Managing duodenal ulcer.
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Biomedical subjects
Publications and source records attributed to J C Meeroff.
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Sir William Osler described the practice of medicine as "an art based on Science." The authors have artfully simplified a frequently needed clinical calculation, using sequential multiplication and obviating the need for logarithmic manipulation.
A significant decrease of the lactose levels (p less than .001) and of the glucose peaks after an overcharge of lactose (p less than .01) were found in 10 patients with duodenal ulcer after a treatment of 35 days with 1,2 daily grams of Cimetidine, when they were compared with a group treated with placebos. Also, a significant increase of the diarrhea associated with the overcharge of lactose (p less than .005) was obtained. The relation between the increase of the pH and the decrease of the lactose values was significant (r = 0,44 - p less than .01).
Two cases of intrinsic factor deficiency with normal hydrochloric acid production are presented. Both patients had markedly reduced intrinsic factor secretion and substantial titers of type I (blocking) intrinsic factor antibodies. No parietal cell antibodies were recognized by immunofluorescence in either case. Three hypotheses are offered to explain these findings: (a) These patients have congenital intrinsic factor deficiency that remained in the preanemic phase until adulthood; (b) they have pernicious anemia detected at a stage before gastric mucosal atrophy and achlorhydria have occurred; or (c) they represent cases of a new syndrome characterized by isolated intrinsic factor deficiency.
Nausea and vomiting occur commonly with gastroenteritis caused by parvovirus-like agents. Infection results in histologic injury to the small bowel mucosa, but the gastric mucosa remains unaffected. We have studied gastric emptying of liquids serially in 10 volunteers before and after ingestion of the parvovirus-like agents, Norwalk and Hawaii viruses. The five subjects who developed illness all showed marked delays in gastric emptying, while the five well subjects had no alteration of emptying. Five addition volunteers who developed Norwalk virus gastroenteritis underwent serial studies of gastric secretion of hydrochloric acid, pepsin, and intrinsic factor. No change was detected in either basal or betazole-stimulated secretion of these three substances during the course of illness. The nausea and vomiting accompanying this type of viral gastroenteritis may result from abnormal gastric motor function.
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A double-blind 4-week trial of sodium oxyferriscorbone versus placebo (distilled water) was conducted in 46 outpatients with endoscopically confirmed gastric ulcer. Ulcer healing occurred in 15 of 20 patients receiving sodium oxyferriscorbone (75%) and in 7 of 20 patients receiving placebo (35%). Patients receiving sodium oxyferriscorbone experienced less pain and required less antacid than those receiving placebo (P less than 0.05). Side effects were reported in 12 patients, 7 while receiving sodium oxyferriscorbone and 5 while receiving placebo. Six patients did not complete the study due to ulcer complications. Routine laboratory tests revealed no persistent abnormalities that could be related to the treatment. Five placebo-treated patients that were therapeutic failures were switched to sodium oxyferriscorbone and healing was observed within 3 weeks. It is concluded that sodium oxyferriscorbone is effective in enhancing healing of gastric ulcers.
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Meperidine is a potent narcotic related chemically and pharmacologically to morphine and atropine. To examine its gastric antisecretory activity a study designed to test the effect of meperidine on basal acid secretion was carried out: 100 mg of meperidine given intramuscularly reduced basal acid output (BAO) by 66.3% at 1 hr (P less than 0.001), 64.9% at 2 hr (P less than 0.001), and 44.9% at 3 hr (P = 0.005). This degree of reduction of BAO by this dose of meperidine did not differ from that produced by 30 mg of propantheline intramuscularly. These results demonstrate that meperidine in standard classical doses is a potent inhibitor of BAO in man.
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Little doubt exists concerning the limited usefulness of gastric analysis as a screening test in unselected populations. Reliable tests, such as those for glycemia, are also of limited value when performed blindly on the general population. When, however, gastric analysis is performed on an adequate preselected population, it has a valuable role in the diagnosis and management of several gastroduodenal diseases. Highly satisfactory results can be obtained when the proper population is selected because errors are minimized due to an increased prevalence of diseases. We have verified the reliability of two types of gastric analyses: the conventional method of gastric analysis based on measurement of acid output alone (CGA) and the so-called gastroionogram (GIG), in 100 consecutive gastric analyses using the method proposed by Kronborg. Gastroionogram increases specificity (even at the risk of decreasing sensitivity) and provides an excellent predictive value of the test. With the same conditions CGA is less useful because of the overlapping among normal and diseased groups. It is useful, however, for separating patients into three groups of normal secretors, hyposecretors and hypersecretors.
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The effect of parenteral sodium acetylsalicylate (Na ASA) on the development of gastric mucosal lesions and bleeding was studied in control rats and in rats subjected to cold-restraint stress. Although both doses of Na ASA studied, 15 and 60 mg/kg intraperitoneally, alone resulted in lesion formation, only with the larger dose did this reach the level of statistical significance. However both doses of Na ASA alone significantly increased blood loss as measured by a decrease in hematocrit value. The administration of Na ASA 15 MG/kg intraperitoneally to animals subjected to cold-restraint significantly increased blood loss, but not lesion formation, while the larger dose of Na ASA significantly increased both parameters. Thus parenteral aspirin not only can cause gastric mucosal damage and bleeding, but it can enhance lesion formation and blood loss produced by cold-restraint. Two mechanisms may be involved: a smaller dose of Na ASA significantly affecting hemostasis but a larger dose being required for gastric mucosal damage.
The study was designed to test whether or not bile reflux is necessary for the development of gastric mucosal lesions during cold-restraint stress in the rat. 40 male Sprague-Dawley rats were studied. They were randomized into 4 groups. Group 1 underwent sham operations with no cold-restraint stress. Group 2 underwent sham operations. Group 3 underwent pyloric ligation. Group 4 underwent bile duct ligation. Groups 2, 3, and 4 were subjected to cold-restraint stress for 3 hours at 4-6 degrees C in a Bollman cage. After the experimental procedure, the stomachs were removed under ether anesthesia, the severity of lesions was recorded, and blood from the hearts was obtained for hematocrit readings. The mean lesion scores of all groups exposed to cold-restraint stress were similar and much higher than that of the unrestrained sham-operated group (P smaller than 0.001). Also, mean hematocrit readings in all groups exposed to cold-restraint stress were lower than in the control group (P smaller than 0.05). There was a correlation between severity of mucosal lesions and hematocrit reading (rs=0.57, P smaller than 0.001). The results obtained allow the following conclusions: (1) Bile reflux is not necessary for formation of cold-restraint stress lesions in the rat. (2) Hematocrit readings appear to be a useful measure of blood loss secondary to experimental mucosal lesions.
Fifty barium-enema studies were performed with glucagon and 50 with a placebo to compare their effect on colonic spasm, patient discomfort, and diagnostic quality. Each drug was administered in a randomized double-blind fashion and was injected intramuscularly 10 minutes before beginning the enema. Bowel relaxation during fluoroscopy was graded. Patients were questioned about discomfort during and immediately after the enema, and radiographs were reviewed blindly for diagnostic quality and degree of spasm. Studies done with glucagon produced significantly less spasm and discomfort and better diagnostic quality compared to the placebo (p less than 0.01).
Glucagon was effective in decreasing acute gastric mucosal lesions, blood loss and gastric acid secretion in the cold restraint stressed rat.
During the steady state perfusion of the duodenum, recovery of a duodenal marker (polyethylene glycol 4000) can be used to quantify intraduodenal volumes. We used this technique to measure and time the recovery from the duodenum of a second nonabsorbable marker, phenol red. When liquid test meals containing phenol red were placed in the stomach, the rate of gastric emptying could be quantified from the appearance of the maker in the duodenum. The osmolality of either test meal or duodenal perfusates was then varied so that the osmotic control of gastric emptying could be examined. Gastric emptying was fastest when duodenal contents were isotonic; nonisotonic duodenal contents slowed emptying whether these conditions were achieved by nonisotonic duodenal perfusates or by emptying of a nonisotonic test meal. However, nonisotonic solutions in the stomach and in the jejunum did not slow gastric emptying, so long as duodenal contents were isotonic. Osomoreceptors, which slow gastric emptying, are present in the duodenum but not in the jejunum or stomach.
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