2015年 · 第49卷第10期

Breast angiosarcoma is a rare non-epithelial tumor, accounting for 0.04% of breast malignancies and 8% of breast sarcomas^[1]With high recurrence rate, extremely poor prognosis and difficult preoperative diagnosis. The author retrospectively analyzed the clinical and imaging manifestations of 5 patients with primary mammary angiosarcoma (PMA) confirmed by surgery and pathology, and combined with literature review, aimed at improving the diagnostic level of this disease.

The patient, a 44-year-old female, presented with dizziness, headache and progressive decrease of bilateral visual acuity for 1 month without obvious trigger. She went to our hospital on August 1, 2014, and no abnormalities were found in the rest of the physical examinations.

A 28-year-old female, G3P2, was seen at 16:00 on 13-Dec-2014 due to disorder of consciousness 1 d after cesarean section. The patient (37 weeks gestation) had headache after waking up on the 11th morning, accompanied by nausea and vomiting. Blood pressure was measured locally at 160/120 mmHg (1 mmHg =0.133 kPa) without treatment. Later, he was referred, and his blood pressure was re-measured at 180/120 mmHg, and he developed abdominal pain and soy sauce-colored urine. The examination found that liver enzymes and bilirubin were elevated, and platelet count was decreased. Emergency cesarean section was performed that night. Prenatal and postpartum limb twitching occurred once each, and was transferred to our hospital due to aggravation of symptoms. Physical examination: anemia appearance, sclera yellow stain. Neurological examination: Moderate coma, asymmetric pupil size, disappearance of direct and indirect light reflections. Routine blood test: white blood cells 19×10⁹/L [normal value (4~10) ×10⁹/L], red blood cells 2.1×10¹²/L [normal value (3.5~5.5) ×10¹²/L], hemoglobin 67 g/L (normal 110-160 g/L), platelets 64×10⁹/L [normal value (100~300) ×10⁹/L]; Alanine aminotransferase 122.9 U/L (normal 0-41.0 U/L), aspartate aminotransferase 399.4 U/L (normal 0-42.0 U/L), D-dimer 9.1 mg/L (normal<0.5 mg/L).

The patient was a 44-year-old male. Pain in the joints of both feet and hands for more than 8 years, blood uric acid increased (examined in another hospital, the specific value is unknown), and the diagnosis was "gout". Two months ago, the patient developed lumbar pain and discomfort accompanied by numbness in both lower limbs, which could not be relieved after rest. He went to the local hospital and was suspected of lumbar disc herniation. He was given symptomatic treatment, but the symptoms did not improve and aggravated, so he went to our hospital for treatment. The patient denied a previous history of tuberculosis. Admission examination: Uric acid was 836 μ mol/L (male normal value 150~420 μ mol/L) in the laboratory, and no obvious abnormalities were found. Physical examination: Spinal pain, which is aggravated with activity, and there is deep tenderness paravertebral pain on the left side of the lower waist. Lumbar spine CT (Philips 256 iCT, Netherlands) and MR (GE 3.0 T MR, USA) were performed. Examination sequence: axial T₂WI (TR 3 560.0 ms, TE 120.0 ms, inversion angle 180°, bandwidth 41.67 Hz, FOV 20 cm ×20 cm, number of excitations 2), sagittal T₁WI (TR460.0 ms, TE 14.0 ms, inversion angle 180°, bandwidth 62.50 Hz, FOV 30 cm ×30 cm, number of excitations 2), fat pressure enhanced axial plane T₁WI (TR 520.0 ms, TE 8.2 ms, inversion angle 180°, bandwidth 31.25 Hz, FOV 20 cm ×20 cm, number of excitations 2), lipid pressure enhanced sagittal T₁WI (TR 500.0 ms, TE 9.1 ms, inversion angle 180°, bandwidth 31.25 Hz, FOV 30 cm ×30 cm, number of excitations 2). Enhanced examination, intravenous Gd-DTPA was administered at a dose of 0.2 ml/kg and a flow rate of 2.0 ml/s. Imaging results: CT scans showed bone destruction of the left facet joint, vertebral body and spinous process of L4 and 5 vertebral bodies, disappearance of structure and shadows of surrounding soft tissue masses, and scattered irregular high-density shadows were seen in the masses (Figure 1,Figure 2）。 MR plain scan axial plane T₂WI showed L4 left vertebral lamina and paraspinous process mass of low intensity (Figure 3), with clear boundaries; Sagittal T₁WI showed: L4 and 5 vertebral bodies left facet joint, vertebral body and spinous process mass-like isohyposignal shadow, partial bone destruction, disappearance of vertebral facet joint structure (Figure 4）； Lipid pressure enhances axial and sagittal T₁WI showed obvious heterogeneous enhancement of the lesion (Figure 5,Figure 6）。 According to the imaging, it was diagnosed as "occupying the left articular process of L4 and 5 vertebral bodies". Under general anesthesia, lumbar 4 and 5 vertebral parabody mass was removed and unilateral nail-bar system internal fixation was performed. Intraoperatively, a 30 cm ×20 cm ×15 cm limestone-like substance was found next to the left vertebral lamina and spinous process of lumbar 4 and 5, and under the latissimus dorsi muscle, which was hard and without envelope, and some vertebral lamina and spinous process were destroyed. Histopathological examination of postoperative lesions showed urate crystals under HE staining microscope, and the formation of foreign body granuloma around it (Figure 7）。 Pathological diagnosis: Gout granuloma with tophi formation.

The patient was a 47-year-old female. He was admitted to hospital on November 9, 2014 due to progressive aggravation of blurred vision in his right eye for more than 6 years. Six years ago, there was no obvious trigger for blurred vision, and the symptoms were persistent and gradually aggravated. There was no headache, dizziness, nausea, vomiting, and no numbness in the limbs. Past health, no history of hypertension, diabetes, coronary heart disease, and no history of genetic diseases, infectious diseases and tumors in the family. Neurological examination: clear mind, fluent speech, bilateral pupils of equal size and round, about 3 mm in diameter, sensitive to light reflection, free movement of both eyes in all directions, negative nystagmus. Laboratory test: White blood cell count 3.30×10⁹/L [Reference value (3.69~9.16) ×10⁹/L)], the percentage of lymphocytes was 42.4% (reference value 20.0% ~40.0%).

The patient was a 21-year-old male. He had blurred vision in his left eye for 3 months and was admitted to the hospital on 6 February 2014. Preoperative routine laboratory tests showed no obvious abnormalities. Neurological examination: clear consciousness, fluent speech, equal size and round pupils in both eyes, sensitive to light reflection, normal visual acuity in right eye, countable fingers within 1 m of visual acuity in left eye, free bilateral eye movement, no nystagmus, symmetric nasolabial folds in bilateral frontal lines, centered tongue extension, normal muscle strength and muscle tone of limbs, bilateral tendon reflex, negative Babinski sign and negative meningeal irritation sign.

The patient was a 28-year-old male. He was admitted to hospital due to dull pain in the right upper abdomen for 2 days. Physical examination: A mass of about 8.0 cm ×10.0 cm was palpable in the right upper abdomen, with unclear boundaries, poor mobility and tenderness. There were no obvious abnormalities in laboratory tests.

The patient was a 4-year-old male. He was found to be deformed in both hands after birth, and went to the orthopedic department of our hospital on July 16, 2008. Physical examination: Generally, the condition is good, the left thumb is not developed, and the right thumb is small, non-functional and floating finger-shaped; The left forearm is bent radially, and the left elbow and wrist joints cannot rotate, so they can only perform flexion and extension movements; Skin sensation and mental development are normal. The patient's parents were unrelated, had a sister, and none of the family members had a history of similar genetic diseases.

Neuroinflammation is widespread in central nervous system (CNS) diseases and aggravates neuronal damage^[1]。 As a new subject, molecular imaging can study the occurrence and development of neuroinflammation by in vivo imaging at the cellular and molecular levels, especially radionuclide imaging and MRI are the main imaging methods for neuroinflammation^[1]。 Therefore, the author reviews the pathophysiological mechanism of neuroinflammation and the research progress of molecular imaging of neuroinflammation in recent years.

Prostate imaging report and data system first published in 2012 (prostate imaging reporting and data system, PI-RADS)^[1]And has attracted widespread attention from experts and scholars. PI-RADS was used to standardize the MRI report of prostate, which has good clinical application value^[2]。 The second edition of PI-RADS (PI-RADS V2) was developed and released in collaboration by the American Radiological Society, the European Society for Genitourinary Radiology and the AdMeTech Foundation at the North American Annual Meeting of Radiology in 2014^[3], supplemented, improved and deleted on the basis of the first version of PI-RADS. PI-RADS V2 provides guiding recommendations on MRI examination equipment and technical requirements, and re-standardizes examination requirements, evaluation classification criteria, technical specifications and scanning parameters. The author compares the contents of the two versions of PI-RADS, and interprets the main points of PI-RADS V2.