New Perspectives in The Management of Peptic
Ulcer Disease.
Professor Javed Akram.
Mb, MEE(Can), MRCP(UK), FRCP(Glasg), FR...
Peptic Ulcer Disease
 A peptic ulcer is a break (an ulceration) in
the protective mucous lining (mucosa) of
the lower eso...
Common Misconceptions
 A peptic ulcer is NOT:
 A stress ulcer
 Chronic gastritis (a symptom as well as a disease state
...
Dyspepsia.
Dyspepsia - Definition
 A group of symptoms which alert
clinicians to consider disease of the upper
gastrointestinal trac...
Symptoms of Functional Dyspepsia
NocturnalNocturnal
painpain
LocalizedLocalized
epigastricepigastric
burningburning
Better...
Quick Stats:Peptic Ulcer
 5-10% lifetime incidence
 1-2% of people have ulcer at any given time
 $5.65 billion industry
Peptic Ulcer Hospitalization RatesPeptic Ulcer Hospitalization Rates
Kurata JH.Kurata JH. Semin Gastrointest DisSemin Gast...
Types
 Gastric
 Slightly more common in men and way more
common in elderly
 Most commonly located in the stomach’s less...
Types
 Duodenal
 Almost always located in the duodenal bulb
 More likely culprit in chronic disease
 No association wi...
Risk Factors
 Smoking
 33-100% more likely to develop duodenal ulcers
 Retards healing of identified ulcers
J Akram& Co...
Risk Factors
 NSAIDS
 Responsible for majority of ulcers not caused
by H.pylori
 Greater risk for complications once ul...
Prevalence of Endoscopic
NSAID-Induced Ulceration
Mean Range
 Gastric Ulcer 15 % 10 to 30%
 Duodenal Ulcer 5 % 4 to 10 %...
Risk Factors for
Serious GI Adverse Events with NSAIDs: Relative Risks
Rodriguez. Lancet. 1994; Guttham. Epidemiology. 199...
NSAID
↑ Leukocyte-Endothelial
Interactions
Capillary
Obstruction
Ischemic
Cell Injury
Proteases +
Oxygen Radicals
Endo/Epi...
Peptic Ulcers and Stress
 Experimental stress results in decreased
upper gastrointestinal blood flow in animals
 (Kauffm...
Peptic Ulcer and Personality
 Studies have found a strong association
between dependency and peptic ulcers
 Patients wit...
Helicobacter pylori
 Gram-negative spiral organism
 Most common and important risk factor for
duodenal ulcer
 Variable ...
Diagnosis of Peptic Ulcer
Diagnosis
 Vague discomfort and feeling of gnawing hunger
 Duodenal usually has predictable food relationship (1-3 hrs a...
Physical Exam
 Epigastric tenderness
 Rectal exam!!
Studies
 Radiography
 Barium swallow with double contrast
 Duodenal-detects 40-80%
 Gastric-detects 65-80%
 Endoscopy...
Diagnosis of H. pylori
 Invasive (if patient requires endoscopy)
 Histologic testing (50-90% sensitive, 100%
specific)
...
Complications
 Perforation
 Reoccurrence
 Obstruction
 Bleeding
 Cancer
Upper GI Bleeding
A common medical condition
 250,000 – 500,000 admissions/year in US
 UGI bleeding incidence 100/100,000 adults
 Inciden...
Bleeding Stats:Mayo J.Akram etal 2001PJGE
Therapy
 Goal is to heal the ulcer and prevent
recurrence
 Both can be accomplished by eradicating H.
pylori if present
...
Nonpharmacologic
 There is no evidence that dietary modifications
changes the course of the disease
 Quit smoking
 Milk...
Treatment of ulcers
 Eradicate H. pylori
 Single antibiotic therapy does not work
 Compliance is key
 More than 60% of...
ULCOCID
(Sucralfate)
Chemical Structure of Sucralfate
Sucrose Octasulphate Poly aluminum Hydroxide
Sucralfate
C12 H6 O11 [SO3 Al2 (OH)5] n H2 O...
ULCOCID
(Sucralfate)
1. Non systemic
2. Cytoprotective
3. Acid related disorders
1. Non systemic
2. Cytoprotective
3. Acid...
PHAMACOKINETICSPHAMACOKINETICS
ABS0RPTION
 Minimal absorption by GIT 3-5%
ABS0RPTION
 Minimal absorption by GIT 3-5%
EXC...
INDICATIONS OF ULCOCID
 Duodenal ulcers
 Gastric ulcers
 treatment of reflux and peptic oesophagitis
 H.pylori
 treat...
AVAILABILITY OF DRUG
1. ULCOCID tablets
( containing 500 mg Sucralfate per tablet ).
2. ULCOCID tablets
( containing 1 g S...
DOSAGE RECOMMENDATION OF ULCOCID
For Ulcer Patients
Morning
2g Ulcocid
Evening
For Non Ulcer Patients
Morning
1 g Ulcocid
...
ULCOCID
ULCOCID should always be
taken 1 hour before meals at
bed time (Monotherapy)
Do not take antacids 1/2 hour
before ...
ANTACIDS Vs ULCOCD
ANTACIDS
 Just symptomatic therapy.
 Intense antacid regimen required
for healing.
 Not safe for hyp...
Ulcocid Vs H2- Receptor AntagonistsUlcocid Vs H2- Receptor Antagonists
Ulcocid
 Less side effects
 Can be administered t...
Human Studies.Human Studies.
Comparative evaluation of Sucralfate &
Cimetidine efficacy in treatment of chronic
erosive ga...
Meta-analysis:Human Studies.Meta-analysis:Human Studies.
Comparative evaluation of Sucralfate &
Cimetidine efficiency in t...
ULCOCID Vs ACID PUMP
INHIBITORS
ULCOCID Vs ACID PUMP
INHIBITORS
Acid Pump Inhibitors
 Jaundice has been reported.
 Hypog...
Anti Helicobacter effects
Omeprazole Vs Ulcocid
(With Clarithromycin and Metronidazole)
75
80
85
90
95
100
4 Weeks
Healing...
Ulcocid Counters the Effect of
H.Pylori on Gastric Mucosa
H.PYLORI
↓ Mucus viscosity
↓ Glycoproteins & lipids
↓ Na+/H+ exc...
HUMAN AND ANIMAL STUDIES
Invitro and clinical data suggest that triple
therapy with SUCRALFATE is effective in
eradicating...
Human StudiesHuman Studies
Glycosulfatase activity of H. Pylori towards human
gastric mucin; effect of Sucrafate.
Results ...
ULCOCID INHIBITS THE EFFECT OF
H.Pylori on gastric mucins
ULCOCID INHIBITS THE EFFECT OF
H.Pylori on gastric mucins
0
200
...
ULCOCID
 Direct binding to ulcer
crater
 Stimulates prostaglandin
production
 Enhances the surface
active phospholipid
...
Recurrent Aphthous Stomatitis (RAS)
 Minor apthae
Recurrent Aphthous Stomatitis (RAS)
 Major apthae
Sucralfate in apthous ulcers.
F.Khan,A.Awan,J.Akram SMJ,Jun,2003
 Statistically significantly better pain relief
 Earlie...
Sucralfate Enema
 Ulcerative Colitis
 Ca.Colon
HUMAN STUDIESHUMAN STUDIES
Management of bleeding in a patient with
colorectal cancer:
SUCRALFATE an oral cytoprotective, ...
WHY ULCOCID ?WHY ULCOCID ?
 Fast pain relief.
 Excellent healing rate.
 Equal good for smokers and non - smokers.
 Goo...
Thank You.
A.P.D. presentation by Prof.JaAkram
A.P.D. presentation by Prof.JaAkram
A.P.D. presentation by Prof.JaAkram
A.P.D. presentation by Prof.JaAkram
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  • So basically this was a presentation to promote ulcocid, a brand of sucralfate made by Don Valley pharm. This is the worth of these professors in Pakistan, they sell themselves for few rupees. Even their undergarments are given by medical reps. Shame on you Javed Akram ...
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  • A.P.D. presentation by Prof.JaAkram

    1. 1. New Perspectives in The Management of Peptic Ulcer Disease. Professor Javed Akram. Mb, MEE(Can), MRCP(UK), FRCP(Glasg), FRCP(Edin), FRCP(London), FACP(USA), FASIM(USA), FACC(USA).
    2. 2. Peptic Ulcer Disease  A peptic ulcer is a break (an ulceration) in the protective mucous lining (mucosa) of the lower esophagus, stomach or duodenum
    3. 3. Common Misconceptions  A peptic ulcer is NOT:  A stress ulcer  Chronic gastritis (a symptom as well as a disease state that may lead to peptic ulcers)  Dyspepsia (the symptoms that may or may not be diagnosed as an ulcer)  Peptic Ulcers cannot be diagnosed solely on the basis of clinical presentation (Werdmuller et al. 1996)
    4. 4. Dyspepsia.
    5. 5. Dyspepsia - Definition  A group of symptoms which alert clinicians to consider disease of the upper gastrointestinal tract (British Society of Gastroenterology, 1996)(British Society of Gastroenterology, 1996)
    6. 6. Symptoms of Functional Dyspepsia NocturnalNocturnal painpain LocalizedLocalized epigastricepigastric burningburning BetterBetter with foodwith food HeartburnHeartburn RetrosternalRetrosternal burningburning NauseaNausea BloatingBloating Early satietyEarly satiety WorseWorse with foodwith food Ulcer-like DominantUlcer-like Dominant Dysmotility-like DominantDysmotility-like Dominant
    7. 7. Quick Stats:Peptic Ulcer  5-10% lifetime incidence  1-2% of people have ulcer at any given time  $5.65 billion industry
    8. 8. Peptic Ulcer Hospitalization RatesPeptic Ulcer Hospitalization Rates Kurata JH.Kurata JH. Semin Gastrointest DisSemin Gastrointest Dis 1993:41993:4 RateRate perper 100,000100,000 Gastric UlcerGastric Ulcer Duodenal UlcerDuodenal Ulcer 70 75 80 85 90 0 20 40 60 80 100 UncomplicatedUncomplicated HemorrhageHemorrhage PerforationPerforation 70 75 80 85 90 0 20 40 YearYear YearYear 30 10 UncomplicatedUncomplicated HemorrhageHemorrhage PerforationPerforation
    9. 9. Types  Gastric  Slightly more common in men and way more common in elderly  Most commonly located in the stomach’s lesser curvature, antrum  1-3% associated with gastric carcinomas  Basic defect is disruption of gastric mucosal barrier (gastritis, duodenal reflux, H. pylori, NSAIDS)
    10. 10. Types  Duodenal  Almost always located in the duodenal bulb  More likely culprit in chronic disease  No association with cancer
    11. 11. Risk Factors  Smoking  33-100% more likely to develop duodenal ulcers  Retards healing of identified ulcers J Akram& Colleagues ..E.J.of Gastrenterology.Nov2003)  Age and Sex  Alcohol  Diet  Milk  Stress  Ramadan fasting
    12. 12. Risk Factors  NSAIDS  Responsible for majority of ulcers not caused by H.pylori  Greater risk for complications once ulcer identified  Risk of GU increases sixfold when taking >three aspirin/day. Buffered coat has no advantage
    13. 13. Prevalence of Endoscopic NSAID-Induced Ulceration Mean Range  Gastric Ulcer 15 % 10 to 30%  Duodenal Ulcer 5 % 4 to 10 %  Clinically Significant Ulcers 2% 1 to 4%
    14. 14. Risk Factors for Serious GI Adverse Events with NSAIDs: Relative Risks Rodriguez. Lancet. 1994; Guttham. Epidemiology. 1997; Shorr. Arch Intern Med. 1993; Piper. Ann Intern Med. 1991. 0 5 10 15 4.4 (2.0-9.7) 12.7 (6.3-25.7) 2.9 (2.2-3.8) 5.8 (4.0-8.6) 5.6 (4.6-6.9) 3.1 (2.5-3.7) 1.6 (1.4-2.0) 13.5 (10.3-17.7) Corticosteroid use Anticoagulant use Low dose NSAIDLow dose NSAID High dose NSAID Age 70-80 Age 60-69 Age 50-59 Prior bleed Relative RiskRelative Risk
    15. 15. NSAID ↑ Leukocyte-Endothelial Interactions Capillary Obstruction Ischemic Cell Injury Proteases + Oxygen Radicals Endo/Epithelial Cell Injury Mucosal Ulceration LossofPG E 2and PG I2m ediated inhibition ofacid secretion and cytoprotectiveeffect Loss of PGI2 induced inhibition of LTB4 mediated endothelial adhesion and activation of neutrophils
    16. 16. Peptic Ulcers and Stress  Experimental stress results in decreased upper gastrointestinal blood flow in animals  (Kauffman, 1997; Livingston 1993)  Effect of stress seems to be reversible  (Levenstein et al., 1996)
    17. 17. Peptic Ulcer and Personality  Studies have found a strong association between dependency and peptic ulcers  Patients with peptic ulcer have significantly more personality disturbances than control subjects (Feldman et al.)  Ulcer patients also more inclined to pessimism and excessive dependence (Akram et al.)
    18. 18. Helicobacter pylori  Gram-negative spiral organism  Most common and important risk factor for duodenal ulcer  Variable risk factor for gastric ulcers  10% healthy people under 30, 60% healthy people over 60.  Will cause disease in 15-20% of infected  Eradication is the key
    19. 19. Diagnosis of Peptic Ulcer
    20. 20. Diagnosis  Vague discomfort and feeling of gnawing hunger  Duodenal usually has predictable food relationship (1-3 hrs after meal)  Gastric ulcer relationship with food more variable  Gastric ulcer-weight loss  Duodenal ulcer-weight gain  Watch for peptic ulceration/bleeding: melena, radiation of pain to back/shoulder
    21. 21. Physical Exam  Epigastric tenderness  Rectal exam!!
    22. 22. Studies  Radiography  Barium swallow with double contrast  Duodenal-detects 40-80%  Gastric-detects 65-80%  Endoscopy  Gold standard  Detects up to 95% gastroduodenal ulcers  Generally considered the study of choice esp. for large ulcers or those not clearly benign
    23. 23. Diagnosis of H. pylori  Invasive (if patient requires endoscopy)  Histologic testing (50-90% sensitive, 100% specific)  Rapid urease (CLO) test (95% sensitive and 95% specific)*  Noninvasive  IgG antibody*  Urea breath test (96% sensitive, 98% specific)
    24. 24. Complications  Perforation  Reoccurrence  Obstruction  Bleeding  Cancer
    25. 25. Upper GI Bleeding
    26. 26. A common medical condition  250,000 – 500,000 admissions/year in US  UGI bleeding incidence 100/100,000 adults  Incidence increases 20-30 fold from third to ninth decade of life  GI bleeding stops spontaneously in 80 %
    27. 27. Bleeding Stats:Mayo J.Akram etal 2001PJGE
    28. 28. Therapy  Goal is to heal the ulcer and prevent recurrence  Both can be accomplished by eradicating H. pylori if present  Treat the acute pain if necessary
    29. 29. Nonpharmacologic  There is no evidence that dietary modifications changes the course of the disease  Quit smoking  Milk intake  Faster healing, lower recurrence, lower complications  Discontinue NSAIDS  COX2 Inhibitors?
    30. 30. Treatment of ulcers  Eradicate H. pylori  Single antibiotic therapy does not work  Compliance is key  More than 60% of the doses must be taken to ensure eradication  If eradicated, maintenance therapy not needed. If recurs, check for H. pylori again  If H. pylori not found, check again and treat with H2- receptor antagonists, PPI’s and sucralfate  Document healing of gastric ulcers with endoscopy
    31. 31. ULCOCID (Sucralfate)
    32. 32. Chemical Structure of Sucralfate Sucrose Octasulphate Poly aluminum Hydroxide Sucralfate C12 H6 O11 [SO3 Al2 (OH)5] n H2 O Sucrose Octasulphate Poly aluminum Hydroxide Sucralfate C12 H6 O11 [SO3 Al2 (OH)5] n H2 O
    33. 33. ULCOCID (Sucralfate) 1. Non systemic 2. Cytoprotective 3. Acid related disorders 1. Non systemic 2. Cytoprotective 3. Acid related disorders
    34. 34. PHAMACOKINETICSPHAMACOKINETICS ABS0RPTION  Minimal absorption by GIT 3-5% ABS0RPTION  Minimal absorption by GIT 3-5% EXCRETION  Approximately 90% is excreted in the stool, very small amount is excreted in the urine. EXCRETION  Approximately 90% is excreted in the stool, very small amount is excreted in the urine.
    35. 35. INDICATIONS OF ULCOCID  Duodenal ulcers  Gastric ulcers  treatment of reflux and peptic oesophagitis  H.pylori  treatment of NSAID & aspirin induced GI symptoms and mucosal damage.  Prevention of stress ulcers and GI bleeding in critically ill patients.  Treatment of oral and oesophageal ulcers due to radiation chemotherapy & sclerotherapy.  Sucralfate enemas in ulcerative colitis & colonic carcinomas  Duodenal ulcers  Gastric ulcers  treatment of reflux and peptic oesophagitis  H.pylori  treatment of NSAID & aspirin induced GI symptoms and mucosal damage.  Prevention of stress ulcers and GI bleeding in critically ill patients.  Treatment of oral and oesophageal ulcers due to radiation chemotherapy & sclerotherapy.  Sucralfate enemas in ulcerative colitis & colonic carcinomas
    36. 36. AVAILABILITY OF DRUG 1. ULCOCID tablets ( containing 500 mg Sucralfate per tablet ). 2. ULCOCID tablets ( containing 1 g Sucralfate per tablet ). 3. ULCOCID Susp. 60 ml ( containing 1 g Sucralfate per 5ml). 1. ULCOCID tablets ( containing 500 mg Sucralfate per tablet ). 2. ULCOCID tablets ( containing 1 g Sucralfate per tablet ). 3. ULCOCID Susp. 60 ml ( containing 1 g Sucralfate per 5ml).
    37. 37. DOSAGE RECOMMENDATION OF ULCOCID For Ulcer Patients Morning 2g Ulcocid Evening For Non Ulcer Patients Morning 1 g Ulcocid Evening For Ulcer Patients Morning 2g Ulcocid Evening For Non Ulcer Patients Morning 1 g Ulcocid Evening
    38. 38. ULCOCID ULCOCID should always be taken 1 hour before meals at bed time (Monotherapy) Do not take antacids 1/2 hour before or after taking ULCOCID (Polytherapy). ULCOCID should always be taken 1 hour before meals at bed time (Monotherapy) Do not take antacids 1/2 hour before or after taking ULCOCID (Polytherapy).
    39. 39. ANTACIDS Vs ULCOCD ANTACIDS  Just symptomatic therapy.  Intense antacid regimen required for healing.  Not safe for hypertensive or cardiac patients.  Non-Palatable.  Not suitable for working class because of frequent dose taken. ANTACIDS  Just symptomatic therapy.  Intense antacid regimen required for healing.  Not safe for hypertensive or cardiac patients.  Non-Palatable.  Not suitable for working class because of frequent dose taken. ULCOCID  Ulcer healing occurs.  None  Palatable  Dosage is convenient. ULCOCID  Ulcer healing occurs.  None  Palatable  Dosage is convenient.
    40. 40. Ulcocid Vs H2- Receptor AntagonistsUlcocid Vs H2- Receptor Antagonists Ulcocid  Less side effects  Can be administered to elderly.  Smokers can use it.  Does not effect hepatic metabolism of drugs.  Does not effect pulmonary functions in patients with pre- existing broncho- pulmonary diseases. Ulcocid  Less side effects  Can be administered to elderly.  Smokers can use it.  Does not effect hepatic metabolism of drugs.  Does not effect pulmonary functions in patients with pre- existing broncho- pulmonary diseases. H2-Receptor Antagonists  More side effects  Causes hallucination and delirium in elderly  Only for non- smokers.  Does effect the metabolism of drugs metabolized by Cytochrome P-450 path-way.  H2 – blockers may worsen the condition. H2-Receptor Antagonists  More side effects  Causes hallucination and delirium in elderly  Only for non- smokers.  Does effect the metabolism of drugs metabolized by Cytochrome P-450 path-way.  H2 – blockers may worsen the condition.
    41. 41. Human Studies.Human Studies. Comparative evaluation of Sucralfate & Cimetidine efficacy in treatment of chronic erosive gastritis. The results of patients with chronic erosive gastritis treated with Sucralfate & Cimetidine were compared. The result of examinations indicate that chronic erosive gastritis is difficult to be heal; Sucralfate proved to be more efficient than Cimetidine. Ref: Au:Kula-Z:Walasek-L So:Pizegl-Lek 1998; 51(2): 73-6 Comparative evaluation of Sucralfate & Cimetidine efficacy in treatment of chronic erosive gastritis. The results of patients with chronic erosive gastritis treated with Sucralfate & Cimetidine were compared. The result of examinations indicate that chronic erosive gastritis is difficult to be heal; Sucralfate proved to be more efficient than Cimetidine. Ref: Au:Kula-Z:Walasek-L So:Pizegl-Lek 1998; 51(2): 73-6
    42. 42. Meta-analysis:Human Studies.Meta-analysis:Human Studies. Comparative evaluation of Sucralfate & Cimetidine efficiency in treatment of chronic erosive gastritis proved that Sucralfate is more efficient than Cimetidine. Ref: Au: Kula-Z:Walasek-L So:Pizegl-Lek 1999; 51(2): 73-6 Comparative evaluation of Sucralfate & Cimetidine efficiency in treatment of chronic erosive gastritis proved that Sucralfate is more efficient than Cimetidine. Ref: Au: Kula-Z:Walasek-L So:Pizegl-Lek 1999; 51(2): 73-6
    43. 43. ULCOCID Vs ACID PUMP INHIBITORS ULCOCID Vs ACID PUMP INHIBITORS Acid Pump Inhibitors  Jaundice has been reported.  Hypoglycaemia, Wt. Gain.  Increased intragastric concentrations of viable bacteria during the T/M. Acid Pump Inhibitors  Jaundice has been reported.  Hypoglycaemia, Wt. Gain.  Increased intragastric concentrations of viable bacteria during the T/M. Ulcocid  No jaundice reported  None  None Ulcocid  No jaundice reported  None  None
    44. 44. Anti Helicobacter effects Omeprazole Vs Ulcocid (With Clarithromycin and Metronidazole) 75 80 85 90 95 100 4 Weeks Healing H.Pylori eradication Omeprazole Ulcocid
    45. 45. Ulcocid Counters the Effect of H.Pylori on Gastric Mucosa H.PYLORI ↓ Mucus viscosity ↓ Glycoproteins & lipids ↓ Na+/H+ exchange of mucus ↓ Mucosal bicarbonate secretion ↓ Cell desquamation ↓ Mucosal microvessel permeability ↓ Mucosal blood flow? ↓ Surface hydrophobicity ↓ Cell membrane permeability ↑ H+ Back diffusion. H.PYLORI ↓ Mucus viscosity ↓ Glycoproteins & lipids ↓ Na+/H+ exchange of mucus ↓ Mucosal bicarbonate secretion ↓ Cell desquamation ↓ Mucosal microvessel permeability ↓ Mucosal blood flow? ↓ Surface hydrophobicity ↓ Cell membrane permeability ↑ H+ Back diffusion. ULCOCID ↑ Mucus viscosity ↑ Glycoproteins & lipids ↑ Na+/H+ exchange of mucus ↑ Mucosal bicarbonate secretion ↑ Mucosal PGE2, Mucosal renewal ↑ Mucosal blood flow ↑ Surface hydrophobicity ↑ Cell membrane permeability ↓ H+ Back diffusion. ULCOCID ↑ Mucus viscosity ↑ Glycoproteins & lipids ↑ Na+/H+ exchange of mucus ↑ Mucosal bicarbonate secretion ↑ Mucosal PGE2, Mucosal renewal ↑ Mucosal blood flow ↑ Surface hydrophobicity ↑ Cell membrane permeability ↓ H+ Back diffusion.
    46. 46. HUMAN AND ANIMAL STUDIES Invitro and clinical data suggest that triple therapy with SUCRALFATE is effective in eradicating HELICOBACTER PYLORI and reducing duodenal ulcer relapse. Ref: Louw- Ja So:Scand-J-Gastroenterol-Suppl. 1998; 191:28-31 Invitro and clinical data suggest that triple therapy with SUCRALFATE is effective in eradicating HELICOBACTER PYLORI and reducing duodenal ulcer relapse. Ref: Louw- Ja So:Scand-J-Gastroenterol-Suppl. 1998; 191:28-31
    47. 47. Human StudiesHuman Studies Glycosulfatase activity of H. Pylori towards human gastric mucin; effect of Sucrafate. Results demonstrate that H. Pylori, through its Glycosulfatase activity affects the sulphated mucin & glycero-gluco-lipid content of the protective mucous layer & that anti-ulcer drug Sucralfate is able to counteract the detrimental action of this enzyme. Ref: Slomiany-BL; Piotrowski-J; Grabska-M; SLOMIANY-a So: Am-j- Gastroenterol. 1999 Sep; 87(9); 1132-7 Glycosulfatase activity of H. Pylori towards human gastric mucin; effect of Sucrafate. Results demonstrate that H. Pylori, through its Glycosulfatase activity affects the sulphated mucin & glycero-gluco-lipid content of the protective mucous layer & that anti-ulcer drug Sucralfate is able to counteract the detrimental action of this enzyme. Ref: Slomiany-BL; Piotrowski-J; Grabska-M; SLOMIANY-a So: Am-j- Gastroenterol. 1999 Sep; 87(9); 1132-7
    48. 48. ULCOCID INHIBITS THE EFFECT OF H.Pylori on gastric mucins ULCOCID INHIBITS THE EFFECT OF H.Pylori on gastric mucins 0 200 400 600 800 1000 1200 Specific binding (dpm/assay) Control 10 40 80 ULCOCID (mg/ml)
    49. 49. ULCOCID  Direct binding to ulcer crater  Stimulates prostaglandin production  Enhances the surface active phospholipid mucosal barrier.  Stimulates growth factors . Epidermal . Transforming . Fibroblast  Anti-helicobacter effects.
    50. 50. Recurrent Aphthous Stomatitis (RAS)  Minor apthae
    51. 51. Recurrent Aphthous Stomatitis (RAS)  Major apthae
    52. 52. Sucralfate in apthous ulcers. F.Khan,A.Awan,J.Akram SMJ,Jun,2003  Statistically significantly better pain relief  Earlier ulcer healing rates  Better QOL
    53. 53. Sucralfate Enema  Ulcerative Colitis  Ca.Colon
    54. 54. HUMAN STUDIESHUMAN STUDIES Management of bleeding in a patient with colorectal cancer: SUCRALFATE an oral cytoprotective, used topically in a patient with colo-rectal cancer resulting in control of bleeding, less localized pain and more freedom & independence for the patient. Ref: Au: Famcombe-M So: Support-care-cancer, 1993 May;1(3):159-60. Management of bleeding in a patient with colorectal cancer: SUCRALFATE an oral cytoprotective, used topically in a patient with colo-rectal cancer resulting in control of bleeding, less localized pain and more freedom & independence for the patient. Ref: Au: Famcombe-M So: Support-care-cancer, 1993 May;1(3):159-60.
    55. 55. WHY ULCOCID ?WHY ULCOCID ?  Fast pain relief.  Excellent healing rate.  Equal good for smokers and non - smokers.  Good for elderly.  Equally good for ulcer and non - ulcer patients.  Economical  Fast pain relief.  Excellent healing rate.  Equal good for smokers and non - smokers.  Good for elderly.  Equally good for ulcer and non - ulcer patients.  Economical
    56. 56. Thank You.
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