Mechanism of Action and Physiological Basis
The action of Betaine Pepsin (Acidin-pepsini) is based on a replacement effect — it artificially compensates for insufficient intrinsic gastric secretion (gaster).
Under physiological conditions, parietal cells secrete hydrochloric acid (HCl). The transport of protons ($H^+$) from the cell cytoplasm across the membrane occurs in exchange for potassium ions ($K^+$). This creates a massive gradient: the intracellular pH is 7.8, while the gastric lumen pH is 0.8.
This sharply acidic environment is absolutely essential for the function of proteolytic enzymes. The main one is pepsin, which performs proteolysis (the breakdown of protein structures). By taking the medication per os, we deliver ready-made enzymes and the substrate to create an acidic environment, initiating the digestive process even in the presence of glandular atrophy.
Pharmacokinetics
The drug exerts its effect prior to systemic absorption. Unlike most pharmacological agents for which the small intestine is the primary site of absorption into the venous bed (the portal vein for the first-pass effect) or the lymphatic duct, Betaine Pepsin acts exclusively within the lumen of the stomach. It interacts with the food bolus and is subsequently broken down or inactivated in the alkaline environment of the intestine.
Indications and Place in Combination Therapy
The primary indication is hypoacid conditions (reduced acidity) and insufficient enzyme production.
Gastric acidity directly affects the efficacy of other drugs. For example, the plant-based preparation nigedase (a lipase from Nigella damascena seeds) is less active at low acidity. In such cases, it is recommended to take it with gastric juice. Betaine Pepsin can serve as a pharmacological alternative, establishing the required pH background for lipases to function.
Furthermore, the drug is conceptually similar to preparations containing bile (where gastric mucosal extract contains pepsin and cathepsin), which are prescribed for complex replacement of gastric and pancreatic secretory deficits.
Mucosal Defense Factors and Adverse Effects
The introduction of exogenous acid and pepsin delivers aggressive factors directly into the stomach. Normally, the epithelium is protected by a robust gastroprotection system regulated by prostaglandins ($E_2$ and $I_2$):
- Mucus: Hydrophilic glycoproteins form a physical gel protecting the wall from acid and pepsin.
- Blood supply: Ensures the "washout" of hydrogen ions (back diffusion).
- Bicarbonates: Neutralize acid at the cell surface.
If the drug is taken on an empty stomach or if doses are exceeded, the aggressive action of pepsin and HCl can overwhelm the mucosal defense potential.
Clinical parallel: Excess acid and pepsin lead to mucosal damage. This is vividly demonstrated during long-term therapy with systemic glucocorticoids, which stimulate HCl and pepsin secretion, causing an ulcerogenic effect ("steroid" ulcers).
In hyperacid conditions and peptic ulcer disease, Betaine Pepsin is strictly contraindicated. In such situations, agents with the opposite effect are used: antacids (magnesium oxide, algeldrate), $H_2$-histamine receptor blockers (reducing basal acid and pepsin secretion), or gastroprotectants (sucralfate, which locally neutralizes HCl and reduces pepsin activity).
Prescribing and Administration Guidelines
The drug is available in 0.25 g tablets.
- Dosage: 0.2–0.5 g per dose orally.
- Frequency: 3–4 times daily.
- Timing with food: Strictly during or immediately after a meal. This is critically important so that the enzyme breaks down dietary proteins rather than attacking the gastric mucosa.