2014年 · 第94卷第06期

With the acceleration of modern life rhythm and the change of lifestyle, various sleep disorders have become a prominent medical and public health problem^[1,2]。 Internationally, after more than 30 years of development, sleep medicine, an emerging marginal interdisciplinary subject mainly focused on the diagnosis and treatment of sleep diseases, has been formed and gradually developed^[3]。 With the continuous improvement of understanding, strengthening the diagnosis and treatment of sleep breathing disorders has become an important link in the discipline construction of sleep medicine in China.

The 81-year-old male was seen at the local county hospital on November 17, 2012 due to repeated left lower abdominal dull pain with fever for 3 days. Three days before the visit, the patient developed dull pain in the left lower abdomen without obvious inducement, accompanied by fever, frequent urination, urgency and painful urination. He complained of obvious fever in the afternoon and night, accompanied by chills, without chills, diarrhea and blood in the stool. Physical examination: left lower abdominal tenderness and rebound pain, blood routine showed: white blood cells 28.8×10⁹/L, neutrophils 0.899, hemoglobin 107 g/L, C-reactive protein (CRP) 156 mg/L; Urine routine: occult blood (±), protein (+); Abdominal B-ultrasound showed: right kidney cyst, large prostate, suggesting peritoneal effusion; Whole abdominal CT showed a soft tissue mass in the left lower abdomen, which was closely related to the small intestine. The diagnosis was: abdominal pain to be examined: small bowel tumor considered; Urinary tract infections. After symptomatic treatment such as anti-infection and analgesia, urinary tract symptoms were relieved, but abdominal pain and fever still existed, so I went to the First Affiliated Hospital of Zhejiang University of Traditional Chinese Medicine for treatment on November 21st. Physical examination on admission: abdominal swelling, left lower abdominal tenderness, rebound pain, no muscle tension, no obvious mass, bowel sounds 3~4 times/min, and positive buckle pain in left kidney area. Blood routine on November 21: white blood cells 29.5×10⁹/L, neutrophils 0.903, hemoglobin 96 g/L, platelets 250×10⁹/L; CRP 138.84 mg/L; Blood biochemistry: albumin 32.30 g/L, alkaline phosphatase 572 U/L, gamma-glutamyltransferase 324 U/L; Tumors: Serum ferritin 1 029.3 μ g/L, squamous cell carcinoma antigen (SCC) 3.40 μ g/L, carcinoembryonic antigen 3.4 μ g/L, sugar chain antigen 19-9 (CA19-9) 12.55×10³U/L, alpha-fetoprotein 2.16 μ g/L; Erythrocyte sedimentation rate (ESR) 87 mm/1 h; There was no abnormality in urine and fecal routine; Chest X-ray showed increased texture in both lungs; Gastroscopy showed no abnormalities; Total abdominal CT plain scan + enhanced (Figure 1) showed that the left lower abdominal sac had solid mass occupation: about 7.1 cm ×6.3 cm ×9.9 cm in size, uneven enhancement after enhancement, blurred fat space between the surrounding intestines, small lymph nodes at the retroperitoneal and mesenteric roots, accompanied by abdominal and pelvic effusion. In order to understand the origin of this abdominal cavity, B-ultrasound of left lower abdomen was performed on November 22 (Figure 2) A regular hypoechoic mass can be seen in the left iliac fossa, about 10.2 cm ×6.2 cm ×6.9 cm in size, with envelope, uneven internal echoes, several irregular small dark areas, and obvious blood flow signals can be seen around and inside. The possibility of retroperitoneal origin is not ruled out, and the occupation of space fluctuates with respiratory movement. In order to understand the relationship between abdominal cavity occupation and intestinal tract, colonoscopy of large intestine on November 24th showed no obvious abnormality; In order to further understand the relationship between abdominal cavity occupation and small intestine, small intestine aerobarium angiography was performed on November 26 (Figure 3) See Group 3 small intestinal external indentation, and dynamically visible contrast medium running along this notch, no sign of leakage outside the intestinal lumen, which clearly confirms that the occupation of space is not related to the intestinal lumen.

Corticosteroids are widely used in various clinical departments, but steroid-related muscle lesions are rare in clinic. With the continuous deepening of research on steroid myopathy at home and abroad in recent years, in order to improve clinicians' identification of such diseases, this article summarizes the related knowledge of steroid myopathy as follows.

Portal vein obstruction is a relatively rare class of hepatic vascular diseases^[1]Its main pathogenesis includes thrombosis, liver cancer invasion, and external compression^[2]。 A Danish study reported that the incidence of portal vein obstruction was less than 4 in 1 million^[3]； Another Swedish study analyzed 23 796 autopsies from 1970 to 1982 and showed a prevalence of up to 1%^[4]。 Growth and development are significantly delayed in children with portal vein occlusion^[5]； For adult patients, portal hypertension complications are more difficult^[6]。 Recent research evidence also suggests that portal vein occlusion will significantly increase the risk of variceal bleeding and death in patients with liver cirrhosis^[7]。 In this paper, the definition, etiology, evolution and treatment strategies of portal vein occlusion are reviewed.

Continuous positive airway pressure (CPAP) is considered the preferred treatment for moderate to severe obstructive sleep apnea syndrome (OSAS). However, in some patients diagnosed with OSAS via polysomnography (PSG) monitoring, the main type of apnea events changed from obstructive to central after the first CPAP pressure titration or longer CPAP treatment. Morgenthaler et al.^[1]For the first time, this phenomenon was defined as complex sleep apnea syndrome (CompSAS), that is, after CPAP titration, while the obstructive respiratory event was substantially eliminated, the residual central apnea index (CAI) ≥5 times/h or Chen-Shi breathing became the dominant respiratory pattern.

A 26-year-old pregnant woman was admitted to Ningbo Women's and Children's Hospital on February 15, 2008 due to the discovery of fetal malformation for 3 days after 31 weeks of menopause. The patient usually has regular menstruation, the cycle is about 30 days, the menstrual period is 3 to 4 days, and there is no obvious nausea and vomiting in the first trimester of pregnancy. The local hospital established a perinatal health care register, and no obvious abnormalities were found in private complaint. 3 days ago, B-ultrasound examination of prenatal examination in Ningbo Women and Children's Hospital showed intrauterine singleton breech pregnancy, fetal survival, amniotic fluid index 5, single umbilical artery, and multiple fetal malformations. On the 7th day of admission, a dead baby with multiple breech deformities was delivered by intrauterine injection of ethacridine (Rivanol). Fetal necropsy findings: malformed fetus, sex unknown. The body length is 30 cm and the body weight is 1.15 kg. Bilateral upper limb deformity, short forearm, absence of both palms, absence of thumb, index finger and middle finger. The legs below the hips are not separated and formed, and they are fused into a vertebral body shape, which resembles a mermaid and is 11 cm long. The umbilical cord is 15 cm long and 0.7 cm in diameter, with a single umbilical artery. There were no obvious abnormalities in the structures of both lungs, heart, liver and spleen, pancreas was absent, esophagus to ileocecal region was normal, sigmoid colon to rectal atresia, no anus, bilateral polycystic kidney and double hydronephrosis, double ureters and bladder were absent, and reproductive system was absent. Absence of pelvis on X-ray of fetal skeleton after delivery, fusion malformation of both lower limbs, only a single femur and a single tibia, spina bifida with abnormal curvature (Figure 1)。 Microscopic examination revealed immature development of each organ, but coincided with the gestational month. Autopsy report: mermaid body sequence sign.

A 40-year-old male was seen in Shaoxing People's Hospital on May 23, 2010 because his liver occupied space for 7 days on physical examination. Previous history of chronic hepatitis B for 20 years. Physical examination: There was no yellowing stain on the skin and sclera of the whole body, no liver palms and spider nevus, flat and soft abdomen, no tenderness and rebound pain, no palpation of the liver and spleen under the costs, no percussion pain in the liver area, and negative mobile voicing. Laboratory tests: hepatitis B virus surface antigen 451.5 μ g/L, hepatitis B virus core antibody 3.7 PEI U/ml, alpha-fetoprotein 4 539.2 μ g/L, sugar chain antigen 242 value 28.5 U/ml, high sensitivity C-reactive protein 172.7 mg/L, alanine aminotransferase 329.9 U/L, aspartate transferase 139.4 U/L. CT showed that the liver capsule was smooth, and irregular low-density shadows were seen in the area under the junction of V and VI segments of the liver, with uneven internal density and unclear boundary, with a size of about 21 mm ×21 mm; After enhancement scan, the arterial phase lesions showed uneven enhancement; No obvious lymph node enlargement was observed, and a malignant tumor of the liver was considered. On June 2, 2010, the right liver tumor was resected under general anesthesia. During the operation, the liver showed small nodular changes, and a mass of about 20 mm was seen between the VI segment of the right liver. Partial hepatic lobectomy specimens, 86 mm ×73 mm ×42 mm in size, showed a gray-white mass 23 mm ×19 mm in size, soft in texture, without capsule. Microscopically: the tumor has unclear boundaries and grows infiltratively in surrounding normal liver tissue; Tumor cells have obvious atypia, large volume, abundant cytoplasm and eosinophilia; The nucleus is large, round or oval, vacuolate, and the nucleolus is distinct, like a somatic cell (FIG. 1A)； The tumor cells showed small focal, nest-like and glandular duct-like structures, in which a large number of mature lymphocytes infiltrated (FIG. 1B)。 Immunohistochemistry: CK7, CK19 (FIG. 2A), CK8/18, Hepatocyte (Figure 2B) positive, whereas AFP, CEA negative; In situ hybridization was negative for EBER. Pathological diagnosis: (right) mixed hepatocellular and cholangiocellular lymphopithelioma-like carcinoma of the liver.