16例瘤壁钙化动脉瘤患者的临床分析

回顾性分析 1 6例瘤壁有钙化的颅内动脉瘤病例的影像学、临床资料及手术治疗 ,分析颅内血管钙化与颅内动脉瘤病理发生机制的关系。 1 6例瘤壁有钙化的颅内动脉瘤的位置 :后交通动脉 3例 ,大脑中动脉 2例 ,前交通动脉 2例 ,椎动脉 5例 ,基底动脉 4例。其中 1 4例动脉瘤直径 >1 .5cm ,9例 >2 .5cm。所有病人的血钙、磷酸盐、血糖、肾功能正常 ;6例病人血脂增高。 1 6例患者均施行动脉瘤夹闭术 ,其中 8例术中切除动脉瘤 ,治疗效果良好。     

Expression of core?binding factor alpha 1 and collagen Ⅱ in patients with chronic kidney disease stage 5

Objective To study the relationship between the medial artery calcification and expression of core?binding factor alpha 1 (Cbfα?1) and collagen Ⅱ (ColⅡ) in chronic kidney disease(CKD) stage 5 patients. Methods Pieces of radial arteries were taken from 40 patients with CKD stage 5 during internal arteriovenous fistula operation. Ten patients with subtotal gastrectomy and normal renal function were chosen as control. The vessels were examined for calcification by von Kossa stain and for the presence of Cbfα?1 and ColⅡ by immunohistochemistry. According to von Kossa stain, CKD stage 5 patients were divided into no calcification group, mild?moderate calcification group and severe calcification group. Other related factors including serum calcium,phosphate, intact parathyroid hormone (iPTH), C?reactive protein (CRP), triglyceride(TG), cholesterol(TC) and low?density lipoproteins(LDL) were also detected. Results Seventeen (42.5%) of CKD Stage 5 patients showed vascular calcification, while calcification was not found in controls. Most calcification occurred in medial layer．Positive immunohistochemical staining of core?binding factor and ColⅡ was found in the smooth muscular cell plasma of medial layer in the vessels with calcification. However, above positive staining was also observed in 78.3% of no calcification group. But there was little staining in control group. Positive staining score of Cbfα?1 and ColⅡ in severe calcification group was significantly higher than that in no calcification group. Same findings were obtained in mild?moderate calcification group, but the difference between them was not statistically significant. CRP and Ca×P were positively correlated with staining score of Cbfα?1 and ColⅡ. Serum phosphate was positively correlated with Cbfα?1 (r=0.786, P<0.01) and ColⅡ (r=0.785, P<0.01) respectively． Conclusions 42.5% of CKD stage 5 patients in our group shows vascular calcification, which occurrs mainly in medial layer. High expression of Cbfα?1 and ColⅡ can be observed in vascular calcification of radial arteries, which is earlier than vascular histological changes. Cbfα?1 and ColⅡ may be involved in the development of vascular calcification.     

Calcification and osteopontin localization in the peritoneum of patients on long-term continuous ambulatory peritoneal dialysis therapy.

BACKGROUND: Peritoneal calcification is an uncommon complication of continuous ambulatory peritoneal dialysis (CAPD), which is mainly observed in patients on long-term therapy. Although some asymptomatic patients must have microscopic calcification in their peritoneum, little information on this topic has been published. Recent studies have revealed active participation of adhesive/chemotactic protein osteopontin (OPN) in dystrophic calcification. METHODS: Peritoneal tissue was obtained by biopsy or at autopsy from 18 CAPD patients (median duration, 122 months), 5 control haemodialysis (HD) patients, and 3 pre-CAPD patients. The distribution of calcium deposits and OPN protein was determined by von Kossa staining and immunohistochemistry, respectively. Smooth muscle cells and macrophages were identified with anti-alpha smooth muscle actin (alpha-SMA) and anti-CD68 antibodies. RESULTS: Calcium deposits with various configurations were observed in specimens from 12 of the 18 CAPD patients. They included massive calcification facing the peritoneal cavity, scattered granular or crystalloid deposits in the submesothelial stroma, and oval-shaped deposits formed within hyalinized vasa. Most were present in highly sclerosed areas and accompanied by extracellular OPN precipitation. Cytoplasmic OPN was detected in infiltrating leukocytes, granulation tissue cells, fibroblast-like cells and mast cells. Computerized tomography examination also detected peritoneal calcification in seven of the CAPD patients. No calcium deposits or OPN staining was detected in control specimens. CONCLUSIONS:The results of our study suggest that microscopic peritoneal calcification is frequent in patients on CAPD for more than 10 years. Myofibroblast infiltration, OPN expression, calcium deposition, and associated OPN precipitation seem to be components of the peritoneal changes in such patients.     

Cardiovascular calcification in end-stage renal disease.

Cardiovascular diseases are common in patients with end-stage renal disease (ESRD) and cardiovascular morbidity and mortality among dialysis patients are substantially higher than in the general population. The reasons for this high incidence are multiple. They include traditional factors such as hypertension, diabetes, dyslipidaemia, sodium overload, and elevated homocysteine levels as well as disturbances of mineral metabolism, specifically abnormalities in phosphorus and calcium homeostasis. This review will describe the specific cardiovascular complications related to calcifications in ESRD, the implications of the abnormalities of mineral metabolism in its pathogenesis and the current imaging techniques available for the detection of cardiovascular calcifications. Excess of calcium load contributes to the development of cardiac calcifications; therefore, alternative strategies to diminish exogenous calcium load should be considered in patients with ESRD.     

Links between cardiovascular disease and osteoporosis in postmenopausal women: serum lipids or atherosclerosis per se?

Introduction and hypothesis Epidemiological observations suggest links between osteoporosis and risk of acute cardiovascular events and vice versa. Whether the two clinical conditions are linked by common pathogenic factors or atherosclerosis per se remains incompletely understood. We investigated whether serum lipids and polymorphism in the ApoE gene modifying serum lipids could be a biological linkage. Methods This was an observational study including 1176 elderly women 60–85 years old. Women were genotyped for epsilon (ɛ) allelic variants of the ApoE gene, and data concerning serum lipids (total cholesterol, triglycerides, HDL-C, LDL-C, apoA1, ApoB, Lp(a)), hip and spine BMD, aorta calcification (AC), radiographic vertebral fracture and self-reported wrist and hip fractures, cardiovascular events together with a wide array of demographic and lifestyle characteristics were collected. Results Presence of the ApoE ɛ4 allele had a significant impact on serum lipid profile, yet no association with spine/hip BMD or AC could be established. In multiple regression models, apoA1 was a significant independent contributor to the variation in AC. However, none of the lipid components were independent contributors to the variation in spine or hip BMD. When comparing the women with or without vertebral fractures, serum triglycerides showed significant differences. This finding was however not applicable to hip or wrist fractures. After adjustment for age, severe AC score (≥6) and/or manifest cardiovascular disease increased the risk of hip but not vertebral or wrist fractures. Conclusion The contribution of serum lipids to the modulators of BMD does not seem to be direct but rather indirect via promotion of atherosclerosis, which in turn can affect bone metabolism locally, especially when skeletal sites supplied by end-arteries are concerned. Further studies are needed to explore the genetic or environmental risk factors underlying the association of low triglyceride levels to vertebral fractures.     

Relationship of Calcification of Atherosclerotic Plaque and Arterial Stiffness to Bone Mineral Density and Osteoprotegerin in Postmenopausal Women Referred for Osteoporosis Screening

Arterial calcification leading to increased arterial stiffness, a powerful risk factor for cardiovascular disease, may underlie the association of osteoporosis with cardiovascular disease in postmenopausal women. Osteoprotegerin (OPG), an indirect inhibitor of osteoclastogenesis, may be involved in arterial calcification. We examined relationships between calcification of subclinical atherosclerotic plaque and arterial stiffness with bone mineral density (BMD) and OPG in a group of 54 postmenopausal women referred for routine osteoporosis screening by dual-energy X-ray absorptiometric scanning of the lumbar spine and hip. Presence of calcified and noncalcified plaque in carotid and femoral arteries was examined using ultrasonography. Pulse wave velocity (PWV), a measure of arterial stiffness, was determined by sequential tonometry over the carotid and femoral region. Fifty-nine percent of osteoporotic women had calcified (echogenic) plaque at one or more sites compared with 42% and 20% for women with osteopenia and normal BMD, respectively (P = 0.04). There was a significant negative correlation between PWV and hip BMD (r = -0.35, P = 0.01), which remained significant when age, mean arterial pressure, and serum lipids were taken into account (P = 0.05). No significant relationships were observed between serum concentrations of OPG and lumbar spine or total hip BMD or with the number of arterial sites with calcified or noncalcified plaque. However, there was a strong correlation between OPG and PWV (r = 0.44, P = 0.001), which remained significant when adjusted for age (P = 0.01). These findings suggest that decreased BMD is associated with arterial calcification and stiffening and raise the possibility that OPG is a marker of arterial stiffening, independent of any association with BMD.     

Associations between vascular calcification, arterial stiffness and bone mineral density in chronic kidney disease.

BACKGROUND: Vascular calcification (VC) and arterial stiffness are major contributors to cardiovascular (CV) disease in chronic kidney disease (CKD). Both are independent predictors of CV mortality and are inversely correlated with bone mineral density (BMD). Few studies have addressed the extent of VC in the pre-dialysis CKD population, with associated measurements of BMD and arterial compliance. METHODS: We report cross-sectional data on 48 patients with CKD (GFR 17-55 ml/min) assessing the prevalence of VC and its associations. All patients had computed tomography (CT) scans through abdominal aorta and superficial femoral arteries (SFAs) to determine VC, pulse wave velocity (PWV) using SphygmoCor device (AtCor PWV Inc., Westmead, Australia) measuring arterial stiffness, and dual-energy X-ray absorptiometry (DEXA) scans to determine BMD, as well as serum markers of renal function and mineral metabolism. RESULTS: Patients, 71% male, 54% diabetic, had a median age 64.5 years. Mean estimated GFR was 35.1 +/- 10 ml/min. Mean PWV was 10.0 +/- 4.5 m/s and mean aortic VC score was 421.5 +/- 244 Hounsfield units, with 90% of subjects having some aortic VC present. In univariate linear regression analysis, aortic VC correlated positively with age (r 0.50, P < 0.001), triglycerides (r 0.47, P = 0.002) and PWV (r 0.33, P = 0.03). There was also greater VC with declining renal function (r -0.28, P = 0.05). There was no significant association between VC and serum markers of mineral metabolism, however phosphate and Ca x P correlated positively with PWV (r 0.35, P = 0.02, r 0.36, P = 0.02, respectively). There was also a positive association between PWV and triglycerides (P = 0.008), and a trend towards greater PWV with increasing age (P = 0.09). In multivariate regression analysis only increasing age and triglyceride levels were significantly associated with aortic VC and PWV. Mean spine and femoral T-scores on DEXA were 0.48 and -1.31 respectively, with 13% of subjects having femoral T-score <-2.5 (osteoporotic range). SFA VC inversely correlated with femoral T-scores (r -0.43, P = 0.004); however, there was a positive (likely false) association between spine T-scores and aortic VC (r 0.37, P = 0.01), related to the limitation of vertebral DEXA in CKD. CONCLUSION: There is a high prevalence of VC in pre-dialysis CKD patients, worse with increasing age, triglycerides and reducing renal function. Correlation exists between VC and PWV and determination of one or both may be useful for CKD patient CV risk assessment. Femoral BMD is inversely associated with SFA VC, but measurement of vertebral BMD by DEXA is unreliable in CKD patients with aortic VC.     

Natural history of paediatric intervertebral disc calcification

This case report concerns a 5-year-old boy who had intervertebral disc calcification with involvement of two disc spaces and herniation of nucleus pulposus in one. The patient’s symptoms resolved completely in a week with conservative measures. At the 4-year follow-up, the child was symptom-free and in full health, the herniation of nucleus pulposus had resolved completely, and calcification had disappeared in one of the disc spaces. Although the cause of this disorder is uncertain, the course is benign and self-limiting, it seldom requires surgical intervention, and the natural history is one of resolution and complete resorption of the calcification. Received: 7 July 2000     

Intervertebral Disc Calcification in Childhood – A Case Report and Review of the Literature

Summary  The authors report the case of a 10-year-old girl with intervertebral disc calcifications from the levels C6/C7 to Th1/Th2, presenting with a herniated calcified intervertebral disc at the C7/Th1 level, causing spinal cord compression with subsequent progressive paresis and sensory loss of her left leg. After anterior cervical discectomy and fusion the neurological deficits completely resolved within 2 weeks. It can be concluded that calcification of an intervertebral disc is a rare syndrome in childhood, causing progressive neurological deficit only in a few reported cases. Although the treatment of choice is conservative, surgery is required in patients who develop progressive neurological deficit.     

Risk factors of the progression of abdominal aortic calcification in patients on chronic haemodialysis

Background. Vascular calcification is an independent determinantof cardiovascular events in maintenance haemodialysis (HD) patients.It is not known whether acute changes of the serum calcium concentrationbefore and after HD (Ca) are associated with the developmentof aortic calcification. Methods. We enrolled 71 patients dialysed with a dialysate with3.0 mEq/l calcium and determined their aortic calcificationindex (ACI) by abdominal computed tomography twice at an intervalof 3 years. To identify the factors contributing to the rateof progression of aortic calcification, we analysed the averagevalues for clinical and laboratory data obtained between thefirst and second evaluations of ACI. Results. The second ACI (mean ± SD: 80.2 ± 63.9)was significantly greater than the first ACI (61.0 ±61.0) after an interval of 35.8 ± 4.2 months. The annualizedchange of ACI (ACI/year) was significantly and directly associatedwith the Ca and C-reactive protein (CRP) (both P < 0.001,P for trend). Stepwise multivariate regression analysis revealedthat ACI/year was positively and independently associated withCRP, presence of diabetes mellitus and Ca, but negatively associatedwith a premenopausal status in women. Similarly, Ca was positivelyand independently associated with ACI/year and the ultrafiltrationrate, but was negatively associated with pre-HD Ca. Conclusion. The increase of serum calcium after HD was relatedto the rate of progression of aortic calcification. Excess calciumis transferred into patients on HD when using a dialysate of3.0 mEq/l calcium. This may be a risk factor for the developmentof vascular calcification.