male gender and allergic disorders, such as food allergy, eczema and asthma. The diagnosis relies on demonstration of increased numbers of eosinophils (>/= 15 per high power field) in esophageal biopsies. There is clinical overlap between EE and gastroesophageal reflux disease (GERD). Patients with EE typically present with reflux symptoms but are unresponsive to proton pump inhibitor therapy. While dysphagia, regurgitation and retrosternal pain are the clinical hallmarks of EE, many patients are asymptomatic. Treatment aims to prevent long-term complications, such as acute food bolus impaction or esophageal strictures. In childhood, treatment relies on elemental or elimination diets. Skin prick and atopy patch testing have proved useful in guiding specific dietary elimination. In adolescents and adults, broad-based elimination diets are commonly not tolerated or may be ineffective. These patients may respond to swallowed corticosteroid aerosols or other immune-modulating drugs. Further prospective clinical trials are needed to outline the most effective long-term treatment of EE.
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PMID:Eosinophilic esophagitis: example of an emerging allergic manifestation? 1971 May 18

Anisakiasis is caused by a fish parasite of the Nematode family. This kind of rare helminthozoonosis can mainly be found in countries where consumption of raw fish is traditionally high like Japan, the Netherlands, Pacific Islands, South Europe, Scandinavia, USA, and Canada. Man is the wrong hoste. Clinical manifestation depends on the localisation of penetration in the GI tract. In Japan, predominantly the stomach is affected in 97 % of cases, probably due to hypo- and achlorhydria; whereas mainly intestinal anisakiasis occurs in Europa. We report on a 67-year-old male patient with a gastric infestation of anisakiasis. The patient was on proton pump inhibitor which migh have caused the localisation of the infestation. The anisakis was an accidental endoscopic finding in a patient for control of an H. p.-positive gastric ulcer. Otherwise the patient was free of pain. The helminth (larva III) was endoscopically extracted. Thereafter, the patient remained in good health. Anisakis serology as well as repeated differential blood counts were without finding. The uneventful medical history and the normal blood findings indicate that our patient had a very early stage of infestation of anisakiasis. The patient reported no stay outside of Austria within the last years. However, he consumed on a regular basis "rolled pickled herring" produced by a well-known Viennese company for canned fish. This is the first documented case of this rare helminthozoonosis acquired in Austria.
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PMID:[The first case of anisakiasis acquired in Austria]. 1980 56

A 67-year-old male and a 43-year-old female were referred to hospital with headaches after intracranial pressure increasing activities, such as coughing. Both patients were diagnosed with primary cough headache. In the case of the first patient, this diagnosis was considered shortly after presentation. His headache disappeared with the standard treatment for primary cough headache, consisting of indomethacin and a proton pump inhibitor. The second patient received medicinal and surgical treatment for rhinosinusitis. These treatments did not improve the headache symptoms. Eventually she was also diagnosed with primary cough headache, and became pain-free with indomethacin and a proton pump inhibitor. Primary cough headache should be differentiated from secondary cough headache, in which the symptoms are caused by structural abnormalities of the brain. Additional investigation is required to differentiate between the two. The diagnosis of primary cough headache is supported by a positive reaction to trial treatment with indomethacin.
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PMID:[Headache after coughing: consider cough headache]. 1985 88


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