MedNexus
2015年 · 第95卷第33期
MedNexus
- 全部
- 医药卫生策略探讨
- 临床研究
- 基础研究
- 流行病学调查
- 荟萃分析
- 疑难病例析评
- 病例报告
- 综述
With the continuous development of information construction of medical institutions and the application of hospital information management and Internet, more and more data generated in medical work are collected and stored by hospital information system. In addition to providing useful information for doctors' clinical diagnosis and treatment, various clinical data collected by hospitals in the process of admission and treatment also provide the most realistic sample data for medical research. How to reasonably manage and apply these data is a new challenge for hospital informatization construction in the future. Therefore, the Department of Neurosurgery of Peking Union Medical College Hospital established a database of non-functional pituitary adenomas to preserve and manage the clinical data of patients completely. Pituitary adenomas are a group of benign intracranial tumors of monoclonal origin of adenopituitary gland, accounting for 10% ~15% of intracranial tumors, and are the third most common intracranial tumors, second only to gliomas and meningiomas[
A 27-year-old female was admitted to the Department of Rheumatology and Immunology of Peking Union Medical College Hospital in June 2013 due to joint pain for 9 years, fever, rash and headache for 4 months. Nine years ago, the patient developed bilateral swelling and pain of wrist, elbow, ankle, knee, multiple metacarpophalangeal joints and proximal interphalangeal joints, accompanied by morning stiffness for about 30 minutes. He was not treated regularly, and intermittently took hormones (specific dosage form unknown) and traditional Chinese medicine, but did not take immunosuppressants. Four months ago, I developed a dark red rash on my cheeks and erythema, ulceration and crusting on both lower limbs, with intermittent fever, with a maximum body temperature of 40 ℃. Without medication, my body temperature dropped to normal spontaneously in 2~3 days, with fever 1~2 times a month, accompanied by headache, mild tingling pain, without nausea, vomiting, rotation of vision, etc. He went to a local hospital and was positive for anti-nuclear antibody, anti-RNP, anti-SM, anti-RO-52 and anti-ribosomal P protein antibody. He was suspected of systemic lupus erythematosus (SLE) and was admitted for further diagnosis and treatment. Since the disease, hair loss is obvious, and body weight decreases by 20 kg. Family history: Both sister and younger sister were diagnosed with SLE, and their parents were in good health. Physical examination: body temperature 38.3 ℃, heart rate 98 beats/min, respiratory rate 18 beats/min, blood pressure 116/80 mmHg (1 mmHg =0.133 kPa); Butterfly pigmentation on both cheeks, scattered crusty rash on lower limbs; The heart rhythm was uniform, the breathing sounds of both lungs were clear, the left upper abdomen was tender, without muscle tension and rebound pain, 5 cm under the costs of the liver and 3 cm under the costs of the spleen. The right wrist joint was swollen and tender (+), the right index finger, middle finger, ring finger and the proximal interphalangeal joint of the left ring finger were swollen and tender (+), and the right knee joint was not swollen and tender (+). Soft neck, Klinefelter sign, Buchner sign (–). Both lower limbs are not swollen. Laboratory test: blood routine: white blood cells 1.52×109/L, lymphocytes 0.35×109/L, hemoglobin 94 g/L, platelets 134×109/L; Negative urine routine; 24 h urine protein quantification 0.15 g; Liver and kidney function: alanine transferase 4 U/L, albumin 25 g/L, creatinine 45 μ mol/L, potassium 2.5 mmol/L; Hypersensitive C-reactive protein 2.95 mg/L, erythrocyte sedimentation rate (ESR) 14 mm/h, complement C3 0.227 g/L, complement C4 0.034 g/L; Immunoglobulin (Ig) G 18.30 g/L, IgA 3.01 g/L, IgM 0.7 g/L; Antinuclear antibody spot type 1:1 280 cytoplasmic type 1:640; Anti-extractable nuclear antigen (ENA) antibodies: anti-SM antibody 1:4, anti-RNP antibody 1:4, anti-SSA antibody 1:4, anti-ribosomal P protein antibody 38 000, 16 500, 15 000. anti-neutrophil cytoplasmic antibodies, anti-cardiolipin antibodies, etc. (-). Procalcitonin<500 ng/L. Electrocardiogram and cardiac ultrasound were basically normal. Abdominal B-ultrasound: diffuse lesions in both kidneys and mild hydrops in both kidneys. There were no obvious abnormalities in chest high-resolution CT and cranial enhanced MRI. Spinal cord puncture was performed, CSF pressure 115 mmH2O (1 mmH2O =0.0098 kPa), CSF routine: colorless and transparent, total number of cells 84×106/L, total number of white blood cells 24×106/L, single core 16×106/L, Multi-core 8×106/L. Cerebrospinal fluid biochemistry: protein 0.95 g/L, glucose 0.9 mmol/L (instant finger blood glucose 7.0 mmol/L), chlorine 131 mmol/L. Cerebrospinal fluid bacteria, fungi, viruses and other etiologic examinations (–). After that, the spinal cord puncture was re-examined twice, the routine biochemistry was roughly the same as before, and the third cerebrospinal fluid bacterial culture: Listeria monocytogenes.
The patient, a 63-year-old female, was admitted to the hospital due to "swelling and pain in both knees for 12 years" and aggravation of pain in the left knee for 2 years ". Physical examination on admission: flexion contracture and varus deformity of the left knee. Range of mobility of the left knee joint: flexion 90° and straightening 30°. X-ray showed: both knee joints were varus, skeletal articular surface sclerosis, and medial space narrowing (
A 23-year-old female was admitted to the Department of Neurology of the First Affiliated Hospital of Zhengzhou University on January 10, 2014 due to "disorder of consciousness for half a month, right limb weakness with unclear speech for 10 days". Half months before admission, the patient suddenly lost consciousness without obvious trigger, accompanied by nausea and vomiting, and the vomit was stomach content, non-jetting, without caffeine-like substances. The local hospital examined 0.5T skull MRI showed: fresh infarction in the left parieto-occipital lobe, and was treated with "mannitol needle" and other drugs. After 7 hours of onset, consciousness gradually recovered, blindness in the left eye, hemiplegia in the right limb, and motor aphasia. After 2 days, reexamination of 1.5T skull MRI showed: multiple acute infarctions in the right cerebellar hemisphere and left parieto-occipital lobe (
Osteoporosis is a disease of the skeletal system characterized by decreased bone strength and increased risk of fractures. Osteoporosis can be divided into primary osteoporosis and secondary osteoporosis, the latter being any disease and/or drug that affects bone metabolism, among which glucocorticoids (GCs) are the most common drugs. Prolonged (more than 3 months) use of any dose of GCs may lead to osteoporosis, i.e. glucocorticoid-induced osteoporosis (GIOP). The proportion of oral glucocorticoids in postmenopausal women is as high as 4.6%[
Endometriosis (EM) has a variety of clinical manifestations due to its biological behaviors such as hyperplasia, infiltration, metastasis and recurrence, and its diagnosis and treatment are complex. There are many staging methods for EM, but there is no staging system that can comprehensively describe the characteristics of EM lesions and predict related factors such as infertility and pain. The ideal EM staging system has complex requirements: based on clinical experience and scientific basis, enjoying expert consensus, clearly defined terminology, applicable to all cases, reflecting the clinical characteristics of the disease, predicting pain relief rate, predicting fertility, predicting the risk of recurrence, guiding treatment, simple communication with patients, etc.[
APOE gene has been widely studied as the most important pathogenic gene in late-onset AD (LOAD). At the same time, recent studies have found that the mutation of the R47H site encoding the type 2 myeloid cell trigger receptor gene (TREM2) is also significantly associated with late-onset Alzheimer's disease. It is suggested that TREM2 gene can inhibit central inflammation and mediate the phagocytosis of A β and apoptotic cell debris by central monocyte phagocytosis system. However, the exact mechanism of its action is not clear at present, and the pathogenesis of its R47H mutation and LOAD pathogenesis is still to be confirmed. This paper reviews the role of TREM2 gene in central inflammation and mediating A β phagocytosis.
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