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PubMed1997

Clinical, radiographic, and pathologic features of medical calcific sclerosis in the breast.

Medial calcific sclerosis (MCS), a nonocclusive calcification of the media of small to medium-sized muscular arteries, may occur in the breast. To ascertain whether MCS causes difficulty with mammographic interpretation of breast calcifications and to determine its clinical and pathologic associations, we reviewed the records and biopsy specimens from 62 patients who had had screening mammography and breast biopsy, lumpectomy, or mastectomy. Ten specimens from 7 patients showed MCS. Average age of patients without MCS was 48.8 years, and that of the 7 patients with MCS was 61.3 years. Microcalcifications were found in 25 of 62 mammograms (34%). Of the 7 patients with MCS, 2 had hypertension, 1 diabetes mellitus, 2 diabetes mellitus and hypertension, and 2 neither hypertension nor diabetes mellitus. In 5 specimens, calcification only was associated with MCS. In 2 of these specimens, the mammographic calcifications were thought to be suggestive of malignancy on the basis of clustering and spiculation. One of the 2 was benign on histopathology; the other was malignant. Overall, carcinoma was identified in 3 of 7 patients with MCS (compared with 11 of 55 patients without MCS) and in 2 of 5 specimens (2 patients) with mammary MCS as the only type of calcification. The mammographic appearance of the microcalcification in MCS may suggest malignancy.

Adult↗
PubMed2003

BMP-7 is an efficacious treatment of vascular calcification in a murine model of atherosclerosis and chronic renal failure.

Chronic renal failure is complicated by high cardiovascular mortality. One key contributor to this mortality is vascular calcification, for which no therapy currently exists. Bone morphogenetic protein 7 is an essential renal morphogen that maintains renal tubular differentiation in the adult and is downregulated in renal failure. Several studies have demonstrated its efficacy in treating various renal diseases in rodents, and it was hypothesized that it would also be an effective treatment of vascular calcification in this setting. Uremia was imposed on LDL receptor null mice (a model of atherosclerosis), which were then treated with bone morphogenetic protein 7 for 15 wk. Uremic animals had increased vascular calcification by histology and chemical analysis. Calcification in treated animals was similar to or less than non-uremic control animals. Cells exhibiting an osteoblast-like phenotype in the vessel wall may be important in the etiology of vascular calcification. Expression of osteocalcin was assessed as a marker of osteoblastic function, and it is shown that it is increased in untreated uremic animals but downregulated to levels similar to non-uremic control animals with treatment. The data are compatible with bone morphogenetic protein 7 deficiency as a pathophysiologic factor in chronic renal failure, and they demonstrate its efficacy as a potential treatment of vascular calcification.

Animals↗
PubMed2003

Vascular calcification: in vitro evidence for the role of inorganic phosphate.

Uremic patients are prone to widespread ectopic extraskeletal calcification resulting from an imbalance of systemic inorganic phosphate (Pi). There can be serious consequences of this process, particularly when it results in the calcification of the vasculature. A recent study examined the response of cultured human aortic smooth muscle cells to varying levels of extracellular Pi. Cells that were exposed to Pi levels similar to those seen in uremic patients (>1.4 mmol/L) showed dose-dependent increases in cell culture calcium deposition. The results of this study also defined the role of elevated phosphate in transforming the vascular phenotype of these cells to an osteogenic phenotype, such that a predisposition for calcification was created. Pi-induced changes included increased expression of the osteogenic markers osteocalcin and core-binding factor-1 genes, the latter of which is considered a "master gene" critical for osteoblast differentiation. These changes occur early after exposure to high phosphate levels and seem to be mediated by a sodium-dependent phosphate co-transporter, Pit-1 (Glvr-1). Calcification of vascular cells also seems to occur in the absence of a mineral imbalance but in the presence of platelet-derived growth factor, a potent atherogenic factor. Taken together, these data suggest that calcification of vascular cells can occur early in a phosphate-rich environment similar to that seen in patients with renal failure and in a platelet-derived growth factor-rich atherosclerotic region under normal phosphorus conditions. From a clinical viewpoint, it seems that early control or prevention of hyperphosphatemia may reduce coronary calcification and its associated morbidity and mortality for patients on dialysis.

Calcinosis↗
PubMed2004

Phenotypic modulation of vascular smooth muscle cells during medial arterial calcification: a role for endothelin?

We have previously shown that an endothelin receptor antagonist can regress medial arterial calcification in a rat model. The aim of this study was to characterize the phenotypic changes of vascular smooth muscle cells during calcification and mineral loss, in order to understand better the underlying mechanisms. Control Wistar rats were compared with rats treated only with warfarin/ vitamin K1 (15 mg/kg per day) for 8 weeks, or in combination with darusentan (30 mg/kg per day) for the final 4 weeks. Vascular smooth muscle cell, bone cell and macrophage phenotypes were evaluated by the local expression of alpha-actin, tartrate-resistant acid phosphatase and ED-1, respectively. Proteins involved in the modulation of bone resorption like osteopontin and osteoprotegerin were also evaluated by immunohistochemistry. The warfarin/vitamin K1 treatment increased medial arterial calcification ninefold (P < 0.05). At sites of calcification, there was a decrease in alpha-actin localization, and an appearance of osteopontin immunostaining. Histochemical and immunostaining for osteoclast and macrophage markers, as well as for osteoprotegerin, were negative. Although the extent of calcification foci was reduced by darusentan, protein localization in the calcified areas was not modified. Thus, the development of medial arterial calcification produces a phenotypic change in vascular smooth muscle cells that does not appear to be normalized in regions remaining calcified during mineral loss.

Animals↗
PubMedDate not supplied

Positive and negative attributes and risk for coronary and aortic calcification in healthy women.

OBJECTIVE: Negative emotions predict the development of clinical coronary events, and some evidence suggests that negative emotions relate to subclinical atherosclerosis. Low levels of positive emotions and cognitions are relatively unexplored as predictors of cardiovascular risk. We tested the hypothesis that low positive and high negative affect and cognitions would be related to risk for coronary and aortic calcification in healthy women. METHODS: One hundred fifty-five healthy women had measures of positive and negative affect/cognitions obtained before or at the time of electron beam tomography scan of coronary and aortic calcification. RESULTS: Coronary calcification was unrelated to women's psychosocial scores. High aortic calcification was consistently associated with low scores on the Pearlin Mastery Scale and Life Engagement Test and high scores on the CES-Depression Inventory and Negative Interactions Scale in multivariate analyses. Odds ratios (OR [95% confidence intervals (CI)]) from the multivariate binary logistic regression analyses for a SD above the mean scales scores were 0.55 (95% CI, 0.35-0.87) for Pearlin Mastery; 0.56 (95% CI, 0.36-0.86) for the Life Engagement Test; 0.63 (95% CI, 0.40-98) for Life Satisfaction; 1.57 (95% CI, 1.04-2.36) for the CES-Depression; 1.77 (95% CI, 1.15-2.74) for the Cook-Medley Hostility; 1.49 (95% CI, 0.98-2.26) for Spielberger Anger-In; and 2.35 (95% CI, 1.49-3.73) for the Negative Interaction scales. CONCLUSIONS: Women's psychosocial attributes were not related to coronary calcification, raising the possibility that psychosocial attributes are less important for early than late stages of coronary atherosclerosis. The observed associations of psychosocial attributes with aortic calcification may be due to somewhat different risk factors being important for atherosclerosis at different vascular beds. Positive attributes may be related to atherosclerosis and should be studied further.

Aged↗
PubMed2004

Quantification of aortic valve calcification with electron beam tomography: a histomorphometric validation study.

RATIONALE AND OBJECTIVES: The exact quantification of the amount of calcification in aortic valves may be useful for the identification of risk factors for the progression of aortic valve calcification and to evaluate new therapeutic approaches for aortic valve disease. Electron beam tomography (EBT) allows the in vivo detection of calcifications in coronary vessels and in the aortic valve. The aim of this study was to validate the quantification of aortic valve calcification by EBT with in vivo and in vitro investigations. METHODS: In 15 patients (aortic stenosis in 13, aortic regurgitation in 2 cases), EBT was performed before aortic valve replacement (40 cross sections, 3-mm slice thickness, matrix 512 x 512, field of view 28 cm, ECG trigger at 40% of the cardiac cycle). EBT was repeated on the explanted aortic valve using the same protocol. In both data sets, the amount of aortic valve calcification was determined using a volumetric score. In serial cuts of the explanted valve (distance 1 mm), the calcified volume was determined by an independent investigator using histomorphometric analysis. RESULTS: The mean calcified volume of the aortic valves as quantified by EBT was 1650.0 +/- 1401.0 mmł in vivo (EBT1) and 1544.4 +/- 1266.5 mmł in vitro (EBT2). Histomorphometric analysis showed a mean calcified volume of 1555.7 +/- 1272.5 mmł. The mean difference between EBT1 and EBT2 was 4.2 +/- 14.7%, between EBT1 and histomorphometry 3.6 +/- 12.1%, and between EBT2 and histomorphometry -0.5 +/- 5.9%. CONCLUSION: EBT allows accurate in vivo quantification of aortic valve calcifications.

Aged↗
PubMed1987

Light and electron microscopic observation on the process of tissue calcification in a case of parathyroid adenoma.

Metastatic calcification in various organs in an autopsy case of parathyroid adenoma was studied by light and electron microscopy. Calcification was observed in kidney, lung, liver, heart, stomach, and thyroid. In the kidney, calcification was found in the tubules and glomeruli. In the liver, calcification was mainly found in Disse's space. The kidney, lung, liver, and heart were examined by electron microscopy. Four forms of early calcification were observed: 1) amorphous dense bodies within the mitochondria; 2) needle-shaped hydroxyapatite; 3) concentric laminated structure; and 4) cytoplasmic vesicles originating in hepatocytes. Calcium phosphate precipitates within the mitochondria were seen as amorphous dense bodies. When calcium phosphate precipitated in the cytoplasmic colloid gel, concentric laminated structures were formed due to Liesegang's phenomenon. Needle-shaped crystals in the amorphous dense bodies of the mitochondria were interpreted as a phenomenon of epitaxy. Calcification in Disse's space was thought to start in cytoplasmic vesicles which were derived from hepatocytes.

Adenoma↗
PubMed2005

Coronary arterial calcification is associated with albuminuria in type 2 diabetic patient.

AIM: Although microalbuminuria has been suggested as an independent risk factor for ischemic heart disease, the relationship between diabetic nephropathy and macroangiopathy remains unclear. Previously, we reported that coronary artery calcification detected by electron beam computed tomography (EBCT) could indicate the degree of coronary atherosclerosis in type 2 diabetic patients. In this study, we examine the association between coronary arterial calcification and microalbuminuria and aortic calcification and microalbuminuria. METHODS: Two hundred and fifty-six patients, including 177 type 2 diabetic patients (106 patients with normoalbuminuria, 71 with microalbuminuria) and 79 non-diabetic patients were evaluated by assessing the urinary albumin excretion rate and using EBCT to determine a coronary calcification score (CCS) and an aortic calcification score (ACS). RESULTS: No differences were observed regarding age, smoking index or BMI. Diabetic patients exhibited a greater CCS than non-diabetic subjects (non-diabetes 33 +/- 75 vs. diabetes 203 +/- 467, p < 0.05). Diabetic patients with microalbuminuria exhibited the most advanced CCS (253 +/- 491, p < 0.05). In contrast, no difference was observed in ACS among three groups. Multiple regression analysis showed that CCS is significantly associated with urinary albumin excretion rate as well as age, duration of diabetes and serum creatinine (R(2) = 0.31), while ACS is strongly associated with age, smoking, serum creatinine, systolic blood pressure and low-density lipoprotein cholesterol level (R(2) = 0.29). CONCLUSION: Increased urinary albumin excretion is associated with coronary arterial calcification in diabetic patients.

Age Factors↗
PubMed2005

Effects of sevelamer and calcium on coronary artery calcification in patients new to hemodialysis.

BACKGROUND: Hemodialysis patients are at increased risk for progressive coronary artery calcification; however, the development and progression of this disease process in patients new to hemodialysis is unknown. METHOD: One hundred and twenty-nine patients new to hemodialysis were randomized to receive calcium containing phosphate binders or the noncalcium phosphate binder sevelamer hydrochloride. Subjects underwent electron beam computed tomography scanning (EBCT) at entry into the study and again at 6, 12, and 18 months. RESULTS: One hundred and nine patients underwent baseline and at least one additional assessment of coronary calcification. At baseline, 37% of sevelamer treated and 31% of calcium treated patients had no evidence of coronary calcification. No subject with a zero coronary artery calcium score (CACS) at baseline progressed to a CACS >30 over 18 months. Subjects with a CACS > 30 at baseline showed progressive increases in CACS in both treatment arms (P < 0.05 for each time point in both groups). Subjects treated with calcium containing phosphate binders showed more rapid and more severe increases in CACS when compared with those receiving sevelamer hydrochloride (P= 0.056 at 12 months, P= 0.01 at 18 months). CONCLUSION: New hemodialysis patients with no evidence of coronary calcification showed little evidence of disease development over 18 months independent of phosphate binder therapy. However, subjects with evidence of at least mild coronary calcification had significant progression at 6, 12, and 18 months. Use of calcium containing phosphate binders resulted in more rapid progression of coronary calcification than did use of sevelamer hydrochloride.

Adult↗
PubMed2005

Calcification and cardiovascular problems in renal failure.

Extraosseus calcification has plagued management of renal failure since the beginning of hemodialysis, but the issue has largely been neglected because the impact on survival was thought to be limited. The recent recognition that hyperphosphatemia is a strong predictor of all-cause mortality, and particularly of cardiac mortality, has transformed the situation. Relatively stringent, though difficult to implement, guidelines have been proposed for the management of hyperphosphatemia. Important recent insights document that, for different reasons, both high and low turnover of bone disease increase the risk of vascular calcifications. Vascular calcification impacts cardiac death not only by complicating coronary atherosclerosis, but also by increasing the stiffness of central arteries, impacting on heart function (increased impedance, reduced coronary perfusion). While in the past extraosseous calcification, including vascular calcification, was thought to be a passive process resulting from transgression of a critical Ca x P product, recent studies show that the adverse effect of hyperphosphatemia is also mediated by active processes (e.g., induction of "osteogenic" genetic programs), and is modulated by calcification inhibitors.

Calcinosis↗
PubMedDate not supplied

Vascular calcifications in uremia: old concepts and new insights.

The annual mortality rate in uremic patients, corrected for age, sex, and race, is significantly higher than in the general population. This is primarily due to cardiovascular events. Vascular calcifications play a vital role in the development of cardiovascular morbidity and subsequent increased mortality. Vascular calcification affects both vascular intima and media layers and its mechanism remains poorly understood. Over the last few years it has been shown that, in addition to traditional cardiovascular risk factors, disturbances in mineral metabolism in the uremic milieu, calcium-containing phosphate binders, and vitamin D treatment of secondary hyperparathyroidism may contribute to the pathogenesis of vascular calcifications. Other uremia-related risk factors (e.g.increased oxidized low-density lipoprotein cholesterol, uremic toxins, increased oxidative stress, dialysis and dialysate-related factors, hemodynamic overload, hyperhomocysteinemia) may also play a role. In uremic patients, apart from these facilitating factors, decreased levels of endogenous calcification inhibitors such as fetuin-Amatrix Gla protein, osteoprotegerin, and osteopontin have also been associated with increased calcium-phosphate precipitation in extraskeletal tissues. Finally, vascular calcification is the outcome of the active and dynamic balance of procalcifying and anticalcifying influences. For the prevention and treatment of vascular calcifications, it is essential to avoid treatment modalities that lead to calcium overload, achieve good metabolic control, and optimize dialysis.

Calcinosis↗
PubMed1982

Basal ganglia calcification on computer tomographic scan. A clinical and radiological correlation.

Computerised tomography of the brain was used to demonstrate basal ganglia calcification which may be of an insufficient degree to be seen on skull X-ray. Cases referred for CT scan from hospitals in Singapore for various reasons over a period of 12 months were studied for basal ganglia calcification. There was a startlingly high incidence of 1.5%, as 47 cases (all except 2 were Chinese) showed such calcification. In 42 cases there was no evidence of basal ganglia calcification on skull X-ray. 16 cases showed neurological affection, fits being the commonest manifestation. An unexpected finding was that no case had abnormality of calcium metabolism or evidence of hypoparathyroidism or pseudohypoparathyroidism. The CT scan is very sensitive in demonstrating minimal basal ganglia calcification and our impression is that such calcification is common.

Adolescent↗
PubMed1984

Post-ischemic calcification in skeletal muscle. A light microscopic study in the rat.

The extent of post-ischemic calcification in skeletal muscle was studied in rats subjected to 5.5 h of ischemia followed by periods of reperfusion ranging from 30 min to 16 h. Sections from the tibialis posterior and soleus muscle were stained with alizarin red S (ARS) and were inspected with light microscopy. The number of ARS-positive cells increased during the first 5 h of reperfusion. The extent of calcification varied between fibers and the pattern of calcification appeared to be dependent on fiber type. In some fast glycogenolytic fibers (FG) central calcifications, probably representing mitochondria, were observed. In fast oxidative glycogenolytic (FOG) and slow oxidative (SO) fibers the most common pattern was an ARS-positive granulation, probably representing calcification of sarcoplasmic reticulum and/or mitochondria. The granulation was more extensive in FOG than in SO fibers. In some areas extracellular ARS-positive material was observed. In such areas, which probably represent areas of no-reflow, no calcification of muscle fibers was observed.

Animals↗
PubMed1991

Whole blood re-calcification time in equine colic.

Whole blood re-calcification times were evaluated as a measure of endotoxin-associated coagulopathy in horses. First, the effects of endotoxin concentration and duration of in vitro incubation of citrated whole blood with endotoxin on the whole blood re-calcification time of blood collected from healthy horses were determined. Increasing concentrations or incubation times of endotoxin accelerated the whole blood re-calcification time. This effect was attributed mainly to increased monocyte thromboplastin activity. Second, whole blood re-calcification time, a clotting profile, plasma factor VII activity and plasma endotoxin concentration on blood samples obtained from 35 equine colic patients and 10 healthy horses were determined. Compared with healthy horses, colic patients had a longer mean whole blood re-calcification and prothrombin time, lower per cent factor VII activity and higher mean fibrin degradation products concentration. Within the colic patient group, horses that did not survive had detectable endotoxin in plasma, longer whole blood re-calcification and prothrombin times, and lower plasma factor VII activity, compared with colic patients that survived. These data indicate that colic patients with endotoxaemia experience hypercoagulable states, followed by consumptive coagulopathy. Although the cause of endotoxin-associated coagulopathy is likely multi-factorial, increased expression of monocyte thromboplastin activity may be involved in the pathogenesis of coagulopathy. The whole blood recalcification time is a simple, fast and inexpensive way to detect coagulopathy during endotoxaemia and determine the prognosis for survival.

Animals↗
PubMed1996

Calcification of the transverse ligament of the atlas in chondrocalcinosis: computed tomography study.

OBJECTIVE: To seek an association between articular chondrocalcinosis (AC) and calcification of the transverse ligament of the atlas (TLA), and to evaluate the frequency and the main computed tomography appearances of such calcification. METHODS: Axial computed tomography slices of the cervico-occipital hinge were performed routinely in 21 patients with AC (three men, 18 women; mean age 79 years, range 67-87) and compared with those from a control group of 21 age and gender matched patients without AC. RESULTS: Calcification of the TLA was present in 14 of the 21 patients (66%) in the AC group and in none of the 21 patients (0%) in the control group (chi 2 test: p < 0.001). Calcification was localised behind the odontoid process, inserted upon the osseous tubercles of the lateral masses of C1, and had a curvilinear profile; it varied in height (1.5 to 9 mm) and appearance (thin = < 1 mm; thick = > 1 mm) and formed either a single or a double band. CONCLUSION: This study has demonstrated a relationship between AC and calcification of the TLA. Although such calcification often remains asymptomatic (nine of 14 patients in our study), it may be associated with attacks of acute neck pain with segmentary stiffness, fever, and an increased erythrocyte sedimentation rate, sometimes revealing AC.

Aged↗
PubMed1993

Limbal and corneal calcification in patients with chronic renal failure.

In patients with chronic renal failure on regular dialysis treatment, limboconjunctival degenerations and calcifications are commonly observed. In this study three groups of patients were followed over a period of 6 years. The first group consisted of 47 patients with renal failure, the second group of 17 patients with renal failure and hyperparathyroidism not controlled by drugs, and the third group seven patients with primary hyperparathyroidism without renal failure. The aim of this study was to determine the progression of the limboconjunctival changes over time. The hypothesis that an increase in serum calcium and phosphorus concentrations, as a result of tertiary hyperparathyroidism, could possibly add a corneal component to the limbal calcification was also tested. All patients with renal failure (in as much as the degenerative limbal features were not obscured by deposits of lime salts), had a type II white limbus girdle of Vogt. This limbal degeneration was observed in only 45% of controls. In all 47 patients with renal failure conjunctival calcification was observed; 26 of them also had limbal calcification. After 6 years 41 patients had developed limbal calcification. This progression was statistically significant. In 15 out of 17 patients with tertiary hyperparathyroidism a band-shaped keratopathy developed in addition to the limboconjunctival calcification.

Calcinosis↗
PubMed2003

On-line detection of cholesterol and calcification by catheter based Raman spectroscopy in human atherosclerotic plaque ex vivo.

BACKGROUND: Raman spectroscopy has the unique potential to detect and quantify cholesterol and calcification in an atherosclerotic plaque in vivo. OBJECTIVE: To evaluate the sensitivity and specificity of this technique for detecting cholesterol or calcification in human coronary artery and aorta specimens ex vivo, using a compact clinical fibreoptic based Raman system developed for in vivo applications. DESIGN: From nine coronary arteries and four aorta specimens, 114 sites were evaluated for the presence of cholesterol and calcification by Raman spectroscopy and standard histology. Raman spectra were acquired and evaluated on-line in around five seconds. RESULTS: The correlation between Raman spectroscopy and histology was r = 0.68 for cholesterol and r = 0.71 calcification in the plaque (p < 0.0001). Sensitivity and specificity for detecting cholesterol and calcification were excellent: receiver operating characteristic (ROC) analysis for each of the components revealed areas under the curves of > 0.92 (p < 0.0001). At the optimal cut-off values determined by ROC analysis, positive predictive values of > 80% and negative predictive values of > 90% were obtained. CONCLUSIONS: On-line real time catheter based Raman spectroscopy detects accumulation of cholesterol and calcification in atherosclerotic plaque with high sensitivity and specificity.

Calcinosis↗
PubMed1981

Myocardial fibre calcification.

Three cases of myocardial fibre calcification found at post-mortem examination are described. In one case there was antemortem hypercalcaemia and hyperphosphataemia and the case was clearly an example of metastatic calcification. In the other two cases there was ischaemic myocardial necrosis and calcification was seen in fibres which were not overtly necrotic, but which were both in proximity to (the majority) and remote from the necrotic zones. Since renal failure with hyperphosphataemia was present in both cases, these were considered to be examples of augmented (by the hyperphosphataemia) dystrophic calcification. The histological, histochemical and ultrastructural features were identical in the three cases. Hydroxyapatite formation was observed initially in mitochondria, followed by spillage of crystals into the cytosol and ultimately into the interstitium. It is suggested that the fundamental lesion is a dysfunction of the fibre membrane; the similarity of this reaction with the calcification seen in skeletal muscle fibres in various myopathies is noted and a unifying hypothesis of the mechanism of skeletal and cardiac muscle fibre calcification is thereby suggested.

Aged↗