Gastroesophageal reflux disease, a condition in which reflux of gastric contents causes uncomfortable symptoms and/or complications. Its esophageal symptoms include typical reflux syndrome (reflux, heartburn), reflux chest pain syndrome; extraesophageal manifestations include: reflux asthma syndrome, reflux cough syndrome, reflux laryngitis syndrome and pharyngitis, sinusitis, recurrent otitis media, etc. It has gradually attracted the attention of clinicians in recent years, and because it is a common, frequent and chronic disease, it is easily recognized and thought of by clinicians. Superior mesenteric artery compression syndrome, a rare disease characterized by postprandial epigastric pain, nausea, vomiting, anorexia and weight loss, is a clinical syndrome caused by compression of the third segment of the duodenum by narrowing of the angle between the superior mesenteric artery (SMA) and the abdominal aorta. Since it was first described by Carl von Rokintansky from Austria in 1842, it has attracted the attention of the medical community. However, because of its low incidence and the intersection of clinical symptoms with other gastrointestinal diseases, it has been repeatedly reported in the literature as an underdiagnosis or misdiagnosis. Superior mesenteric artery compression syndrome: also known as benign duodenal stasis, duodenal vascular compression syndrome, tubular plaster clamp syndrome, Wilkie syndrome, etc. Etiology and pathology: The ascending duodenal segment crosses the third lumbar vertebra, abdominal aorta and paravertebral muscle from right to left, and passes between the superior mesenteric artery and abdominal aorta. When the angle between the two arteries is too small, the superior mesenteric artery can cause narrowing and obstruction of the intestinal lumen by compressing the duodenum over the conus and abdominal aorta. Clinical manifestations are divided into two types: acute obstruction and chronic obstruction. The former mainly manifests as acute gastric dilatation, and physical examination reveals epigastric distention, gastric peristaltic waves, and audible vibrohydraulic sounds. The latter is common clinically, with long-term intermittent epigastric pain, vomiting (vomit is often mixed with bile), anorexia and other manifestations, and malnutrition such as wasting, weakness, weight loss and anemia in those with a long history. In acute attacks of chronic obstruction, the manifestations are the same as those of acute obstruction, and there are often no obvious signs during the remission period, which can be easily misdiagnosed as gastroesophageal reflux disease, chronic gastritis, peptic ulcer, etc. Barium X-ray examination shows dilatation of the proximal duodenum, even gastric dilatation, frequent retroperistalsis, and dilatation of the proximal horizontal part of the duodenum. In this case, barium is seen in the third segment of the duodenum with sudden truncation, and then another truncation vaguely appears in the left side of the vertebral body, both of which are in a vertical line without barium, which is clinically called “penumbral sign&rdquo. diagnosis is obtained by abdominal ultrasound, CTA examination, by measuring the angle and distance between the abdominal aorta and SMA. However, there is no unified standard, domestic reports SMAS patients with two arteries angle 15°-20° (normal people average 40°- 60°), foreign reports two arteries angle 7°- 22° (normal people 25°-60°), two arteries between the distance of about 2- 8mm (normal people 10-28mm) . We found that the superior mesenteric artery syndrome is often misdiagnosed as gastroesophageal reflux disease in clinical practice for the following reasons: 1. The high intestinal obstruction formed in patients with SMAS often causes food retention and frequent retroperistalsis at the proximal end of the duodenal obstruction, which naturally produces a gradual decreasing pressure gradient of duodenum-gastric-esophagus, with a conceivable end of regurgitation of gastrointestinal contents into the esophagus along the pressure gradient; 2. The high intestinal obstruction can cause duodenal and gastric dilatation, and the ventral segment of the lower esophageal sphincter shortens after gastric dilatation, resulting in a decrease in LES length, a decrease in LES resting pressure, and a weakening of the anti-reflux effect of the LES, causing gastroesophageal reflux; 3. Some studies have pointed out that gastric dilatation is the main cause of inducing transient lower esophageal sphincter relaxation, and TLESR is now known to be the main mechanism for the occurrence of gastroesophageal reflux; 4. SMAS-induced gastro Gastroduodenal reflux caused by SMAS is different from the reflux of simple gastric contents. The former reflux not only contains gastric acid and pepsin, but also often mixed with bile salts and pancreatic juice that reflux into the esophagus at the same time, and some studies have found that gastric and duodenal fluids are jointly involved in damage to the mucosa of the digestive tract. 5. It is found that most SMAS patients are long and lean, and often have the problems of insufficient gastrointestinal motility and delayed gastric emptying, which keep the stomach filled for a long time, thus increasing the intragastric pressure and gastric dilatation, and promoting the occurrence of reflux. For all these reasons, SMAS is prone to secondary gastroesophageal reflux, which objectively leads to the development of GERD.