Internal drug therapy is the most basic treatment for peptic ulcer disease, and there is a wide variety of anti-ulcer drugs, with more than two drugs being used in most cases. The problem of drug interactions is becoming more and more prominent, so this paper discusses the rational application of anti-ulcer drugs in combination with several common drug combinations that currently exist.
The first is the use of a new drug, which can be used in the same way as a new drug, which can be used in the same way as a new drug, which can be used in the same way as a new drug, which can be used in the same way as a new drug, which can be used in the same way as a new drug, which can be used in the same way as a new drug, which can be used in the same way as a new drug, which can be used in the same way as a new drug, which can be used in the same way as a new drug, which can be used in the same way as a new drug, which can be used in the same way as a new drug.
2, H2RA + choline receptor blockers: choline receptor blockers such as pirenzepine, tilenazepine (Telenzepine) are selective M1R blockers, but these drugs on the inhibition of gastric acid secretion is not strong, the combination of two types of drugs through different mechanisms of action can synergistically inhibit gastric acid secretion, enhance the efficacy of acid suppression; H2RA stimulates the release of gastrin, with pirenzepine to inhibit the release of gastrin, can also reduce the adverse effects. The combination of H2RA stimulates the release of gastrin and pirenzepine inhibits the release of gastrin, which also reduces the adverse effects. The combination of H2RA to stimulate gastrin release and pirenzepine to inhibit gastrin release can also reduce adverse effects. Because it has been recently shown that the choline receptor on the gastric wall cells is M3R, long-term application of anticholinergic drugs does not change the incidence of duodenal ulcer complications, and the long-term use of drugs can cause changes in symptoms or even mask them, thus delaying the recognition of recurrence. Therefore, anticholinergics alone should never be used to treat duodenal ulcer disease, and anticholinergics should only be used as an adjunct to antacid therapy.
3. H2RA + other classes of drugs.
(1) Cimetidine has obvious inhibition of liver drug enzymes, affecting the metabolism of a variety of drugs, more adverse reactions. For example, cimetidine can cause heart block and heart failure when used in combination with insulin, phenytoin sodium and other central depressants, which can lead to central inhibition due to increased blood concentration. Should be avoided or reduced in combination with the application.
(2) Metronidazole’s 2-position methyl hydroxylation and 1-position hydroxyethyl oxidation are inhibited by cimetidine, which decreases the clearance rate by 30% and prolongs t1/2 by 27%, and the combination of the two drugs may cause ataxia, vertigo, peripheral neuropathy and other adverse effects. The combination of the two drugs may cause adverse effects such as ataxia, dizziness and peripheral neuropathy. Ranitidine and famotidine, which have weak effects on hepatic enzymes, can be used.
(3) Cimetidine has similar myoneural blocking effect as aminoglycosides, and the combination of the two may lead to respiratory depression or arrest.
(4) Lactase acid production reduces the absorption of cimetidine by 20%-30%, which may reduce the efficacy of cimetidine.
4, proton pump inhibitor (PPI) + a variety of antibiotics to eradicate HP bacteria: most antibacterial drugs in an alkaline environment to stabilize and enhance antibacterial activity. PPI inhibits gastric acid secretion, raises PH and enhances the function of antibiotics many times; and can directly inhibit bacteria. For example, amoxicillin in PH5, the minimum inhibitory concentration is 0.5mg/L. When PH is 5, it is 0.06mg/L, which increases more than 10 times; it can enhance the antibacterial effect of erythromycin up to more than 60 times. Therefore, the combination of the two can improve the antibacterial efficacy. Omeprazole has good antibacterial activity against metronidazole-resistant HP in vitro and can improve the sensitivity of drug-resistant HP to metronidazole. The mechanism is related to the inhibition of ATPase, which increases the accumulation of drugs in the body of bacteria, and the combined use of drugs to treat HP infection can also improve the efficacy. When used in combination, it is advisable to take acid-suppressing drugs first and then antibacterial drugs.
5.PPI + other drugs.
(1) Omeprazole can inhibit hepatic cytochrome P450 enzyme activity, thus reducing the decomposition of bicoumarin anticoagulants, desipramine, phenytoin sodium and other drugs in the liver. Pantoprazole does not inhibit hepatocyte P450 enzyme activity and does not affect the metabolism of bicoumarins, desipramine, phenytoin sodium, theophyllines, and non-steroidal anti-inflammatory drugs.
(2) When combined with quinolones, because PPI inhibits gastric acid secretion and reduces the absorption of quinolones, it should be avoided to be taken together.
6, bismuth + acid suppressants: bismuth forms various forms of insoluble complexes in acidic environment, which are deposited on the gastric mucosa and play a role in protecting the mucosa. Acid suppressants can reduce the efficacy of bismuth, so when combined, bismuth can be used first, and then take acid suppressants after 1 hour, or take acid suppressants before bedtime.
7, bismuth + a variety of antibiotics: bismuth and a variety of antibiotics together can enhance the antibacterial efficacy, after the addition of 1-2 antibiotics Hp eradication rate can reach 80%-90%.
8.Pay attention to prevent bismuth poisoning
(1) During the treatment period of bismuth and within 2 months after stopping the drug, you should not take any bismuth-containing drugs (such as Gastric Biotec, Lodegastric, Gastric Speed, etc.).
(2) Milk and alcoholic beverages should not be taken during the taking period, while drinking less tea and coffee.
9.Aluminium thioglycollate + acid suppressants and alkaline antacids: The adhesion of aluminium thioglycollate to gastric mucosa and the amount of bile acid salt combined with local PH have obvious relationship, the best PH of its adhesion and ulcer surface is 2~3, when PH>4, this adhesion is weakened and the amount of bile acid salt combined is reduced. Alkaline antacids make the PH in the stomach rise, can reduce the efficacy of aluminum thioglycollate, and should not be taken at the same time with antacids; acid inhibitors can reduce the efficacy of aluminum thioglycollate, ranitidine and other acid inhibitors due to adhesion, absorption is reduced and reduce the efficacy of the combination should be taken first aluminum thioglycollate, more than 2 hours apart.
10.Aluminium thioglycollate + other types of drugs.
(1) aluminum thiosulfate + a variety of antibacterial drugs: aluminum thiosulfate can enhance the anti-Hp effect of antibiotics such as metronidazole, erythromycin, tetracycline and amoxicillin, which can enhance the antibacterial effectiveness of metronidazole by 1.5 times, increase amoxicillin by 2 times, tetracycline by 3 times and erythromycin by 8 times. It is believed that the efficacy of triple therapy containing aluminum thioglycollate for HP eradication is approximately the same as that of triple therapy containing bismuth.
(2) Aluminum thioglycollate can interfere with the absorption of phenytoin sodium, tetracycline, quinolone antibacterial drugs, digoxin, theophylline, lipid tolerant vitamins and other drugs, and when combined with these drugs, they should be taken separately at intervals of more than 2 hours.
11, prokinetic drugs + acid suppressants: 1 therapeutic amount of acid suppressants [Foreign Medical Digestion 99 -1 50] [simethicone, ranitidine, loxacid] have an effect on both gastric motility and gastric emptying. Mechanism.
(1), decreased secretion of gastric acid and increased secretion of gastrin, which increases the contraction of the gastric sinus and slows gastric emptying.
(2), decreased gastric acid, decreased gastric enzyme activity, decreased food hydrolysis, and large food particles do not easily pass through the pylorus.
(3), reduced gastric acid is often accompanied by reduced secretion of body fluids, increased food viscosity, and slowed emptying. Prokinetic drugs can correct the inhibitory effect of acid-suppressing drugs on gastrointestinal motility. Because both types of drugs are metabolized by the hepatic P450 enzyme system, and prokinetic drugs can increase the bioavailability of H2 receptor blockers, the blood concentration increases when combined, the toxic side effects also increase, and should be reduced. The combination of Prebux with some slow and controlled release formulations that act or are absorbed in the stomach, such as controlled release tablets of gentamicin, leads to a short residence time of the latter in the stomach, thus reducing efficacy and absorption.12 Macrolides such as isoniazid, metronidazole, ketoconazole, ciprofloxacin, enoxacin, and erythromycin can inhibit the metabolism of Prebux and cause prolongation of the O-T interval, and the combination of the two drugs may cause arrhythmia.