pared before and after eradication
of H. pylori using the present gold
standard endoscopy and
13
C UBT
(75mg
13
C Urea).
7
200 dyspeptic patients were en-
doscopied and subsequently ei-
ther tested with the tablet (50 and
100 mg) or with the conventional
urea test. H. pylori infected patients
were treated and then given another
endoscopy and rechecked.
The sensitivity and specificity of the
conventional UBT were 100%. The
sensitivity and specificity of the tab-
let test (100 mg) were 100% and
98.85%. In post treatment monitor-
Possible Treatment Regimens
Provided that no penicillin allergy is
present, the following regimens are
possible:
•
First line treatment:
PPI + Amoxicillin +
Clarithromycin for 7 days
Alternative:
PPI + Metronidazole +
Amoxicillin for 7 days
•
Second line treatment:
Rabeprazol + Amoxicillin +
Clarithromycin for 14 days
Alternative:
Rabeprazol + Amoxicillin +
Metronidazole for 14 days
•
Third line treatment:
PPI + Levofloxacin + Amoxicillin
for 10 days
In case of penicillin allergy:
PPI + Clarithromycin +
Metronidazol for 7 days
In counties with high
Clarithromycin resistance:
PPI + Metronidazone + Bismuth
+ Tetracycline for 10–14 days
These tested treatment regimens
produce an eradication rate of 80 to
90%.
Observation after successful eradi-
cation
The time for testing the success of
H. pylori eradication after the end
of treatment should be at least 4 – 6
weeks. In special cases where a gas-
tric ulcer or gastric MALT lymphoma
has been diagnosed, follow-up is
necessary with endoscopy. In cases
of a bleeding ulcer, a UBT or antigen
stool test should be carried out 4 to 8
weeks after bleeding has ceased, due
to potential false-negative results.
Second generation
13
C Urea Breath
test shows precision in studies
Studies have proven the reliability of
the modern Diabact
®
UBT. The diag-
nostic precision of this test was com-
3
How Diabact UBT
®
works
1. A base line breath sample is taken from the fasting patient. The
patient then takes the 50 mg Diabact
®
UBT tablet with water.
2. When the tablet containing the
13
C isotope labelled urea is swal-
lowed, it breaks down immediately in the stomach and releases
13
C
urea. A second breath sample is taken 10 minutes after swallowing
the tablet.
3. In presence of an H. pylori infection,
13
C urea is metabolised to car-
bon dioxide and ammonia by the urease produced by H. pylori.
4. The
13
C isotope diffuses into the blood as CO
2
and is transported to
the lungs where it is exhaled into a sample tube.
5. An increased level of
13
C is an indication of H. pylori colonisation of
the stomach.
6. If there is no H. pylori present in the stomach, the urea is simply
eliminated by the gastrointestinal tract (see also the interview with
Prof. Strowski in this issue).
High Infection Rates in the Population
Corea 1988, Cancer Res. 48; 3554
Developmental stages of gastric carcinoma
(acc. to Corea)
Normal gastric mucosa
Superficial gastritis
Atrophic gastritis
Metaplasia
Dysplasia
Carcinoma
H. pylori
Precancerous
lesions
1,2 4,5,6,7,8