gastrins and Lung-Diseases--Obstructive

The ability of H2 receptor antagonists and continuous enteral alimentation to maintain high intragastric pH in patients with chronic obstructive pulmonary disease (COPD) requiring mechanical ventilation was evaluated by continuously monitoring intragastric pH prior to and following sequential addition of ranitidine or continuous enteral alimentation (or both) to their therapeutic regimen. Prior to therapy, intragastric pH was less than 4.0 for 75 +/- 10 percent of the time, but never less than 1.0. Nevertheless, this moderate gastric acidity was associated with evidence of mucosal injury. Ranitidine failed to continuously maintain a high intragastric pH (pH less than 4.0 for 35 +/- 11 percent of the time; p greater than 0.2 compared to patients treated with placebo). Following administration of continuous enteral alimentation, intragastric pH fell, and ranitidine therapy only partially blocked this increase in gastric acidity induced by continuous enteral alimentation. We conclude that without treatment, patients with COPD who have acute respiratory failure may develop gastric mucosal injury despite the presence of only moderate intragastric acidity; however, ranitidine and continuous enteral alimentation are not effective in maintaining a high intragastric pH.

Topics: Acute Disease; Adult; Aged; Combined Modality Therapy; Enteral Nutrition; Female; Gastric Acidity Determination; Gastric Juice; Gastrins; Humans; Hydrogen-Ion Concentration; Lung Diseases, Obstructive; Male; Middle Aged; Ranitidine; Respiration, Artificial; Respiratory Insufficiency; Time Factors

The gastrin gene is known to be expressed in all classes of bronchogenic carcinomas. Furthermore, high levels of gastrin have been reported in both the bronchoalveolar lavage (BAL) fluid and serum of patients with lung cancer. Based on these preliminary data a study was conducted to evaluate the usefulness of gastrin measurements in the diagnosis and staging of lung cancer.. Thirty-five patients with lung cancer (26 non-small cell (NSCLC) and nine small cell (SCLC)) and 25 patients with chronic obstructive pulmonary disease underwent fibreoptic bronchoscopy and BAL. Gastrin levels were determined in both BAL fluid and the serum and compared with each other and with staging.. No difference was found between the gastrin levels in the BAL fluid or serum of the study groups. There was no correlation with the stage in NSCLC and no correlation was found between the gastrin levels in the serum and the BAL fluid. A significant difference was seen in gastrin levels in BAL fluid between extensive and limited SCLC (p < 0.05).. There is no evidence of clinical usefulness for gastrin measurements in lung cancer.

Topics: Adult; Aged; Bronchoalveolar Lavage Fluid; Carcinoma, Non-Small-Cell Lung; Carcinoma, Small Cell; Female; Gastrins; Humans; L-Lactate Dehydrogenase; Lung Diseases, Obstructive; Lung Neoplasms; Male; Middle Aged; Neoplasm Staging

Increased basal and/or pentagastrin-stimulated gastric acid secretion was observed in 31 of 40 cystic fibrosis (CF) patients as compared to 13 age-matched control volunteers. Fasting serum gastrin level for 20 CF patients of 67.7 +/- 11.1 pg/ml (ranging from 10 to 145 pg/ml) was normal. Meal-stimulated serum gastrin concentrations were not significantly higher for seven CF patients as compared to nine normal subjects. In a rat bioassay, serum extracts from six CF patients produced gastric acid secretion comparable to 250 ng/ml of pentagastrin; significantly (p less than 0.01) greater than the responses produced by serum extracts from six normal subjects. There was no significant correlation of severity of pulmonary disease or steatorrhea with acid secretory results. Fourteen of 16 CF patients biopsied had evidence of proximal small intestinal injury which correlated with basal acid output elevation. Gastric acid hypersecretion in CF patients is due to nongastrin secretagogues and is a cause of proximal small intestinal injury.

Topics: Adolescent; Adult; Animals; Celiac Disease; Child; Child, Preschool; Cystic Fibrosis; Duodenum; Female; Gastric Acid; Gastrins; Humans; Infant; Intestinal Diseases; Lung Diseases, Obstructive; Male; Pentagastrin; Rats; Rats, Inbred Strains; Time Factors

Nine patients with chronic obstructive pulmonary disease were given oral aminophylline, intravenous aminophylline, and various inhaled and oral adrenergic bronchodilators to determine the effect of these agents on gastric acid secretion and gastrin release. Inhaled epinephrine hydrochloride resulted in an increase in basal acid output of borderline significance (.05 less than P less than .10). Oral aminophylline caused a significant increase in basal acid output from 2.43 to 4.06 mEq (P less than .05). Intravenous aminophylline also caused a significant increase in basal acid output from 0.66 to 2.19 mEq (P less than .01). There were no statistically significant changes in serum gastrin levels after administration of any of the bronchodilators. Aminophylline should be used with caution, if at all, in patients with peptic ulcer disease. In these patients, a beta agonist should be used for initial therapy. If the addition of aminophylline is necessary, antacids should be given.

Topics: Administration, Oral; Aminophylline; Bronchodilator Agents; Gastric Juice; Gastrins; Humans; Infusions, Parenteral; Lung Diseases, Obstructive; Male; Peptic Ulcer