Effects and efficacy of Mucosta tablets
gastric ulcer
Improvement of gastric mucosal lesions (erosion, bleeding, redness, edema) in the following diseases
Acute gastritis, acute exacerbation of chronic gastritis
Usage and dosage of Mucosta tablets
<Gastric ulcer>
The usual adult dose is 100 mg of rebamipide (Mucosta Tablets 100 mg: 1 tablet, Mucosta Granules 20%: 0.5 g) orally 3 times a day in the morning, evening and before bedtime.
<Improvement of gastric mucosal lesions (erosion, bleeding, redness, edema) in the following diseases
Acute gastritis, acute exacerbation of chronic gastritis>
The usual adult dose is 100 mg of rebamipide (Mucosta Tablets 100 mg: 1 tablet, Mucosta Granules 20%: 0.5 g) orally three times a day.
People who need attention
pregnant woman
Pregnant women or women who may be pregnant should only be administered if the therapeutic benefits are judged to outweigh the risks. Fetal transfer has been reported in animal studies (rats).
lactating woman
Consider the therapeutic benefit and the benefit of breastfeeding and consider continuing or discontinuing breastfeeding. Excretion into milk has been reported in animal experiments (rats).
Children, etc.
No clinical trials have been conducted in children, etc.
senior citizen
Pay attention to side effects such as gastrointestinal symptoms. Physiological function is generally decreased.
Side effects
0.1% to less than 0.5%
Rash, constipation, bloating, diarrhea, dysgeusia
Less than 0.1%
Itching, hypersensitivity symptoms such as drug-eruption-like eczema, nausea, heartburn, abdominal pain, belching, increased AST and ALT
Frequency unknown
Urticaria, numbness, dizziness, drowsiness, dry mouth, vomiting, increased γ-GTP, Al-P, thrombocytopenia, leukopenia, granulocytopenia, mammary gland swelling, breast pain, gynecomastia, lactation induction, palpitations, Fever, hot flush, numbness of the tongue, cough, difficulty breathing, hair loss, abnormal menstruation, increased BUN
Pharmacology of Mucosta Tablets
Mechanism of action
Protects gastric mucosa, accelerates wound healing
Rebamipide is recognized to have a gastric mucosa protective effect and a healing promoting effect on damaged gastric mucosa by increasing endogenous prostaglandin and gastric mucus volume.
Inhibition of gastric mucosa inflammation
Rebamipide has been found to have the effect of suppressing inflammation of the gastric mucosa by suppressing free radicals, suppressing the production of inflammatory cytokines, and the like.
Suppressive effect and healing promoting effect on experimental gastric ulcer
Water immersion restraint stress ulcers, aspirin ulcers, indomethacin ulcers, histamine ulcers, serotonergic ulcers, pylorus ligation ulcers and ischemia-reperfusion thought to be associated with reactive oxygen species, platelet activating factor (PAF), diethyl Dithiocarbamate (DDC) inhibited gastric mucosa injury induced by stress indomethacin. It also promoted the healing of rat acetic acid ulcers and suppressed the recurrence and recurrence seen 120-140 days after ulcer formation.
Suppressive effect and healing promoting effect on experimental gastritis
In rats, it inhibited the development of experimental gastritis induced by taurocholic acid, one of the major bile acids, and had healing promoting effects.
Gastric mucosa prostaglandin increasing action
It increased gastric mucosal prostaglandin E2 content in rats. It also increased prostaglandin E2 and I2 in gastric juice, as well as 15-keto-13,14-dihydroprostaglandin E2, a metabolite of prostaglandin E2.
In healthy adult males, it increased gastric mucosal prostaglandin E2 content and inhibited gastric mucosal damage caused by ethanol loading.
gastric mucosa protection
In rats, it suppressed gastric mucosal injury caused by ethanol, strong acid and strong alkali 19), 22). It also inhibited cytotoxicity caused by aspirin and taurocholic acid (one of the main components of bile acid) in cultured rabbit fetal gastric epithelial cells (in vitro).
In healthy adult males, it inhibited gastric mucosal damage caused by aspirin, ethanol, and hydrochloric acid-ethanol loading.
Gastric mucus volume increasing effect
In rats, it enhanced the biosynthetic enzyme activity of mucus macromolecular glycoproteins and increased the amounts of gastric mucosal lining mucus and soluble mucus. Endogenous prostaglandins were not involved in the increase in soluble mucus.
Gastric mucosal blood flow increasing action
In rats, it increased gastric mucosal blood flow and ameliorated the hemodynamic disturbance caused by blood removal.
Action on the gastric mucosal barrier
In rats, it had almost no effect on the gastric potential difference, but inhibited the ethanol-induced decrease in the gastric potential difference.
Gastric alkaline secretion enhancing effect
It enhanced gastric alkaline secretion in rats.
Activation of gastric mucosa cell turnover
In rats, it stimulated gastric mucosal cell neogenesis and increased the number of tegmental epithelial cells.
Damaged gastric mucosa repair effect
In a wound repair model using cultured rabbit gastric epithelial cells, bile acids and hydrogen peroxide normalized the delayed repair process.
Effects on gastric acid secretion
In rats, it had little effect on basal gastric secretion and no inhibitory effect on stimulated gastric acid secretion.
Action on active oxygen
Rebamipide directly scavenged hydroxyl radicals and inhibited superoxide production in polymorphonuclear leukocytes. It also inhibited Helicobacter pylori-mediated gastric mucosal cell damage caused by reactive oxygen species production from neutrophils (in vitro).
Indomethacin-stressed rats inhibited gastric mucosal injury and reduced lipid peroxide content in gastric mucosa.
Effects on inflammatory cell infiltration into gastric mucosa
It inhibited inflammatory cell infiltration in rat taurocholic acid (one of the main components of bile acid)-induced gastritis model, NSAIDs gastric mucosal injury model, and ischemia-reperfusion model.
Effects on inflammatory cytokines (interleukin-8) in gastric mucosa
It suppressed the increase in interleukin-8 (IL-8) production from human gastric epithelial cells caused by Helicobacter pylori 39). It also suppressed the activation of NF-κB in epithelial cells and the expression of IL-8 mRNA (in vitro).