Abstract
Objective This aim is to evaluate the effect of Sijunzi decoction (SJZD) treating chronic atrophic gastritis (CAG). Methods We performed searches in seven databases. The randomized controlled trials (RCTs) comparing SJZD with standard medical care or inactive intervention for CAG were enrolled. Combined therapy of SJZD plus conventional therapies compared with conventional therapies alone was also retrieved. The primary outcome included the incidence of gastric cancer and the improvement of atrophy, intestinal metaplasia, and dysplasia based on the gastroscopy and pathology. The secondary outcomes were Helicobacter pylori clearance rate, quality of life, and adverse event/adverse drug reaction. Results Six RCTs met the inclusion criteria. The research quality was low in the trials. For the overall effect rate, pooled analysis from 4 trials showed that modified SJZD plus conventional medications exhibited a significant improvement (OR = 4.86; 95% CI: 2.80 to 8.44; P < 0.00001) and without significant heterogeneity compared with the conventional medications alone. None reported the adverse effect. Conclusions Modified SJZD combined with conventional western medicines appears to have benefits for CAG. Due to the limited number and methodological flaw, the beneficial and harmful effects of SJZD for CAG could not be identified. More high-quality clinical trials are needed to confirm the results.
Highlights
Chronic atrophic gastritis (CAG) is a common inflammatory condition typically characterized by the loss of gastric glandular structures or by glandular structures metaplastic atrophy [1]
It is worth noting that helicobacter pylori (HP) infection has a remarkable influence on the incidence of CAG
The results indicated that modified Sijunzi decoction (SJZD) plus conventional medications could improve significantly the histologic scores of atrophy, intestinal metaplasia, and dysplasia compared with the conventional medications alone (P < 0.05)
Summary
Chronic atrophic gastritis (CAG) is a common inflammatory condition typically characterized by the loss of gastric glandular structures or by glandular structures metaplastic atrophy [1]. It is worth noting that helicobacter pylori (HP) infection has a remarkable influence on the incidence of CAG. A systematic review published in 2010 reported that the rate ratio between HP infection and CAG incidence ranged from 2.4 to 7.6 [4]. A small subset of CAG cases eventually progress to gastric neoplasia [5, 6]. The severity of CAG has been demonstrated to be a key risk factor for the development of gastric cancer from a 10-year prospective cohort study in Japan [7]. The proper management of CAG will contribute to the prevention of gastric cancer
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