Prilosec

[Omeprazole]

The antisecretory effect thus lasts far longer than would be expected from the very short (less than one hour) plasma half-life, apparently due to prolonged binding to the parietal H + /K + ATPase enzyme. When the drug is discontinued, secretory activity returns gradually, over 3 to 5 days. The inhibitory effect of omeprazole on acid secretion increases with repeated once-daily dosing, reaching a plateau after four days.

Results from numerous studies of the antisecretory effect of multiple doses of 20 mg and 40 mg of omeprazole in normal volunteers and patients are shown below. The "max" value represents determinations at a time of maximum effect (2-6 hours after dosing), while "min" values are those 24 hours after the last dose of omeprazole.
Range of Mean Values from Multiple Studies
of the Mean Antisecretory Effects of Omeprazole
After Multiple Daily Dosing

Parameter
Omeprazole
20 mg
Omeprazole
40 mg
% Decrease in
Basal Acid Output
Max
78 *
Min
58-80
Max
94 *
Min
80-93
% Decrease in
Peak Acid Output 79 * 50-59 88 * 62-68
% Decrease in 24-hr. Intragastric

Text Continues Below

---

Acidity
80-97 92-94

* Single Studies

Single daily oral doses of omeprazole ranging from a dose of 10 mg to 40 mg have produced 100% inhibition of 24-hour intragastric acidity in some
patients.
Enterochromaffin-like (ECL) Cell Effects In 24-month carcinogenicity studies in rats, a dose-related significant increase in gastric carcinoid tumors and ECL cell hyperplasia was observed in both male and female animals (see PRECAUTIONS, Carcinogenesis, Mutagenesis, Impairment of Fertility). Carcinoid tumors have also been observed in rats subjected to fundectomy or long-term treatment with other proton pump inhibitors or high doses of H2-receptor antagonists.

Human gastric biopsy specimens have been obtained from more than 3000 patients treated with omeprazole in long-term clinical trials. The incidence of ECL cell hyperplasia in these studies increased with time; however, no case of ECL cell carcinoids, dysplasia, or neoplasia has been found in these patients. (See also CLINICAL PHARMACOLOGY, Pathological Hypersecretory Conditions.)

However, these studies are of insufficient duration and size to rule out the possible influence of long-term administration of omeprazole on the development of any premalignant or malignant conditions. Serum Gastrin Effects In studies involving more than 200 patients, serum gastrin levels increased during the first 1 to 2 weeks of once-daily administration of therapeutic doses of omeprazole in parallel with inhibition of acid secretion. No further increase in serum gastrin occurred with continued treatment. In comparison with histamine H2-receptor antagonists, the median increases produced by 20 mg doses of omeprazole were higher (1.3 to 3.6 fold vs. 1.1 to 1.8 fold increase). Gastrin values returned to pretreatment levels, usually within 1 to 2 weeks after discontinuation of therapy.

Other Effects Systemic effects of omeprazole in the CNS, cardiovascular and respiratory systems have not been found to date. Omeprazole, given in oral doses of 30 or 40 mg for 2 to 4 weeks, had no effect on thyroid function, carbohydrate metabolism, or circulating levels of parathyroid hormone, cortisol, estradiol, testosterone, prolactin, cholecystokinin or secretin.

No effect on gastric emptying of the solid and liquid components of a test meal was demonstrated after a single dose of omeprazole 90 mg. In healthy subjects, a single I. V. dose of omeprazole (0.35 mg/ kg) had no effect on intrinsic factor secretion. No systematic dose-dependent effect has been observed on basal or stimulated pepsin output in humans. However, when intragastric pH is maintained at 4.0 or above, basal pepsin output is low, and pepsin activity is decreased. As do other agents that elevate intragastric pH, omeprazole administered for 14 days in healthy subjects produced a significant increase in the intragastric concentrations of viable bacteria.

The pattern of the bacterial species was unchanged from that commonly found in saliva. All changes resolved within three days of stopping treatment. The course of Barrett's esophagus in 106 patients was evaluated in a U. S. double-blind controlled study of PRILOSEC 40 mg b. i. d. for 12 months followed by 20 mg b. i. d. for 12 months or ranitidine 300 mg b. i. d. for 24 months. No clinically significant impact on Barrett's mucosa by antisecretory therapy was observed. Although neosquamous epithelium developed during antisecretory therapy, complete elimination of Barrett's mucosa was not achieved.

No significant difference was observed between treatment groups in development of dysplasia in Barrett's mucosa and no patient developed esophageal carcinoma during treatment. No significant differences between treatment groups were observed in development of ECL cell hyperplasia, corpus atrophic gastritis, corpus intestinal metaplasia, or colon polyps exceeding 3 mm in diameter (see also CLINICAL PHARMACOLOGY, Enterochromaffin-like (ECL) Cell Effects).

Clinical Studies
Duodenal Ulcer Disease Active Duodenal Ulcer—

In a multicenter, double-blind, placebo-controlled study of 147 patients with endoscopically documented duodenal ulcer, the percentage of patients healed (per protocol) at 2 and 4 weeks was significantly higher with PRILOSEC 20 mg once a day than with
placebo (p £ 0.01).

Treatment of Active Duodenal Ulcer
% of Patients Healed

PRILOSEC
20 mg a. m.
(n = 99)

Placebo
a. m.
(n = 48)
Week 2 Week 4 * 41 * 75 13 27

* (p £ 0.01)

Complete daytime and nighttime pain relief occurred significantly faster
(p £ 0.01) in patients treated with PRILOSEC 20 mg than in patients treated with placebo. At the end of the study, significantly more patients

who had received PRILOSEC had complete relief of daytime pain (p £ 0.05) and nighttime pain (p £ 0.01).

In a multicenter, double-blind study of 293 patients with endoscopically documented duodenal ulcer, the percentage of patients healed (per
protocol) at 4 weeks was significantly higher with PRILOSEC 20 mg once a day than with ranitidine
150 mg b. i. d. (p < 0.01). 7

Treatment of Active Duodenal Ulcer
% of Patients Healed

PRILOSEC
20 mg a. m.
(n = 145)

Ranitidine
150 mg b. i. d.
(n = 148) Week 2

Week 4
42 *
82
34
63 *
(p < 0.01)

Healing occurred significantly faster in patients treated with PRILOSEC than in those treated with ranitidine 150 mg b. i. d. (p < 0.01).

In a foreign multinational randomized, double-blind study of 105 patients with endoscopically documented duodenal ulcer, 20 mg and 40 mg of PRILOSEC were compared to 150 mg b. i. d. of ranitidine at 2, 4 and 8 weeks. At 2 and 4 weeks both doses of PRILOSEC were statistically superior (per protocol) to ranitidine, but 40 mg was not superior to 20 mg of PRILOSEC, and at 8 weeks there was no significant difference between any of the active drugs.

Treatment of Active Duodenal Ulcer
% of Patients Healed

PRILOSEC Ranitidine
20 mg
(n = 34)
40 mg
(n = 36)
150 mg b. i. d.
(n = 35) Week 2

Week 4
Week 8

* 83
* 97

100

* 83
* 100

100

53
82
94 *
(p £ 0.01)

H. pylori Eradication in Patients with Duodenal Ulcer Disease Triple Therapy( PRILOSEC/ clarithromycin/ amoxicillin)— Three U. S., randomized, double-blind clinical studies in patients with H. pylori infection and duodenal ulcer disease (n = 558) compared PRILOSEC plus clarithromycin plus amoxicillin to clarithromycin plus amoxicillin. Two studies (126 and 127) were conducted in patients with an active duodenal ulcer, and the other study (M96-446) was conducted in patients with a history of a duodenal ulcer in the past 5 years but without an ulcer present at the time of enrollment. The dose regimen in the studies was PRILOSEC 20 mg b. i. d. plus clarithromycin 500 mg b. i. d. plus amoxicillin 1 g b. i. d. for 10 days; or clarithromycin 500 mg b. i. d. plus amoxicillin 1 g b. i. d. for 10 days. In studies 126 and 127, patients who took the omeprazole regimen also received an additional 18 days of PRILOSEC 20 mg q. d. Endpoints studied were eradication of H. pylori and duodenal ulcer healing (studies 126 and 127 only). H. pylori status was determined by CLOtest ® , histology and culture in all three studies. For a given patient, H. pylori was considered eradicated if at least two of these tests were negative, and none was positive.

The combination of omeprazole plus clarithromycin plus amoxicillin was effective in eradicating H. pylori.
Per-Protocol and Intent-to-Treat H. pylori Eradication Rates
% of Patients Cured [95% Confidence Interval]
PRILOSEC +clarithromycin
+amoxicillin
Clarithromycin +amoxicillin

Per-Protocol * Intent-to-Treat * Per-Protocol * Intent-to-Treat *
Study 126 *77 [64, 86]
(n = 64)
*69 [57, 79]
(n = 80)
43 [31, 56]
(n = 67)
37 [27, 48]
(n = 84)

Study 127 *78 [67, 88]
(n = 65)
*73 [61, 82]
(n = 77)
41 [29, 54]
(n = 68)
36 [26, 47]
(n = 83)

Study M96-446 *90 [80, 96] (n = 69) *83 [74, 91] (n = 84) 33 [24, 44] (n = 93) 32 [23, 42] (n = 99)
* Patients were included in the analysis if they had confirmed duodenal ulcer disease (active ulcer, studies 126 and 127; history of ulcer within 5 years, study M96-446) and H. pylori infection at baseline defined as at least two of three positive endoscopic tests from CLOtest â , histology, and/ or culture. Patients were included in the analysis if they completed the study. Additionally, if patients dropped out of the study due to an adverse event related to the study drug, they were included in the analysis as failures of therapy. The impact of eradication on ulcer recurrence has not been assessed in patients with a past history of ulcer.

* Patients were included in the analysis if they had documented H. pylori infection at baseline and had confirmed duodenal ulcer disease. All dropouts were included as failures of therapy. *
(p < 0.05) versus clarithromycin plus amoxicillin.

Dual Therapy (PRILOSEC/ clarithromycin)— Four randomized, double-blind, multicenter studies (M93-067, M93-100, M92-812b, and M93-058) evaluated PRILOSEC 40 mg q. d. plus clarithromycin 500 mg t. i. d. for 14 days, followed by PRILOSEC 20 mg q. d. (M93-067, M93-100, M93-058) or by PRILOSEC 40 mg q. d. (M92-812b) for an additional 14 days in patients with active duodenal ulcer associated with H. pylori. Studies M93-067 and M93-100 were conducted in the U. S. and Canada and enrolled 242 and 256 patients, respectively. H. pylori infection and duodenal ulcer were confirmed in 219 patients in Study M93-067 and 228 patients in Study M93-100.

These studies compared the combination regimen to PRILOSEC and clarithromycin monotherapies. Studies M92-812b and M93-058 were conducted in Europe and enrolled 154 and 215 patients, respectively. H. pylori infection and duodenal ulcer were confirmed in 148 patients in study M92-812b and 208 patients in Study M93-058. These studies compared the combination regimen to omeprazole monotherapy. The results for the efficacy analyses for these studies are described below. H. pylori eradication was defined as nonpositive test (culture or histology) at 4 weeks following the end of treatment, and two negative tests were required to be considered eradicated of H. pylori.

In the per-protocol analysis, the following patients were excluded: dropouts, patients with missing H. pylori tests post-treatment, and patients that were not assessed for H. pylori eradication because they were found to have an ulcer at the end of treatment.
The combination of omeprazole and clarithromycin was effective in eradicating H. pylori.
H. pylori Eradication Rates (Per-Protocol Analysis at 4 to 6 Weeks)
% of Patients Cured [95% Confidence Interval]
PRILOSEC +
Clarithromycin PRILOSEC Clarithromycin

U. S. Studies Study M93-067 74 [60, 85] **

(n = 53) 0 [0, 7] (n = 54) 31 [18, 47] (n = 42)
Study M93-100 64 [51, 76] **
(n = 61)
0 [0, 6]
(n = 59)
39 [24, 55]
(n = 44)
Non U. S. Studies Study M92-812b 83 [71, 92] *

(n = 60)
1 [0, 7]
(n = 74)
N/ A

Study M93-058 74 [64, 83] *
(n = 86)
1 [0, 6]
(n = 90)
N/ A

* Statistically significantly higher than clarithromycin monotherapy (p < 0.05)
* Statistically significantly higher than omeprazole monotherapy (p < 0.05)

Ulcer healing was not significantly different when clarithromycin was added to omeprazole therapy compared to omeprazole therapy alone.

The combination of omeprazole and clarithromycin was effective in eradicating H. pylori and reduced duodenal ulcer recurrence.
Duodenal Ulcer Recurrence Rates by
H. pylori Eradication Status
% of Patients with Ulcer Recurrence
H. pylori eradicated # H. pylori not eradicated #

U. S. Studies * 6 months post-treatment
Study M93-067 * 35 (n = 49) 60 (n = 88)
Study M93-100 * 8
(n = 53)
60
(n = 106)
Non U. S. Studies * 6 months post-treatment

Study M92-812b * 5
(n = 43)
46
(n = 78) Study M93-058 * 6

(n = 53)
43
(n = 107)
12 months post-treatment
Study M92-812b * 5 (n = 39) 68 (n = 71)

# H. pylori eradication status assessed at same timepoint as ulcer recurrence
* Combined results for PRILOSEC + clarithromycin, PRILOSEC, and clarithromycin treatment arms *
Combined results for PRILOSEC + clarithromycin and PRILOSEC treatment arms *
(p £ 0.01) versus proportion with duodenal ulcer recurrence who were not H. pylori eradicated Gastric Ulcer In a U. S. multicenter, double-blind, study of omeprazole 40 mg once a day, 20 mg once a day, and placebo in 520 patients with endoscopically diagnosed gastric ulcer, the following results were obtained.

Treatment of Gastric Ulcer
% of Patients Healed
(All Patients Treated)

PRILOSEC
20 mg q. d.
(n = 202)

PRILOSEC
40 mg q. d.
(n = 214)
Placebo
(n = 104)
Week 4 Week 8 47.5 ** 74.8 ** 55.6 ** 82.7 **,+ 30. 8 48.1

** (p < 0.01) PRILOSEC 40 mg or 20 mg versus placebo
+ (p < 0.05) PRILOSEC 40 mg versus 20 mg

For the stratified groups of patients with ulcer size less than or equal to 1 cm, no difference in healing rates between 40 mg and 20 mg was detected
at either 4 or 8 weeks. For patients with ulcer size greater than 1 cm, 40 mg was significantly more effective than 20 mg at 8 weeks.

In a foreign, multinational, double-blind study of 602 patients with endoscopically diagnosed gastric ulcer, omeprazole 40 mg once a day, 20
mg once a day, and ranitidine 150 mg twice a day were evaluated.
Treatment of Gastric Ulcer
% of Patients Healed
(All Patients Treated)

PRILOSEC
20 mg q. d. (n = 200)
PRILOSEC
40 mg q. d. (n = 187)
Ranitidine
150 mg b. i. d. (n = 199)

Week 4
Week 8
63.5
81.5
78.1 **,++
91.4 **,++
56.3
78.4 **
(p < 0.01) PRILOSEC 40 mg versus ranitidine ++
(p < 0.01) PRILOSEC 40 mg versus 20 mg

Gastroesophageal Reflux Disease (GERD) Symptomatic GERD
A placebo controlled study was conducted in Scandinavia to compare the efficacy of omeprazole 20 mg or 10 mg once daily for up to 4 weeks in the
treatment of heartburn and other symptoms in GERD patients without erosive esophagitis. Results are shown below.

% Successful Symptomatic Outcome a
PRILOSEC
20 mg a. m.
PRILOSEC
10 mg a. m.
Placebo
a. m.
All patients

Patients with
confirmed GERD

46 *,*
(n = 205) 56 *,*

(n = 115)

31 * (n = 199)
36 *
(n = 109)

13 (n = 105)
14
(n = 59) a
Defined as complete resolution of heartburn *
(p < 0.005) versus 10 mg *
(p < 0.005) versus placebo

Erosive Esophagitis In a U. S. multicenter double-blind placebo controlled study of 20 mg or 40 mg of PRILOSEC Delayed-Release Capsules in patients with symptoms of GERD and endoscopically diagnosed erosive esophagitis of grade 2 or above, the percentage healing rates (per protocol) were as follows:
Week
20 mg PRILOSEC
(n = 83)
40 mg PRILOSEC
(n = 87)
Placebo
(n = 43)
4
8
39 **
74 **
45 **
75 **
7
14 **
(p < 0.01) PRILOSEC versus placebo.

In this study, the 40 mg dose was not superior to the 20 mg dose of PRILOSEC in the percentage healing rate. Other controlled clinical trials have also shown that PRILOSEC is effective in severe GERD. In comparisons with histamine H2-receptor antagonists in patients with erosive esophagitis, grade 2 or above, PRILOSEC in a dose of 20 mg was significantly more effective than the active controls. Complete daytime and nighttime heartburn relief occurred significantly faster (p < 0.01) in patients treated with PRILOSEC than in those taking placebo or histamine H2-receptor antagonists.

In this and five other controlled GERD studies, significantly more patients taking 20 mg omeprazole (84%) reported complete relief of GERD symptoms than patients receiving placebo (12%). Long Term Maintenance Treatment of Erosive Esophagitis In a U. S. double-blind, randomized, multicenter, placebo controlled study, two dose regimens of PRILOSEC were studied in patients with endoscopically confirmed healed esophagitis. Results to determine maintenance of healing of erosive esophagitis are shown below.
Life Table Analysis

PRILOSEC
20 mg q. d.
(n = 138)

PRILOSEC
20 mg 3 days
per week
(n = 137)
Placebo
(n = 131)
Percent in
endoscopic
remission at 6 months *

70 34 11 * (p < 0.01) PRILOSEC 20 mg q. d. versus PRILOSEC 20 mg 3 consecutive days per week or placebo.

In an international multicenter double-blind study, PRILOSEC 20 mg daily and 10 mg daily were compared to ranitidine 150 mg twice daily in patients with endoscopically confirmed healed esophagitis. The table below provides the results of this study for maintenance of healing of erosive esophagitis.
Life Table Analysis
PRILOSEC
20 mg q. d.
(n = 131)

PRILOSEC
10 mg q. d.
(n = 133)

Ranitidine
150 mg b. i. d.
(n = 128)
Percent in
endoscopic
remission at
12 months * 77 * 58 46 *
(p = 0.01) PRILOSEC 20 mg q. d. versus PRILOSEC 10 mg q. d. or Ranitidine. *
(p = 0.03) PRILOSEC 10 mg q. d. versus Ranitidine.

In patients who initially had grades 3 or 4 erosive esophagitis, for maintenance after healing 20 mg daily of PRILOSEC was effective, while
10 mg did not demonstrate effectiveness.

Pathological Hypersecretory Conditions

In open studies of 136 patients with pathological hypersecretory conditions, such as Zollinger-Ellison (ZE) syndrome with or without multiple endocrine adenomas, PRILOSEC Delayed-Release Capsules significantly inhibited gastric acid secretion and controlled associated symptoms of diarrhea, anorexia, and pain. Doses ranging from 20 mg every other day to 360 mg per day maintained basal acid secretion below 10 mEq/ hr in patients without prior gastric surgery, and below 5 mEq/ hr in patients with prior gastric surgery. Initial doses were titrated to the individual patient need, and adjustments were necessary with time in some patients (see DOSAGE AND ADMINISTRATION).

PRILOSEC was well tolerated at these high dose levels for prolonged periods (> 5 years in some patients). In most ZE patients, serum gastrin levels were not modified by PRILOSEC. However, in some patients serum gastrin increased to levels greater than those present prior to initiation of omeprazole therapy. At least 11 patients with ZE syndrome on long-term treatment with PRILOSEC developed gastric carcinoids. These findings are believed to be a manifestation of the underlying condition, which is known to be associated with such tumors, rather than the result of the administration of PRILOSEC. (See ADVERSE REACTIONS.)

Microbiology Omeprazole and clarithromycin dual Studies 126, 127)
Susceptible b 171 153 7 3 8
Intermediate b
Resistant b 14 4 1 6 3 a
Includes only patients with pretreatment clarithromycin susceptibility test results b
Susceptible (S) MIC £ 0.25 mg/ mL, Intermediate (I) MIC 0.5 -1.0 µg/ mL, Resistant (R) MIC ³ 2 mg/ mL

Patients not eradicated of H. pylori following omeprazole/ clarithromycin/ amoxicillin triple therapy or omeprazole/ clarithromycin dual therapy will likely have clarithromycin resistant H. pylori isolates. Therefore, clarithromycin susceptibility testing should be done, if possible. Patients with clarithromycin resistant H. pylori should not be treated with any of the following:

omeprazole/ clarithromycin dual therapy, omeprazole/ clarithromycin/ amoxicillin triple therapy, or other regimens which include clarithromycin as the sole antimicrobial agent. Amoxicillin Susceptibility Test Results and Clinical/ Bacteriological Outcomes

In the triple therapy clinical trials, 84.9% (157/ 185) of the patients in the omeprazole/ clarithromycin/ amoxicillin treatment group who had pretreatment amoxicillin susceptibletherapy and omeprazole,
clarithromycin and amoxicillin triple therapy have been shown to be active against most strains of Helicobacter pylori in vitro and in clinical infections as described in the INDICATIONS AND USAGE section.

Helicobacter Helicobacter pylori Pretreatment Resistance

Clarithromycin pretreatment resistance rates were 3.5% (4/ 113) in the omeprazole/ clarithromycin dual therapy studies (M93-067, M93-100) and 9.3% (41/ 439) in omeprazole/ clarithromycin/ amoxicillin triple therapy studies (126, 127, M96-446).

Amoxicillin pretreatment susceptible isolates (£ 0.25 µg/ mL) were found in 99.3% (436/ 439) of the patients in the omeprazole/ clarithromycin/ amoxicillin triple therapy studies (126, 127, M96-446). Amoxicillin pretreatment minimum inhibitory concentrations (MICs) > 0.25 µg/ mL occurred in 0.7% (3/ 439) of the patients, all of whom were in the clarithromycin and amoxicillin study arm. One patient had an unconfirmed pretreatment amoxicillin minimum inhibitory concentration (MIC) of > 256 µg/ mL by Etest ® .
Clarithromycin Susceptibility Test Results and Clinical/ Bacteriological Outcomes
Clarithromycin Susceptibility Test Results and Clinical/ Bacteriological Outcomes a
Clarithromycin
Pretreatment Results
Clarithromycin Post-treatment Results

H. pylori negative -
eradicated
H. pylori positive -not eradicated

Post-treatment susceptibility results S b I b R b No MIC
Dual Therapy -(omeprazole 40 mg q. d./ clarithromycin 500 mg t. i. d. for 14 days followed by omeprazole 20 mg q. d. for another 14 days) (Studies M93-067, M93-100)
Susceptible b 108 72 1 26 9
Intermediate b 1 1
Resistant b 4 4
Triple Therapy -(omeprazole 20 mg b. i. d./ clarithromycin 500 mg b. i. d./ amoxicillin 1 g b. i. d. for
10 days -Studies 126, 127, M96-446; followed by omeprazole 20 mg q. d. for another 18 days -
MICs (£ 0.25 µg/ mL) were eradicated of H. pylori and 15.1% (28/ 185) failed therapy. Of the 28 patients who failed triple therapy, 11 had no post-treatment susceptibility test results and 17 had post-treatment H. pylori isolates with amoxicillin susceptible MICs. Eleven of the patients who failed triple therapy also had post-treatment H. pylori isolates with clarithromycin resistant MICs.

Susceptibility Test for Helicobacter pylori The reference methodology for susceptibility testing of H. pylori is agar dilution MICs 1 . One to three microliters of an inoculum equivalent to a No. 2 McFarland standard (1 x 10 7 -1 x 10 8 CFU/ mL for H. pylori) are inoculated directly onto freshly prepared antimicrobial containing Mueller-Hinton agar plates with 5% aged defibrinated sheep blood (³ 2 weeks old).

The agar dilution plates are incubated at 35° C in a microaerobic environment produced by a gas generating system suitable for campylobacters. After 3 days of incubation, the MICs are recorded as the lowest concentration of antimicrobial agent required to inhibit growth of the organism. The clarithromycin and amoxicillin MIC values should be interpreted according to the following criteria:

Clarithromycin MIC (mg/ mL) a Interpretation
£ 0.25 Susceptible (S) 0.5 Intermediate (I)

³ 1.0 Resistant (R)

Amoxicillin MIC (mg/ mL) a, b Interpretation
£ 0.25 Susceptible (S)
a These are tentative breakpoints for the agar dilution methodology and they should not be used to interpret results obtained using alternative methods.
b There were not enough organisms with MICs > 0.25 mg/ mL to determine a resistance breakpoint.

Standardized susceptibility test procedures require the use of laboratory control microorganisms to control the technical aspects of the laboratory
procedures. Standard clarithromycin and amoxicillin powders should provide the following MIC values:

Microorganism Antimicrobial Agent MIC (mg/ mL) a
H. pylori ATCC 43504 Clarithromycin 0.016-0.12 (mg/ mL)
H. pylori ATCC 43504 Amoxicillin 0.016-0.12 (mg/ mL) a
These are quality control ranges for the agar dilution methodology and they should not be used to control test
results obtained using alternative methods.

1 National Committee for Clinical Laboratory Standards. Summary Minutes, Subcommittee on Antimicrobial Susceptibility
Testing, Tampa FL, January 11-13, 1998.

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