PubMed · 13668178
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J M MANZANARES. 1959. [Normal spirogram].. https://pubmed.ncbi.nlm.nih.gov/13668178/
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The urea breath test is a noninvasive and very accurate test for the diagnosis of Helicobacter pylori infection. However, false negative urea breath test results have been reported to occur in a considerable percentage of the individuals taking proton pump inhibitors; the interval needed to be completely confident that false negative tests had been excluded has varied among the different studies between 6 and 14 days. The impact of H(2)-receptor antagonists on the accuracy of urea breath test remains controversial, although, in contrast with proton pump inhibitors, the data suggest that H(2)-receptor antagonists, for the most part, have little effect on the result of the urea breath test. The urea breath test does not represent a suitable tool for estimating the density of H. pylori colonization. The only quantitative information to be obtained from the urea breath test is that the higher the delta value, the lower the probability of a false-positive urea breath test result. Although some authors have demonstrated a correlation between urea breath test values and histological lesions of the gastric mucosa, the practical utility of this relationship remains unclear. It has been suggested that the pretreatment urea breath test has the potential to identify patients who require modification of the standard therapeutic regimen (for example, prolonging the duration of treatment or increasing the pharmacological dose when bacterial density is high), but other studies could not confirm this relationship. Some studies have shown that the urea breath test is less accurate in patients who have undergone partial gastrectomy. Finally, in contrast with biopsy-based methods, which are responsible for a high number of false-negative results when used to diagnose H. pylori infection in patients with upper gastrointestinal bleeding, urea breath test seems not to be negatively influenced by the presence of this complication.
The relationship between eNO and events in the alveolar-capillary unit in acute lung injury remains to be established. Since endogenous eNO largely originates from the airway epithelium, but nitroglycerin (GTN)-induced eNO is due to microvascular/alveolar metabolism, we have proposed to use basal and GTN-induced eNO as metabolic markers of the airway--and microvascular/alveolar function, respectively. The current work investigates the relationship between basal and GTN-induced eNO and oxygenation parameters (PaO(2)/FiO(2) ratio) in patients undergoing cardiac surgery utilising cardiopulmonary bypass (CPB). Breath by breath eNO measurements were made in 10 patients before, and 1 and 3 h after CPB either under basal conditions or following intravenous administration of GTN (1, 2 and 3 microg/kg). Basal eNO remained unchanged, whereas GTN-induced eNO was reduced following CPB. Also, there was a transient reduction in PaO(2)/FiO(2) ratio 1 h after CPB (32+/-4 vs. 44+/-3 kPa). A negative correlation was found between oxygenation and basal eNO by Pearson's correlation test and linear regression analysis suggesting that decreased oxygenation was associated with increased basal eNO. In contrast, a decrease in GTN-induced eNO positively correlated with reduced oxygenation index (R=0.533, p=0.002). These data suggest that differential relationships exist between basal and nitrovasodilator-induced eNO and oxygenation indices during subclinical lung injury in patients following CPB and that GTN-induced eNO evolution may reflect better microvascular events and injury.
BACKGROUND: Ghrelin, the endogenous ligand of the growth hormone secretagogue receptor, is released from the stomach. Animal studies suggest that ghrelin stimulates gastrointestinal motor activity. AIM: To investigate the influence of ghrelin on gastric emptying rate and meal-related symptoms in idiopathic gastroparesis. METHODS: In six patients with idiopathic gastroparesis, a breath test was used to measure gastric emptying rates (t(1/2)) for solids and liquids after administration of saline or ghrelin 40 microg/30 min in a double-blind, randomized fashion. At each breath sampling, the patient was asked to grade the intensity of six different symptoms (epigastric pain, bloating, postprandial fullness, nausea, belching and epigastric burning) and these were added to obtain meal-related symptom severity score. RESULTS: Ghrelin significantly enhanced liquid emptying (t(1/2): 86 +/- 7 vs. 53 +/- 6 min, P = 0.02) and tended to enhance solid emptying (144 +/- 45 vs. 98 +/- 15 min, P = 0.06). Ghrelin pre-treatment significantly decreased cumulative meal-related symptom score (196 +/- 30 vs. 136 +/- 23, P = 0.04) and individual scores for fullness (55 +/- 8 vs. 39 +/- 8, P = 0.02), and for pain (40 +/- 8 vs. 16 +/- 5, P < 0.05). CONCLUSIONS: In idiopathic gastroparesis, administration of ghrelin enhances gastric emptying and improves meal-related symptoms. These observations suggest a potential for ghrelin receptor agonists in the treatment of gastroparesis.