Trial | NCT02524262  Report issue

Title

L-cysteine Prevents Stomach Exposure to Carcinogenic Acetaldehyde
Slow-release L-cysteine Capsule Prevents Carcinogenic Gastric Acetaldehyde Exposure in Helicobacter-associated Atrophic Gastritis

  • Phase

    Phase 2

  • Study Type

    Interventional

  • Status

    Completed No Results Posted

  • Intervention/Treatment

    l-cysteine ...

  • Study Participants

    8
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.
Study Started
Dec 31
2012
Primary Completion
Sep 30
2015
Study Completion
Sep 30
2015
Last Update
Jan 25
2016
Estimate

Dietary Supplement Slow-release L-cysteine

Bind and inactivate acetaldehyde formed from ethanol by covalent binding to L-cysteine

  • Other names: Acetium

Slow-release L-cysteine Experimental

Oral intake of slow-release L-cysteine 200 mg before challenge with ethanol.

Placebo Placebo Comparator

Oral intake of identically-looking placebo capsules

Criteria 

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
No Results Posted