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From may 2000 to may 2006 •1704 upper GI endoscopies were done at RNH endoscopy unit, Riyadh, KSA

Link between h. pylori and human disease

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From may 2000 to may 2006

• 1704 upper GI endoscopies were done at RNH endoscopy unit, Riyadh, KSA

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1400

Males

Femles• Males 1210

( 71%)

• Females 494 ( 29%)

INDICATIONS

INDICATIONS

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1000• Dyspep 903 (53%)• Reflux 443 (26%)• Haemat 145 (8.5%)• Melaena 58 (3.4%)• Both 43 (2.5%)• Vomiting 58 (3.4%)• Dysphag 29 (1.7%)• Anaemia 15 (0.9%)• Wt loss 5 (0.3%)• Diarrhoea 5 (0.3%)

FINDINGS

Gastritis 699 (41%)GERD 238 (14%)NERD 208 (12.2%)Duodenitis 199 (11.7%)BRG 177 (10.4%)DU 116 (6.8%)Gastr erosions 106 (6.2%)Bleed DU 68 (4%)GERD/H hernia 65 (3.8%)

Varices 49 (2.9%)GU 44 (2.6%)NERD/H hernia 43 (2.5%)Mallory-Weiss 22 (1.3%)Bleed GU 15 (0.9%)Ca stomach 5 (0.3%)G Lymphoma 5 (0.3%)Ca oesophagus 7 (0.4%)Gastric polyp 3 (0.2%)Oesophageal eros 3 (0.2%)Villous atrophy 3 (0.2%)

Lieomyoma 1 (0.1%)Zollinger-Ellison 1 (0.1%)FB 3 (0.2%)Achalasia 1 (0.1%)Dieulafoy lesion 1 (0.1%)

# Gastritis is the commonest finding, 41% followed by GERD and or NERD in 32.5%.

# About 50% of patients with reflux symptoms had no oesophagitis but NERD.

# Hiatus hernia present in only 19.4% of patients with GERD/ or NERD.

# BRG is a common cause of dyspepsia and reflux symptoms(>10%) specially post-cholecystectomy.

# Peptic ulcer (DU or GU), is present in about 27% of patients presented with dyspepsia.

# DU is about three times more common than GU .

# Bleeding DU is more common than bleeding GU .

• # The 3 cases of esophageal erosions were drug induced ( Tabucine and Fosamax).

• # The 3 cases of gastric polyps were treated with polypectomy and both were benign.

• # The 3 cases of villous atrophy were due to celiac disease in 2 and giardiasis infection in one patient.

# 1635 (96%) patients had biopsies for H. pylori testing, either by rapid urease test (CLO) or by histopathology

# 69 (4%) patients did not have biopsies (coagulopathy)

FINDINGS……continue

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H. pyl pos

H. pyl neg

• H. pylori positive 1170 (71.6%)

• H. pylori negative 465(28.4%)

# More than 97% of patients with DU are H. pylori positive.# About 70% of patients with GU are H. pylori positive.

# 4 of the 10 patients with gastric malignancy tested positive

# Positive males were 73%# Positive females were 67%

FINDINGS………continue

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Pos DU

Neg DU

Pos GU

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• H. pylori positive DU 179 ( 97% )

• H. pylori negative DU 5 ( 3% )

• H.pylori positive GU 41 ( 70% )

• H. pylori negative GU 18 ( 30% )

DISTRIBUTION OF PEPTIC ULCER

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90SA

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yem

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Turk

• SA 85 (35%)• Jord 39 (16%)• Ind 39 (16%)• Yem 29 (12%)• Egy 17 (7%)• Flip 17 (7%)• Sud 15 (6%)• Turk 2 (1%)

AGE DISTRIBUTION in 1704 patients

10 - 19 years 48

20 - 29 371

30 - 39 489

40 - 49 426

50 - 59 189

60 - 69 81

70 - 79 62

80 and over 38

TREATMENT OF H.pylori

• Different regimens for H. pylori eradication were used in 1170 patients and these were chosen from the literature:

# 350 patients received (OCA);

Omeprazole 20 mg +

Clarithromycin 500 mg +

Amoxil 1000 mg, both twice daily for 1 week

# 475 patients received (PCA);

Pantoprazole 40 mg +

Clarithromycin 500 mg +

Amoxil 1000 mg, both twice daily for 1 week

# 185 patients received (LCA);

Lansoprazole 30 mg +

Clarithromycin 500 mg +

Amoxil 1000 mg, both twice daily for 1 week

# 35 patients received (OMA);

Omeprazole 20 mg +

Metronidazole 500 mg +

Amoxil 1000 mg, both twice daily for 1 week

# 125 patients received (EAL);

The most recent regimen;

Esomeprazole (Nexium) 20 mg +

Azithromycin (Zithromax) 500 mg+

Levofloxacin (Tavanic) 500 mg, both once daily for 1 week

RESULTS OF TREATMENT

• We were using 13C-UBT/ 14C-UBT or HpSAg to confirm H.pylori eradication 4 weeks after completing the course of the triple therapy in 850 patients

• The eradication rate was as follow:

• LCA regimen…………………….88%

• OCA regimen…………………….87%

• EAL regimen (once daily)……..87%

• PCA regimen……………………. 75%

• OMA regimen…………………….28.5%

This rate of eradication is similar to that seen in most studies (80-90%), although the eradication rate for metronidazole based regimens was much lower than other studies(28.5%).

This could be explained by higher H.pylori resistance to metronidazole in our locality due to abuse of metronidazole.

246 out of the 1704 gastroscopy (14.5%) were done as emergency procedures for acute upper GI bleeding ( haematemesis

and/or melaena).

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80 DU 28%

G/D eros 26%

Varices 20%

MW tear 8%

GU 6%

GERD 6%

Ca stom 2%

Leiomyo 0.8%

ZE synd 0.8%

Dieulafoy 0.5%

Causes of haematemesis and/or melaena in 246 patients

OUTCOME IN THE 246 PATIENTS8 patients were referred for surgery, ( 6 for bleeding

DU, 1 for leiomyoma, 1 for Dieulafoy leison), one of these ulcer patients developed cardiac arrest before surgical intervention and this is the only patient who died representing mortality of 0.4% ( was referred for endoscopy 3 days after haematemesis)!!!.

OUTCOME IN 246 PATIENTS cont…

17 patients with Ca stomach and Ca oesophagus were referred to specialist centers

# The other 221 patients(90%) were treated successively medically with sclerotherapy, adrenaline injection, heat coagulation, Sengstaken tube and drugs.

• How does gastric H. pylori colonization increase risk for DU? One explanation is that antral H. pylori colonization diminishes the number of somatostatin-producing cells; somatostatin-mediated inhibition of gastrin release leads to hypergastrinemia. Individuals with antral-predominant gastritis (and thus a normally functioning acid-producing gastric corpus) develop increased acid secretion, which may increase the risk of DU per se or may induce gastric metaplasia in the duodenum, which becomes colonized by H. pylori, then inflamed, and finally ulcerated. After eradication of H. pylori from patients with DU disease, the level of acid secretion often falls.

Eradication of H. pylori eliminates DU recurrence

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H. pylori -H. pyolri +

Huang et al, Am J Gastroenterol 1996;91(9):125

• The effect of H. pylori eradication on 24 H esophageal acid secretion is variable, but most treatment trials with PPI do not find that H. pylori status adversely affects symptom relief or healing of GERD in the majority of patients.

Relationship between H. pylori and extra-gastric gastrointestinal malignancies

• H. pylori role in extra-gastric gastrointestinal malignancies, such as esophageal cancer, is controversial. Doctors from Greece explored the relationship of H. pylori infection, and H. pylori cagA-positive strain with this malignancy by performing meta-analysis of all relevant studies through 2007.

• The researchers found that in adenocarcinoma patients there were inverse significant relationships with both the H. pylori prevalence, and the prevalence of H. pylori cagA-positive strain i.e there is a temporal relationship between a falling prevalence of H. pylori colonization and a rising incidence of these conditions Similarly in patients with Barrett's esophagus, there were inverse significant relationships, which might suggest a protective role of the infection in these entities.

• The research team noted that in patients with squamous cell carcinoma there were no significant relationships with both H. pylori prevalence, and the prevalence of H. pylori cagA-positive strains.

Clinical Gastroenterology and Hepatology; 2007: 5(12): 1413-7

• Several extra-gastrointestinal pathologies have been linked epidemiologically with H. pylori colonization. The most notable are ischemic heart disease and cerebrovascular disease. The associations have been found more commonly in small than in large studies, and most authorities consider them to be noncausal and due to confounding factors.

HOME TAKE MESSAGE

# Most H. pylori-colonized persons do not develop clinical sequelae. That some persons develop overt disease whereas others do not is probably due to a combination of bacterial strain differences, host susceptibility to disease, and environmental factors; of these, bacterial factors are best studied.

# Clinicians should continue to eradicate H. pylori when found and not be concerned about aggravating coexisting reflux disease which should easily respond to PPI therapy specially in patients who are candidates

for long term PPI. (Gut 2004;53:310-313)