Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes mellitus has been associated with a variety of gastrointestinal motor disturbances. Pyloric activity, however, has not been specifically investigated. We have quantified the pyloric manometric profile in 24 diabetics with recurrent nausea or vomiting, or both, without evidence of mechanical obstruction. Twelve healthy volunteers served as controls. A multilumen pneumohydraulic perfusion assembly with five side openings, each 1 cm apart, was positioned fluoroscopically across the antroduodenal junction and used to monitor pressure activity for 5 h (3 h fasting and 2 h fed). Three patterns of pyloric activity were defined and quantified: (a) baseline elevation of greater than or equal to 3 mmHg for greater than or equal to 1 min (tonic pattern); (b) antral-type phasic pressure activity mixed with duodenal phasic activity (phasic pattern); and (c) phasic pattern superimposed on tonic activity (combined tonic-phasic pattern). The duration of the total pyloric activity before and after the meal was greater in diabetics than in controls (p less than 0.005). Furthermore, episodes of unusually prolonged (greater than or equal to 3 min) and intense (greater than or equal to 10 mmHg) tonic contraction, "pylorospasm," were observed in 14 of 24 diabetics but in only 1 control (p = 0.025). In diabetics, episodes of pylorospasm had a peak amplitude of tonic activity of 13 +/- 1 mmHg and a duration of 7 +/- 0.7 min (mean +/- SE). We conclude that pyloric dysmotility forms part of the widespread disruption of gut motility that affects some patients with diabetes.
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PMID:Pyloric dysfunction in diabetics with recurrent nausea and vomiting. 369 9

Gastroparesis, or delayed gastric emptying, is a common cause of chronic nausea and vomiting as seen in a gastroenterology practice. Diabetic, postsurgical, and idiopathic causes remain the three most common forms of gastroparesis. In addition to nausea and vomiting, symptoms of gastroparesis may include early satiety, postprandial fullness, and abdominal pain. Physiologic changes that may explain symptoms in patients with gastroparesis, in addition to delayed gastric emptying, include impaired fundic accommodation, antral hypomotility, gastric dysrhythmias, pylorospasm, and perhaps visceral hypersensitivity. Diagnosis of gastroparesis is best determined using a radioisotope-labeled solid meal with scintigraphic imaging for at least 2 hours, and preferably 4 hours, postprandially. Most commonly, a 99mTc sulfur colloid-labeled egg sandwich with imaging at 0, 1, 2, and 4 hours is used. Extension of the gastric emptying test to 4 hours improves the accuracy of the test, but unfortunately, this is not commonly performed at many centers. Emptying of liquids remains normal until the late stages of gastroparesis and is less useful. The aims of treatment should be to control symptoms and maintain adequate nutrition and hydration. Patients should be advised to eat small meals and to limit their intake of fat and fiber. Additional dietary recommendations may include increasing caloric intake in the form of liquids. For diabetic patients, control of blood glucose levels is important, as symptom exacerbation is frequently associated with poor glycemic control. Specific treatment often begins with metoclopramide, 10 mg, up to four times daily, after a discussion of possible side effects with the patient. An antiemetic agent, such as prochlorperazine, 5 to 10 mg orally or 25 mg by suppository, can be added on an as-needed basis every 4 to 6 hours to control nausea. If these antiemetic medications are not effective, or if side effects develop, orally dissolving ondansetron, 8 mg every 8 to 12 hours, can be tried on an as-needed basis. If this regimen is unsuccessful, then alternative prokinetic agents--erythromycin, 125 mg, or tegaserod, 6 mg, prior to meals--can be tried. For cases refractory to these treatments, referral to a center with US Food and Drug Administration permission to use domperidone should be considered. Alternatively, symptom modulators such as low-dose tricyclic antidepressants can be tried to reduce symptoms, but these do not improve gastric emptying. In patients for whom all medical therapy fails, other options that are tried at experienced centers include the injection of botulinum toxin into the pylorus, placement of a feeding jejunostomy, and/or placement of a gastric electrical stimulator.
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PMID:Delayed gastric emptying: whom to test, how to test, and what to do. 1683 48