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PubMed2003

The progression of vascular calcification and serum osteoprotegerin levels in patients on long-term hemodialysis.

BACKGROUND: The aortic calcification index (ACI), estimated on abdominal computed tomographic scans, has been associated with the extent of arteriosclerosis in hemodialysis patients. However, the contribution of biochemical markers to the progression of vascular calcification in patients undergoing hemodialysis is not fully understood. METHODS: We examined the relationship between coronary risk factors; metabolic factors, including serum osteoprotegerin (OPG) concentration; and progression of vascular calcification in 26 dialysis patients. RESULTS: Mean patient age was 52.6 +/- 8.7 (SD) years, and mean duration of dialysis therapy was 7.7 +/- 5.8 years. ACI was measured twice in each patient, and the mean interscan period was 4.9 +/- 0.3 years. Mean ACI changed from 22.2 +/- 24.2 to 33.9 +/- 28.8 overall, and mean change in ACI (DeltaACI) was 12.0 +/- 9.9. Patients were divided into 2 groups: slow progressors, with DeltaACI of 4.1 +/- 3.2 (n = 13), and rapid progressors, with DeltaACI of 19.8 +/- 7.9 (n = 13). Serum fasting glucose and CRP levels of rapid progressors were high, and their serum albumin and intact parathyroid hormone levels were low. Multiple regression analyses showed that serum OPG levels were independently associated with vascular calcification in the hemodialysis patients studied. CONCLUSION: Rapid progression of vascular calcification was associated with dose of calcium carbonate prescribed and serum OPG concentration. The clinical significance of these observations remains to be determined.

Aortic Diseases↗
PubMed2003

Heterotopic calcification in burn scars and non-healing ulcers.

Heterotopic calcification (HC) is abnormal deposition of calcium salts in tissues other than bone and enamel. The heterotopic calcification in the burn patients is commonly found either in periarticular region or in the muscles, but the occurrence of heterotopic calcification of the burn scar itself in the presence of normal serum calcium, phosphate and alkaline phosphatase is not reported earlier. We present four adult male patients of lower limbs heterotopic calcification in burn scars with unusual presentation of non-healing ulcers with a latent period of 15-20 years. In one of the patient it was Marjolin's ulcer although the lesion was away from the calcified area. Excision of the calcified scars and the release of contracture have cured the non-healing ulcers and this may prevent re-calcification in future.

Adult↗
PubMed1987

Postmortem and intraoperative balloon valvuloplasty of calcific aortic stenosis in elderly patients: mechanisms of successful dilation.

Percutaneous balloon dilation of the aortic valve has recently been proposed as a palliative procedure for treating nonsurgical candidates with calcific aortic stenosis. To assess the safety, efficacy and mechanisms of successful balloon valvuloplasty, postmortem (n = 33) and intraoperative (n = 6) balloon aortic valvuloplasty was performed in the hearts of 39 elderly patients with calcific aortic stenosis. The cause of aortic stenosis was degenerative nodular calcification in 28 cases, calcific bicuspid aortic stenosis in 8 cases and rheumatic heart disease in 3 cases. Balloon dilation was performed with 15 to 25 mm balloons in the postmortem specimens, and with 18 to 20 mm balloons in the operating room immediately before aortic valve replacement. After balloon dilation, valve orifice dimensions and leaflet mobility increased in all patients. The mechanisms of successful dilation included fracture of calcified nodules in 16 aortic valves, separation of fused commissures in 5 valves, both in 6 valves and grossly inapparent microfractures in 12 valves. Valve leaflet avulsion occurred in one heart after inflation with a clearly oversized balloon. Liberation of calcific debris, valve ring disruption or midleaflet tears did not occur in any heart. In conclusion, there are at least three mechanisms of successful aortic valvuloplasty, depending on the origin of valvular stenosis. Embolic phenomena and acute valvular regurgitation do not appear to be likely events associated with this procedure.

Aged↗
PubMed1998

Insertion/deletion polymorphism of the angiotensin I-converting enzyme gene is associated with coronary artery plaque calcification as assessed by intravascular ultrasound.

OBJECTIVES: We evaluated the influence of the insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene on coronary plaque morphology and calcification in patients with angiographically documented coronary artery disease (CAD). BACKGROUND: The ACE I/D polymorphism has been associated with an increased risk of myocardial infarction in patients with the DD genotype but not with the presence of native CAD. METHODS: We studied 146 patients undergoing percutaneous transluminal coronary angioplasty for stable angina pectoris by means of preinterventional intravascular ultrasound (IVUS). Qualitative and quantitative criteria were used to classify the target lesions as poorly or highly echoreflective or as calcified. Genomic deoxyribonucleic acid was analyzed by polymerase chain reaction (PCR) to identify the I/D polymorphism, with a second insertion-specific PCR in DD genotypes to prevent mistyping. RESULTS: The ACE genotype groups (DD 46, ID 68, II 32) were well matched for the basic characteristics. Patients with the DD genotype had significantly more calcified lesions (DD 80%, ID 57%, II 66%; unadjusted odds ratio [OR] 2.88, 95% confidence interval [CI] 1.30 to 6.92, p = 0.008) and more calcifications >180 degrees of the vessel circumference (DD 22%, ID 10%, II 6%; OR 2.80, 95% CI 1.05 to 7.63, p = 0.03). The prevalence of myocardial infarction was not significantly associated with coronary calcification (OR 1.44, 95% CI 0.72 to 2.88, p = 0.31). CONCLUSIONS: Patients with CAD and the ACE DD genotype have a significantly higher incidence and greater extent of coronary lesion calcification, as determined by IVUS. This finding indicates that the ACE I/D gene polymorphism is related to the development or progression of atherosclerotic plaque calcification.

Aged↗
PubMed1997

Osteopontin is associated with bioprosthetic heart valve calcification in humans.

Calcification of non-osseous tissues such as heart valves or vessels is a major concern in clinical practice. The exact mechanism is still unknown. Numerous studies have shown that mineral deposits of crystalline hydroxyapatite within these tissues were associated with increased non-collagenous protein content. More recently osteopontin was found to be associated with calcification in living tissues such as vessels and native human aortic valves. The aim of this study was to determine whether or not non-collagenous proteins can also be found in non-living tissues such as glutaraldehyde-pretreated porcine valves after implantation in humans. Thirty-eight glutaraldehyde pretreated porcine bioprostheses were studied: 16 not implanted and 22 after 11 years of implantation in the aortic and mitral valve position in humans. In areas of calcification vizualized by Von Kossa staining and microradiography, immunostaining using polyclonal antibodies against calcium-binding proteins showed osteopontin positive staining and no staining for osteocalcin, bone sialoprotein or osteonectin. In uncalcified areas and in non-implanted values, staining for osteopontin or other calcium-binding proteins was negative. Western blot analysis of macroscopically calcified and uncalcified areas showed that several proteins were adsorbed in implanted values and confirmed the presence of osteopontin in the calcified areas, while no immunolabelling was found in non-calcified areas, in uncalcified valves and in non-implanted valves. Thus the presence of osteopontin in the calcified areas of bioprosthetic heart valves implanted in human indicates that this protein is associated with bioprosthetic valvular calcification. Since these values are made of non-living connective tissue, and no cell immunostained for osteopontin was found around the calcified area, this suggests that a non-cellular mediated mechanism involving protein adsorption may play a role in bioprosthetic valvular calcification.

Bioprosthesis↗
PubMedDate not supplied

Thyroid calcifications: sonographic patterns and incidence of cancer.

We investigated the incidence of cancer in surgically resected 151 thyroid nodules in 101 patients according to their calcification patterns on preoperative ultrasonography (US). Calcification was detected in 57 (38%) nodules, 31 (54%) of which was histologically diagnosed as cancer. According to the calcification types, 9 of 11 nodules with microcalcifications, 15 of 29 nodules with intranodular coarse calcification, 6 of 14 nodules with peripheral calcification and 1 of 3 calcified spots without surrounding tumor were diagnosed as cancer.

Adult↗
PubMedDate not supplied

Regulation of cardiovascular calcification.

Vascular calcification is highly correlated with cardiovascular disease (CVD) and is a significant predictor of cardiovascular events, especially in high risk patients such as the end stage renal disease (ESRD) population. Vascular calcification can lead to serious problems including valve stenosis, decreased vascular compliance, calciphylaxis, and even sudden death. However, the contribution of vascular calcification to progression of atherosclerosis is unknown and needs more study. Biochemical, histological, and genetic studies indicate that vascular calcification is actively regulated and involves both positive and negative modulators. Several nonmutually exclusive theories to account for vascular calcification based on current studies are discussed.

Animals↗
PubMed1997

Calcifications of the basal ganglia in children with brain tumours.

Calcifications in the basal ganglia have been found in nine (5.4%) of all children treated for any kind of brain tumour in our department. This has occurred over a mean period of 2.8 years after diagnosis. The group of patients has been compared with a group of other children, matched for age, sex, histologic diagnosis and tumour treatment, but without calcifications of the basal ganglia. The groups differ from each other with respect to a significantly higher incidence of hypothyroidism and growth hormone deficiency in the group of children with calcifications in the basal ganglia. Moreover the children with calcifications show a larger IQ-loss. Although the pathogenesis of the calcifications of the basal ganglia is not known, an association of damage to the vascular bed of the basal ganglia due to periods of increased intracranial pressure, together with endocrine deficiencies is discussed. We advise an adequate supplementation in cases of endocrine deficiencies in children treated for brain tumours as early as possible.

Basal Ganglia Diseases↗
PubMed2001

Six cases of cervical ligamentum flavum calcification in Blacks in the French West Indies.

OBJECTIVE: Calcification of the ligamentum flavum at the cervical spine is an uncommon condition reported mainly in Japanese patients. We describe the clinical manifestations, imaging study findings, and outcomes in six cases seen in the French West Indies. MATERIAL AND METHODS: We retrospectively reviewed the medical charts of six patients admitted to an orthopedics department for spinal cord compression shown upon computed tomography to be caused by calcification of the ligamentu flavum. There were five women and one man, mean age at admission was 71.7 years (range, 64-79 years) and all six patients were Black. RESULTS: Five patients had cervical myelopathy and one was asymptomatic. All five symptomatic patients had cervical spinal stenosis, explaining the rapid symptom onset (within six and a half months) and severe motor loss. Computed tomography reconstruction in the sagittal plane ruled out ossification of the ligamentum flavum. Magnetic resonance imaging of the neck failed to demonstrate the calcifications but was useful in evaluating the severity of the spinal cord compression. One patient had articular chondrocalcinosis in both knees and another had calcifications in the basal ganglia. Surgical decompression by the posterior route was performed in two patients and was effective in both, whereas two of the three symptomatic patients who did not have surgery experienced worsening neurological loss. Analysis of the operative specimens from the two surgically treated patients showed a mixture of calcium pyrophosphate dihydrate crystals and apatite microcrystals. CONCLUSION: Calcification of the ligamentum flavum is probably underrecognized in blacks. This condition causes severe neurological loss. Imaging studies provide the diagnosis. The pathogenesis remains unclear.

Aged↗
PubMed2006

Paraneoplastic hypercalcemia with metastatic calcification--clinicopathologic studies.

Hypercalcemia is a common paraneoplastic syndrome that may result in metastatic calcification. We report here on four autopsy cases with paraneoplastic hypercalcemia with metastatic calcification, to evaluate the clinicopathologic manifestations. All were males, aged 37-63 years old. Primary tumors included one transitional cell carcinoma of the urinary bladder, one multiple myeloma, and two squamous cell carcinomas of the esophagus. Calcium concentrations ranged from 3.3 to 5.9 mmol/L. Chronic hypercalcemia resulted in metastatic calcification. The kidney and stomach were the most vulnerable organs. Only case 1 presented with an increase in plasma calcium above 5 mmol/L (about twice the normal value); the metastatic calcification involved the capillary walls of his lungs, and he died of fulminant pulmonary edema. Our conclusion is that judicious treatment for paraneoplastic hypercalcemia is important with respect to the occurrence of pulmonary edema associated with metastatic calcification.

Adult↗
PubMed1999

Polyethylene glycol-grafted bovine pericardium: a novel hybrid tissue resistant to calcification.

Calcification is a frequent cause of the clinical failure of bioprosthetic heart valves fabricated from glutaraldehyde pretreated bovine pericardium (GATBP). An investigation was made of the grafting of different molecular weight polyethylene glycol (PEG 600, 1500, 4000 and 6000) via glutaraldehyde (GA) linkages to bovine pericardium (BP) and of their stability and calcification. The process of the calcification profile was studied by in vitro experiments via incubating pericardial samples in a metastable solution of calcium phosphate. Calcification of bovine pericardium grafted with PEG 6000 was significantly decreased compared to low molecular weight PEG grafts or Sodium dodecyl sulphate- (SDS) and GA-treated tissues. The mechanical properties of these modified tissues after enzyme (Trypsin) digestion and calcification were investigated. The biocompatibility aspects of grafted tissues were also established by monitoring the platelet adhesion, octane contact angle and water of hydration. PEG 6000-grafted tissues retained the maximum strength in trypsin buffer and calcium phosphate solutions. Scanning electron micrographs revealed that the PEG-grafted bovine pericardium had substantially inhibited the platelet-surface attachment and their spreading. It is conceivable that high molecular weight polyethylene glycol-grafted pericardium (a hybrid tissue) may be a suitable calcium-resistant material for developing prosthetic valves due to their stability and biocompatibility.

Journal Article↗
PubMed2004

Invasive measurements of pulse wave velocity correlate with the degree of aortic valve calcification and severity associated with matrix metalloproteinases in elderly patients with aortic valve stenosis.

The aim of the present study was to assess the association between invasive PWV (pulse wave velocity), serum levels of MMPs (matrix metalloproteinases) and the echocardiographic severity and calcification score of degenerative AS (aortic stenosis). We enrolled 30 patients (16 males; age, 61.3+/-8.2 years) diagnosed with degenerative AS and an additional 30 age- and sex-matched control patients. Invasive PWV methods with a pigtail catheter and double-channel recording were performed in both groups in our catheterization laboratory. We scored the severity of calcification at the AV (aortic valve) during two-dimensional echocardiography. The association between the trans-valvular pressure gradient, the severity of calcification of the AV and the value of PWV were analysed. We also analysed the serum levels of MMP-9, MMP-3 and TIMP-1 (tissue inhibitor of metalloproteinases-1) in these patients. In the group with degenerative AS, mean AV pressure gradients (56.0 compared with 9.5 mmHg; P<0.001) and calcified AV scoring (3.3+/-1.2 compared with 2.1+/-0.9; P<0.001) were higher than in the control group. In addition, PWV was faster in the group with degenerative AS (15.5+/-3.8 compared with 8.0+/-2.7 m/s; P=0.001). After being adjusted for age, sex, mean blood pressure and left ventricular function, both the AV pressure gradient and the severity of calcification were strongly correlated with PWV (R=0.706, P<0.0001, and R=0.561, P=0.03 respectively). In addition, the serum levels of MMP-9, MMP-3 and TIMP-1 were all significantly higher and correlated with PWV in the group with AS (all P<0.05). With higher serum levels of MMPs and their inhibitors, we found that this invasive measurement of PWV was associated strongly with the pressure gradient and calcification of AV. More advanced degenerative changes in AV was probably associated with more severe aortic arteriosclerosis.

Aged↗
PubMed2000

Warfarin exposure and calcification of the arterial system in the rat.

There is evidence from knock-out mice that the extrahepatic vitamin K-dependent protein, matrix gla protein, is necessary to prevent arterial calcification. The aim of this study was to determine if a warfarin treatment regimen in rats, designed to cause extra-hepatic vitamin K deficiency, would also cause arterial calcification. Sprague-Dawley rats were treated from birth for 5-12 weeks with daily doses of warfarin and concurrent vitamin K1. This treatment causes an extrahepatic vitamin K deficiency without affecting the vitamin K-dependent blood clotting factors. At the end of treatment the rats were killed and the vascular system was examined for evidence of calcification. All treated animals showed extensive arterial calcification. The cerebral arteries and the veins and capillaries did not appear to be affected. It is likely that humans on long-term warfarin treatment have extrahepatic vitamin K deficiency and hence they are potentially at increased risk of developing arterial calcification.

Animals↗
PubMed2001

Gastric carcinoma with psammomatous calcification after Billroth II reconstruction: case report and literature review.

A case of gastric carcinoma with psammomatous calcification arising in the remnant stomach after Billroth II reconstruction is reported. Borrmann type 1 gastric carcinoma was detected in the remnant stomach of an 82-year-old woman, who had a past history of distal partial gastrectomy for a perforated gastric ulcer, with Billroth II reconstruction at 40 years of age. Histologically, the tumor was a tubular adenocarcinoma that invaded the muscularis propria. Numerous psammoma bodies were found in the lumens of the tumor glands. Dystrophic calcification of gastric cancer is rare and psammomatous calcification of gastric cancer has only been reported in five cases previously. To our knowledge, this is the first case of gastric carcinoma with psammomatous calcification arising in the remnant stomach. We also review previously published reports regarding gastric carcinoma with psammomatous calcification.

Adenocarcinoma↗
PubMed2003

Sevelamer hydrochloride prevents ectopic calcification and renal osteodystrophy in chronic renal failure rats.

BACKGROUND: Hyperphosphatemia is associated with severe complications, including ectopic calcification of soft tissues, secondary hyperparathyroidism, and renal osteodystrophy (ROD). Sevelamer hydrochloride is a nonabsorbed calcium- and metal-free phosphate binder that lowers serum phosphorus levels in hemodialysis patients. This study examined the efficacy of sevelamer in preventing ectopic calcification of soft tissues and ROD in adenine-induced renal failure rats. METHODS: Male, 12-week-old Wistar-Jcl rats were freely fed an adenine diet (0.75 g adenine in 100 g normal diet) for four weeks. After three weeks of the adenine diet, when serum phosphorus levels had significantly increased, the rats were freely fed a normal diet that contained 1% or 2% of sevelamer for another five weeks. Time course changes of serum levels of phosphorus, calcium, and parathyroid hormone (PTH) were measured. At the end of the study, calcium and phosphorus levels in the heart and aorta were measured, and the calcification of kidney, heart, aorta, and stomach were histopathologically examined. The severity of ROD was evaluated by a histopathologic and morphometric analysis of the femurs. RESULTS: Compared with the adenine controls (N = 10), the sevelamer-treated (1%, N = 6; and 2%, N = 10) groups of adenine-induced renal failure rats had reduced serum phosphorus, serum calcium x phosphorus product, and serum PTH levels. Moreover, in the treatment groups, sevelamer suppressed calcification of the aorta media, and also the osteoid volume, fibrosis volume, and porosity ratio of femurs. CONCLUSION: These results suggest that sevelamer treatment might contribute to the suppression of ectopic calcification and ROD.

Animals↗
PubMed2003

Sevelamer hydrochloride attenuates kidney and cardiovascular calcifications in long-term experimental uremia.

BACKGROUND: In chronic renal failure (CRF), hyperphosphatemia and an elevated calcium-phosphate product are associated with vascular calcification and increased cardiovascular morbidity and mortality. Previous data have demonstrated that 3-month treatment of uremic rats with sevelamer was associated with less nephrocalcinosis compared to calcium carbonate (CaCO3), despite similar control of serum phosphorus, calcium-phosphorus product (Ca x P product), and secondary hyperparathyroidism. There was no evidence of aortic calcification after 3 months of uremia (J Am Soc Nephrol 13:2299-2308, 2002). The present studies explore the influence of sevelamer and CaCO3 on cardiovascular and kidney calcifications in long-term experimental uremia over 6 months. METHODS: Normal and 5/6 nephrectomized rats (U) were fed a high phosphorus (HP) diet for 6 months. Two phosphate binders, CaCO3 and sevelamer, were administered and their influence on hyperphosphatemia, secondary hyperparathyroidism, kidney/myocardial/aortic calcification, and renal function was compared. RESULTS: All uremic rats began the study with the same degree of renal failure. Sevelamer was as effective as CaCO3 in reducing serum phosphorus, Ca x P product, and attenuating secondary hyperparathyroidism. Despite similar serum cholesterol levels, rats in the U-HP + sevelamer group had markedly lower calcium deposition in the myocardium and aorta (myocardium, 72 +/- 4 microg/g wet tissue; aorta, 736 +/- 156 microg/g wet tissue) compared to rats in either the U-HP + CaCO3 group (myocardium, 179 +/- 48, P < 0.05; aorta, 1308 +/- 343, P < 0.05) or the U-HP group (myocardium, 98 +/- 10, NS; aorta, 2150 +/- 447, P < 0.05). Dual immunohistochemical analysis for calcium and endothelial cell markers demonstrated that myocardial calcium deposition was intravascular within capillaries. Furthermore, calcium deposition in the kidney of uremic rats treated with sevelamer (582 +/- 111 microg/g wet tissue) was lower than that found in uremic rats treated with CaCO3 (1196 +/- 180 microg/g wet tissue). Sevelamer-treated rats had less deterioration in renal function with an associated lower serum creatinine, higher creatinine clearance, and less proteinuria. There was no difference in overall mortality between the three experimental groups. CONCLUSION: In long-term experimental CRF, in addition to controlling serum phosphorus and secondary hyperparathyroidism as efficiently as CaCO3, treatment with the phosphate-binder sevelamer attenuates vascular and kidney calcification.

Animals↗
PubMed2003

Deficiencies of calcium-regulatory proteins in dialysis patients: a novel concept of cardiovascular calcification in uremia.

Dialysis patients suffer a manifold increase in cardiovascular mortality when compared to a nonuremic population, while this phenomenon is not sufficiently explained by an increased prevalence of traditional risk factors, such as hypercholesterolemia and hypertension. The presence of hyperphosphatemia, of an increased calcium x phosphate product, as well as the magnitude of vascular and valvular calcifications, were recently identified as specific major risk factors of cardiovascular mortality in the uremic population. Furthermore, hyperphosphatemia and an increased calcium x phosphate product could be quantitatively linked to the burden of coronary artery calcification in young dialysis patients, suggesting the correction of hyperphosphatemia as the central target for preventive therapeutic intervention. Recent studies in knockout mice, however, point to the alternative possibility that deficiencies in calcium-regulatory proteins may represent important pathomechanisms leading to extraosseous calcifications. alpha 2-Heremans Schmid glycoprotein (Ahsg/fetuin) and matrix Gla protein (MGP) are strong inhibitors of calcification in vivo. Novel evidence that deficiencies of such proteins may be involved in the pathogenesis of cardiovascular calcifications in dialysis patients will be discussed.

Animals↗
PubMed1999

Microcystic Calcifications at Stereotactic Breast Biopsy.

Calcifications in breast microcysts frequently exhibit characteristic layering in 90-degree horizontal beam mammographic images. This observation is sufficiently predictive of a benign process that biopsy can be avoided. We report our experience with nine patients in whom stereotactic biopsy was attempted for clustered calcifications which failed to convincingly layer in true lateral magnification views. Two cases are described and illustrated. In all nine patients, layering of calcifications was more convincingly suggested on preliminary digital images prior to stereotactic biopsy. The effect of compression and dependent breast position may explain this observation. Calcification was sparse or absent in extracted cores yet diminished or disappeared in postbiopsy mammograms. Radiologists are alerted to these possible results when stereotactic biopsy of microcystic calcification is attempted.

Journal Article↗