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Thursday, May 14, 2009

MANAGEMENT IN PEPTIC ULCER DISEASE


MANAGEMENT IN PEPTIC ULCER DISEASE
T. Jijinu, Sujith Varma
National College of Pharmacy, Manassery, Calicut
Cite this: T. Jijinu, Sujith Varma, "MANAGEMENT IN PEPTIC ULCER DISEASE", B. Pharm Projects and Review Articles, Vol. 1, pp. 514-542, 2006. (http://farmacists.blogspot.in/)
 
DEFINITION
    Ulcers are the open sore in the skin or mucous membrane. Usually ulcers are seen in duodenum, which is the first pact of intestine, in stomach refused as gastric ulcer and esophagus called esophageal ulcers.

 
    Peptic ulcers are generally caused by an acid resistant bacteria called Helicobacter pylori (H pylori) which infect the stomach. H pylori is Gram negative spiral shaped bacteria. In human it colonizes in stomach and the likelihood of infections increases with age. Peptic ulcer describes a condition in which there is a discontinuity in the entire thickness of the gastric mucosa that persist as a result of acid and pepsin in the gastric juice. The word peptic refers to the pepsin i.e., stomach enzyme, which helps in breakdown of proteins.

 
Figure 1
EPIDEMOLOGY

 
    Prevalence of H pylori infection correlates with socio-economic status rather than race with a prevalence of 80% in developing countries compared to prevalence of 20-90% in developed countries. Peptic ulcer is common among older age individual and females.

 
    H pylori infection is commonly seen in adult population. H pylori infections occur in 10% of children annually between the ages of 2 and 8 years. It is clear from the surveys conducted that the majority of person in the world are infected with H pylori.

 
    H pylori infection was diagnosed in 82% of all peptic ulcer patients and also seen in 75% of Non steroidal anti-inflammatory drugs (NSAID) users. 5-10% of the adult population have peptic ulcer in life time.

 
ETIOLOGY

 
        Although H pylori is the major cause for peptic ulcers, other factors which cause peptic ulcer include:
  • Non steroidal anti inflammatory drugs, Aspirin
  • Zollinger Ellison Syndrome (Gastreinoma)
  • Severe stress (e.g.: Trauma, Burns)
  • Alcohol, smoking
  • Bile reflux
  • Pancreatic enzyme reflux
  • Radiation
  • Staphylococcus aureus exotoxin
  • Bacterial or viral infection

 
Figure 2: Peptic ulcer disease

 
        The most important one is the H pylori infection, non steroidal anti-inflammatory drugs, smoking and alcohol consumption.

 
ZOLLINGER -ELLISON SYNDROME

 
        Zollinger Ellison syndrome occurs from a gastrienoma, a tumor in the pancreas. Zollinger Ellison syndrome is characterized by gastric acid hyper secretion and also by the recurrent peptic ulceration that results from a gastrin producing tumor (gastrinoma). This disease can be distinguished from peptic ulcer by the demonstration of fasting hyper gastrinoma. This tumor may be localized or diffuse tumor. The presence of hyper gastrinoma leads to hyper secretion. The treatment is based on the presence or absence of peptic ulcers, esophagitis, diarrhoea, and gastrinoma, which may be malignant. The major drug of choice is the proton pump inhibitors for managing hyper secretion of gastric acid. Treatment should be instituted with omeprazole 60 mg/d.

 
SIGNS AND SYMPTOMS ASSOCIATED WITH PEPTIC ULCER

 
  • Burning pain mainly abdominal pain. Pain may get better or worse after eating a meal.
  • Nausea, vomiting
  • Weight lose
  • Fatigue
  • Belching
  • Chest pain
  • Anorexia
  • Vomiting blood
In children certain medical condition can contribute to the development of ulcer.

 
PATHOPHYSIOLOGY
Gastric acid secretion

 
        A minimal level of gastric acid secretors is necessary for the formation of peptic ulcers. Thus gastric acid serves as a cofactor with H pylori infection or use of non steroidal anti inflammatory drugs. Basal or nocturnal acid secretion is generally increased in a patient with duodenal ulcer. Factor responsible for acid hyper secretion include increased parietal cell mass, increased basal secretory drive and increased post-prandial secretory drive. Acid hyper secretions may also be a consequence of H pylori infection.

 
Figure 3: Peptic ulcer disease
Pepsin

 
        It appears to play a critical role in the proteolytic activity involved in ulcer formation. Gastric mucosal cell secrete two types of proteolytic proenzymes. Pepsinogen is produced only in the chief and mucous neck cells of the acid secreting mucosa, where as pepsinogen II is found in antral mucosa. Pepsin is activated by acidic pH, inactivated reversibly at pH 4 and irreversibly destroyed at pH 7. Pepsinogen I secretion is directly proportional to the rate of acid secretion.

 
Helicobacter pylori

 
        It is a spiral shaped pH sensitive, gram negative micro aerophilic bacterium that resides between the mucous layer and surface epithelial cells in the stomach or any location where gastric type epithelium is found.

 
        The combination of its spiral shape and flagella permits the H pylori to move from the lumen of the stomach, where the pH is low to the mucous layer where the local pH is neutral. The acute infection is accompanied by transient hypochlorhydria, which permits the organism to survive in the acidic gastric juice. The exact method by which H pylori initially induces hypochlorhydria is unclear. One theory is that H pylori produces large amount of urease, which hydrolyse urea in the gastric juice and converts it to ammonia and carbon dioxide. The local buffering effect of ammonia protects the organism from the lethal effect of acid. H pylori also produces acid inhibiting proteins which allow it to adapt to the low pH environment of the stomach. H pylori attaches itself to gastric type epithelium by adherence pedestals, which prevent the organism from being shed during cell turn over and mucus secretion.

 
        H pylori contributes to gastric mucosal injury by
  1. Direct mechanisms
  2. Alteration in the immune / inflammatory response
  3. Hyper gastrinemia leading to increased acid secretion.

 
Direct mucosal damage is produced by elaborating bacterial enzymes (lipases, proteases and urease), virulence factors like (vacuolating cytotoxin, cytotoxin associated gene proteins and growth inhibiting factor) and adherence. Lipases and protease degrade gastric mucus, ammonia produced by urease may be toxic to gastric epithelial cells, and bacterial adherence enhances the uptake of toxins into gastric epithelial cells.

 
        H pylori infection alter the inflammatory response and damages epithelial cells directly by cell mediated immune mechanisms or indirectly by activated neutrophils or macrophages attempting to phagocytose bacteria or bacterial products. H pylori infection may increase gastric acid secretion in patients with duodenal ulcer, or diminish acid output in patients with gastric cancer infection of gastric antrum leads to post prandial hypergastrinemia and hyper secretion of gastric acid. Responsible mechanisms includes (1) Cytokines, such as tumor necrosis factor (TNF) a released in H pylori gastritis; (2) products of H pylori, such as ammonia; and diminished expression of somatostatin.

 
Non Steroidal Anti Inflammatory Drugs
        Non steroidal anti inflammatory drugs cause gastric mucosal damage by two important mechanisms (a) direct or topical irritation of the gastric epithelium and (b) Systemic inhibition of endogenous GI mucosal prostaglandin synthesis

 
    Systemic inhibition of prostaglandin play the predominant role in the development of gastric ulcer. Cycloxygenase (COX) is the rate limiting enzyme in the conversion of arachidonic acid to PGs and is inhibited by Non steroidal anti inflammatory drugs.

 
DIAGNOSIS
Test for H Pylori

 
    The diagnosis of H pylori can be made using invasive or non invasive tests. The invasive method requires upper GI endoscopy with a mucosal biopsy taken for histology, culture or detection of urease activity.

 
    The non invasive tests for H pylori do not require endoscopy or a mucosal biopsy and include the urea breath test and antibody detection test. These are less expensive than endoscopic tests. Various tests for detection of H pylori is given in table below.
Table:1
Tests 
Description
Advantages 
Disadvantages 
Antibody detection (Laboratory based) 
Detects antibodies to H pylori in serum 
  • Endoscopy not required
  • Inexpensive
  • Most accurate 
  • Low specificity  
Antibody detection 
Qualitative detection of IgG antibody to H pylori in whole blood
  • Quick
  • Inexpensive  
  • May yield invalid results 
Urea breath test
H pylori urease breaks down ingested labeled (urea, patients exhales labeled CO2)
  • Endoscopy not required
  • Less expensive 
  • Results are not immediate
Histology
Microbial examination
  • High specificity and sensitivity
  • Require endoscopy
  • Expensive
Culture
Culture of biopsy
  • Used to test for antibiotic resistance
  • High specificity  
  • Require endoscopy
  • Patient discomfort
  • Expensive 
Biopsy urease
Urease of H pylori generates ammonia which causes a colour change
  • High specificity and sensitivity
  • Require endoscopy
  • expensive 

 

 
    In case of invasive test histological identification has a sensitivity and specificity greater than 95% and allows classification of gastritis that may be present. Culture has a specificity of 100% and enables susceptibility testing of anti microbial agents to detect resistance and permit appropriate treatments.

 
    The sensitivity and specificity of Biopsy urease test which detect H pylori urease enzyme activity are above 90%. Urea breath test is based on urease production by H pylori. The carbon 13 (Non radio active isotope) and carbon 14 (Radio active isotope) tests require that the patient ingest labeled urea, which is broken down in the stomach to ammonia and labeled bicarbonate. The labeled bicarbonate is absorbed in the blood and excreted in breath.

 
    Antibody detection test are used to detect circulating immuno globulin IgG directed against H pylori.

 
    ELISA (Enzyme Linked Immuno Sorbent Assay) have been approved for use and have a sensitivity and specificity of 90%. The method use an enzyme to detect the binding of Ag & Ab. This enzyme converts colorless substrate to colored product indicate the presence of Ag-Ab binding. (Ag-Antigen & Ab-Antibody).

 
    Tests for H pylori (with the exception of antibody detection) may produce false negative results. If antibiotics or bismuth are taken with in the previous four weeks, or if a proton pump inhibitor is taken with in the previous two weeks. These agents temporarily suppresses H pylori and cause false negative results.

 
    The selection of a specific H pylori test depends on patient specific factor and the clinical situation. Antibody (Ab) detection tests are the initial screening test of choice because they are quick, inexpensive and less invasive than endoscopic biopsy tests.

 
TREATMENT

 
Recommended treatment may include:

 
Life Style Changes
    Doctors used to recommend eating bland foods with milk and only small amount of food with each meal. People who find that certain foods cause irritation should discuss the problem with their physicians. Smoking has been shown to delay ulcer healing and has been linked to ulcer recurrence. Therefore people with ulcer should not smoke.

 
Medications

 
    Several types of medication are given for the treatment of stomach and duodenal ulcer. Which include,

 

 
  • H2 blockers to reduce the amount of acid in the stomach by blocking histamine, which is a powerful stimulant of acid secretion.

 
  • Acid pump inhibitors which completely block stomach acid production by stopping the stomachs acid pump the final step of acid secretion.

 
  • Mucosal protective agents to shield the stomach's mucous lining from the damage of acid and they do not inhibit the release of acid.

 
    When treating H pylori, these medications are often used in combination with antibiotics.

 
Surgery

 
    In most cases, antiulcer medicines heal ulcers quickly and effectively, and eradication of Helicobacter pylori prevents most ulcers from recurring. However, people who do not respond to medication or who develop complications may require surgery.

 
    At present, laparoscopic surgery is performed to treat ulcers and include,

 
  • Vagotomy: A procedure that involves cutting parts of the vagus nerve (a nerve that transmits message from the brain to the stomach) to interrupt messages sent through it and thereby, reducing the acid secretion.

 
  • Antrectomy: An operation to remove the lower part of the stomach (antrum), which produces a hormone that stimulates the stomach to secrete digestive juices. Sometimes a surgeon may also remove an adjacent part of the stomach that secretes pepsin and acid. The vagotomy is usually done in conjunction with an antrectomy.

 
  • Pyloroplasty: A surgical procedure that may be performed along with a vagotomy, in which the opening in to the duodenum and small intestine (pylorus) are enlarged, enabling contents to pass more freely from the stomach. In the future laproscopic methods may become the standard surgical treatment.

 
GOALS OF TREATMENT

 
    Treatment goals are the relief of discomfort and protection of the gastric mucosal barrier to promote healing. Cessation of the causative agent and antacids may be sufficient for treating mild cases. Most patients require an H2 receptor antagonist or a pump inhibitor, which has proved to provide a faster and more reliable healing than antacids. Either an H2 receptor blocker or a proton pump inhibitor can be used as a first line agent. In refractory cases, sucralfate also may be indicated.

 
CLASSIFICATION OF DRUGS USED IN TREATMENT

 
  1. Reduction of gastric acid secretion
    a. H2 antihistamines            : Cimetidine, Famotidine, Nizatidine,                   Rantidine
    b. Proton pump inhibitors     : Lansoprazole, Omeprazole, Esomeprazole,                          Rabe prazole, Pantoprazole.
    c. Anticholenergics              :Pirenzepine, Propantheline, Oxyphenonium.
    d. Prostaglandin analogues     : Misoprostol, Enprostil, Rioprostil.

 
  1. Neutralization of gastric acid (Antacids)
    a. Systemic antacid            : Sodium bicarbonate, Sodium citrate
    b. Non systemic antacids         : Magnesium hydroxide, Magnesium
                        trisilicate, Magaldrate, Aluminium
                        hydroxide gel, Calcium carbonate.

 
  1. Ulcer protectives         : Sucralfate, Colloidal bismuth sub citrate                      (CBS).

 
  1. Ulcer healing drugs            : Carbenxolone sodium.
  2. Anti H pylori drugs            : Amoxicillin, Clarithromycin,
                        Metronidazole, Tinidazole, Tetracyclin.
Table 2
Drug Category:
Antacids
Aluminium containing and magnesium containing antacids can be helpful in relieving symptoms of gastritis by neutralizing gastric acids. These agents are inexpensive and safe
Drug Name
Aluminium and magnesium hydroxide (Maalox, Mylanta). It neutralizes gastric acidity, resulting in increase in stomach and duodenal bulb pH. Aluminium ions inhibit smooth muscle contraction, thus inhibiting gastric emptying. Magnesium and aluminum antacid mixtures are used to avoid bowel function changes.
Adult dose 
2 – 4 tsp PO qid prn.
Pediatric Dose 
0.5 ml/kg PO qid prn
Contraindictions 
Documented hypersensitivity 
Interactions
Both drugs reduce efficacy of fluoroquinolones, contricosteroids, benzodiazepines, and phenothiazines; aluminum and magnesium potentiate effects of valproic acid, sulfonylurea, quinidine, and levodopa 
Pregnancy 
C-Safety for use during pregnancy has not been established
Precautions  
Use aluminum containing antacids with caution in patients who have recently suffered a massive upper GI hemorrhage
Drug Category
H2-receptor antagonists – inhibit the action of histamine on the parietal cell, which inhibits acid secretion. The four drugs in this class are all equally effective and are available over the counter in half prescription strength for heartburn treatment. Although the IV administration of H2 blockers may be used to tret acute complications, the benefits are yet to be proven.
Drug Name 
Cimetidine (Tagamet) – inhibits histamine at H2 receptors of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.
Adult Dose 
150 mg PO qid; not exceed 600 mg/d 50 mg/dose IV/IM q6-8h; not to exceed 400 mg/d.
Pediatric Dose 
Not established. Suggested Dose: 20-40mg/kg/d PO/IV/IM divided q4h.
Contrindications 
Documented hypersensitivity.
Interactions 
Can increase blood levels of theophylline, warfrain, tricyclic antidepressants, triamterene, phenytoin, quinidine, propranolol, metronidazole, procainamide, and lidocaine.
Pregnancy
B-Usually safe but benefits must outweigh the risks.
Precautions 
Elderly patients may experience confusional states; may cause impotence and gynecomastia in young makes; may increase levels of many drugs; adjust dose or discontinue treatment if changes in renal function occur.
Drug Name 
Famotidine (Pepcid) – competitively inhibits histamine at the H2 receptor of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.
Adult Dose
40mg PO qhs
20mg/dose IV qhs; not to exceed 40 mg/d
Pediatric dose
Not established
Suggested dose: 1-2 mg/kg/d PO/IV divided qhs; not to exceed 40 mg/dose
ContraindicationsDocumented hypersensitivity
InteractionsMay decrease effects of ketoconazole and itraconazole
PregnancyB - Usually safe but benefits must outweigh the risks.
PrecautionsIf changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment
Drug NameNizatidine (Axid) - Competitively inhibits histamine at H2 receptors of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.
Adult Dose300 mg PO hs or 150 mg PO bid
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity
InteractionsNone reported
PregnancyB - Usually safe but benefits must outweigh the risks.
PrecautionsCaution in renal or liver impairment; if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment

 

Drug NameRanitidine (Zantac) - Competitively inhibits histamine at the H2 receptors of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.
Adult Dose150 mg PO bid or 300 mg PO qhs; not to exceed 300 mg/d
50 mg/dose IM/IV qhs
Pediatric Dose<12 years: Not established
>12 years: 1.25-2.5 mg/kg/dose PO qhs; not to exceed 300 mg/d
0.75-1.5 mg/kg/dose IV/IM qhs; not to exceed 400 mg/d
ContraindicationsDocumented hypersensitivity
InteractionsMay decrease effects of ketoconazole and itraconazole; may alter serum levels of ferrous sulfate, diazepam, nondepolarizing muscle relaxants, and oxaprozin
PregnancyB - Usually safe but benefits must outweigh the risks.
PrecautionsCaution in renal or liver impairment; if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment
Drug Category: Proton pump inhibitors - Bind to the proton pump of parietal cell, inhibiting secretion of hydrogen ions into gastric lumen. Proton pump inhibitors relieve pain and heal peptic ulcers more rapidly than H2 antagonists do. Drugs in this class are equally effective. They all decrease serum concentrations of drugs that require gastric acidity for absorption, such as ketoconazole or itraconazole. Five drugs are now FDA approved in this category. Omeprazole will soon go off patent and be available as a generic. Side effect is achlorhydria
Drug Name Lansoprazole (Prevacid) - Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump.
Used for up to 4 week to treat and relieve symptoms of active duodenal ulcers. Physicians may prescribe for up to 8 wk to treat all grades of erosive esophagitis.
Adult Dose 30 mg qid for 4-8 week
Pediatric Dose Not established  
Contraindications Documented hypersensitivity  
Interactions May decrease effects of ketoconazole and itraconazole; may increase theophylline clearance
Pregnancy B - Usually safe but benefits must outweigh the risks.  
Precautions Adjust dose in liver impairment 
Drug Name Omeprazole (Prilosec) -- Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump.
Used for up to 4 week to treat and relieve symptoms of active duodenal ulcers. Physicians may prescribe for up to 8 wk to treat all grades of erosive esophagitis.
Adult Dose 20 mg PO qid for 4-8 week
Pediatric Dose Not established
Contraindications Documented hypersensitivity  
Interactions May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin  
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Bioavailability may be increased in elderly patients 
Drug Name Esomeprazole (Nexium) - S-isomer of omeprazole. Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump.
Used for up to 4 week to treat and relieve symptoms of active duodenal ulcers. Physicians may prescribe for up to 8 week to treat all grades of erosive esophagitis.
Adult Dose 20-40 mg PO qid
Pediatric Dose Not established  
Contraindications Documented hypersensitivity  
Interactions Amoxicillin or clarithromycin may increase plasma levels of esomeprazole when used concurrently; may reduce absorption of dapsone; may increase levels of diazepam and GI absorption of digoxin; may decrease absorption of iron, ketoconazole and itraconazole
PregnancyC - Safety for use during pregnancy has not been established.  
Precautions Symptomatic relief with proton pump inhibitors may mask symptoms of gastric malignancy 
Drug Name Rabeprazole (Aciphex) -Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump. For short-term (4-8 week) treatment and symptomatic relief of gastritis.
Used for up to 4 week to treat and relieve symptoms of active duodenal ulcers. Physicians may prescribe for up to 8 wk to treat all grades of erosive esophagitis.
Adult Dose 20 mg tab PO qid 4-8 week
Pediatric Dose Not established  
Contraindications Documented hypersensitivity  
Interactions May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin  
PregnancyB - Usually safe but benefits must outweigh the risks.  
Precautions Symptomatic relief with proton pump inhibitors may mask symptoms of gastric malignancy 
Drug Name Pantoprazole (Protonix) -Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump. For short-term (4-8 week) treatment and symptomatic relief of gastritis.
Used for up to 4 week to treat and relieve symptoms of active duodenal ulcers. Physicians may prescribe for up to 8 week to treat all grades of erosive esophagitis.
Adult Dose 40 mg PO qid
Pediatric Dose Not established  
Contraindications Documented hypersensitivity  
Interactions May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin  
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Symptomatic relief with proton pump inhibitors may mask symptoms of gastric malignancy 
Drug Category: Gastrointestinal agents - Are effective in the treatment of peptic ulcers and in preventing relapse. Their mechanism of action is not clear. Multiple doses are required, and they are not as effective as the other options. Side effects are constipation, dry mouth and nausea.
Drug Name Sucralfate (Carafate) - Binds with positively charged proteins in exudates and forms a viscous adhesive substance that protects the GI lining against pepsin, peptic acid, and bile salts. Used for short-term management of ulcers.
Adult Dose 1 g PO qid  
Pediatric Dose Not established
Suggested dose: 40-80 mg/kg/ divided qhs
Contraindications Documented hypersensitivity  
Interactions May decrease effects of ketoconazole, ciprofloxacin, tetracycline, phenytoin, warfarin, quinidine, theophylline, and norfloxacin  
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Caution in renal failure and impaired excretion of absorbed aluminum 
Drug Name Misoprostol (Cytotec) - A prostaglandin analog that protects the lining of the GI tract by replacing depleted prostaglandin E1 in prostaglandin inhibiting therapies.
Adult Dose 200 mcg PO qid with food; if not tolerated, decrease to 100 mcg qid or 200 mcg bid with food  
Pediatric Dose Not established  
Contraindications Documented hypersensitivity  
Interactions None reported  
PregnancyX - Contraindicated in pregnancy  
Precautions Caution with elderly patients and in renal impairment 

 

 
AYURVEDIC MEDICATION

 
  • Aloe M.P Plus
    Aloe M.P Plus is a powerful natural, 100% organic aloe mucilaginous polysaccharides (AMP) based non toxic supplement. Aloevera polysaccharides are believed to neutrilise harmful enzymes and proteins and work together with your body to reverse stomach disorders, immune disease and many other common aliments.
        
  • Manuka honey
    Manuka honey has been found to inhibit the growth of the bacteria, Helicobacter pylori.

 
    The procedure to take summerglow UMF 16 + Manuka honey for digestive health is given as

 
    i. Take a teaspoon to a table spoon of summerglow UMF 16 + Manuka honey three-four times a day. Ideally one hour before meals and again at bed time.

 
    ii. Should not drink water immediately after having the honey so as not to dilute the honey.

 
    iii. Take honey with bread, toast or cracker biscuit holds the honey in the stomach for as long as possible.

 
    iv. Many people have experienced good results if they have the honey straight from the teaspoon.

 
    v. Summerglow UMF 16 + Manuka honey is pure honey. So it does not interfere with regular medications.

 
    vi. Adjust the amount and frequency to suit your own needs. Most people have a generous amount of the honey initially they reduce it as they feel warranted.

 
    vii. A little discomfort was experienced by a few for a very short period.

 
    Summer glow UMF 16 + Manuka honey is 100% pure honey so it is safe to have as much as desired and as often as wished. (excepts for diabetics)

 
  • Extra virgin Siberian pine nut oil

 
    Extra virgin Siberian pine nut oil stops ulcer related stomach and duodenal ulcer quickly. It has got natural antioxidant property. Clinical studies proves that peptic ulcer are also caused by free radicals. So this oil acts as an effective healing agent for such type of ulcers.

 
HERBS

 
    Certain herbs are recommended by herbal specialist for peptic ulcers. They are
  • Astragalus (Astragalus membranaceus): Used traditionally to treat stomach ulcers.
  • Barberry (Berberis vulgaris): This herbs contains active substances called berberine alkaloids. These substances have been shown to combat infection and bacteria. For this reason barberry is used to ease inflammation and infection of the gastro intestinal tract. Barberry has also been used traditionally to improve apetite.

 
  • Bilberry (Vaccinium myrtillus): Bilberry fruits helps to prevent stomach ulcer related to a variety of factors including stress, medications and alcohol.

 
  • Cat's claw (Uncaria tomentosa): The back and root of this herb have been used among indigenous people of the rainforest for centuries to treat a variety of health problems including ulcers and other gastro intestinal disorders. The benefits of this herb may be due to its ability to reduce inflammation.

 
  • Cranberry (Vaccinium spp): May have properties that help to prevent
    H pylori infection.

 
  • Dong Quai (Angelica sinensis): Animal studies with dong quai, soothe ulcers, but studies in needed before a definitive conclusion can be drawn.

 
  • Garlic (Allium sativum): Some studies suggest that high amounts of garlic may protect against stomach cancer, which is a potential complication of H pylori peptic ulcers. This is controversial, however and high amounts of garlic may infact cause gastro intestinal distress.

 
  • Licorice (glycyrrhiza glabra): This herb is a demulcent (soothing, coating agent) that has long been valued for its use in food and medicinal remedies, including treatment of ulcers. Some licorice root extracts, known as deglycyrrhizenated licorice (DGL), still have the healing properties of licorice without the harmful effects. DGL may be better for stomach or duodenal ulcers than Glycyrrhia glabra and may even prove as effective as some prescription drugs for stomach ulcers.

 
  • Slippery elm (ulmus fulva): Although there has been little scientific research on slippery elm, it has along history of use based on clinical experience. Gastritis (stomach inflammation) and peptic ulcer are among the conditions that seem to respond well to slippery elm.

 
  • Turmeric (curcuma longa): Turmeric has long been used in both Ayurvedic and Chinese medicine to treat digestive disorders. In an animal study, for example, extracts of turmeric root reduced the release of acid from the stomach and protect intestinal walls and ulsers from injuries such as gastritis or inflammation. Further studies are needed to know to what extend these protective effects apply to human volunteer as well (Note: at very high doses, turmeric may induce ulcers). It is very important to stick with the dose recommended by an herbal specialist.

 
  • Angelica (Angelica archangelica)

 
  • German chamomile (Matricaria recutita)

 
  • Lemon balm (Melissa officinalis)

 
  • Licorice

 
  • Milk thistle (Silybum marianum)

 
  • Peppermint (Mentha piperita)

 
Additional herbs that have been used clinically by herbal specialist to treat peptic ulcers include;

 
  • Calendula (calendula officinalis): Used in the United States during the 19th century to treat stomach ulcers.
  • Capsaicin: The active ingredient in cryenne (capsicum frutescens/capsicum Spp)
  • Marshmallow (althea officinalis)

 
HELICOBACTER PYLORI ERADICATION
Effective treatment
    
    Treatment regimens which have been shown in randomized controlled trials (RCTS) to be most effective consist of two antibiotics combined with either bismuth or a proton pump inhibitor or H2 antagonist. Three regimens are mentioned here.

 
  1. Standard triple therapy
    Consist of a two week course of bismuth subcitrate (4 ´ 120mg daily) with metronidazole (3 ´ 400 mg daily) and tetracycline (4 ´ 500mg daily). It is cheap and has been shown to eradicate H pylori in almost 95% of patients. This standard triple therapy have given along with H2 antagonist or proton pump inhibitor, but the benefit of this have not been evaluated. The H2 antagonist or proton pump inhibitor is stopped once healing has occurred.

     
  2. Other triple therapies
    Five new regimen which has found to achieve eradication rates of 95% or over have been evaluated. One week of omeprazole (2 ´ 20mg daily), Amoxicillin (2 ´ 1000mg daily), clarithromycin (2 ´ 500mg daily).
        
        Alternatively one week of : Omeprazole (2 ´ 20 mg daily), metronidazole (2 ´ 400 mg daily), clarithromycin (2 ´ 250mg daily). These treatment have not been compared directly to the standard triple therapy. Several other alternative regimens have been proposed.

     
  3. Success of eradication therapy
    Success depends on:
        Patient compliance: Patient should be counseled concerning the importance of completing the course of therapy and warn against the possible side effects they may experience. Metronidazole and Tinidazole medications are not effective in populations with resistance to H pylori organisms.

     
        The standard triple therapy has proven to be very effective and its low cost make it a choice of treatment.

 
HEALING OPTIONS
Table 3
Herbal Home Remedy        : Banana
                 Chandan
                 Lime
                 Vegetable juice
                 Almond milk
Ayurvedic supplements    : Avucid
                 Avipattikar churna
                 Mahashankha Bati
                 Prawal Bhasma 
Diet     : The diet of the patient suffering from a peptic ulcer should be planned so as to provide adequate nutrition, while affording rest to the disturbed organs, maintaining the neutralization of excess gastric acid and there by inhibiting the production of acid and reducing mechanical and chemical irritation. Milk, cream, butter, fruits, fresh raw and boiled vegetables, natural foods and natural vitamin supplements constitute the best diet.
Yoga    : Yoga will also help in the healing of peptic ulcer disease.
  • Vajrasana
  • Padmasana
  • Pawanmuktasan
  • Bhujangasana
  • Paschl mothanasana 

 
LIFE STYLE:

 
    Doctors generally recommend eating bland foods with mild and only small amounts of food with each meal. Dietary and other life style measures that should help include;
  • Eat a diet rich in fiber, especially from fruits and vegetables; this may reduce the risk of developing an ulcer in the first place and may speed up the recovery. The vitamin A may be an added benefit from these foods.

 
  • Foods containing flavanoids, like apples, celery, cranberries (including cranberry juice), onions, and tea may inhibit the growth of Helicobacter pylori.

 
  • Quit smoking

 
  • Receive treatment for alcohol abuse

 
  • Avoid coffee, including decaffeinated coffee, as well as carbonated beverages all of which can increase the production of stomach acid

 
  • Reduce stress with regular use of relaxation techniques such as yoga or medication. These practices may help to lessen pain and reduce the need for non steroidal anti inflammatory agent.

 
Nutrition and dietary supplements

 
    Dietary measures that should help are,
  • Eat a diet rich in fiber, especially from fruits (including fruit juices) and vegetables. It may reduce the risk of developing ulcer. The vitamin A may be an added benefit from these foods.
  • Foods containing flavanoids, like apples celery, cranberries onions and tea may inhibit the growth of H pylori.
  • Avoid beverages that should irritate the lining of the stomach or increase acid production including coffee, alcohol and carbonated beverages.

 
Gamma-linolenic acid (GLA)

 
    Gamma linolenic acid (GLA) from evening primrose oil (EPO) may have anti ulcer properties. Gamma linolenic acid is an essential fatty acid (EFA) in the Omega 6 family that is found primarily in plant based oils, including EPO and borage seed oil.

 
Omega-3-fatty acids

 
    Treatment with Omega-3-fatty acids reduced the risk of ulcers caused by NSAIDS.

 
Probiotics

 
    Probiotics inhabit the lining of the intenstine and protect from the entry of bad infections that can cause disease. Lactobacillus acidophilus is the most commonly used probiotics.

 
Vitamin C

 
    High dose of vitamin C treatment for four weeks are effectively in the treatment of H pylori infection in some people.

 


 

CONCLUSION

 
    Peptic ulcer can be cured. The incidence can be reduced by proper diet control. Research are carried out for the development of optimal and most cost effective drug regimen. Future research will surely provide us with safer drug with minimal side effect regimen and perhaps a vaccine. Newer drug that spare the GI tract and decrease NSAID related morbidity and mortality will be soon available in market.

 

 

 

BIBLIOGRAPHY

 
  1. James.M. Crawford M.D, PhD, Associate professor of pathology, Director – Programme in gastro intestinal pathology. Yale University School of Medicine, New Haven.
  2. Robbins and Cotran pathological basis of disease, 7th edition. Kumar Abbas Fausto, Page No: 816-820.
  3. Robbins pathological basis of disease, Cotran, Kumar, Collins Sixth edition Page No: 793-796.
  4. Text book of pathology, Harsh Mohan, Page No: 556-568.
  5. Blaser M.J Parsonnet J: The bacteria behind ulcers Sci. AM 274, 104, 1996.
  6. MacGowan et al: Helicobacter Pylori and gastric acid, biological and therapeutic implication, Gastro enecology 110; 926; 1996.
  7. Morson DC et al: Gastro intestinal Pathology 3rd edition, Oxford Black well Scientific Publications 1992.
  8. White head R: Gastro intestinal and Oesophageal Pathology; 2nd edition London, Churchill Livingstone, 1995.
  9. Fifth edition, Pharmacotherapy, A pathophysiologic Approach., Joseph.T.Dipiro, Robert.L.Talbert, Gary.C.Yee, Gary.R.Matzke, Barbara.G.Wells, L.Mechael Posey.
  10. Issel bacher K.J, Podolsky D.K: Approach to the patient with GI disease in Wilson JD, Braunwald E. et al, Harrison's principles of internal medicine, New York, MC. GrawHill, 1991: 1213-1216.
  11. Janowitz HD: Approach to the patient with GI symptoms in Sachar DB, Waye J.D et.al eds. Pocket guide to Gastro enterology Baltimore, Williams and Wilkins 1989: 1-7.
  12. Walsh JH, Peterson WL. The treatment of Helicobecter Pylori infection in the management of ulcer disease 1995, 333, 984-991.
  13. Del.Valle J. Cohen H, Laine L et.al. Acid peptic disorders In Yamada.T, Aplers DH, Laine L et.al, eds. Textbook of Gastro enterology 3rd edition Philadelphia, Lippin cott Williams and Wilkins 1999; 1370-1444.
  14. Yardely JH, Hendrix T.R Gastrites, duodenitis and associated ulcerative lesions. In Yamada T, Aplers DH, Laine L et.al, eds. Text book of gastro enterology, 3rd ed. Philadelphia, Lippin cott Williams and Wilkins; 1999; 1463-1499.
  15. Talley N.J, Holtmann G. Approach to the patient with dyspepsia and related functional GI complaints in Yamada T, Aplers DH, Laine L et. al, eds. Text book of Gastroenterology, 3rd edition, Philadelphia, Lippin cott Williams and Wilkins 1999; 660-693.
  16. Barr.M.Buckley M,O. Moracin Non Steroidal anti inflammatory drugs and H pylori, Aliment pharmacol
  17. Ng TM, Fock K.M, Khor J.L, et. al NSAIDS, H pylori and bleeding Gastric ulcer. Aliment Pharmacol Ther 2000; 14; 203-209.
  18. Sachs G. Shin M, Munson K et.al. The controlof gastric acid and H pylori eradication. Aliment pharmacol ther 2000; 14; 1384-401 Review.
  19. Vaira. D, Menegatti M, Migloioli M. Gastro entrology 1997, 113 (suppl); S78-S84.
  20. Vaira D, Holton J, Menegatiic M. et. al. Invasive and non invasive test for H pylori infection Aliment pharmacol ther 2000, (suppl), 13-22 Review.
  21. Megrand. F: How should H pylori infection be diagnosed? Gastro entrology 1997, 113 (suppl); S93-S98.
  22. Graham Dy. Therapy of H pylori; Current status and issues. Gastro enterology 2000; 118 (suppl) S2-S8.
  23. Anderson J, Gona Zales. J.H. Pylori infection Review of the guidelines for diagnosis and treatment. 2000, 55; 44-49.
  24. Delvalle J, Scherman J.M. Zollenger – Ellison syndrome 1999, 1445-1462.
  25. Williams M.P, Pounder RE H.Pylori, from the benign to the malignant Am J. Gastro enterol 1999, 94 (suppl); S11-S16.
  26. Kuipers E.J: Exploring the link between H pylori and gastric cancers. Aliment pharmacol ther 1993; 13 (suppl); 3-11.
  27. Huang J2, Hunt RH H-pylori and gastric cancer – Alimetn pharmacol ther 2000 (suppl 3); 48-54; Review.
  28. Danesh J. H pylori infection and gastric cancer systematic review of the epidemiological studies. Aliment pharmacol ther 1999; 13; 851-856.
Dundan W.G et.al; Virulence factor of H pylori int. j. med- microbial 290; 647, 2001.



Cite this: T. Jijinu, Sujith Varma, "MANAGEMENT IN PEPTIC ULCER DISEASE", B. Pharm Projects and Review Articles, Vol. 1, pp. 514-542, 2006. (http://farmacists.blogspot.in/)
 

2 comments:

sukhwinder kaur said...

plz tell me that where u refferred all material
and which refferces are u right in biblography that are not mention in end of paragarph in no. form.

Dr Health Clinic said...

very nice and good blog
dermatologist in Bangalore