L-cysteine Prevents Stomach Exposure to Carcinogenic Acetaldehyde
L-cysteine Prevents Stomach Exposure to Carcinogenic Acetaldehyde
Atrophic gastritis with hypochlorhydric milieu is a risk factor for gastric cancer. Microbes
 colonizing the acid-free stomach oxidize ethanol into acetaldehyde, a group 1 carcinogen. The
 aim is to assess gastric production of acetaldehyde and its inert condensation product,
 non-toxic 4-methyltiazolidine-2-carboxylic acid (MTCA), after alcohol intake under treatment
 with slow-release L-cysteine or placebo.

 Patients with biopsy-confirmed atrophic gastritis, low serum pepsinogen and high gastrin-17
 are studied. On separate days, patients will be randomly assigned to receive 200 mg
 slow-release L-cysteine or placebo, then have intragastric instillation of 15% (0.3 g/kg)
 ethanol. After intake, gastric concentrations of acetaldehyde, ethanol, L-cysteine and MTCA
 are analysed for 4 hours.

 Expected results show mitigated exposure of the gastric mucosa to acetaldehyde.
Gastric infection with Helicobacter pylori induces chronic active gastritis which over the
 years develop atrophic gastritis with a hypochlorhydric milieu which is a risk factor for
 gastric cancer. Microbes colonizing acid-free stomach oxidize ethanol into acetaldehyde,
 considered a group 1 carcinogen.

 The aim of the study is to assess the gastric production of acetaldehyde and its inert
 condensation product, non-toxic 4-methyltiazolidine-2-carboxylic acid (MTCA), after alcohol
 intake under treatment with slow-release L-cysteine. Identical placebo tablets will be used
 for comparison.

 Patients with biopsy-confirmed atrophic gastritis, low serum pepsinogen and high gastrin-17
 will be studied with case-control design. All subjects will be their own control. On separate
 days, patients are randomly assigned to receive 200 mg slow-release L-cysteine or placebo,
 then have intragastric instillation of 15% (0.3 g/kg) ethanol (corresponding to two glasses
 of wine). After intake, gastric sampling of fluid for a period of four hours is done and
 concentrations of acetaldehyde, ethanol, L-cysteine and MTCA are analysed.

 L-cysteine is expected to decrease gastric acetaldehyde concentrations and increase the MTCA
 level. Gastric L-cysteine and MTCA concentrations are expected to be maintained over the
 study period. With placebo, acetaldehyde is expected to be elevated along with ethanol
 concentrations.

 Based on these assumptions slow-release L-cysteine binds acetaldehyde to form inactive MTCA,
 which remains in gastric juice resulting in reduced local exposure of the gastric mucosa to
 carcinogenic acetaldehyde.
Inclusion Criteria:

 -  Helicobacter-associated chronic gastritis

 -  Hypochlorhydria

 -  Hypergastrinemia

 -  Hypopepsinogenemia

 Exclusion Criteria:

 -  Active peptic ulcer disease

 -  Other inflammatory gastrointestinal disease

 -  Gastrointestinal bleeding

 -  Gastrointestinal surgery

 -  Neurological disease

 -  Alcohol abuse

 -  Mental disorder

 -  Not able to sign informed consent