Obtained from Medical Marijuana.com
Posted by "Jan"
Medical Marijuana and Peptic Ulcers
Medical benefits of marijuana for people with gastrointestinal disorders were backed up by the United States Institute of Medicine medical marijuana study. According to the Institute, “For patients who suffer simultaneously from severe pain, nausea, and appetite loss, cannabinoid drugs might offer broad-spectrum relief not found in any other single medication."
Medical marijuana can be used to treat a variety of diseases and symptoms related to the gastrointestinal system. Cannabis helps combat cramping that accompanies many GI disorders because cannabinoids relax contractions of the smooth muscle of the intestines. Research shows that the body’s own cannabinoids, known as anandamides, affect neurological systems that control the gastrointestinal system. External and internal cannabinoids strongly control gastrointestinal motility and inflammation. They also have the ability to decrease gastrointestinal fluid secretion and inflammation. This means that cannabis can be useful to stop ulcers and other syndromes.
Studies indicate that cannabinoids in marijuana bind with cannabinoid receptors in the digestive tract, especially the small and large intestine, causing muscle relaxation, reduction of inflammation, analgesia, increased nerve-muscle coordination, anti-emesis, and relief of spasms such as those that cause nausea.
The overall opinion of enlightened people in the medical community is that medical cannabis can interact with the endogenous cannabinoid system to reduce problems associated with nausea, vomiting, gastric ulcers, irritable bowel syndrome, Crohn's disease, secretory diarrhea, paralytic ileus and gastroesophageal reflux disease.
There are no clinical studies with cannabinoids in gastric ulcers. However, THC and other substances that bind to the cannabinoid-1-receptor (CB1 receptor agonists) inhibited the gastric acid production in humans and the formation of ulcers in animals.
The nervous system of the bowel of several species, including the mouse, rat, guinea pig and humans, contains cannabinoid CB1 receptors that depress motility of stomach and intestine.
Gastric acid secretion is also inhibited in response to CB1 receptor activation, although the detailed underlying mechanism has yet to be elucidated. Cannabinoid receptor agonists delay gastric emptying in humans as well as in rodents and probably also inhibit human gastric acid secretion.
The extent to which the effects on gastrointestinal function of cannabinoid receptor agonists or antagonists/inverse agonists can be exploited therapeutically has yet to be investigated as has the extent to which these drugs can provoke unwanted effects in the gastrointestinal tract when used for other therapeutic purposes.
Modified according to: Pertwee RG. Cannabinoids and the gastrointestinal tract. Gut 2001;48(6):859-867
In anaesthetized rats the non selective CB-receptor agonist WIN 55,212-2 and the selective CB(1)-receptor agonist HU-210 dose-dependently decreased the acid secretion. (...) Our results indicate that the antisecretory effects of cannabinoids on the rat stomach are mediated by suppression of the activity of the vagus nerve on the stomach through activation of CB1 receptors.
Modified according to: Adami M, et al. Gastric antisecretory role and immunohistochemical localization of cannabinoid receptors in the rat stomach. Br J Pharmacol 2002;135(7):1598-1606.
In 90 volunteers participating in a vaccine-development programme consumption of beer more than 3 days a week was linked with high stomach acid output, and smoking of cannabis greater than 2 days a week was linked with low acid output. in one word less protection againt helico and pepsin.
Source: Nalin DR, et al. Cannabis, hypochlorhydria, and cholera. Lancet 1978;2(8095):859-862.
Increasing number of evidence suggest that gastric mucosal protection can be induced also centrally. Several neuropeptides, such as TRH, amylin, adrenomedullin, enkephalin, -endorphin, nociceptin, nocistatin, ghrelin or orexin given centrally induce gastroprotection and the dorsal vagal complex and vagal nerve may play prominent role in this centrally initiated effect. Since also cannabinoid receptors are present in the dorsal vagal complex, we aimed to study whether activation of central cannabinoid receptors result in gastric mucosal defense and whether there is an interaction between cannabinoids and endogenous opioids. Gastric mucosal damage was induced by 100% ethanol in rats. The cannabinoids were given intravenously (i.v.) or intracerebroventricularly (i.c.v.), while the antagonists were given i.c.v or intracisternally (i.c.). Gastric lesions were evaluated macroscopically 60 min later. Anandamide, methanandamide and WIN55,212-2 reduced ethanol-induced mucosal lesions after both peripheral (0.28-5.6 µmol/kg, 0.7-5.6 µmol/kg and 0.05-0.2 µmol/kg i.v., respectively) and central (2.9-115 nmol/rat, 0.27-70 nmol/rat and 1.9-38 nmol/rat i.c.v., respectively) administration. The gastroprotective effect of anandamide and methanandamide given i.c.v. or i.v.was reversed by the CB1 receptor antagonist SR141716A (2.16 nmol i.c.v.). Naloxone (27.5 nmol i.c.v.) also antagonized the effect of i.c.v. or i.v. injected anandamide
and WIN55,212-2, but less affected that of methanandamide. The gastroprotective effect of anandamide was diminished also by endomorphin-2 antiserum. In conclusion it was first demonstrated that activation of central CB1 receptors results in gastroprotective effect. The effect is mediated at least partly by endogenous opioids.
Can cannabis be helpful in gastric ulcers?
Answers:
• Franjo Grotenhermen
There are no clinical studies with cannabinoids in gastric ulcers. However, THC and other substances that bind to the cannabinoid-1-receptor (CB1 receptor agonists) inhibited the gastric acid production in humans and the formation of ulcers in animals.
• Roger Pertwee
The nervous system of the bowel of several species, including the mouse, rat, guinea pig and humans, contains cannabinoid CB1 receptors that depress motility of stomach and intestine. (...)
Gastric acid secretion is also inhibited in response to CB1 receptor activation, although the detailed underlying mechanism has yet to be elucidated. Cannabinoid receptor agonists delay gastric emptying in humans as well as in rodents and probably also inhibit human gastric acid secretion. (...)
The extent to which the effects on gastrointestinal function of cannabinoid receptor agonists or antagonists/inverse agonists can be exploited therapeutically has yet to be investigated as has the extent to which these drugs can provoke unwanted effects in the gastrointestinal tract when used for other therapeutic purposes.
Modified according to: Pertwee RG. Cannabinoids and the gastrointestinal tract. Gut 2001;48(6):859-867.
• Adami et al.
In anaesthetized rats the non selective CB-receptor agonist WIN 55,212-2 and the selective CB(1)-receptor agonist HU-210 dose-dependently decreased the acid secretion. (...) Our results indicate that the antisecretory effects of cannabinoids on the rat stomach are mediated by suppression of the activity of the vagus nerve on the stomach through activation of CB1 receptors.
Modified according to: Adami M, et al. Gastric antisecretory role and immunohistochemical localization of cannabinoid receptors in the rat stomach. Br J Pharmacol 2002;135(7):1598-1606.
Sofia et al.
Delta-9-tetrahydrocannabinol (THC) inhibited ulcer formation in the rat. However, this antiulcer activity of THC was substantially less than for tridihexethyl chloride.
Modified according to: Sofia RD, et al. Evaluation of antiulcer activity of delta9-tetrahydrocannabinol in the Shay rat test. Pharmacology 1978;17(3):173-177.
Nalin et al.
In 90 volunteers participating in a vaccine-development programme consumption of beer more than 3 days a week was linked with high stomach acid output, and smoking of cannabis greater than 2 days a week was linked with low acid output.
Source: Nalin DR, et al. Cannabis, hypochlorhydria, and cholera. Lancet 1978;2(8095):859-862.
The current state of knowledge of the biochemistry of cannabinoids is increasing at an exponential rate and, with discoveries of cannabinoid receptors in unexpected areas of the body, new potential research/treatment avenues are appearing at an increasing rate.
Grinspoon reports anecdotal use of cannabis to control bowel movements in multiple sclerosis, and relief from the symptoms of Crohn"s disease. Mikuriya[ii] records irritable bowel syndrome, as well as other inflammatory gastrointestinal conditions (principally among AIDS patients), as one of a wide variety of conditions for which cannabis has been prescribed or recommended for therapeutic use in California. Consroe et al[iii], in an anonymous survey of 112 MS patients, found a large proportion reported improvements in bowel and bladder dysfunction from smoked cannabis. There are no clinical trials currently published, although I understand GW trials of cannabis extracts on patients with bowel disorders are either under way or at an advanced stage of planning.
However, there does appear to be some scientific support for claimed therapeutic benefits, from the research literature concerning the actions and metabolism of cannabinoids and cannabinoid receptors. The wall of the intestine is composed of a type of muscle known as "smooth muscle", also found lining the walls of arteries and in other involuntary functions. Cannabinoids relax smooth muscles.
Intestinal Motility and Irritable Bowel Syndrome:
The CB1 cannabinoid receptor has specifically been found to inhibit motility of the intestine in a variety of laboratory and farm animals. The effect is specific, indicating that endogenous cannabinoids to be responsible for regulating smooth muscle tone in the intesting, and the rate of peristalsis.
Summary - Cannabinoids and the GI Tract:
While I am not aware of any published results from controlled human studies of medical use of cannabis in the treatment of conditions such as gastric ulcers or irritable bowel syndrome, there appears to be sufficient animal evidence of the potential efficacy of cannabis in reducing intestinal spasms, ulceration and gastric acid secretion to merit further research into this and related indications.
Any symptomatic relief obtained from smoking cannabis, or use via inhalers or sublingual sprays, would occur far more rapidly than with oral preparations.
“Given this verified list of problems that can be created by prescription drugs used to treat gastrointestinal disorders, and the lack of such problems caused by medical marijuana which provides better relief, it’s amazing that medical marijuana is not already the most popularly prescribed medication for such disorders.”
Licensed medical marijuana grower-patients who grow medical marijuana using organic ingredients and properly engineered synthetic ingredients have told us that cannabis provides a wide range of relief, without severe side-effects, in ways that other drugs, treatment and surgery do not.
Recommendation: Indica x Sativa hybrid. Whole plant extracts. Vaporizer, Tinctures (under the tongue), Suppositories, Edibles (maybe), CannaButter.
Get the medicine into the system as quickly as possible.
____________________________________________________________________________
References
Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary; HAS Institute of Experimental Medicine, Budapest, Hungary;
Department of Pathophysiology, Faculty of Medicine,
Semmelweis University, Budapest, Hungary References
Grinspoon L & Bakalar JB (1997) Marijuana - The Forbidden Medicine (2nd Ed) Yale University Press
[ii] Mikuriya TH (1998) International Classification of Diseases 9-CM 1996 - Conditions treated with cannabis, encountered 1994-1998.
[iii] Consroe P, Musty R, Rein J, Tillery W, Pertwee R. [1997] The perceived effects of smoked cannabis on patients with multiple sclerosis. Eur Neurol 38(1):44-8
[iv] Rosell S, Agurell S & Martin B (1976) Effects of cannabinoids on isolated smooth muscle preparations. Ch in Nahas (Ed) Marijuana, Chemistry, Biochemistry & Cellular Effects. pp 397-406. Springer-Verlag
[v] Pertwee RG, Fernando SR, Nash JE, Coutts AA. (1996). Further evidence for the presence of cannabinoid CB1 receptors in guinea pig small intestine. Br. J. Pharmacol. 118:2199•205
[vi] Kazuhisa K, Natsuo U, Yuko K, Hiroshi S, Shozo Y, Itsuo K (1997) Distribution of anandamide amidohydrolase in rat tissues with special reference to small intestine, BBA - Lipids And Lipid Metabolism (1347) 2-3 pp. 212-218
[vii] Katayama K, Ueda N, Kurahashi Y, Suzuki H, Yamamoto S, Kato I. [1997] Distribution of anandamide amidohydrolase in rat tissues with special reference to small intestine. Biochim Biophys Acta 1347(2-3):212-8
[viii] Martin BR, Thomas BF & Razdan K (1995) Structural requirements for cannabinoid receptor probes. Ch in Pertwee RG (Ed) Cannabinoid Receptors. London: Academic Press
[ix] Lan R, Liu Q, Fan P, Lin S, Fernando SR, McCallion D, Pertwee R, Makriyannis A. [1999] Structure-activity relationships of pyrazole derivatives as cannabinoid receptor antagonists. J Med Chem 42(4):769-76
[x] Shook JE, and Burks TF (1989) Psychoactive cannabinoids reduce gastrointestinal propulsion and motility in rodents J Pharmacol Exp Ther 249 (2): 444-449.
[xi] Cadas H, Gaillet S, Beltramo M, Venance L, and Piomelli D (1996) Biosynthesis of an Endogenous Cannabinoid Precursor in Neurons and its Control by Calcium and cAMP J Neurosci 16 (12) pp. 3934-3942
[xii] Coutts AA, Irving AJ, Mackie K, Pertwee RG, Anavi-Goffer S [2002] Localisation of cannabinoid CB(1) receptor immunoreactivity in the guinea pig and rat myenteric plexus. J Comp Neurol 448(4):410-22
[xiii] Lopez-Redondo F, Lees GM, Pertwee RG. [1997] Effects of cannabinoid receptor ligands on electrophysiological properties of myenteric neurones of the guinea-pig ileum. Br J Pharmacol 122(2):330-4
[xiv] Pinto L, Izzo AA, Cascio MG, Bisogno T, Hospodar-Scott K, Brown DR, Mascolo N, Di Marzo V, Capasso F. [2002] Endocannabinoids as physiological regulators of colonic propulsion in mice. Gastroenterology 123(1):227-34
[xv] Izzo AA, Fezza F, Capasso R, Bisogno T, Pinto L, Iuvone T, Esposito G, Mascolo N, Di Marzo V, Capasso F. [2001] Cannabinoid CB1-receptor mediated regulation of gastrointestinal motility in mice in a model of intestinal inflammation. Br J Pharmacol 134(3):563-70
[xvi] Izzo AA, Mascolo N, Tonini M, Capasso F. [2000] Modulation of peristalsis by cannabinoid CB(1) ligands in the isolated guinea-pig ileum. Br J Pharmacol 129(5):984-90
[xvii] Mancinelli R, Fabrizi A, Del Monaco S, Azzena GB, Vargiu R, Colombo GC, Gessa GL. [2001] Inhibition of peristaltic activity by cannabinoids in the isolated distal colon of mouse. Life Sci 69(1):101-11
[xviii] Ueda N, Goparaju SK, Katayama K, Kurahashi Y, Suzuki H, Yamamoto S. [1998] A hydrolase enzyme inactivating endogenous ligands for cannabinoid receptors. J Med Invest 45(1-4):27-36
[xix] Croci T, Manara L, Aureggi G, Guagnini F, Rinaldi-Carmona M, Maffrand JP, Le Fur G, Mukenge S, Ferla G. [1998] In vitro functional evidence of neuronal cannabinoid CB1 receptors in human ileum. Br J Pharmacol 125(7):1393-5
[xx] Tyler K, Hillard CJ, Greenwood-Van Meerveld B [2000] Inhibition of small intestinal secretion by cannabinoids is CB1 receptor-mediated in rats. Eur J Pharmacol 409(2):207-11
[xxi] Nalin DR, Levine MM, Rhead J, Bergquist E, Rennels M, Hughes T, O'Donnel S, Hornick RB. [1978] Cannabis, hypochlorhydria, and cholera. Lancet 2(8095):859-62
[xxii] Izzo AA, Mascolo N, Borrelli F, Capasso F. [1999] Defaecation, intestinal fluid accumulation and motility in rodents: implications of cannabinoid CB1 receptors. Naunyn Schmiedebergs Arch Pharmacol 359(1):65-70
[xxiii] Winn M, Arendsen D, Dodge P, Dren A, Dunnigan D, Hallas R, Hwang K, Kyncl J, Lee YH, Plotnikoff N, Young P, Zaugg H. [1976] Drugs derived from cannabinoids. 5. delta6a,10a-Tetrahydrocannabinol and heterocyclic analogs containing aromatic side chains. J Med Chem 19(4):461-71
[xxiv] Turker RK, Kaymakcalan S, Ercan ZS. [1975] Antihistaminic action of (--)-trans-delta 9-tetrahydrocannabinol. Arch Int Pharmacodyn Ther 214(2):254-62
[xxv] Kulkarni-Narla A, Brown DR. [2000] Localization of CB1-cannabinoid receptor immunoreactivity in the porcine enteric nervous system. Cell Tissue Res 302(1):73-80
[xxvi] Pertwee RG [2001] Cannabinoids and the gastrointestinal tract. Gut 48(6):859-67
[xxvii] Landi M, Croci T, Rinaldi-Carmona M, Maffrand J, Le Fur G, Manara L. [2002] Modulation of gastric emptying and gastrointestinal transit in rats through intestinal cannabinoid CB(1) receptors. Eur J Pharmacol 450(1):77
[xxviii] Izzo AA, Mascolo N, Capasso R, Germano MP, De Pasquale R, Capasso F. [1999] Inhibitory effect of cannabinoid agonists on gastric emptying in the rat. Naunyn Schmiedebergs Arch Pharmacol 360(2):221-3
[xxix] Krowicki ZK, Moerschbaecher JM, Winsauer PJ, Digavalli SV, Hornby PJ. [1999] Delta-9-tetrahydrocannabinol inhibits gastric motility in the rat through cannabinoid CB1 receptors. Eur J Pharmacol 371(2-3):187-96
[xxx] Bateman DN. [1983] Delta-9-tetrahydrocannabinol and gastric emptying. Br J Clin Pharmacol 15(6):749-51
[xxxi] Adami M, Frati P, Bertini S, Kulkarni-Narla A, Brown DR, de Caro G, Coruzzi G, Soldani G. [2002] Gastric antisecretory role and immunohistochemical localization of cannabinoid receptors in the rat stomach. Br J Pharmacol 135(7):1598-606
[xxxii] Izzo AA, Mascolo N, Capasso F [2001] The gastrointestinal pharmacology of cannabinoids. Curr Opin Pharmacol 1(6):597-603
[xxxiii] Coruzzi G, Adami M, Coppelli G, Frati P, Soldani G. [1999] Inhibitory effect of the cannabinoid receptor agonist WIN 55,212-2 on pentagastrin-induced gastric acid secretion in the anaesthetized rat. Naunyn Schmiedebergs Arch Pharmacol 360(6):715-8
[xxxiv] Nalin DR, Levine MM, Rhead J, Bergquist E, Rennels M, Hughes T, O'Donnel S, Hornick RB. [1978] Cannabis, hypochlorhydria, and cholera. Lancet 2(8095):859-62
[xxxv] Germano MP, D'Angelo V, Mondello MR, Pergolizzi S, Capasso F, Capasso R, Izzo AA, Mascolo N, De Pasquale R. [2001] Cannabinoid CB1-mediated inhibition of stress-induced gastric ulcers in rats. Naunyn Schmiedebergs Arch Pharmacol 363(2):241-4
[xxxvi] De Souza H, Trajano E, de Carvalho FV, Palermo Neto J. [1978] Effects of acute and long-term cannabis treatment of restraint-induced gastric ulceration in rats. Jpn J Pharmacol 28(3):507-10
^ a b "GI Consult: Perforated Peptic Ulcer". Retrieved 2007-08-26.
^ a b "Peptic Ulcer". Retrieved 2010-06-18.
^ "Peptic ulcer". Retrieved 2010-06-18.
^ "Ulcer Disease Facts and Myths". Retrieved 2010-06-18.
^ Cullen DJ, Hawkey GM, Greenwood DC, et al. (1997). "Peptic ulcer bleeding in the elderly: relative roles of Helicobacter pylori and non-steroidal anti-inflammatory drugs". Gut 41 (4): 459–62. doi:10.1136/gut.41.4.459. PMC 1891536. PMID 9391242.
^ "Peptic Ulcer: Peptic Disorders: Merck Manual Home Edition". Retrieved 2007-10-10.
^ Diverticulitis - Digestive Disorders - Merck Manuals Consumer Version
^ Johannessen T. "Peptic ulcer disease". Pasienthandboka.
^ Kato, Ikuko; Abraham M. Y. Nomura, Grant N. Stemmermann and Po-Huang Chyou (1992). "A Prospective Study of Gastric and Duodenal Ulcer and Its Relation to Smoking, Alcohol, and Diet". American Journal of Epidemiology 135 (5): 521–530. PMID 1570818. Retrieved 2010-03-18.
^ a b Salih, Barik; M Fatih Abasiyanik, Nizamettin Bayyurt, Ersan Sander (June 2007). "H pylori infection and other risk factors associated with peptic ulcers in Turkish patients: A retrospective study". World Journal of Gastroenterology 13 (23): 3245–3248. PMID 17589905.
^ Martin, U.S.A.F.M.C. (Major), David F.; Captain Elizabeth Montgomery, U.S.A. M.C., Arthus S, Dobek, Ph.D., Geoffrey A, Patrissi, M.A., Colonel David A, Peura, U.S.A. M.C., F.A.C.G. (28 June 2008). "Campylobacter pylori, NSAIDS, and Smoking: Risk Factors for Peptic Ulcer Disease". American Journal of Gastroenterology 84 (10): 1268–1272. doi:10.1111/j.1572-0241.1989.tb06166.x. PMID 2801677. Retrieved 2010-03-18.[dead link]
^ Kurata Ph.D., M.P.H., John H.; Nogawa, Aki N. M.S. (Jan 1997). "Meta-analysis of Risk Factors for Peptic Ulcer: Nonsteroidal Antiinflammatory Drugs, Helicobacter pylori, and Smoking". Journal of Clinical Gastroenterology 24 (1): 2–17. doi:10.1097/00004836-199701000-00002.PMID 9013343. Retrieved 2010-03-18.
^ For nearly 100 years, scientists and doctors thought that ulcers were caused by stress, spicy food, and alcohol. Treatment involved bed rest and a bland diet. Later, researchers added stomach acid to the list of causes and began treating ulcers with antacids. National Digestive Diseases Information Clearinghouse
^ A, Sonnenberg; Müller-Lissner SA, Vogel E, Schmid P, Gonvers JJ, Peter P, Strohmeyer G, Blum AL (1981). "Predictors of duodenal ulcer healing and relapse.". Journal of Gastroenterology 81 (6): 1061–1067. PMID 7026344. Retrieved 2010-03-18.
^ Kim YH, Lee JH, Lee SS, et al. (2002). "Long-term stress and Helicobacter pylori infection independently induce gastric mucosal lesions in C57BL/6 mice". Scand. J. Gastroenterol. 37 (11): 1259–64. doi:10.1080/003655202761020515. PMID 12465722.
^ Wachirawat W, Hanucharurnkul S, Suriyawongpaisal P, et al. (2003). "Stress, but not Helicobacter pylori, is associated with peptic ulcer disease in a Thai population". J Med Assoc Thai 86 (7): 672–85. PMID 12948263.
^ "Peptic ulcer". Retrieved 2010-06-18.
^ "Tests and diagnosis". Retrieved 2010-06-18.
^ "ATLAS OF PATHOLOGY". Retrieved 2007-08-26.
^ Peptic Ulcer Symptoms. Retrieved on 2011-02-20
^ "Ranitidine in Peptic Ulcer".
^ "Sucralfate for Peptic Ulcer".
^ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved Nov. 11, 2009.
^ Snowden FM (October 2008). "Emerging and reemerging diseases: a historical perspective". Immunol. Rev. 225 (1): 9–26. doi:10.1111/j.1600-065X.2008.00677.x. PMID 18837773.
^ Brown LM (2000). "Helicobacter pylori: epidemiology and routes of transmission.". Epidemiol. Rev. 22 (2): 283–97. PMID 11218379.
^ "Peptic ulcer disease". Retrieved 2010-06-18.
^ "Epidemiology of peptic ulcer disease". Retrieved 2010-06-18.
^ Marshall B.J., ed. (2002), "Helicobacter Pioneers: Firsthand accounts from the scientists who discovered helicobacters, 1892–1982", ISBN 0-86793-035-7. Basil Rigas, Efstathios D. Papavasassiliou. John Lykoudis. The general practitioner in Greece who in 1958 discovered the etiology of, and a treatment for, peptic ulcer disease.
^ Marshall B.J. (1983). "Unidentified curved bacillus on gastric epithelium in active chronic gastritis". Lancet 1 (8336): 1273–75. PMID 6134060.
^ Marshall B.J., Warren J.R. (1984). "Unidentified curved bacilli in the stomach patients with gastritis and peptic ulceration". Lancet 1 (8390): 1311–15. doi:10.1016/S0140-6736(84)91816-6. PMID 6145023.
^ Kathryn Schulz (2010-09-09). "Stress Doesn't Cause Ulcers! Or, How To Win a Nobel Prize in One Easy Lesson: Barry Marshall on Being ... Right". The Wrong Stuff. Slate. Retrieved 2011-07-17.
^ Van Der Weyden MB, Armstrong RM, Gregory AT (2005). "The 2005 Nobel Prize in physiology or medicine". Med. J. Aust. 183 (11–12): 612–4.PMID 16336147.
^ Ulcer, Diagnosis and Treatment - CDC Bacterial, Mycotic Diseases
^ Medicine for Nurses (Toohey, 1974)
^ Huwez FU, Thirlwell D, Cockayne A, Ala'Aldeen DA (December 1998). "Mastic gum kills Helicobacter pylori [Letter to the editor, not a peer-reviewed scientific article"]. N. Engl. J. Med. 339 (26): 1946. doi:10.1056/NEJM199812243392618. PMID 9874617. Retrieved 2008-09-06. See also their corrections in the next volume.
^ Loughlin MF, Ala'Aldeen DA, Jenks PJ (February 2003). "Monotherapy with mastic does not eradicate Helicobacter pylori infection from mice". J. Antimicrob. Chemother. 51 (2): 367–71. doi:10.1093/jac/dkg057. PMID 12562704.
^ Bebb JR, Bailey-Flitter N, Ala'Aldeen D, Atherton JC (September 2003). "Mastic gum has no effect on Helicobacter pylori load in vivo". J. Antimicrob. Chemother. 52 (3): 522–. doi:10.1093/jac/dkg366. PMID 12888582.
Ramakrishnan K, Salinas RC. Peptic ulcer disease. Am Fam Physician. 2007;76:1005-1012]
Chey WD, Wong BC. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. Aug 2007;102:1808-1825]
Malagelada JR, Kuipers EJ, Blaser MJ. Acid peptic disease: clinical manifestations, diagnosis, treatment, and prognosis. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 142.
Lanza FL, Chan FK, Quigley EM; Practice Parameters Committee of the American College of Gastroenterology. Guidelines for prevention of NSAID-related ulcer complications. Am J Gastroenterol. 2009;104:728-738. [
Posted by "Jan"
Medical Marijuana and Peptic Ulcers
Medical benefits of marijuana for people with gastrointestinal disorders were backed up by the United States Institute of Medicine medical marijuana study. According to the Institute, “For patients who suffer simultaneously from severe pain, nausea, and appetite loss, cannabinoid drugs might offer broad-spectrum relief not found in any other single medication."
Medical marijuana can be used to treat a variety of diseases and symptoms related to the gastrointestinal system. Cannabis helps combat cramping that accompanies many GI disorders because cannabinoids relax contractions of the smooth muscle of the intestines. Research shows that the body’s own cannabinoids, known as anandamides, affect neurological systems that control the gastrointestinal system. External and internal cannabinoids strongly control gastrointestinal motility and inflammation. They also have the ability to decrease gastrointestinal fluid secretion and inflammation. This means that cannabis can be useful to stop ulcers and other syndromes.
Studies indicate that cannabinoids in marijuana bind with cannabinoid receptors in the digestive tract, especially the small and large intestine, causing muscle relaxation, reduction of inflammation, analgesia, increased nerve-muscle coordination, anti-emesis, and relief of spasms such as those that cause nausea.
The overall opinion of enlightened people in the medical community is that medical cannabis can interact with the endogenous cannabinoid system to reduce problems associated with nausea, vomiting, gastric ulcers, irritable bowel syndrome, Crohn's disease, secretory diarrhea, paralytic ileus and gastroesophageal reflux disease.
There are no clinical studies with cannabinoids in gastric ulcers. However, THC and other substances that bind to the cannabinoid-1-receptor (CB1 receptor agonists) inhibited the gastric acid production in humans and the formation of ulcers in animals.
The nervous system of the bowel of several species, including the mouse, rat, guinea pig and humans, contains cannabinoid CB1 receptors that depress motility of stomach and intestine.
Gastric acid secretion is also inhibited in response to CB1 receptor activation, although the detailed underlying mechanism has yet to be elucidated. Cannabinoid receptor agonists delay gastric emptying in humans as well as in rodents and probably also inhibit human gastric acid secretion.
The extent to which the effects on gastrointestinal function of cannabinoid receptor agonists or antagonists/inverse agonists can be exploited therapeutically has yet to be investigated as has the extent to which these drugs can provoke unwanted effects in the gastrointestinal tract when used for other therapeutic purposes.
Modified according to: Pertwee RG. Cannabinoids and the gastrointestinal tract. Gut 2001;48(6):859-867
In anaesthetized rats the non selective CB-receptor agonist WIN 55,212-2 and the selective CB(1)-receptor agonist HU-210 dose-dependently decreased the acid secretion. (...) Our results indicate that the antisecretory effects of cannabinoids on the rat stomach are mediated by suppression of the activity of the vagus nerve on the stomach through activation of CB1 receptors.
Modified according to: Adami M, et al. Gastric antisecretory role and immunohistochemical localization of cannabinoid receptors in the rat stomach. Br J Pharmacol 2002;135(7):1598-1606.
In 90 volunteers participating in a vaccine-development programme consumption of beer more than 3 days a week was linked with high stomach acid output, and smoking of cannabis greater than 2 days a week was linked with low acid output. in one word less protection againt helico and pepsin.
Source: Nalin DR, et al. Cannabis, hypochlorhydria, and cholera. Lancet 1978;2(8095):859-862.
Increasing number of evidence suggest that gastric mucosal protection can be induced also centrally. Several neuropeptides, such as TRH, amylin, adrenomedullin, enkephalin, -endorphin, nociceptin, nocistatin, ghrelin or orexin given centrally induce gastroprotection and the dorsal vagal complex and vagal nerve may play prominent role in this centrally initiated effect. Since also cannabinoid receptors are present in the dorsal vagal complex, we aimed to study whether activation of central cannabinoid receptors result in gastric mucosal defense and whether there is an interaction between cannabinoids and endogenous opioids. Gastric mucosal damage was induced by 100% ethanol in rats. The cannabinoids were given intravenously (i.v.) or intracerebroventricularly (i.c.v.), while the antagonists were given i.c.v or intracisternally (i.c.). Gastric lesions were evaluated macroscopically 60 min later. Anandamide, methanandamide and WIN55,212-2 reduced ethanol-induced mucosal lesions after both peripheral (0.28-5.6 µmol/kg, 0.7-5.6 µmol/kg and 0.05-0.2 µmol/kg i.v., respectively) and central (2.9-115 nmol/rat, 0.27-70 nmol/rat and 1.9-38 nmol/rat i.c.v., respectively) administration. The gastroprotective effect of anandamide and methanandamide given i.c.v. or i.v.was reversed by the CB1 receptor antagonist SR141716A (2.16 nmol i.c.v.). Naloxone (27.5 nmol i.c.v.) also antagonized the effect of i.c.v. or i.v. injected anandamide
and WIN55,212-2, but less affected that of methanandamide. The gastroprotective effect of anandamide was diminished also by endomorphin-2 antiserum. In conclusion it was first demonstrated that activation of central CB1 receptors results in gastroprotective effect. The effect is mediated at least partly by endogenous opioids.
Can cannabis be helpful in gastric ulcers?
Answers:
• Franjo Grotenhermen
There are no clinical studies with cannabinoids in gastric ulcers. However, THC and other substances that bind to the cannabinoid-1-receptor (CB1 receptor agonists) inhibited the gastric acid production in humans and the formation of ulcers in animals.
• Roger Pertwee
The nervous system of the bowel of several species, including the mouse, rat, guinea pig and humans, contains cannabinoid CB1 receptors that depress motility of stomach and intestine. (...)
Gastric acid secretion is also inhibited in response to CB1 receptor activation, although the detailed underlying mechanism has yet to be elucidated. Cannabinoid receptor agonists delay gastric emptying in humans as well as in rodents and probably also inhibit human gastric acid secretion. (...)
The extent to which the effects on gastrointestinal function of cannabinoid receptor agonists or antagonists/inverse agonists can be exploited therapeutically has yet to be investigated as has the extent to which these drugs can provoke unwanted effects in the gastrointestinal tract when used for other therapeutic purposes.
Modified according to: Pertwee RG. Cannabinoids and the gastrointestinal tract. Gut 2001;48(6):859-867.
• Adami et al.
In anaesthetized rats the non selective CB-receptor agonist WIN 55,212-2 and the selective CB(1)-receptor agonist HU-210 dose-dependently decreased the acid secretion. (...) Our results indicate that the antisecretory effects of cannabinoids on the rat stomach are mediated by suppression of the activity of the vagus nerve on the stomach through activation of CB1 receptors.
Modified according to: Adami M, et al. Gastric antisecretory role and immunohistochemical localization of cannabinoid receptors in the rat stomach. Br J Pharmacol 2002;135(7):1598-1606.
Sofia et al.
Delta-9-tetrahydrocannabinol (THC) inhibited ulcer formation in the rat. However, this antiulcer activity of THC was substantially less than for tridihexethyl chloride.
Modified according to: Sofia RD, et al. Evaluation of antiulcer activity of delta9-tetrahydrocannabinol in the Shay rat test. Pharmacology 1978;17(3):173-177.
Nalin et al.
In 90 volunteers participating in a vaccine-development programme consumption of beer more than 3 days a week was linked with high stomach acid output, and smoking of cannabis greater than 2 days a week was linked with low acid output.
Source: Nalin DR, et al. Cannabis, hypochlorhydria, and cholera. Lancet 1978;2(8095):859-862.
The current state of knowledge of the biochemistry of cannabinoids is increasing at an exponential rate and, with discoveries of cannabinoid receptors in unexpected areas of the body, new potential research/treatment avenues are appearing at an increasing rate.
Grinspoon reports anecdotal use of cannabis to control bowel movements in multiple sclerosis, and relief from the symptoms of Crohn"s disease. Mikuriya[ii] records irritable bowel syndrome, as well as other inflammatory gastrointestinal conditions (principally among AIDS patients), as one of a wide variety of conditions for which cannabis has been prescribed or recommended for therapeutic use in California. Consroe et al[iii], in an anonymous survey of 112 MS patients, found a large proportion reported improvements in bowel and bladder dysfunction from smoked cannabis. There are no clinical trials currently published, although I understand GW trials of cannabis extracts on patients with bowel disorders are either under way or at an advanced stage of planning.
However, there does appear to be some scientific support for claimed therapeutic benefits, from the research literature concerning the actions and metabolism of cannabinoids and cannabinoid receptors. The wall of the intestine is composed of a type of muscle known as "smooth muscle", also found lining the walls of arteries and in other involuntary functions. Cannabinoids relax smooth muscles.
Intestinal Motility and Irritable Bowel Syndrome:
The CB1 cannabinoid receptor has specifically been found to inhibit motility of the intestine in a variety of laboratory and farm animals. The effect is specific, indicating that endogenous cannabinoids to be responsible for regulating smooth muscle tone in the intesting, and the rate of peristalsis.
Summary - Cannabinoids and the GI Tract:
While I am not aware of any published results from controlled human studies of medical use of cannabis in the treatment of conditions such as gastric ulcers or irritable bowel syndrome, there appears to be sufficient animal evidence of the potential efficacy of cannabis in reducing intestinal spasms, ulceration and gastric acid secretion to merit further research into this and related indications.
Any symptomatic relief obtained from smoking cannabis, or use via inhalers or sublingual sprays, would occur far more rapidly than with oral preparations.
“Given this verified list of problems that can be created by prescription drugs used to treat gastrointestinal disorders, and the lack of such problems caused by medical marijuana which provides better relief, it’s amazing that medical marijuana is not already the most popularly prescribed medication for such disorders.”
Licensed medical marijuana grower-patients who grow medical marijuana using organic ingredients and properly engineered synthetic ingredients have told us that cannabis provides a wide range of relief, without severe side-effects, in ways that other drugs, treatment and surgery do not.
Recommendation: Indica x Sativa hybrid. Whole plant extracts. Vaporizer, Tinctures (under the tongue), Suppositories, Edibles (maybe), CannaButter.
Get the medicine into the system as quickly as possible.
____________________________________________________________________________
References
Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary; HAS Institute of Experimental Medicine, Budapest, Hungary;
Department of Pathophysiology, Faculty of Medicine,
Semmelweis University, Budapest, Hungary References
Grinspoon L & Bakalar JB (1997) Marijuana - The Forbidden Medicine (2nd Ed) Yale University Press
[ii] Mikuriya TH (1998) International Classification of Diseases 9-CM 1996 - Conditions treated with cannabis, encountered 1994-1998.
[iii] Consroe P, Musty R, Rein J, Tillery W, Pertwee R. [1997] The perceived effects of smoked cannabis on patients with multiple sclerosis. Eur Neurol 38(1):44-8
[iv] Rosell S, Agurell S & Martin B (1976) Effects of cannabinoids on isolated smooth muscle preparations. Ch in Nahas (Ed) Marijuana, Chemistry, Biochemistry & Cellular Effects. pp 397-406. Springer-Verlag
[v] Pertwee RG, Fernando SR, Nash JE, Coutts AA. (1996). Further evidence for the presence of cannabinoid CB1 receptors in guinea pig small intestine. Br. J. Pharmacol. 118:2199•205
[vi] Kazuhisa K, Natsuo U, Yuko K, Hiroshi S, Shozo Y, Itsuo K (1997) Distribution of anandamide amidohydrolase in rat tissues with special reference to small intestine, BBA - Lipids And Lipid Metabolism (1347) 2-3 pp. 212-218
[vii] Katayama K, Ueda N, Kurahashi Y, Suzuki H, Yamamoto S, Kato I. [1997] Distribution of anandamide amidohydrolase in rat tissues with special reference to small intestine. Biochim Biophys Acta 1347(2-3):212-8
[viii] Martin BR, Thomas BF & Razdan K (1995) Structural requirements for cannabinoid receptor probes. Ch in Pertwee RG (Ed) Cannabinoid Receptors. London: Academic Press
[ix] Lan R, Liu Q, Fan P, Lin S, Fernando SR, McCallion D, Pertwee R, Makriyannis A. [1999] Structure-activity relationships of pyrazole derivatives as cannabinoid receptor antagonists. J Med Chem 42(4):769-76
[x] Shook JE, and Burks TF (1989) Psychoactive cannabinoids reduce gastrointestinal propulsion and motility in rodents J Pharmacol Exp Ther 249 (2): 444-449.
[xi] Cadas H, Gaillet S, Beltramo M, Venance L, and Piomelli D (1996) Biosynthesis of an Endogenous Cannabinoid Precursor in Neurons and its Control by Calcium and cAMP J Neurosci 16 (12) pp. 3934-3942
[xii] Coutts AA, Irving AJ, Mackie K, Pertwee RG, Anavi-Goffer S [2002] Localisation of cannabinoid CB(1) receptor immunoreactivity in the guinea pig and rat myenteric plexus. J Comp Neurol 448(4):410-22
[xiii] Lopez-Redondo F, Lees GM, Pertwee RG. [1997] Effects of cannabinoid receptor ligands on electrophysiological properties of myenteric neurones of the guinea-pig ileum. Br J Pharmacol 122(2):330-4
[xiv] Pinto L, Izzo AA, Cascio MG, Bisogno T, Hospodar-Scott K, Brown DR, Mascolo N, Di Marzo V, Capasso F. [2002] Endocannabinoids as physiological regulators of colonic propulsion in mice. Gastroenterology 123(1):227-34
[xv] Izzo AA, Fezza F, Capasso R, Bisogno T, Pinto L, Iuvone T, Esposito G, Mascolo N, Di Marzo V, Capasso F. [2001] Cannabinoid CB1-receptor mediated regulation of gastrointestinal motility in mice in a model of intestinal inflammation. Br J Pharmacol 134(3):563-70
[xvi] Izzo AA, Mascolo N, Tonini M, Capasso F. [2000] Modulation of peristalsis by cannabinoid CB(1) ligands in the isolated guinea-pig ileum. Br J Pharmacol 129(5):984-90
[xvii] Mancinelli R, Fabrizi A, Del Monaco S, Azzena GB, Vargiu R, Colombo GC, Gessa GL. [2001] Inhibition of peristaltic activity by cannabinoids in the isolated distal colon of mouse. Life Sci 69(1):101-11
[xviii] Ueda N, Goparaju SK, Katayama K, Kurahashi Y, Suzuki H, Yamamoto S. [1998] A hydrolase enzyme inactivating endogenous ligands for cannabinoid receptors. J Med Invest 45(1-4):27-36
[xix] Croci T, Manara L, Aureggi G, Guagnini F, Rinaldi-Carmona M, Maffrand JP, Le Fur G, Mukenge S, Ferla G. [1998] In vitro functional evidence of neuronal cannabinoid CB1 receptors in human ileum. Br J Pharmacol 125(7):1393-5
[xx] Tyler K, Hillard CJ, Greenwood-Van Meerveld B [2000] Inhibition of small intestinal secretion by cannabinoids is CB1 receptor-mediated in rats. Eur J Pharmacol 409(2):207-11
[xxi] Nalin DR, Levine MM, Rhead J, Bergquist E, Rennels M, Hughes T, O'Donnel S, Hornick RB. [1978] Cannabis, hypochlorhydria, and cholera. Lancet 2(8095):859-62
[xxii] Izzo AA, Mascolo N, Borrelli F, Capasso F. [1999] Defaecation, intestinal fluid accumulation and motility in rodents: implications of cannabinoid CB1 receptors. Naunyn Schmiedebergs Arch Pharmacol 359(1):65-70
[xxiii] Winn M, Arendsen D, Dodge P, Dren A, Dunnigan D, Hallas R, Hwang K, Kyncl J, Lee YH, Plotnikoff N, Young P, Zaugg H. [1976] Drugs derived from cannabinoids. 5. delta6a,10a-Tetrahydrocannabinol and heterocyclic analogs containing aromatic side chains. J Med Chem 19(4):461-71
[xxiv] Turker RK, Kaymakcalan S, Ercan ZS. [1975] Antihistaminic action of (--)-trans-delta 9-tetrahydrocannabinol. Arch Int Pharmacodyn Ther 214(2):254-62
[xxv] Kulkarni-Narla A, Brown DR. [2000] Localization of CB1-cannabinoid receptor immunoreactivity in the porcine enteric nervous system. Cell Tissue Res 302(1):73-80
[xxvi] Pertwee RG [2001] Cannabinoids and the gastrointestinal tract. Gut 48(6):859-67
[xxvii] Landi M, Croci T, Rinaldi-Carmona M, Maffrand J, Le Fur G, Manara L. [2002] Modulation of gastric emptying and gastrointestinal transit in rats through intestinal cannabinoid CB(1) receptors. Eur J Pharmacol 450(1):77
[xxviii] Izzo AA, Mascolo N, Capasso R, Germano MP, De Pasquale R, Capasso F. [1999] Inhibitory effect of cannabinoid agonists on gastric emptying in the rat. Naunyn Schmiedebergs Arch Pharmacol 360(2):221-3
[xxix] Krowicki ZK, Moerschbaecher JM, Winsauer PJ, Digavalli SV, Hornby PJ. [1999] Delta-9-tetrahydrocannabinol inhibits gastric motility in the rat through cannabinoid CB1 receptors. Eur J Pharmacol 371(2-3):187-96
[xxx] Bateman DN. [1983] Delta-9-tetrahydrocannabinol and gastric emptying. Br J Clin Pharmacol 15(6):749-51
[xxxi] Adami M, Frati P, Bertini S, Kulkarni-Narla A, Brown DR, de Caro G, Coruzzi G, Soldani G. [2002] Gastric antisecretory role and immunohistochemical localization of cannabinoid receptors in the rat stomach. Br J Pharmacol 135(7):1598-606
[xxxii] Izzo AA, Mascolo N, Capasso F [2001] The gastrointestinal pharmacology of cannabinoids. Curr Opin Pharmacol 1(6):597-603
[xxxiii] Coruzzi G, Adami M, Coppelli G, Frati P, Soldani G. [1999] Inhibitory effect of the cannabinoid receptor agonist WIN 55,212-2 on pentagastrin-induced gastric acid secretion in the anaesthetized rat. Naunyn Schmiedebergs Arch Pharmacol 360(6):715-8
[xxxiv] Nalin DR, Levine MM, Rhead J, Bergquist E, Rennels M, Hughes T, O'Donnel S, Hornick RB. [1978] Cannabis, hypochlorhydria, and cholera. Lancet 2(8095):859-62
[xxxv] Germano MP, D'Angelo V, Mondello MR, Pergolizzi S, Capasso F, Capasso R, Izzo AA, Mascolo N, De Pasquale R. [2001] Cannabinoid CB1-mediated inhibition of stress-induced gastric ulcers in rats. Naunyn Schmiedebergs Arch Pharmacol 363(2):241-4
[xxxvi] De Souza H, Trajano E, de Carvalho FV, Palermo Neto J. [1978] Effects of acute and long-term cannabis treatment of restraint-induced gastric ulceration in rats. Jpn J Pharmacol 28(3):507-10
^ a b "GI Consult: Perforated Peptic Ulcer". Retrieved 2007-08-26.
^ a b "Peptic Ulcer". Retrieved 2010-06-18.
^ "Peptic ulcer". Retrieved 2010-06-18.
^ "Ulcer Disease Facts and Myths". Retrieved 2010-06-18.
^ Cullen DJ, Hawkey GM, Greenwood DC, et al. (1997). "Peptic ulcer bleeding in the elderly: relative roles of Helicobacter pylori and non-steroidal anti-inflammatory drugs". Gut 41 (4): 459–62. doi:10.1136/gut.41.4.459. PMC 1891536. PMID 9391242.
^ "Peptic Ulcer: Peptic Disorders: Merck Manual Home Edition". Retrieved 2007-10-10.
^ Diverticulitis - Digestive Disorders - Merck Manuals Consumer Version
^ Johannessen T. "Peptic ulcer disease". Pasienthandboka.
^ Kato, Ikuko; Abraham M. Y. Nomura, Grant N. Stemmermann and Po-Huang Chyou (1992). "A Prospective Study of Gastric and Duodenal Ulcer and Its Relation to Smoking, Alcohol, and Diet". American Journal of Epidemiology 135 (5): 521–530. PMID 1570818. Retrieved 2010-03-18.
^ a b Salih, Barik; M Fatih Abasiyanik, Nizamettin Bayyurt, Ersan Sander (June 2007). "H pylori infection and other risk factors associated with peptic ulcers in Turkish patients: A retrospective study". World Journal of Gastroenterology 13 (23): 3245–3248. PMID 17589905.
^ Martin, U.S.A.F.M.C. (Major), David F.; Captain Elizabeth Montgomery, U.S.A. M.C., Arthus S, Dobek, Ph.D., Geoffrey A, Patrissi, M.A., Colonel David A, Peura, U.S.A. M.C., F.A.C.G. (28 June 2008). "Campylobacter pylori, NSAIDS, and Smoking: Risk Factors for Peptic Ulcer Disease". American Journal of Gastroenterology 84 (10): 1268–1272. doi:10.1111/j.1572-0241.1989.tb06166.x. PMID 2801677. Retrieved 2010-03-18.[dead link]
^ Kurata Ph.D., M.P.H., John H.; Nogawa, Aki N. M.S. (Jan 1997). "Meta-analysis of Risk Factors for Peptic Ulcer: Nonsteroidal Antiinflammatory Drugs, Helicobacter pylori, and Smoking". Journal of Clinical Gastroenterology 24 (1): 2–17. doi:10.1097/00004836-199701000-00002.PMID 9013343. Retrieved 2010-03-18.
^ For nearly 100 years, scientists and doctors thought that ulcers were caused by stress, spicy food, and alcohol. Treatment involved bed rest and a bland diet. Later, researchers added stomach acid to the list of causes and began treating ulcers with antacids. National Digestive Diseases Information Clearinghouse
^ A, Sonnenberg; Müller-Lissner SA, Vogel E, Schmid P, Gonvers JJ, Peter P, Strohmeyer G, Blum AL (1981). "Predictors of duodenal ulcer healing and relapse.". Journal of Gastroenterology 81 (6): 1061–1067. PMID 7026344. Retrieved 2010-03-18.
^ Kim YH, Lee JH, Lee SS, et al. (2002). "Long-term stress and Helicobacter pylori infection independently induce gastric mucosal lesions in C57BL/6 mice". Scand. J. Gastroenterol. 37 (11): 1259–64. doi:10.1080/003655202761020515. PMID 12465722.
^ Wachirawat W, Hanucharurnkul S, Suriyawongpaisal P, et al. (2003). "Stress, but not Helicobacter pylori, is associated with peptic ulcer disease in a Thai population". J Med Assoc Thai 86 (7): 672–85. PMID 12948263.
^ "Peptic ulcer". Retrieved 2010-06-18.
^ "Tests and diagnosis". Retrieved 2010-06-18.
^ "ATLAS OF PATHOLOGY". Retrieved 2007-08-26.
^ Peptic Ulcer Symptoms. Retrieved on 2011-02-20
^ "Ranitidine in Peptic Ulcer".
^ "Sucralfate for Peptic Ulcer".
^ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved Nov. 11, 2009.
^ Snowden FM (October 2008). "Emerging and reemerging diseases: a historical perspective". Immunol. Rev. 225 (1): 9–26. doi:10.1111/j.1600-065X.2008.00677.x. PMID 18837773.
^ Brown LM (2000). "Helicobacter pylori: epidemiology and routes of transmission.". Epidemiol. Rev. 22 (2): 283–97. PMID 11218379.
^ "Peptic ulcer disease". Retrieved 2010-06-18.
^ "Epidemiology of peptic ulcer disease". Retrieved 2010-06-18.
^ Marshall B.J., ed. (2002), "Helicobacter Pioneers: Firsthand accounts from the scientists who discovered helicobacters, 1892–1982", ISBN 0-86793-035-7. Basil Rigas, Efstathios D. Papavasassiliou. John Lykoudis. The general practitioner in Greece who in 1958 discovered the etiology of, and a treatment for, peptic ulcer disease.
^ Marshall B.J. (1983). "Unidentified curved bacillus on gastric epithelium in active chronic gastritis". Lancet 1 (8336): 1273–75. PMID 6134060.
^ Marshall B.J., Warren J.R. (1984). "Unidentified curved bacilli in the stomach patients with gastritis and peptic ulceration". Lancet 1 (8390): 1311–15. doi:10.1016/S0140-6736(84)91816-6. PMID 6145023.
^ Kathryn Schulz (2010-09-09). "Stress Doesn't Cause Ulcers! Or, How To Win a Nobel Prize in One Easy Lesson: Barry Marshall on Being ... Right". The Wrong Stuff. Slate. Retrieved 2011-07-17.
^ Van Der Weyden MB, Armstrong RM, Gregory AT (2005). "The 2005 Nobel Prize in physiology or medicine". Med. J. Aust. 183 (11–12): 612–4.PMID 16336147.
^ Ulcer, Diagnosis and Treatment - CDC Bacterial, Mycotic Diseases
^ Medicine for Nurses (Toohey, 1974)
^ Huwez FU, Thirlwell D, Cockayne A, Ala'Aldeen DA (December 1998). "Mastic gum kills Helicobacter pylori [Letter to the editor, not a peer-reviewed scientific article"]. N. Engl. J. Med. 339 (26): 1946. doi:10.1056/NEJM199812243392618. PMID 9874617. Retrieved 2008-09-06. See also their corrections in the next volume.
^ Loughlin MF, Ala'Aldeen DA, Jenks PJ (February 2003). "Monotherapy with mastic does not eradicate Helicobacter pylori infection from mice". J. Antimicrob. Chemother. 51 (2): 367–71. doi:10.1093/jac/dkg057. PMID 12562704.
^ Bebb JR, Bailey-Flitter N, Ala'Aldeen D, Atherton JC (September 2003). "Mastic gum has no effect on Helicobacter pylori load in vivo". J. Antimicrob. Chemother. 52 (3): 522–. doi:10.1093/jac/dkg366. PMID 12888582.
Ramakrishnan K, Salinas RC. Peptic ulcer disease. Am Fam Physician. 2007;76:1005-1012]
Chey WD, Wong BC. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. Aug 2007;102:1808-1825]
Malagelada JR, Kuipers EJ, Blaser MJ. Acid peptic disease: clinical manifestations, diagnosis, treatment, and prognosis. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 142.
Lanza FL, Chan FK, Quigley EM; Practice Parameters Committee of the American College of Gastroenterology. Guidelines for prevention of NSAID-related ulcer complications. Am J Gastroenterol. 2009;104:728-738. [
