Poor dilation of esophageal peristalsis and retention of barium in the pyriform fossa

Introduction Poor esophageal peristalsis, dilatation and retention of piriform sputum are digestive symptoms of dermatomyositis and polymyositis. Dermatomyositis (DM) and polymyositis (PM) are currently considered to be autoimmune diseases. category. DM is characterized by diffuse inflammation of the skin and muscles, erythema and edema of the skin, weakness, pain and swelling of the muscles, which can be accompanied by joint pain and multiple organ damage such as lung and heart muscle. PM has no skin damage, and the etiology and pathogenesis of DM and PM are not yet clear.

Cause

The etiology and pathogenesis of DM and PM are not known and may be related to the following factors:

1. Infection: A variety of infections (bacteria, viruses, protozoa, etc.) have been found to be associated with this disease. More definitely JDM, there is often upper respiratory tract infection before the onset, anti-streptococcus "O" value is elevated, it is considered to be related to allergic reactions after bacterial infection. In the nucleus of the myocytes, a variety of virus-like particles are found in the cytoplasm and nucleus of vascular endothelial cells, perivascular tissue cells and fibroblasts, and elevated viral antibodies, especially paramyxoviruses, can also be detected in the serum of some patients. However, the transfer of muscle and plasma from these infected patients to animals did not cause inflammation in the muscles of the animals. Jo-1 (histidyl-tRNA synthetase) is unique to PM, and the Jo-1 antigen is similar to some viral antigens in the protein sequence. Whether or not there is a "molecular simulation" effect remains to be further studied.

2, tumor: the disease associated with a higher incidence of malignant tumors, especially DM, and some reports as high as 43%. Excision of the tumor lesion can alleviate the disease, and the patient's tumor solution is used for intradermal test, which is positive, and the passive transfer test is also positive. Anti-tumor antibodies are found in the serum of the patient. The tumor tissue and the normal muscle fibers, tendon sheath, blood vessels, and connective tissue of the human body have cross-antigenicity. These normal tissues can also react with anti-tumor antibodies as antigens, leading to lesions of these tissues. However, there is also a contrary view that the incidence of malignant tumors in DM/PM patients is not significantly higher than that in the normal population.

3. Immunization: Although the diseased organs of DM and PM are mainly muscles, they have not known what muscle-specific autoantigens are.

an examination

Related inspection

Esophagography esophageal barium meal perspective

Skin and muscle are the main symptoms of the two groups. The skin often precedes the muscles for several weeks to several years. It can also have myositis or muscle and skin at the same time. Skin and muscle symptoms are often not parallel, but one can be heavy and the other lighter. In some cases, the first symptom of the organ may not be skin or muscle, but the heart, lung or pleura, manifested as pericardial tamponade, pulmonary fibrosis or pleurisy.

1. Skin symptoms: The typical skin lesions are edematous purple-red spots on the upper eyelids, which spread to the periorbital area and gradually expand to the V-shaped area of the face, neck and upper chest. The elbow and elbow, especially the metacarpophalangeal joint and the metatarsophalangeal joint, appear purple-red papules with telangiectasia, hypopigmentation, overlying fine scales, called Gottron (Gordon) sign or Grottron papules. The edematous purplish red spot and Gottron sign of the upper eyelid are an important basis for the diagnosis of DM, especially the former, the earliest, and meaningful for early diagnosis. Most patients have a painless, itchy, etc. skin lesion. Other skin damage types of DM include heterochromia, erythroderma, cutaneous vasculitis, urticaria, and calcium deposition. There is an increased likelihood of cutaneous heterochromia with malignant tumors. Skin vasculitis and skin calcification occur mostly in JDM. Patients with cutaneous vasculitis are prone to systemic vasculitis at the same time. The symptoms are often severe, and the prognosis is poor when the treatment is not correct. Patients with cutaneous calcium are often associated with mild organ damage and good prognosis, but there are also reports of acute abdomen and intra-abdominal hemorrhage caused by extensive calcinosis of the abdominal wall. The rare types of skin lesions are plaque-like skin mucin deposition and blister or bullous damage. Mucin deposits are prone to occur in middle-aged and elderly women and may be the first symptom of DM. The prognosis of vesicles or bullae is poor.

2, muscle symptoms: involving the striated muscle, but the involvement of skeletal muscle is much more common than the myocardium. Smooth muscle is rarely affected. The proximal muscles of the extremities are most vulnerable, such as deltoid and quadriceps. Multiple symmetric onset. The diseased muscles have symptoms such as weakness and pain, and exhibit corresponding dyskinesias. The upper limbs are difficult to lift, and the lower limbs cannot lift and squat and cannot stand up. Heavier ones have difficulty lifting their heads and can't turn over, showing the involvement of the neck and trunk muscles. In severe cases, the limbs cannot move in the bed or can only move a few centimeters, or even a slight muscle contraction. When the esophagus and throat muscles are involved, there are difficulty in swallowing, eating cough, and changing pronunciation. Respiratory muscle involvement can cause shortness of breath and difficulty breathing. Eye muscles are affected by diplopia. A small number of patients may have no muscle pain and only manifest as muscle weakness.

3, other systemic symptoms, digestive system: the most common symptoms of digestive tract in systemic damage, manifested as abdominal distension, loss of appetite, digestion and malabsorption, constipation or diarrhea. Nearly one-third of patients have dysphagia, mainly difficulty in swallowing solid food; esophageal barium meal in the supine position, 2/3 patients can find abnormalities, such as esophageal dilation, poor peristalsis, contrast agent passing slowly and pear-shaped The sputum agent is retained. JDM can also cause intestinal necrosis due to vasculitis, gastrointestinal ulcers and bleeding. Abnormal liver function is more common during disease activity. Individual patients may have gallbladder cirrhosis, cholestatic hepatitis, and anti-mitochondrial antibodies can be detected at this time.

Differential diagnosis

Esophageal varices: The function of the portal system due to excessive blood supply to one of the liver's main sources of blood supply is abnormal. The venous blood that should have been introduced into the system and returned to the heart cannot flow in. The siltation in the lumen causes the vein to expand abnormally and cannot be retracted to normal, the so-called varicose veins. The source of blood from the portal venous system includes the esophageal vein, umbilical vein, and iliac vein. These vasodilatation will form varicose veins in the corresponding part, that is, esophageal varices, vein dilation near the navel, and hemorrhoids.

Pressure trails formed on the left wall of the esophagus: Esophageal barium meal examination of congenital aortic coarctation is often shown in the aortic constriction, the enlarged thoracic descending aorta or the enlarged right intercostal artery, and the pressure on the left wall of the esophagus Footprint, called the "E" sign.

Partial peristalsis of esophageal smooth muscle and decreased esophageal sphincter tone: typical in patients with scleroderma esophageal involvement. Scleroderma esophagus, referred to as scleroderma, involves the dysplasia of the esophageal muscle layer. Esophageal involvement manifests difficulty in swallowing, heartburn, vomiting, and a feeling of fullness behind the sternum or upper abdomen.

Esophageal peristalsis is weakened: esophagitis can weaken esophageal peristalsis, and esophagitis is inflammation of the esophagus. The clinical manifestation is post-sternal pain during swallowing, which can also cause esophageal spasm and temporary dysphagia.

Esophageal dilation: divided into primary and secondary. The expansion that occurs above the esophageal stricture is a secondary expansion, and the primary expansion is divided into two types: extensive expansion and limited expansion. Extensive expansion, also known as congenital expansion, the cause of the disease is unknown, esophageal neuromuscular dysfunction caused by full esophageal dilation. The full expansion of the esophagus is also called giant esophageal disease. The limited expansion is due to dilatation of the diverticulum. The limited expansion of the esophagus, that is, the diverticulum is often divided into two types: bulging (true) diverticulum and traction (pseudo) diverticulum. The bulging diverticulum protrudes more from the posterior wall, and the sag is sag in front of the spine due to the increase of the diverticulum. Traumatic diverticulum often causes scar contraction due to chronic inflammation of the tissues around the esophagus (such as lymph node tuberculosis), which is formed by pulling the esophageal wall, and occurs mostly in the anterior wall of the esophagus.

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