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Pay attention to post-stroke pneumonia-mucosal protective agents, safe and effective treatment options

Pay attention to post-stroke pneumonia-mucosal protective agents, safe and effective treatment options

  • Categories:Stomach healthy
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  • Time of issue:2020-12-01
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(Summary description)

Pay attention to post-stroke pneumonia-mucosal protective agents, safe and effective treatment options

(Summary description)

  • Categories:Stomach healthy
  • Author:
  • Origin:
  • Time of issue:2020-12-01
  • Views:0
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Pay attention to post-stroke pneumonia-mucosal protective agents, safe and effective treatment options  

   Pneumonia is the most common infection after stroke, and it is also the main cause of early and long-term mortality and morbidity after stroke. Therefore, determining the risk factors for pneumonia is very important to prevent stroke complications and improve the long-term prognosis after stroke. Proton pump inhibitor (PPI) and H₂ receptor antagonist (H2RA) play a protective role by reducing the secretion of gastric acid and reducing the acidity of the stomach. However, the acidity of gastric juice is one of the main bactericidal barriers. Considering its biological principle, the bactericidal barrier of gastric acid and the antacid properties of PPI and H2RA, the use of acid inhibitors may lead to the risk of pneumonia, especially those with dysphagia Patients with stroke are very prone to respiratory infections. However, patients with ischemic stroke usually need to take antiplatelet drugs or anticoagulants throughout their lives to prevent cardiovascular events. Aspirin and non-steroidal anti-inflammatory drugs inhibit prostaglandin-endoperoxidase synthase, thereby reducing the basic protective effects of the cytoprotective prostaglandin E₂ and prostaglandin I₂ in the gastric mucosa. Decreased prostaglandin levels can mediate gastrointestinal mucosal damage by reducing mucosal blood flow, bicarbonate and mucus secretion, impaired proliferation and repair functions, and increased inflammatory molecules such as gastric acid and leukotrienes. Clopidogrel, another commonly used antiplatelet drug, can also cause a similar degree of damage to the gastrointestinal mucosal barrier. There have been a large number of research reports in the early stage. A hospital-based cohort study studied 1676 patients with acute stroke. The results showed that the degree of exposure to PPI during hospitalization was significantly related to the risk of hospital-acquired pneumonia. In addition, a Taiwanese study based on A retrospective study of the National Health Insurance Research Database also showed that among 355 acute stroke patients, the risk of using H2RA and PPI pneumonia increased significantly. And an observational study conducted in Japan using the National Diagnostic Procedures and the Inpatient Database also showed that PPI and H2RA pneumonia after acute stroke also increased significantly, and the incidence of pneumonia in the two groups was similar. The relevant guidelines of the American Heart Association also clearly pointed out that for the treatment or prevention of gastrointestinal mucosal damage caused by NSAIDs, it is recommended to choose PPI therapy, and PPI and H2RA should also be considered to increase the risk of pneumonia. In summary, for patients who need long-term anticoagulation therapy after stroke, are there other better drug treatment options?

   This study is a retrospective cohort study based on the national population based on the National Health Insurance Database in South Korea to evaluate the risk of post-stroke pneumonia caused by PPI, H2RA and mucosal protective agents. This study analyzed 8,319 patients with acute ischemic stroke, and determined the use of PPI, H2RA, and mucosal protective agents after stroke according to prescription records. These records were used as variables that change over time. The primary endpoint was the occurrence of post-stroke pneumonia. The average follow-up time was 3.95 years after stroke.

   This study is a retrospective cohort study based on the national population based on the National Health Insurance Database in South Korea to evaluate the risk of post-stroke pneumonia caused by PPI, H2RA and mucosal protective agents. This study analyzed 8,319 patients with acute ischemic stroke, and determined the use of PPI, H2RA, and mucosal protective agents after stroke according to prescription records. These records were used as variables that change over time. The primary endpoint was the occurrence of post-stroke pneumonia. The average follow-up time was 3.95 years after stroke.

  01

   Research object

   A cohort study based on a national population sample using NHIS-NSC. From 2002 to 2013, we collected 8,319 patients, aged ≥20 years, who were diagnosed as acute ischemic stroke for the first time. The primary endpoint was the onset time of pneumonia after discharge. The standard flow of entry and discharge is shown in Figure 1.

   Figure 1. Flow chart of included patients

  02

  research method

  According to the prescription records, the patients' exposure to PPI, H2RA and mucosal protective agents were recorded every day during the follow-up period and collected as time-related variables. According to the daily dosage of PPI and H2RA, it is divided into low-dose and high-dose groups. If the daily dosage is higher than the following: omeprazole 20 mg, pantoprazole 40 mg, lansoprazole 30 mg, Beprazole 20 mg, esomeprazole 30 mg, dexlansoprazole 20 mg, ilaprazole 20 mg, cimetidine 800 mg, famotidine 40 mg, lamotidine 20 mg, Nizatidine 300 mg, ranitidine 300 mg, and rosatidine 150 mg are considered high-dose groups, and their cut-off values ​​are determined by the World Health Organization; mucosal protective agents used include polyprezinc and rebamipide , Teprenone, isoladine, icafibrate, sofelone, sucralfate and misoprostol. The statistical analysis method uses PPI, H2RA and mucosal protective agent exposure as variables, gender, age, history of hypertension, DM, MI, AF, COPD, use of thrombolysis, family income, length of stay, hospital type and year are associated Variables; analyze the hazard ratio (HR) and 95% confidence interval (CI) through the time-related Cox proportional hazards regression model; test the proportional hazard assumptions of the Cox model by evaluating the proportionally drawn Schonfeld residuals. Using PostgreSQL 10.1 and R software 3.4.4 for data processing and statistical analysis, two-way p<0.05 was statistically significant.

  03

  Result analysis

   Finally, 8319 patients with acute ischemic stroke were included.

   Table 1. Baseline characteristics of enrolled patients

  

   Figure 2 shows the proportion of patients who received PPI, H2RA and mucosal protective agents during the entire follow-up period after stroke. The proportion of patients receiving medication during the follow-up period was relatively consistent. The number of patients given PPI, H2RA, and mucosal protective agent were 147 (2.2%), 971 (14.5%) and 1131 (16.9%), respectively.

   Figure 2. Proportion of patients receiving medication after stroke

   During the follow-up of 3.95 ± 3.01 years (mean ± standard deviation), 2035 (24.5%) patients developed pneumonia after stroke and discharge. Figure 3 is an estimated probability curve of no pneumonia, and PPI, H2RA and mucosal protective agents are used as time-related variables during follow-up. The analysis found that among the anti-ulcer drugs, treatment with PPI and H2RA was associated with an increased risk of pneumonia (Figure 3A and Figure 3B), and the application of mucosal protective agent treatment group had no correlation with the risk of pneumonia (Figure 3C).

  

In the multivariate time-correlated Cox regression model (Table 2), PPI (HR [95%CI], 1.56 [1.24–1.96], p <0.001) and H2RA (HR [95%CI], 1.40 [1.25-1.58] ], p <0.001) patients have a significantly increased risk of pneumonia, and the use of mucosal protective agents is not associated with the occurrence of pneumonia (HR [95%CI], 0.89 [0.78-1.01], p = 0.055).

   Table 2. The effect of drugs on the risk of pneumonia after stroke

  

   At the same time, the risk of pneumonia was further analyzed based on the daily dose of PPI and H2RA (Table 3). There is a significant dose-response relationship between the risk of pneumonia and the daily dose of antacid drugs (high doses of PPI and H2RA cause a higher risk of pneumonia)

  Table 3. The effect of antacids on the risk of pneumonia based on the strength of the dose

  

   Discussion

   This study confirmed that the use of PPI and H2RA antacids was significantly associated with the occurrence of pneumonia after stroke. The average follow-up time was 3.95±3.01 years, and 24.5% of the patients had pneumonia. However, compared with antacid drugs, the application of mucosal protective agents has no correlation with the risk of pneumonia. At present, mucosal protective agents have been widely used in the protective treatment of gastroduodenal mucosa, such as polyprezinc, which increases gastric blood flow, inhibits the production of inflammatory factors, and reduces free oxygen without affecting gastric acid. It has a variety of mucosal protection mechanisms to treat gastrointestinal-related symptoms or prevent ulcers. The dose of PPI and H2RA is dose-related with the risk of pneumonia. It also reminds the worsening effect of antacid drugs on the risk of pneumonia. Considering the potential risk of pneumonia, clinicians should exercise caution when taking antacid drugs for a long time. Therefore, the American Heart Association should refer to relevant guidelines for patients with a low risk of gastrointestinal bleeding and no clear indication for PPI therapy. In order to use antacids to minimize the potential risk of pneumonia after stroke, mucosal protective agents are also a safe and effective alternative for gastrointestinal symptom control or mucosal protection for stroke patients susceptible to pneumonia.

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