SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: We designed a new method of measuring gastric emptying and orocecal transit time (OCTT) at the same time to assess the influence of gastric emptying upon OCTT. METHODS: Twenty-five dyspeptic patients (6 men, 19 women) with a mean age of 64.8 years (range, 25-80 years) were studied. The patients received a liquid test meal, containing 100 mg of 13C-acetate and 12g of lactulose, while they were in the sitting position after an overnight fast. Breath samples were collected at 10-min intervals of 120 min and both 13CO2 and hydrogen (H2) levels were measured. Subsequently, H2 concentrations were measured at 30-min intervals, for a total of 240 min. RESULTS: The results of gastric emptying were expressed as the time of peak 13CO2 excretion. OCTT was defined as the period between the ingestion of lactulose and a H2 peak rise of 5 ppm above the baseline value. The onset of H2 enrichment in the breath began at 90-110 min, whereas 13CO2 levels increased from the beginning, with peak enrichment values being reached after 60-80 min. OCTT was related to 13CO2 peak time. In 5 of the 25 patients, H2 breath enrichment in the 10-min sample was more than 5 ppm over the baseline value. All these 5 patients had double or triple peaks in serial breath H2 concentrations. CONCLUSIONS: The combination of the lactulose hydrogen breath test (LHBT) with the 13C-acetate breath test, which requires only breath samples, provides us with much information on the gastrointestinal tract; gastric emptying, OCTT, bacterial overgrowth in the small intestine, colonic fermentation, and oropharyngeal flora. The 13C-acetate breath test can be useful as an adjuvant test when LHBT is performed for measuring OCTT.
Gastroesophageal reflux disease, achalasia and esophageal spasms are the most frequent esophageal motility disorders and are associated with dysphagia and non-cardiac chest pain. The diagnosis of achalasia is based on manometric criteria. Pneumatic dilatation, laparoscopic myotomy, and the minimal invasive injection of botulinum toxin are therapeutic options. Long-term-pH-metry is the gold standard to diagnose gastroesophageal reflux disease. Proton pump inhibitors (PPI) are the first-line therapy in reflux disease. Esophageal manometry and pH-metry are essential investigations prior to an antireflux operation. The evaluation of chronic constipation refractory to medical treatment should include anal manometry, and MR-defecography for the diagnosis of anorectal outlet obstruction such as anismus which could be treated successfully by biofeedback therapy.
A new congenital syndrome characterized by the simultaneous failure of control of ventilation (Ondine's curse) and intestinal motility (Hirschsprung's disease) is reported in three infants, all of whom died in the first few months of life; two were siblings. Detailed studies in one also revealed markedly decreased esophageal motility and abnormal control of heart rate. In one infant, minute ventilation was lower in quiet than in REM sleep and lower in both states of sleep than in wakefulness. Although the mean inspiratory flow was decreased in quiet sleep, the hypoventilation resulted primarily from a decrease in respiratory frequency. Intravenous doxapram increased ventilation but did not reverse respiratory failure. Aminophyllin, progesterone, physostigmine and chlorpromazine did not change ventilation significantly; imipramine resulted in a significant decrease. Both long and short-term variability of the heart rate were markedly decreased when compared with the normal infant. Although neuropathologic studies postmorten did not reveal an anatomic defect, we postulate that a developmental abnormality in serotonergic neurons is responsible for this new syndrome.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We found colitis in 11 of 14 children, 4 months to 7 yr after surgical diversion of the colon for chronic intestinal pseudo-obstruction. Colonoscopic examination was incidental during placement of a catheter for colon manometry and transit studies. All 14 children had complained of diffuse, poorly localized abdominal pain, but only three had a history of bloody stools. Diversion colitis had not previously been suspected in six of eight affected children without hematochezia. Biopsies showed a nonspecific acute and chronic inflammation and/or nodular lymphoid hyperplasia. There was no correlation between the duration of the colonic diversion and the severity of the colitis. Diversion colitis may be an indolent inflammatory nidus and a potential cause for repeated bacteremia, abdominal pain, and bleeding.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Gastrointestinal side effects still constitute a major drawback in both acute and chronic use of opioids. The exact mechanism behind the gastrointestinal effects is not known, but experimental studies indicate both central and peripheral actions. In an attempt to clarify to what extent the systemic effects of morphine after epidural administration contribute to the action on gastrointestinal motility, a study aiming to resemble the situation with epidural morphine was designed. Twenty healthy male volunteers were randomly allocated to two groups. Group one (n = 10) received intrathecal (0.4 mg) and intramuscular (4 mg) morphine (IT-IM-group). Group two (n = 10) received intrathecal (0.4 mg) morphine and i.m. saline (IT-group). Gastroduodenal activity was assessed by gastric emptying, manometry and electrogastrography. The plasma and urine concentrations of morphine and its inactive metabolite morphine-3-and active metabolite morphine-6-glucuronide were also determined. During the fasted state the gastrointestinal activity is characterised by a cyclic pattern with a duration of 80-120 min in the duodenum comprising three different phases with intense activity during Phase III. This pattern was seen in all volunteers. After the intrathecal administration the Phase III activity occurred significantly earlier in the IT-IM group (median 31 min; IR 34 min) compared to IT group (82 min; 37 min) (P < 0.01). The number of Phase IIIs was higher in the IT-IM group during the first 4 h after the morphine administration, compared to the IT group. However, after 6 h, there was no difference between the groups. The propagation velocity of Phase III decreased significantly in both groups (P < 0.001), but there was no difference between the groups. Tachygastria increased significantly with time in both groups. The acetaminophen absorption test showed that the area under the concentration curve (120 min) was significantly smaller in the IT-IM group compared to the IT group (P < 0.05). There were no measurable plasma concentrations of morphine or the glucoronidated metabolites M3G and M6G in the group that only received intrathecal morphine. This study showed that intrathecal morphine (0.4 mg) influenced gastroduodenal motility and that intramuscular morphine (4 mg) gave additional effects. These results might be applicable to the epidural situation and are indirect evidence that the gastroduodenal effects of epidural morphine are caused by both central and systemic effects of morphine.
Gastrointestinal motor abnormalities occur frequently in patients with diabetes mellitus. The gastrointestinal motor dysfunction in these patients has been associated with the presence of autonomic neuropathy. Recently, however, several studies have shown that the gastrointestinal motor responses to various stimuli are impaired during acute hyperglycemia in both healthy subjects and diabetic patients. It has been demonstrated that acute hyperglycemia impairs esophageal peristalsis, reduces the lower esophageal sphincter pressure, delays gastric emptying, slows intestinal transit, and reduces the gallbladder contraction in response to various stimuli in healthy subjects. In diabetic patients gastric emptying and gallbladder contraction have been shown to be impaired during hyperglycemia. With regard to the mechanisms of action, it has been suggested that hyperglycemia may affect gastrointestinal function through vagal-cholinergic inhibition, by alterations in serum osmolality, or perhaps by alterations in gastrointestinal hormone secretion.