L-cysteine Prevents Stomach Exposure to Carcinogenic Acetaldehyde
Condition: Gastritis, Atrophic
MeSH terms: Gastritis; Gastritis, Atrophic; Atrophy
Study type: Interventional
Phase: Phase 2

Summary: 
      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.
    

Detailed description: 
      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.
    

Intervention name(s): Slow-release L-cysteine
Intervention type(s): Dietary Supplement
Intervention description(s): Bind and inactivate acetaldehyde formed from ethanol by covalent binding to L-cysteine
Other intervention name(s): Acetium
Allocation: Randomized
Intervention model: Crossover Assignment
Masking: Single (Participant)
Primary purpose: Prevention
Keywords: atrohpic gastritis; acetaldehyde; ethanol; L-cysteine