Displaying publications 1 - 20 of 23 in total

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  1. The cause of pyloric stenosis of infancy: A hyperacidity pathogenesis
    Rogers IM
    Med Hypotheses, 2020 Aug;141:108116.
    PMID: 26654484 DOI: 10.1016/j.mehy.2015.11.023
    The cause of pyloric stenosis of infancy (PS) is at present unknown. A theory of causation is proposed which is consistent with all the known clinical features of this condition. It is based on the knowledge that PS babies are hypersecretors of acid which pre-dates the development of PS and is an inherited constitutional feature. This acidity will become temporarily and dangerously high due to an insensitivity of the negative feed-back between gastrin and gastric acidy within the first few weeks of life. Normal babies who have inherited normal acidity will also experience peak acid secretions at that time but will be much less acid than babies destined to develop PS. Acid entering the duodenum causes contraction of the pyloric sphincter. Hyperacidity will naturally lead to repeated pyloric sphincter contractions and sphincter hypertrophy. Inappropriate repeated feeding of the vomiting PS baby by a first-time overanxious mother to her ever hungry baby, by provoking feed related sphincter contraction is considered to play a significant part in pathogenesis. Should the baby with PS survive beyond the age of around 6weeks, the matured negative feed-back between gastrin and acid will ensure that dangerous hyperacidity is kept in check. This coupled with the natural pyloric canal widening with age, will lead then to an long lasting cure. This theory explains satisfactorily all the known and hitherto unexplained features of this condition.
    Matched MeSH terms: Gastric Acid
  2. Fulltext The Perilous PPI: Proton Pump Inhibitor as a Cause of Clinically Significant Hypomagnesaemia
    Tai YT, Tong CV
    J ASEAN Fed Endocr Soc, 2020;35(1):109-113.
    PMID: 33442177 DOI: 10.15605/jafes.035.01.18
    Proton pump inhibitors (PPIs) are the mainstay of therapy for all gastric acid related diseases and are commonly used in current clinical practice. Although widely regarded as safe, PPIs have been associated with a variety of adverse effects, including hypomagnesaemia. The postulated mechanism of PPI-related hypomagnesaemia involves inhibition of intestinal magnesium absorption via transient receptor potential melastin (TRPM) 6 and 7 cation channels. PPIinduced hypomagnesaemia (PPIH) has become a well recognized phenomenon since it was first reported in 2006. Clinical concerns arise from growing number of case reports presenting PPIH as a consequence of long-term PPI use, with more than 30 cases published to date. In this article, we report 2 cases of PPIH associated with the use of pantoprazole. Both patients presented with severe hypomagnesaemia and hypocalcaemia. One of them had associated hypokalemia and cardiac arrhythmia. A casual relation with PPIs postulated and supported by resolution of electrolyte abnormalities after discontinuation of PPIs.
    Matched MeSH terms: Gastric Acid
  3. Synergistic effects of tocopherol, tocotrienol, and ubiquinone in indomethacin-induced experimental gastric lesions
    Nafeeza MI, Kang TT
    Int J Vitam Nutr Res, 2005 Mar;75(2):149-55.
    PMID: 15929636
    Nonsteroidal anti-inflammatory drugs and their adverse effects on the gastric mucosa are yet another set of unresolved medical problems. This study examined the effects of various antioxidants on several gastric parameters after a single exposure to indomethacin. Forty-eight male rats of the Sprague-Dawley (200-250 g) strain were randomly divided to receive a single antioxidant (tocopherol, tocotrienol, or ubiquinone) or a combination of two (tocopherol-tocotrienol, tocopherol-ubiquinone or tocotrienol-ubiquinone) for 28 days. The rats were then challenged with a single dose of indomethacin and killed six hours later. Findings showed that the severity of gastric lesions was comparable in all groups. Only groups that received a combination of antioxidants exhibited reduced lipid peroxidation compared with all other groups (p < 0.05). The combination groups had a higher level of gastric prostaglandin E2 (PGE2) content compared with all other groups (p < 0.05). There was no significant difference among the groups in the gastric acid concentration and the glutathione/oxidized glutathione (GSH/GSSG) ratio. We conclude that although supplementation of these antioxidants in combination had desirable effects on lipid peroxidation and gastric PGE2 level, they did not reduce the lesions produced by indomethacin.
    Matched MeSH terms: Gastric Acid
  4. Fulltext Randomised clinical trial: the effectiveness of Gaviscon Advance vs non-alginate antacid in suppression of acid pocket and post-prandial reflux in obese individuals after late-night supper
    Deraman MA, Abdul Hafidz MI, Lawenko RM, Ma ZF, Wong MS, Coyle C, et al.
    Aliment Pharmacol Ther, 2020 06;51(11):1014-1021.
    PMID: 32343001 DOI: 10.1111/apt.15746
    BACKGROUND: Late-night supper increases the risk of postprandial reflux from the acid pocket especially in obesity. An alginate-based, raft-forming medication may be useful for obese patients with GERD.

    AIMS: To compare the efficacy of Gaviscon Advance (Reckitt Benckiser, UK) and a non-alginate antacid in post-supper suppression of the acid pocket and post-prandial reflux among obese participants.

    METHODS: Participants underwent 48 h wireless and probe-based pH-metry recording of the acid pocket and lower oesophagus, respectively, and were randomised to single post-supper (10 pm) dose of either Gaviscon Advance or a non-alginate antacid on the second night. Primary outcomes were suppression of median pH of acid pocket and lower oesophagus, measured every 10-minutes post-supper for 1 h. Secondary outcomes were suppression of % time pH acid pocket but not the lower oesophagus was suppressed with Gaviscon Advance vs antacid (all P acid pocket. (Clinical trial registration unique identifier: NCT03516188).

    Matched MeSH terms: Gastric Acid/metabolism
  5. Palm vitamin E and the healing of ethanol-induced gastric lesions
    Ismail NM, Jaarin K, Ahmad A, Marzuki A, Ng WK, Gapor MT
    Asia Pac J Clin Nutr, 1999 Dec;8(4):258-62.
    PMID: 24394225
    The main focus of the study was to examine the effect of palm vitamin E (a tocotrienol-enriched fraction of palm oil) on the healing of ethanol-induced gastric mucosal lesions. The study was divided into three sections.Study 1 determined the gastric content of vitamin E after dietary supplementation with palm vitamin E for 3 weeks. Seven rats were fed a normal diet and another 7 were fed a palm vitamin E-enriched diet (150 mg/kg food). The gastric content of vitamin E levels were higher in rats fed with a palm vitamin E-enriched diet (p<0.01). Study 2 determined the time-dependent effects of palm vitamin E on gastric lesions and gastric acidity postethanol administration. Two groups of rats were fed either a normal rat diet or a palm vitamin E-enriched diet (150 mg/kg food). After 3 weeks, the control and a treated group received a single intragastric dose of 100% ethanol. Assessment of gastric lesions after 1 week showed a lower gastric lesion index in the palm vitamin E group compared with the controls (p<0.05) but there was no difference in the gastric acid content after 1 week between the two groups. Study 3 determined the effects of palm vitamin E on the gastric tissue content of malondialdehyde (MDA), PGE2 and gastric acidity without ethanol administration. The MDA content was lower in the palm vitamin E-treated group (p<0.05). However, the gastric acid and PGE2 content in both groups did not differ. The findings suggest that feeding with a palm vitamin E-enriched diet (150 mg/kg food) for 3 weeks resulted in a significant concentration of vitamin E in the gastric tissue. It was concluded that palm vitamin E may promote the healing of ethanol-induced gastric lesions through minimizing the lipid preoccupation process in the gastric mucous.
    Matched MeSH terms: Gastric Acid
  6. Fulltext Mechanisms of Gastroprotective Effects of Ethanolic Leaf Extract of Jasminum sambac against HCl/Ethanol-Induced Gastric Mucosal Injury in Rats
    Alrashdi AS, Salama SM, Alkiyumi SS, Abdulla MA, Hadi AH, Abdelwahab SI, et al.
    Evid Based Complement Alternat Med, 2012;2012:786426.
    PMID: 22550543 DOI: 10.1155/2012/786426
    Jasminum sambac is used in folk medicine as the treatment of many diseases. The aim of the present investigation is to evaluate the gastroprotective effects of ethanolic extracts of J. sambac leaves against acidified ethanol-induced gastric ulcers in rats. Seven groups of rats were orally pre-treated with carboxymethylcellulose (CMC) as normal group, CMC as ulcer group, 20 mg/kg of omeprazole as positive group, 62.5, 125, 250, and 500 mg/kg of extract as the experimental groups, respectively. An hour later, CMC was given orally to normal group and acidified ethanol solution was given orally to the ulcer control, positive control, and the experimental groups. The rats were sacrificed after an hour later. Acidity of gastric content, the gastric wall mucus, ulcer areas, and histology and immunohistochemistry of the gastric wall were assessed. Gastric homogenates were determined for prostaglandin E(2) (PGE(2)), superoxide dismutase (SOD), andmalondialdehyde (MDA) content. Ulcer group exhibited significantly severe mucosal injury as compared with omeprazole or extract which shows significant protection towards gastric mucosal injury the plant promotes ulcer protection as it shows significant reduction of ulcer area grossly, and histology showed marked reduction of edema and leucocytes infiltration of submucosal layer compared with ulcer group. Immunohistochemistry showed overexpression of Hsp70 protein and downexpression of Bax protein in rats pretreated with extract. Significant increased in the pH, mucus of gastric content and high levels of PGE(2), SOD and reduced amount of MDA was observed.
    Matched MeSH terms: Gastric Acid
  7. Histamine dosage for maximal gastric secretion in Asians - a reappraisal
    Ti TK
    Ann Acad Med Singap, 1981 Apr;10(2):198-200.
    PMID: 7332283
    Paired augmented histamine tests using 40 microgram 60 microgram histamine acid phosphate (HAP) per kg body weight were conducted on each of 57 Asian subjects. The mean peak acid output (PAO) for the total series to the two different doses of HAP was 22.3 mEq/hr and 23.3 mEq/hr respectively and the difference was not statistically significant according to the paired t test. There were similarly no significant difference in PAO to the two doses of HAP in the following groups of subjects: 26 Chinese, 17 Indians, 14 Malays; 24 subjects with duodenal ulcer, 16 controls; 28 subjects with body weight below 50 kg, 19 between 50-60 kg and 10 exceeding 60 kg. These findings differ from earlier reports that for maximal gastric secretion Asians required a higher dosage of histamine compared with Caucasian subjects.
    Matched MeSH terms: Gastric Acid/metabolism*
  8. Fulltext Helicobacter pylori and peptic ulcer disease--a causal link
    Goh KL
    Med J Malaysia, 1997 Jun;52(2):161-8.
    PMID: 10968075
    The link between Helicobacter. pylori and peptic ulcer disease in 1997 is an irrefutable one. The association between infection and ulcerogenesis has been shown to be biologically plausible with induction of epithelial inflammation and cell damage and its effect on gastrin/acid homeostasis. The association of H. pylori infection and peptic ulcer disease is a close and consistent one. There is ample evidence indicating that H. pylori eradication results in virtual abolition of ulcer relapse. Several studies have demonstrated that eradication of H. pylori results in ulcer healing and there is evidence showing a temporal relationship between infection and development of peptic ulcer disease.
    Matched MeSH terms: Gastric Acid/secretion
  9. Gastroprotective activities of Turnera diffusa Willd. ex Schult. revisited: Role of arbutin
    Taha MM, Salga MS, Ali HM, Abdulla MA, Abdelwahab SI, Hadi AH
    J Ethnopharmacol, 2012 May 7;141(1):273-81.
    PMID: 22374081 DOI: 10.1016/j.jep.2012.02.030
    Turnera diffusa Willd. ex Schult. has been used for the treatment of several human disorders including peptic ulcer.
    Matched MeSH terms: Gastric Acid/metabolism
  10. Gastric acid secretion in duodenal ulcer disease in the Malaysia-Singapore region
    Ti TK
    Ann Acad Med Singap, 1983 Oct;12(4):507-17.
    PMID: 6678134
    Basal and pentagastrin stimulated acid output was measured in 80 normal and 179 duodenal ulcer subjects of Chinese, Indian and Malay origin. Basal and maximally stimulated acid output was significantly higher in duodenal ulcer patients compared with normal subjects. There was however considerable overlap and less than one in four duodenal ulcer patients were hypersecretors. The acid output (and hence the parietal cell mass) was lower than in Caucasian subjects and this was possibly related to weight differences. The acid output did not differ significantly in the Chinese, Indian and Malay subjects, suggesting that parietal cell mass in the three racial groups is closely similar. The difference in frequency of duodenal ulcer disease in the three racial groups is thus not related to gastric secretory capacity.
    Matched MeSH terms: Gastric Acid/metabolism*; Gastric Acidity Determination
  11. Eurycoma longifolia in Radix for the treatment of ethanol-induced gastric lesion in rats
    Qodriyah HM, Asmadi AY
    Pak J Biol Sci, 2013 Dec 01;16(23):1815-8.
    PMID: 24506055
    The effect of treatment with Radix on ethanol-induced gastric lesions was investigated. The main ingredient of Radix is Eurycoma longifolia. Twenty-four rats of the Sprague-Dawley species were randomly divided into four groups. Three groups were given 0.5 mL 100% ethanol orally. Another group was used as a control and was given only distilled water orally (control). After 6 h all the rats were fed with normal diet. One group that was administered with ethanol was only given distilled water orally (no treatment). Another two groups that were administered with ethanol were treated with oral Radix 0.128 mg g(-1) b.wt. (Radix) and oral ranitidine 21.4 mg kg(-1) b.wt. (Ranitidine), respectively. After one week, all the rats were fasted overnight and sacrificed. The stomach was isolated and examined for the presence and severity of gastric lesions. Measurements for malondialdehyde content and gastric acid concentration were also done. It is found that the ulcer index was lower in the Radix and ranitidine group compared to the no treatment group whereas in the control group there was no lesion. There was no difference in ulcer index between the Radix and ranitidine group. The gastric MDA content was significantly higher in all the groups that were induced with ethanol compared to the control group but no difference between all the ethanol-induced groups. There was no difference in the gastric acid concentration in all groups. Hence it is concluded that Eurycoma longifolia in Radix is as effective as ranitidine in the treatment of ethanol-induced gastric lesions in rats.
    Matched MeSH terms: Gastric Acid/metabolism
  12. Effect of palm vitamin E on the healing of ethanol-induced gastric injury in rats
    Jaarin K, Renuvathani M, Nafeeza MI, Gapor MT
    Int J Food Sci Nutr, 2000;51 Suppl:S31-41.
    PMID: 11271855
    The effect of palm vitamin E on the healing of ethanol-induced gastric lesions and various biochemical parameters were investigated. The study was divided into two phases. In the first phase of the study, 42 rats of Sprague Dawley species (200-250 gm weight) were randomly divided into two groups fed with a normal diet (control) or palm vitamin E enriched diet (150 mg/kg) for 3 weeks. The rats were killed after 3 weeks of feeding. Gastric tissue contents of malondialdehyde (MDA), prostaglandin E2 and acid were measured. In the second phase of the study 42 rats were divided into two groups. Group 1 was fed normal rat pellets (control) and group 2 was fed palm vitamin E enriched pellets (150 mg/kg food) for 3 weeks. After 3 weeks of feeding gastric mucosal injury was induced by an orogastric tube administration of 0.5 ml 100% ethanol. The rats were killed at 1 hour, 4 hours and 1 week after ethanol exposure for semiquantitative determination of ulcer index and gastric acid concentration. Gastric tissue MDA and mucus were measured only at 1 week after ethanol exposure. In the first phase of the study we found that palm vitamin E only caused a significant reduction in gastric MDA. However, it showed no significant effects on prostaglandin E2 and gastric acid concentration. In the second phase of the study, the mean ulcer index of palm vitamin E supplemented group killed after 1 week of ethanol exposure was significantly lower compared to the respective control. However, there was no significant difference in ulcer index in rats killed at 1 hour and 24 hours after ethanol exposure. The gastric acid concentration was significantly higher in the group treated with palm vitamin E killed 1 week after ethanol exposure compared to control. The gastric tissue MDA was significantly lower in the palm vitamin E supplemented group compared to control. There was no significant difference in gastric mucus content of the both groups. The ulcer healing which occurred in the presence of a high gastric acid suggests that the effect of palm vitamin E on the healing of gastric lesions was not mediated via a reduction in gastric acid nor was it mediated through increasing prostaglandin E2 or mucus production. The most probable mechanism is via reducing lipid peroxidation as reflected by a significant decreased in gastric tissue MDA content.
    Matched MeSH terms: Gastric Acid
  13. Fulltext Does oral lansoprazole really reduce gastric acidity in VLBW premature neonates?
    Tham SY, Rogers IM, Samuel KF, Singh A, Ong KK
    Med J Malaysia, 2012 Jun;67(3):284-8.
    PMID: 23082418 MyJurnal
    Premature neonates of very low birth weight (VLBW) whose treatment required the use of naso-gastric tube feeding were investigated. 10 infants suspected of having GERD (gastroesophageal reflux) received oral lansoprazole therapy by tube administration. 9 other infants formed a control group. In the treated group a fasting pH was determined before treatment and again after 7 days treatment. The control group was similarly assessed at an interval of 7 days. Despite acid reduction, the post-treatment pH mean of 1.31 would continue to pose a threat to the esophageal mucosa. The physiology of neonatal acid secretion is discussed to explain these findings.
    Matched MeSH terms: Gastric Acid/secretion*; Gastric Acid/chemistry
  14. Fulltext Comparison between tocotrienol and omeprazole on gastric growth factors in stress-exposed rats
    Nur Azlina MF, Qodriyah HMS, Chua KH, Kamisah Y
    World J Gastroenterol, 2017 Aug 28;23(32):5887-5894.
    PMID: 28932080 DOI: 10.3748/wjg.v23.i32.5887
    AIM: To investigate and compare the effects of tocotrienol and omeprazole on gastric growth factors in rats exposed to water-immersion restraint stress (WIRS).

    METHODS: Twenty-eight male Wistar rats were randomly assigned to four groups of seven rats. The two control groups were administered vitamin-free palm oil (vehicle) and the two treatment groups were given omeprazole (20 mg/kg) or tocotrienol (60 mg/kg) by oral gavage. After 28 d of treatment, rats from one control group and both treated groups were subjected to WIRS one time for 3.5 h. Gastric lesions were measured and gastric tissues were obtained to measure vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), and transforming growth factor-alpha (TGF-α) mRNA expression.

    RESULTS: Rats exposed to WIRS for 3.5 h demonstrated the presence of considerable ulcers in the form of gastric erosion. The lesion index in the stressed control (S) group was increased (P < 0.001) compared to the tocotrienol treated and omeprazole treated groups. Stress led to a decrease in gastric VEGF (P < 0.001), bFGF (P < 0.001) and TGF-α (P < 0.001) mRNA levels and caused an increase in EGF mRNA (P < 0.001) that was statistically significant compared to the non-stressed control group. Although both treatment agents exerted similar ulcer reducing ability, only treatment with tocotrienol led to increased expression of VEGF (P = 0.008), bFGF (P = 0.001) and TGF-α (P = 0.002) mRNA.

    CONCLUSION: Tocotrienol provides gastroprotective effects in WIRS-induced ulcers. Compared to omeprazole, tocotrienol exerts a similar protective effect, albeit through multiple mechanisms of protection, particularly through up-regulation of growth factors that assist in repair of gastric tissue injuries.

    Matched MeSH terms: Gastric Acid/secretion
  15. Fulltext Comparative effects of a tocotrienol-rich fraction and tocopherol in aspirin-induced gastric lesions in rats
    Nafeeza MI, Fauzee AM, Kamsiah J, Gapor MT
    Asia Pac J Clin Nutr, 2002;11(4):309-13.
    PMID: 12495264
    This study examined the effects of a tocotrienol-rich fraction (TRF) obtained from palm oil on the healing of aspirin-induced gastric mucosal lesions. Thirty-six male Sprague-Dawley rats (200-250 g) were randomly divided into three groups. Group I was fed a vitamin E-deficient diet (control), Group II was fed a vitamin E-deficient diet supplemented with tocopherol (300 mg/kg food) and Group III was fed a vitamin E-deficient diet supplemented with TRF (300 mg/kg food). After eight weeks, the control and treated groups received a single intragastric dose of 400 mg/kg body weight aspirin. The rats were killed 24 h after exposure to aspirin. Assessment of gastric lesions showed a lower gastric lesion index in the TRF (P = 0.0005) and tocopherol groups (P = 0.0008) compared to the control. The gastric malondialdehyde (MDA) content was also lower in the TRF (P = 0.025) and tocopherol groups (P = 0.025) compared to control. There were, however, no significant differences in the gastric lesion index and gastric MDA content between the TRF and tocopherol-fed groups. There were no significant differences in the adherent gastric mucous concentration and gastric acid concentration among all groups. We conclude that the TRF and tocopherol are equally effective in preventing aspirin-induced gastric lesions. The most probable mechanism is through their ability to limit lipid peroxidation, which is involved in aspirin-induced gastric lesions.
    Matched MeSH terms: Gastric Acid/secretion
  16. Coatless alginate pellets as sustained-release drug carrier for inflammatory bowel disease treatment
    Md Ramli SH, Wong TW, Naharudin I, Bose A
    Carbohydr Polym, 2016 Nov 05;152:370-381.
    PMID: 27516284 DOI: 10.1016/j.carbpol.2016.07.021
    Conventional alginate pellets underwent rapid drug dissolution and failed to exert colon targeting unless subjected to complex coating. This study designed coatless delayed-release oral colon-specific alginate pellets for ulcerative colitis treatment. Alginate pellets, formulated with water-insoluble ethylcellulose and various calcium salts, were prepared using solvent-free melt pelletization technique which prevented reaction between processing materials during agglomeration and allowed reaction to initiate only in dissolution. Combination of acid-soluble calcium carbonate and highly water-soluble calcium acetate did not impart colon-specific characteristics to pellets due to pore formation in fragmented matrices. Combination of moderately water-soluble calcium phosphate and calcium acetate delayed drug release due to rapid alginate crosslinking by soluble calcium from acetate salt followed by sustaining alginate crosslinking by calcium phosphate. The use of 1:3 ethylcellulose-to-alginate enhanced the sustained drug release attribute. The ethylcellulose was able to maintain the pellet integrity without calcium acetate. Using hydrophobic prednisolone as therapeutic, hydrophilic alginate pellets formulated with hydrophobic ethylcellulose and moderately polar calcium phosphate exhibited colon-specific in vitro drug release and in vivo anti-inflammatory action. Coatless oral colon-specific alginate pellets can be designed through optimal formulation with melt pelletization as the processing technology.
    Matched MeSH terms: Gastric Acid/chemistry
  17. Fulltext Chitosan Nanoparticles as Carriers for the Delivery of ΦKAZ14 Bacteriophage for Oral Biological Control of Colibacillosis in Chickens
    Adamu Ahmad K, Sabo Mohammed A, Abas F
    Molecules, 2016 Mar 14;21(3):256.
    PMID: 26985885 DOI: 10.3390/molecules21030256
    The use of chitosan as a delivery carrier has attracted much attention in recent years. In this study, chitosan nanoparticles (CS-NP) and chitosan-ΦKAZ14 bacteriophage-loaded nanoparticles (C-ΦKAZ14 NP) were prepared by a simple coercavation method and characterized. The objective was to achieve an effective protection of bacteriophage from gastric acids and enzymes in the chicken gastrointestinal tract. The average particle sizes for CS-NP and C-ΦKAZ14 NP were 188 ± 7.4 and 176 ± 3.2 nm, respectively. The zeta potentials for CS-NP and C-ΦKAZ14 NP were 50 and 60 mV, respectively. Differential scanning calorimetry (DSC) of C-ΦKAZ14 NP gave an onset temperature of -17.17 °C with a peak at 17.32 °C and final end set of 17.41 °C, while blank chitosan NP had an onset of -20.00 °C with a peak at -19.78 °C and final end set at -20.47. FT-IR spectroscopy data of both CS-NP and C-ΦKAZ14 NP were the same. Chitosan nanoparticles showed considerable protection of ΦKAZ14 bacteriophage against degradation by enzymes as evidenced in gel electrophoresis, whereby ΦKAZ14 bacteriophage encapsulated in chitosan nanoparticles were protected whereas the naked ΦKAZ14 bacteriophage were degraded. C-ΦKAZ14 NP was non-toxic as shown by a chorioallantoic membrane (CAM) toxicity assay. It was concluded that chitosan nanoparticles could be a potent carrier of ΦKAZ14 bacteriophage for oral therapy against colibacillosis in poultry.
    Matched MeSH terms: Gastric Acid/metabolism
  18. Capsaicin and gastric ulcers
    Satyanarayana MN
    Crit Rev Food Sci Nutr, 2006;46(4):275-328.
    PMID: 16621751
    In recent years, infection of the stomach with the organism Helicobacter Pylori has been found to be the main cause of gastric ulcers, one of the common ailments afflicting humans. Excessive acid secretion in the stomach, reduction in gastric mucosal blood flow, constant intake of non-steroid anti-inflammatory drugs (NSAIDS), ethanol, smoking, stress etc. are also considered responsible for ulcer formation. The prevalent notion among sections of population in this country and perhaps in others is that "red pepper" popularly known as "Chilli," a common spice consumed in excessive amounts leads to "gastric ulcers" in view of its irritant and likely acid secreting nature. Persons with ulcers are advised either to limit or avoid its use. However, investigations carried out in recent years have revealed that chilli or its active principle "capsaicin" is not the cause for ulcer formation but a "benefactor." Capsaicin does not stimulate but inhibits acid secretion, stimulates alkali, mucus secretions and particularly gastric mucosal blood flow which help in prevention and healing of ulcers. Capsaicin acts by stimulating afferent neurons in the stomach and signals for protection against injury causing agents. Epidemiologic surveys in Singapore have shown that gastric ulcers are three times more common in the "Chinese" than among Malaysians and Indians who are in the habit of consuming more chillis. Ulcers are common among people who are in the habit of taking NSAIDS and are infected with the organism "Helicobacter Pylori," responsible for excessive acid secretion and erosion of the mucosal layer. Eradication of the bacteria by antibiotic treatment and avoiding the NSAIDS eliminates ulcers and restores normal acid secretion.
    Matched MeSH terms: Gastric Acid/metabolism*
  19. Antiulcer activity of the chloroform extract of Bauhinia purpurea leaf
    Hisam EE, Zakaria ZA, Mohtaruddin N, Rofiee MS, Hamid HA, Othman F
    Pharm Biol, 2012 Dec;50(12):1498-507.
    PMID: 22954284 DOI: 10.3109/13880209.2012.685945
    CONTEXT: Bauhinia purpurea L. (Fabaceae) is a native plant species of many Asian countries, including Malaysia and India. In India, the root, stem, bark, and leaf of B. purpurea are used to treat various ailments, including ulcers and stomach cancer.
    OBJECTIVE: In an attempt to establish its pharmacological potential, we studied the antiulcer activity of lipid-soluble extract of B. purpurea obtained via extraction of air-dried leaves using chloroform.
    MATERIALS AND METHODS: The rats were administered the chloroform extract (dose range of 100-1000 mg/kg) orally after 24 h fasting. They were subjected to the absolute ethanol- and indomethacin-induced gastric ulcer, and pyloric ligation assays after 30 min. The acute toxicity study was conducted using a single oral dose of 5000 mg/kg extract and the rats were observed for the period of 14 days. omeprazole (30 mg/kg) was used as the standard control.
    RESULTS: At 5000 mg/kg, the extract produced no sign of toxicity in rats. The extract exhibited significant (p < 0.05) dose-dependent antiulcer activity for the ethanol-induced model. The extract also significantly (p < 0.05) increased the gastric wall mucus production and pH of gastric content, while significantly (p < 0.05) reducing the total volume and total acidity of the gastric content in the pylorus ligation assay.
    DISCUSSION AND CONCLUSION: The extract possesses antiulcer, antisecretory and cytoprotective activities, which could be attributed to its flavonoid and tannin content. These findings provide new information regarding the potential of lipid-soluble compounds of B. purpurea for the prevention and treatment of gastric ulcers.
    Matched MeSH terms: Gastric Acid/secretion; Gastric Acidity Determination
  20. Anti-acid secretion activity of drugs cimetidine, ranitidine, tiotidine D 15,144 in dogs fixed with gastric fistulae
    Ridzwan BH, Waton NG, Jais AM
    Gen. Pharmacol., 1989;20(2):133-6.
    PMID: 2565846
    1. Acid secretion for each dog has reached a near maximum (100%) at the 6th samples, 90 min after the intravenous infusion of histamine (10 mu ghr-1, or approximately equal to 0.3 mghr-1). 2. 0.5 mgkg-1 Cimetidine had produced a mean inhibition of 47% on the stomach. 3. 0.1 mgkg-1 Ranitidine (D 14,951) could only inhibit a maximum of 28%, and the secretion had return to normal in just 30 min. 4. 0.025 mgkg-1 Tiotidine (D 15,104) had inhibited 53% acid secretion within 15 min of exposure. Recovery was quite similar to that of Cimetidine, at 150 min. 5. At a dosage one fifth of Cimetidine (0.1 mgkg-1) D 15,144 had depressed 35% of acid secretion at the first 15 min. The inhibition is gradually increased to about 43% (at 30 min), and was maintained for the next 105 min.
    Matched MeSH terms: Gastric Acid/metabolism*
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