Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A double-blind, cross-over comparison of Naprosyn (naproxen) 750 mg daily and Butacote (enteric-coated phenylbutazone) 300 mg daily was carried out in a multi-centre trial. Twenty-five patients, mostly male and under 40 years of age, were entered. After a 2-week period in which any existing anti-inflammatory drugs were tailed off, patients were entered into the trial and treated for 1 month with each drug. Patients were assessed at 4-weekly intervals. Both drugs significantly reduced morning stiffness. Morning pain and discomfort and wall-tragus distance were also significantly reduced by both drugs during the trial. Results of the Schober test showed improvement during both treatment periods. There were no overall statistically significant differences between the effects of the 2 drugs on objective parameters. However, overall subjective assessment of symptoms showed a greater improvement on Butacote. Treatment preferences by physician and subjective assessment by the patient both favoured Butacote but the difference between the 2 drugs was not statistically significant. Side effects were mostly of a minor nature. One patient had to discontinue the trial, due to indigestion while taking Butacote.
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PMID:A comparative study of Butacote and Naprosyn in ankylosing spondylitis. 36 71

Seven patients with hyperlipoproteinemia (HLP) type II (four patients with type II A and three patients with type II B), who were experienced to be resistant to hypolipidemic drugs, were treated for 6 months with etofibrate, a double-ester of nicotinic acid and clofibrinic acid, at a dose of 0.3 g t.i.d. Mean serum cholesterol level decreased by up to 18% from a pre-treatment value of 7.7 +/- 1.4 mmol/l. The reduction of serum cholesterol was due both to a decrease in very low density (VLDL) and low density (LDL) lipoprotein cholesteral by 61 and 25%, respectively (after 6 months). Furthermore alpha-LP (HDL) cholesterol increased by 8%, (after 6 months). All seven patients had previously received clofibrate and had obtained a mean decrease in plasma cholesterol by 6%. There was a slight transient increase in S-ASAT and S-ALAT simultaneous with in increase in serum urate. However, these values returned after 3 months to pre-treatment level. No influence on glucose tolerance was recorded. There were no bothersome side effects except a transient discomfort in the form of flushing or acid indigestion which occurred after 1--2 months of treatment with etofibrate.
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PMID:Treatment of hyperlipoproteinemia type II with etofibrate. 52 96

An open study was carried out in general practice to assess the analgesic effectiveness, tolerance and side-effects of salsalate when given at a dosage of 3 g per day for 6 weeks. Sixty-six patients who were known long-term analgesic users were treated: they included 16 with active inflammatory disease of rheumatoid type, 20 with degenerative joint disease, and 27 with other musculo-skeletal conditions. Three patients were withdrawn during the study because of gastro-intestinal upset. Assessments, using rating scale scores, were made pre-trial and at 2-weekly intervals of joint pain, other musculo-skeletal pain, and duration of morning stiffness. The results showed that there was marked improvement in joint pain and morning stiffness, particularly in those patients with inflammatory joint disease. Improvement in musculo-skeletal discomfort was less evident. Side-effects were reported on 24 occasions, the most frequent being dyspepsia. Faecal occult blood tests showed that there were 7 patients with probable blood loss during treatment, 4 of them, however, had no other clinical signs or symptoms of gastrointestinal intolerance.
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PMID:The use of salsalate for control of long-term musculo-skeletal pain: an open, non-comparative assessment. 65 29

Motility-like dyspepsia, a clinical subgroup of functional dyspepsia, refers to the cluster of symptoms which suggests an underlying motility disturbance of the upper gut. Characteristic symptoms, in addition to upper abdominal pain or discomfort, are nausea, vomiting, early satiety, anorexia, postprandial abdominal bloating and excessive repetitive postprandial belching. Patients with concomitant symptoms of irritable bowel syndrome are currently excluded from this clinical entity. Delayed gastric emptying of solids and/or liquids, postprandial antral hypomotility and antroduodenal incoordination, gastric myoelectrical arrhythmias and dysfunction of visceral afferents are the major alterations in upper gut sensorimotor activity which have been described. An empirical trial of medical therapy is warranted if there are no "alarm" symptoms at presentation. If symptoms are not relieved after 2-4 weeks, then investigations of the upper gastrointestinal tract, preferably by endoscopy, to exclude the presence of organic disease, is advisable. Management approaches are then reassurance, dietary manipulations and attention to psychosocial aspects. Prokinetic agents appear to be useful as short-term medical therapy in some patients, but optimum long-term treatment strategies, including the use of medications which may improve a diminished tolerance to gut distension, are not established.
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PMID:Motility-like dyspepsia. Current concepts in pathogenesis, investigation and management. 144 83

Because non-ulcer dyspepsia is associated with stress and motility disturbances it is now called functional dyspepsia. Compared with healthy persons, patients with functional dyspepsia are characterized by poor vagal tone, wider gastric antrum both fasting and postprandially, lack of stress-related repression of antral motility and meal-induced dyspeptic symptoms. Postprandial discomfort is related to antral distension. Poor vagal tone may cause antral distension and dysmotility as well as symptoms in these patients. Treatment programmes or drugs which improve vagal tone may be beneficial.
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PMID:[Functional dyspepsia--a stress disease]. 141 45

Dyspepsia can be defined as the presence of upper abdominal pain or discomfort; other symptoms referable to the proximal gastrointestinal tract, such as nausea, early satiety, and bloating, may also be present. Symptoms may or may not be meal related. To be termed chronic, dyspepsia should have been present for three months or longer. Over half the patients who present with chronic dyspepsia have no evidence of peptic ulceration, other focal lesions, or systemic disease and are diagnosed as having non-ulcer (or functional) dyspepsia. Non-ulcer dyspepsia is a heterogeneous syndrome. It has been proposed that this entity can be subdivided into a number of symptomatic clusters or groupings that suggest possible underlying pathogenetic mechanisms. These groupings include ulcer-like dyspepsia (typical symptoms of peptic ulcer are present), dysmotility (stasis)-like dyspepsia (symptoms include nausea, early satiety, bloating, and belching that suggest gastric stasis or small intestinal dysmotility), and reflux-like dyspepsia (heartburn or acid regurgitation accompanies upper abdominal pain or discomfort). The aetiology of non-ulcer dyspepsia is not established, although it is likely a multifactorial disorder. Motility abnormalities may be important in a subset of dyspepsia patients but probably do not explain the symptoms in the majority. Epidemiological studies have not convincingly demonstrated an association between Helicobacter pylori and non-ulcer dyspepsia. Other potential aetiological mechanisms, such as increased gastric acid secretion, psychological factors, life-event stress, and dietary factors, have not been established as causes of non-ulcer dyspepsia. Management of non-ulcer dyspepsia is difficult because its pathogenesis is poorly understood and is confounded because of a high placebo response rate. Until more data are available, it seems reasonable that treatment regimens target the clinical groupings described above. Antacids are no more effective than placebo in non-ulcer dyspepsia, although a subgroup of non-ulcer dyspepsia patients with reflux-like or ulcer-like symptoms may respond to H2-receptor antagonists. However, there is no significant benefit of these agents over placebo in many cases. Bismuth has been shown to be superior to placebo in patients with H. pylori in a number of studies, but these trials had several shortcomings and others have reported conflicting findings. Sucralfate was demonstrated in one study to be superior to placebo, but this finding was not confirmed by another group of investigators. Prokinetic drugs appear to be efficacious, and may be most useful in patients with dysmotility-like and reflux-like dyspepsia.
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PMID:Non-ulcer dyspepsia: myths and realities. 188 33

The definition of the term dyspepsia and of derived terms such as organic dyspepsia, functional dyspepsia, reflux-like dyspepsia, and non-ulcer dyspepsia continues to provoke controversy. In recent literature, however, it is apparent that a measure of agreement is now emerging with regard to 'dyspepsia', which is considered simply to denote episodic or persistent symptoms that include abdominal pain or discomfort and which are referable to the upper gastrointestinal tract. Particular symptom patterns may justify the use of descriptions such as reflux-like dyspepsia, ulcer-like dyspepsia, or dysmotility-like dyspepsia, but these terms should not carry any implication that the symptom patterns can be attributed to particular pathogenetic processes. In many patients with dyspepsia, clinical assessment and investigation fail to identify any abnormality to which the symptoms can reasonably be attributed. The label of 'functional dyspepsia' is well-established medical parlance in these circumstances and is generally accepted as the converse of 'organic dyspepsia', which denotes dyspepsia for which a responsible disease process has been identified.
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PMID:Definitions of dyspepsia. 189 23

110 patients who presented dyspeptic complaints to their general practitioner were interviewed using a questionnaire. Most patients had a long history of dyspeptic symptoms. 36 had been treated before for a peptic ulcer. Only 12 patients had a history of dyspepsia lasting less than three months. It is difficult to distinguish between organic and non-organic dyspepsia from the symptoms, and long-standing symptoms at any rate should be investigated further. The effect of medical treatment varies. Many patients have to live with their discomfort.
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PMID:[Dyspepsia in general practice]. 192 81

In this era of H2-inhibitors, the available evidence does not support the need to place peptic ulcer disease patients on restrictive diets. The major goal of diet is to avoid extreme elevations of gastric acid secretion and the direct irritation of gastric mucosa. In view of this, only slight modifications in the patient's usual diet are recommended. Table 1 depicts a sample menu for chronic peptic ulcer disease. Frequent milk ingestion as previously prescribed is not encouraged. This is owing to the transient buffering effect and significant gastric acid secretion effect of milk. The fat content of milk has no influence on these effects. Spices, in particular black pepper, red pepper, and chili powder, may produce dyspepsia. One study shows red chili powder to have no detrimental effect on duodenal ulcer healing. It has also been proposed that daily pepper ingestion may have a beneficial adaptive cytoprotective response. While still controversial and under evaluation, peptic ulcer patients should avoid any spice that causes discomfort, especially during exacerbation of peptic disease. Currently, studies indicate that it is prudent to avoid alcohol. This is especially true for the concentrated forms, such as 40% (80 proof) alcohol. Coffee should be avoided on the basis of its strong acid secretagogue property. Coffee can induce dyspepsia. Whether noncoffee caffeine-containing beverages (tea, soft drinks) induce peptic ulcer is unknown, but they are acid secretion stimulators. Decaffeinated coffee has an acid stimulating effect as well. It is reasonable to have peptic ulcer patients restrict decaffeinated coffee and all caffeine-containing beverages. There appears to be no evidence to restrict dietary fiber. Some fiber-containing foods may possess factors that are protective against ulcer disease. According to the Mayo Clinic Diet Manual, previously recommended small frequent feedings have not been shown to be more effective than three meals per day in the treatment of chronic peptic ulcer disease. This reference cites authorities advising against extra feedings because of increased acid secretion and unnecessary complication of eating patterns. However, some patients claim to be relieved of symptoms with more frequent feedings, especially during acute phases. Citric acid juices may induce reflux and cause discomfort in selective patients. Stomach distention with large quantities of food should be discouraged. Although there is now little role for dietary therapy, one should note that bland and ulcer diets probably are not detrimental to most persons if they are used for a short time and may have some psychological benefit.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diet and nutrition in ulcer disease. 207 99

We studied the prevalence of gallstones in patients with upper abdominal pain, heaviness, or discomfort by ultrasound examination of the gallbladder. The actual ultrasound examination was performed by a clinical gastroenterologist blinded to the symptoms. Of 1,680 consecutive dyspeptic patients, 500 (29.8%) had gallstones. The gallbladder was contracted in 450 (91.2%), normal-size in 36 (7.2%), and distended in 8 (1.6%). Biliary colic was more frequently the presenting complaint in patients with a contracted gallbladder than in those with normal size gallbladder (p less than 0.001). Dyspepsia was more frequent in the presence of a normal size gallbladder than a contracted one (p less than 0.001). We conclude that ultrasonography of the gallbladder by the clinician has a high diagnostic yield, and the symptom complex has an excellent correlation with the sonographic appearance.
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PMID:Gallstone disease in north India: clinical and ultrasound profile in a referral hospital. 222 98


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