Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined 66 patients with pain of possible esophageal origin for sensitivity to intraesophageal infusions of coffee, orange juice, spicy tomato drink, or HCl of varying concentrations as an addendum to their acid infusion (Bernstein) tests. Compared to Berstein-negative subjects, acid-sensitive patients were sensitive to infusion of coffee (P less than 0.01), orange juice (P less than 0.001), and tomato drink (P less than 0.001). Patients were largely insensitive to HCl solutions with a titratable acidity of 1 mEq per liter or less, less than the least acidic food solution tested. However, Berstein-positive patients were still highly sensitive to infusions of coffee, orange juice, and tomato drink adjusted to pH 7 (P less than 0.001). Patients were unable to differentiate symptoms caused by acid or food infusions, and solutions did not differ in the duration of infusion needed either to cause symptoms or to relieve them by saline. We conclude that the pain of esophagitis is nonspecific and can be precipitated by variety of seemingly unrelated substances.
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PMID:Food sensitivity in reflux esophagitis. 2 14

Antacids can reduce gastroduodenal acidity for long periods if taken in substantial quantities after food. Their healing effect on gastric ulcer is minimal, if present at all, and easily overwhelmed by the benefit obtained from admission to hospital. Intensive antacid therapy appears effective in healing duodenal ulcer and preventing haemorrhage from stress ulcer, and is comparable in these respects with cimetidine but with a higher incidence of side-effects. Clinical impression strongly suggests that antacids relieve pain in peptic ulcer but objective confirmation is lacking.
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PMID:Antacids and peptic ulcer--a reappraisal. 3 92

Studies in which the numbers of healed or unhealed ulcers and their correlation with symptoms are availabel are summarized in Table 1. A review of the data and inspection of the Table show that the correlation of GU or DU healing with symptomatic remission is generally poor. The reasons for this are unknown and reflect the very incomplete understanding of the mechanism of ulcer pain and of the pathways through which the pain is mediated. The pathogenesis of pain in GU or DU may be due to the action of acid and pepsin, or of bile, on the tissues exposed in the ulcer crater, to abnormal motility, to normal motility acting on inflamed tissue, to areas of inflammation surrounding the ulcer crater, or to a combination of these factors. The relative importance of each of these variables in DU or GU, or in individual patients (because the mechanism of pain may not be the same in each patient) is not known. Nor is it known how much the pathogenesis of ulcer pain is the result of local release of histamine, kinins, and prostaglandins. These biogenic factors are known to be associated with inflammation and produce, or enhance, somatic pain. Their importance in peptic ulcer in man needs to be studied. Relief of pain after neutralization or buffering of gastric contents with alkali or food suggests strongly that acid must play an important part in the pathogenesis of the ulcer symptoms. The rapidity with which relief of symptoms occurs points towards the direct involvement of hydrogen ions in at least one type of ulcer symptom. Lowering of intragastric acidity by histamine H2- receptor antagonists or high-dose alkali may contribute to the observed discrepancies between ulcer healing and the remission of pain, by creating an environment in the gastroduodenal lumen which favours symptomatic improvement, even in the presence of an unhealed crater. This idea, however, does not explain why there is a discordance between healing and symptoms in patients receiving placebo, or in those treated with other drugs, such as carbenoxolone sodium. In the absence of endoscopic evidence, the presence or absence of symptoms cannot be assumed to indicate with certainty the presence or the absence of a peptic ulcer.
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PMID:Peptic ulceration and its correlation with symptoms. 36 2

The results from a short-term (28 days) treatment of patients with duodenal ulcer are reported. The average surface of the ulcers from 40.4 mm2 (initial average value) diminished to 7.3 mm2 by the 14 th day of the treatment. The graphic study of the kinetics of healing of the ulcer process revealed that in a treatment with 0.8--1.0 g Simetidin, a diminution of the ulcer by half (t/2) could be expected by the seventh day. In 16, out of the 21 treated, the ulcer epithelized by the 14th day of the treatment. In one patient a prolonged treatment of 42 days proved to be necessary to guarantee the epithelization of the ulcer. In 2/3 of treated patients, the pain complaints, the sensation of warmth and acidity disappeared by the end of the first week of the treatment. The average values of the basic and peak acid output (BAO and PAO), the N-acetyl neuramine acid output, the gastrin basic level, GOT, GPT and creatinine in serum do not change after the treatment. A significant reduction of hemoglobin concentration in the gastric juice is established after the treatment with Simetidin.
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PMID:[Results of the short-term (28 days) cimetidine treatment of duodenal ulcer]. 38 Jan 69

The results are reported from the treatment of 30 patients with gastric and 13 with diodenal ulcers with biogastrone in the course of 20 days (300 mg were given the first week, where on -- 150 mg daily). A more favourable effect upon the clinical symptoms and ulcer were observed in the patients with gastric ulcer (the symptoms disappeared in 87 per cent whereas the ulcer -- in 32 per cent) as compared with the duodenal ulcer (the symptoms disappeared in 46 per cent, whereas -- the ulcer in none). Biogastrone treatment influences the pain in a higher per cent as compared with Caved-S and oxyferroscorbon (p greater then 0.05), whereas regards the rest of the clinical symptoms -- no statistically significant difference was established. As compared with the treatment with oxyferroscorbon, Caved-A and cimetidin, biogastrone has a slower effect on the subjective complaints and the ulcer niche. After biogastrone treatment, the indices of gastric secretion and acidity decrease and the sialic acid in gastric juice is increased only in the gastric ulcer, but does not change considerably in the duodenal ulcer. The rest of the laboratory indices do not change with biogastrone treatment. In two of the patients, in the course of biogastrone treatment, light edema appeared on the face and the arterial blood pressure was elevated in other two, disappearing after the treatment without any additional treatment. Biogastrone treatment is indicated mainly in cases with gastric ulcer, with decreased sialic acid in gastric juice.
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PMID:[Treatment of peptic ulcer with Biogastrone (carbenoxolone)]. 51 51

Serum creatine phosphokinase (CPK) concentrations were determined in healthy volunteers for the first 48 hours after intramuscular injection of 50 mg chlordiazepoxide hydrochloride or of its solvent alone. Intramuscular injection of both the drug solution and its solvent was painful and caused CPK elevations. The CPK rise due to the drug solution was 33 per cent higher than that due to the solvent alone, but the difference was not significant. The pH of the solvent preparation is low and it contains high concentrations of propylene glycol. The pain and muscle damage due to injection of the solvent could be due to its acidity and its high osmolarity. Problems associated with intramuscular injections of water-insoluble drugs are not resolved by the use of such solvent preparations.
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PMID:Serum creatine phosphokinase concentrations after intramuscular chlordiazepoxide and its solvent. 94 24

PZ-177 was found to have potent analgesic, anti-inflammatory and mild central depressive actions. In the present work, the general pharmacological actions of PZ-177 were tested in order to investigate other significant actions and to determine the side effects. PZ-177 showed no significant pharmacological activities on the respiratory and cardiovascular system, on the renal function, on the autonomic nervous system, on the sugar level and coagulation in blood and on local irritation. Volume and acidity of gastric juice were decreased and turn over was not inhibited in the connective tissure. Thus PZ-177 was considered to have no ulcerogenic action on the gastric mucosa. The compound relaxed the tonus of isolated small intestine, tracheal muscles and uterus and stopped spontaneous movement. Moreover the contraction of those smooth muscles by such spasmogens as acetylcholine, histamine serotonin, BaCl2 and oxytocin was inhibited by PZ-177 and the activity was almost the same with each spasmogen. It was found therefore to have spasmolytic activity and no specific antagonistic action on the chemical mediators. PZ-177 showed also wear relaxant activity on the skeletal muscle. Those actions on the muscles may have a curative effect on inflammation in bronchotracheal and gastrointestinal tracts or on pain with contraction of skeletal muscle. From the above results, it may be considered that PZ-177 is a relatively safe and useful analgesic and anti-inflammatory compound.
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PMID:[General pharmacological actions of l-(m-chlorophenyl)-3-N,N-dimethylcarbamoyl-5-methoxypyrazole (PZ-177)]. 98 49

A randomized controlled study comparing once-a-day morning and once-a-day bedtime administration of 40 mg famotidine in treating duodenal ulcers was carried out in 99 Japanese patients. Endoscopic examinations were performed at the baseline and repeated at 3-week intervals until healing was confirmed. Eighty-two patients fulfilled the evaluation criteria (38 in the morning group and 44 in the bedtime group). In 13 of these patients the antisecretory effects of these regimens were also assessed by 24 h intragastric pH monitoring. The healing rates were 66% after 3 weeks and 95% after 6 weeks in the morning group, and 57% after 3 weeks and 80% after 6 weeks in the bedtime group. The differences were insignificant between the two groups, but there was a higher healing rate tendency after 6 weeks in the morning group (0.05 less than P less than 0.10). Regarding pain subsidence, there were no significant differences between the two groups. Both treatments were significantly superior to the control group in increasing 24 h intragastric pH. The morning regimen was significantly superior to the bedtime regimen in suppression of daytime acidity. On the contrary, the bedtime regimen was significantly superior to the morning regimen in suppression of nocturnal acidity. These findings suggest that suppression of nocturnal acidity is important but not essential to promote duodenal ulcer healing and suppression of daytime acidity is equally important. Thus, once-a-day morning administration of 40 mg famotidine seems to be at least as effective as once-a-day bedtime administration of 40 mg famotidine in treating duodenal ulcers.
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PMID:A comparative study of once-a-day morning and once-a-day bedtime administration of 40 mg famotidine in treating duodenal ulcers. 157 22

The aim of this study was to compare the duodenal ulcer healing effects of morning (08.00 hours) vs. single bedtime (22.00 hours) doses of 40 mg famotidine, bearing in mind that the known efficacy of bedtime doses of H2-antagonists is regarded as evidence of the predominance of nocturnal gastric acidity in the pathogenesis of duodenal ulcer. This randomized double-blind multicentre trial was conducted in a total of 127 patients with endoscopically proven active duodenal ulcer. Nine patients dropped out and thus 118 were included in the final analysis. The duration of treatment was 4 weeks, and this was extended to 8 weeks in patients whose ulcers failed to heal by week 4. The patients in the two treatment groups were well matched for age and sex. The therapeutic efficacy parameters were endoscopic healing of the ulcer lesion and disappearance of pain. Results were compared using the chi-square method. The 4- and 8-week (cumulative) ulcer healing rates in the patients treated with the morning dose of famotidine were 77.2% and 86%, respectively, compared with 78.6% and 91.8% in those who received the bedtime dose. The differences failed to prove statistically significant either at week 4 (P = 0.85) or at week 8 (P = 0.31). The percentages of patients with ulcer pain, evaluated weekly, were similar in the two treatment groups. The equivalent efficacy of the morning and bedtime famotidine regimens raises doubts concerning the predominance of nocturnal gastric acidity in the pathogenesis of duodenal ulcer.
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PMID:Comparison between single morning and bedtime doses of 40 mg famotidine for the treatment of duodenal ulcer. 252 Jun 24

In a randomized, double-blind, placebo-controlled, comparative cross-over study, we studied the effect of four H2-receptor antagonists on intragastric 24-hour acidity, nocturnal volume and acid output. Ten healthy male volunteers were administered 300 mg or 150 mg nizatidine, 800 mg cimetidine, 300 mg ranitidine, 40 mg famotidine, or placebo on several days, in each case at 9:000 PM. Nocturnal intragastric H+ concentration (mmol/l) (11:00 PM to 7:00 AM) was significantly reduced by all H2 blockers compared with placebo. We obtained the following inhibition rates: Cimetidine 67%; ranitidine 95%; famotidine 89%; nizatidine 80% (300 mg) and 69% (150 mg). Nocturnal acid (mmol/l) and volume output (ml/h) were also significantly (compared with placebo) inhibited by all four H2-receptor antagonists. Inhibition of nocturnal acid secretion was almost identical on nizatidine 300 mg nocte, ranitidine 300 mg nocte, famotidine 40 mg nocte, and cimetidine 800 mg nocte. Nizatidine 300 mg nocte and 150 mg nocte exclusively reduced acid secretion at night, without an aftereffect into the following day (8:00 AM to 6:00 PM). These results suggest that the clinical efficacy of these H2-receptor antagonists is identical with respect to healing peptic ulcer disease and providing freedom from pain. It is generally accepted today that gastric acid inhibitors used in the treatment of peptic ulcer disease should interfere with daytime gastric acid secretion as little as possible, particularly since the acid protects the stomach from bacteria ingested with the food during the day.
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PMID:[Inhibition of 24-hour acidity by nizatidine]. 256 71


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