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PubMed2002

Changes in size of periarthritis calcifications in patients with painful shoulder treated with injectable disodium-clodronate.

Calcific periarticular disease is characterized by the deposition of calcium phosphate crystals in many tendons and particularly in the rotator cuff tendons. Calcifications of any size may be accompanied by painful shoulder syndrome and tendon tears. Ecographic assessment of changes in the size of calcifications may be a marker of tissue changes in evolving shoulder periarthropathies. The aim of this study was to compare variations in pain and ultrasound dimensions in the calcifications in the tendons of the rotator cuff in patients treated with disodium-clodronate compared with those treated with paracetamol and nimesulide. In all groups, pain reduction occurred over a 6-month period, but was significantly greater in patients administered disodium-clodronate than in those administered nimesulide or paracetamol. A significant reduction in the size of calcifications was also observed in all three groups, but this reduction was more marked in the disodium-clodronate group.

Acetaminophen↗
PubMed2003

Detoxification on top of enhanced, diamine-extended glutaraldehyde fixation significantly reduces bioprosthetic root calcification in the sheep model.

BACKGROUND AND AIM OF THE STUDY: Increased concentrations of glutaraldehyde (GA), diamine-extension (DA) of crosslinks and subsequent extraction of excess GA all reduce bioprosthetic calcification in the subdermal rat model. The study aim was to demonstrate the combined effect of all three treatments in a circulatory sheep model. METHODS: Two fixation treatments were used for GA detoxification (urazole in acetate buffer, 0.1 M; pH 4.5; 37 degrees C; 7 days): (i) conventional 0.2% GA fixation (4 degrees C; 7 days); and (ii) enhanced 3.0% GA fixation (4 degrees C; 2 days, followed by a DA interim step; 100 mM L-lysine; 37 degrees C; 2 days, followed by GA; 3.0%; 37 degrees C; 5 days). Entire porcine root prostheses were implanted in the distal aortic arch of young sheep for 12 weeks (n = 5 per group). Non-detoxified 0.2% GA-treated roots served as controls (n = 5). Calcium analysis was based on atomic absorption spectrophotometry; morphology was assessed using light and transmission electron microscopy. RESULTS: Detoxification alone resulted in an 83% reduction of leaflet calcification (p = 0.086), but achieved only 23% (p = 0.145) and 12% (p = 0.362) mitigation of calcification in aortic wall and sinus tissue, respectively. When combined with DA-enhanced 3% GA fixation, detoxification led to a 95% reduction in leaflet calcification (p = 0.057), followed by 79% in sinus (p = 0.003) and 79% in aortic wall tissue (p = 0.0003). Morphologically, detoxification primarily affected leaflets and the subadventitial layer of aortic wall tissue, whereas enhanced fixation seemed to affect all structures. CONCLUSION: It was shown in a circulatory sheep model that a combination of DA-enhanced fixation with an extraction process of excess GA leads to a distinct mitigation of leaflet and aortic wall calcification.

Animals↗
PubMed2003

Bioprosthetic tissue calcification: influence of blood contact and arterial pressure. an experimental study in rats and sheep.

BACKGROUND AND AIM OF THE STUDY: Several animal models are currently used to study bioprosthetic tissue calcification. The study aim was to evaluate the influence of species and environmental factors (blood contact and arterial pressure) on valve tissue mineralization. METHODS: Glutaraldehyde-fixed porcine cusps and aortic wall samples were implanted subcutaneously in rats (n = 6) and sheep (n = 18). In sheep, similar samples were also implanted into the jugular vein (blood contact) and carotid artery (blood contact and arterial pressure). Tissue was explanted at intervals up to three months and evaluated macroscopically, and by X-radiography, light and electron microscopy and calcium content measurement. RESULTS: After eight weeks in the subcutaneous position, glutaraldehyde-fixed cusps were severely calcified in rats, but not in sheep (78.6 +/- 28.3 and 0.3 +/- 0.5 microg Ca/mg, respectively; p <0.001). Aortic wall samples were calcified in both species, but less in sheep (p <0.001). In sheep, blood contact without arterial pressure (venous implants) significantly increased the calcification of cusp and even more of aortic wall tissue. Arterial pressure had no effect on calcification of aortic wall tissue. CONCLUSION: Major inter-species inconsistencies were found in valve tissue calcification after subcutaneous implantation. In sheep, blood contact increased tissue calcification significantly, mainly in aortic wall samples. Arterial pressure did not enhance mineralization of aortic wall tissue.

Animals↗
PubMed2003

[Cardiovascular calcifications in hemodialysis patients. Prevalence and risk factors].

OBJECTIVES: Cardiovascular diseases are the leading cause of morbidity and mortality in chronic hemodialysed patients. The aim of our study was to determine the prevalence of cardiovascular calcifications in dialysed patients and to evaluate their risk factors. METHODS: We did a transversal study in 86 chronically hemodialysed patients in the hemodialysis department, Ibn Sina university hospital (Rabat). All patients, 44 men and 42 females, mean age 42 +/- 15.5 years were hemodialysed for more than one year. FINDINGS: The prevalence of cardiovascular calcifications was 24.5%. Chronic hemodialysed patients with cardiovascular calcifications were older (50.5 years +/- 15.4 vs 39 years +/- 14.6; p = 0.003). They had a long hemodialysis duration (81 months +/- 51 vs 59 months +/- 43; p = 0.05) and a higher calcium plasmatic concentration (2.27 +/- 0.15 vs 2.1 +/- 0.19 mmol/l; p = 0.03). We noted a male gender predominance (sex ratio M/W = 18/3 vs 26/39; p = 0.0002). Multivariate analysis showed, as an independent predictor of cardiovascular calcifications, the old age (p = 0.01). Cardiovascular calcifications seem uncommon in our hemodialysis patients. Older age, longer hemodialysis duration and male gender are risk factors. The use of low doses of calcium carbonate, vitamin D and low milk products diet may explain this low prevalence.

Adult↗
PubMed2003

Mathematical analysis of calcifications in stented, antibiotic sterilized and cryopreserved sheep biological valves implanted for one year in tricuspid position.

UNLABELLED: The aim of the study was morphometric and mathematic analysis of calcification profiles present in the leaflets of a cryopreserved and alive heart valve depending on the diagnosed pathologic process. Sheep antibiotic sterilised and cryopreserved biological valves were implanted in tricuspid position in young sheeps for one-year period. After this time the valves removed and studied morphologically. The control group consisted of 7 intact valves, the comparative group, so called group of valves after the processing antibiotic sterilization and cryopreservation consisted of 7 valves after mentioned procedures. Histologic investigations were based on paraffin sections of formalin-fixed valve cusps, stained with H&E and Masson trichrome, calcium deposits were stained von Kossa technique. The measured values included: 1. area and equivalent diameter, 2. length, 3. breadth, 4. perimeter, 5. elongation, 6. roundness, 7. fullness coefficient. CONCLUSIONS: 1. A process of initial processing and cryopreservation of biological valve increases a dimension and disturbs a shape of microcalcifications. 2. Cryopreserved biological valves explanted after one-year implantation into an animal in a tricuspid position possess microcalcifications and calcification foci. The size of microcalcifications decreases together with an intensification of degenerative processes of the connective tissue, especially in hyalinization. Hyalinization of the biological valve tissue seems to be favorable for a valve durability and as a pathological process decreasing calcification. 3. Mathematic analysis of morphometric features defining differences in size and shape of each calcification indicate morphologic and morphometric autonomy of calcifications, characteristic for the analyzed group of valve pathologic changes.

Animals↗
PubMed2003

Von Willebrand factor in type 1 diabetes: its production and coronary artery calcification.

BACKGROUND: Von Willebrand factor (vWF) has generally been regarded as a good predictor of vascular risk. However, no previous studies have examined its relationship with coronary calcification. The aim of this study was to determine whether vWF activity is higher in type 1 diabetic patients than controls; its relationship with cardiovascular risk factors; and to endothelial nitric oxide production and coronary artery calcification. MATERIAL/METHODS: Von Willebrand factor activity was measured in 181 type 1 diabetic patients and 188 controls. Coronary artery calcification was measured by Electron Beam Computed Tomography. Forearm blood flow was measured by venous plethysmography in response to intra-brachial infusion of bradykinin, glyceryl trinitrate, noradrenaline and NG-monomethyl-L-arginine (L-NMMA) in 149 subjects. RESULTS: Von Willebrand factor was significantly increased in diabetic patients compared to controls (median 100% vs 87%, p=0.001). Von Willebrand factor activity was significantly higher in diabetic patients with micro/macroalbuminuria than those with normoalbuminuria (109% vs 93%, p<0.001). Among diabetic subjects, being in the top quartile for vWF was associated with a lower response to L-NMMA (p=0.009). There was no association between vWF activity and coronary artery calcification in either the diabetic (p=0.9) or control group (p=0.8). CONCLUSIONS: Cardiovascular risk factors including albuminuria do not explain the high vWF activity in type 1 diabetic patients. There is some evidence that vWF correlates with endothelial nitric oxide production. The lack of correlation with coronary artery calcification indicates that vWF is not a useful marker of atheroma burden.

Adult↗
PubMed1992

Decrease of tumor-like calcification in uremia despite aggravation of secondary hyperparathyroidism: a case report.

Extraskeletal pseudotumoral calcifications generally develop in uremic patients with a high calcium x phosphorus (Ca x P) product and severe secondary hyperparathyroidism. In the present case report we describe a chronic hemodialysis patient presenting with a massive calcification of the left shoulder region, severe aluminum (Al) intoxication and moderate hyperparathyroidism. Her initial serum Ca x P product was only slightly elevated: 5.01 mmol2/l2. Under deferoxamine treatment during the subsequent 4 months, Al overload decreased. On the other hand, parathyroid overfunction worsened, as reflected by an increase of the serum immunoreactive parathyroid hormone [1-84] level from initially 690 to 1052 pg/ml (normal, 15-60 pg/ml) and an increase of alkaline phosphatase activity, and plasma calcitriol increased from undetectable to a low-normal value. Predialysis serum total Ca levels decreased rapidly from 2.9 to 2.5 mM but serum P concentrations remained elevated: 1.6-2.5 mM. Unexpectedly, the extent of the periarticular calcification diminished considerably during the same time period. The present observation shows that in a subset of uremic patients with Al overload, pseudotumoral calcifications may regress during Al chelation therapy despite progression of hyperparathyroidism. Since Al may predispose collagen to develop dystrophic or metastatic calcification, it is suggested that this process is reversible by correcting Al intoxication.

Aluminum↗
PubMed1955

THE RELATION of tuberculin sensitivity to pulmonary calcifications as an index of tuberculosis infection.

A single intradermal tuberculin test of 10 TU was arbitrarily selected for use in the Danish mass antituberculosis campaign of 1950-52. The present report discusses how efficiently this test can distinguish tuberculosis-infected and uninfected members of the adult population; it is based on the relation between size of tuberculin reaction and frequency of intrathoracic (presumably tuberculous) calcifications in 50,000 adults.Frequency distributions by size of 10 TU reactions for the study population, divided into 10-year age-groups, show a very consistent pattern for all age-groups: a smooth bimodal curve with a zone of low frequency around the 6 mm point of induration clearly separating persons with large reactions from those with very small or no reactions.In persons 15-34 years old the frequency of pulmonary calcifications is very low for those with tuberculin reactions measuring 0-7 mm of induration; for those with reactions of 8-9 mm the frequency rises sharply and reaches a maximum for those with reactions 18 mm or larger. In the age-groups up to 54 years the frequency of calcifications remains very low in persons with no reactions to the tuberculin test; the sudden steep rise in frequency is displaced with age from right to left on the tuberculin-reaction scale, and there is a progressive increase in the frequency of calcifications with the increase in reaction size. In the age-group 55 years or more persons with no reaction also have a high frequency of calcifications, and there is only a very slight rise in the frequency from 0-1 mm to the largest reactions.Up to the age of about 50 years, probably few persons not reacting to the 10 TU test are tuberculosis-infected. For persons over this age, however, division of the population into two groups according to the tuberculin-reaction size apparently does not correspond to a division into infected and uninfected.

Adult↗
PubMedDate not supplied

[Inflammation and subcutaneous calcification of venous origins].

There have been few descriptions up to now of calcifications in chronic venous insufficiency, other than in cases where venous insufficiency is complicated be severe trophic disorders and in particular ulcers. It was therefore felt to be of interest to assess the presence of calcifications in venous insufficiency without trophic disorders. This study was based upon 40 cases recruited in the phlebology out-patient clinic of the Notre Dame de Bon Secours Hospital. Calcifications of the lower limbs were found in 7 patients, either by palpation, routine X-rays or ultrasonography. The etiopathogenic mechanisms of this occurrence not having been elucidated, a number of hypotheses are put forward on the basis of acquired data concerning: the process of formation of ectopic calcifications, changes in subcutaneous tissue, the ultimate consequences of venous stasis and of raised venous pressure, due essentially to anoxia and inflammation. One hypothesis can thus be put forward: that of inflammation. The release of cells and mediators of inflammation, the production of free radicals, causing damage to the cells of connective tissue and to the organic framework (collagen fibres) and changes in the chemical environment could combine to result in the formation of calcifications in subcutaneous tissue. However, inflammation has not been proven to be the primary etiological factor.

Adult↗
PubMed2004

Expression of bone sialoprotein and bone morphogenetic protein-2 in calcific aortic stenosis.

BACKGROUND AND AIM OF THE STUDY: Calcific aortic stenosis, the major heart valve disease encountered in the elderly, leads to massive calcium deposition in the valve leaflets that morphologically resembles bone formation. Recent studies have demonstrated the expression of various bone-associated proteins in stenotic valves, suggesting that valvular calcification may be an actively regulated process. Bone sialoprotein (BSP), a non-collagenous bone matrix protein, and bone morphogenetic protein-2 (BMP-2), a member of the transforming growth factor cytokine superfamily, are known to participate in the regulation of bone development and maturation. Their pathogenetic role in calcific aortic stenosis is unknown. METHODS: Using an immunoperoxidase technique and antibodies against BSP and BMP-2, the expression of BSP and BMP-2 was examined in 16 human aortic valves with calcific aortic stenosis obtained at valve replacement, and in seven normal autopsy controls without signs of aortic stenosis. RESULTS: By semiquantitative scoring, stenotic valves showed a significantly increased staining of BSP in cells and extracellular matrix as compared to control valves (2.7 +/- 0.1 versus 0.6 +/- 0.2 score units, p <0.001). Marked BMP-2 expression was detected in stenotic valves, mostly in cell-rich areas associated with focal calcium deposits, but no specific staining for BMP-2 was detected in control valves (1.5 +/- 0.2 versus 0.0 +/- 0.0 score units, p <0.001). CONCLUSION: These results demonstrate for the first time that BSP and BMP-2 are differentially expressed in normal aortic valves and in aortic stenosis, thereby supporting the concept that valvular calcification might be based on an actively regulated process involving BSP and BMP-2.

Aged↗
PubMed2004

Inhibition of calcification with citric acid in pericardial bioprosthetic heart valve material: a preliminary report.

BACKGROUND AND AIM OF THE STUDY: Although current bioprosthetic heart valves have low thrombogenicity and favorable hemodynamic properties, their durability remains unsatisfactory. Valve failure usually occurs from calcific degeneration. The study aim was to investigate the effect of a chelating agent, citric acid (CA), on calcification in bovine pericardium. METHODS: Freshly excised bovine pericardium was dissected free from adhering fat tissue and cut into 1- cm2 pieces; these were rinsed in phosphate-buffered saline solution (PBS), transferred into +4 degrees C PBS containing 0.625% glutaraldehyde (GA) for initial fixation, and then allocated to two groups. Control samples received the same treatment in a fresh solution for 5 days. The other samples underwent an additional fixation step in PBS (pH = 7.4, 37 degrees C) containing 3.8% CA for a period of 48 h (30 ml/g tissue) and were then transferred into freshly prepared PBS + 0.625% GA solution at 37 degrees C for a further 3 days. To investigate calcification rate, pericardial patches were inserted into the dorsal pouches of 15 juvenile male Wistar rats for 42 days. Tissue calcium levels were measured with atomic absorption spectrophotometer, and also assessed histopathologically. RESULTS: The calcium content of CA-treated pericardium was significantly lower than that of controls (66.4 +/- 33.5 and 111.4 +/- 27.2 mg/g, respectively; p = 0.000). In general, the degree of calcification in histological sections agreed well with results of the chemical analyses. Control pericardial tissues showed moderate to severe solid mineral depositions, predominantly parallel to the implant surface, whereas only minor traces of calcium were found in CA-treated tissues. CONCLUSION: These preliminary data suggest that calcific degeneration in bovine pericardium may be reduced by using CA as a chelating agent.

Animals↗
PubMed2004

[Evaluation of the correlation between calcifications in the aortic valve and in the coronary arteries using MSCT].

INTRODUCTION: Calcium score is the subject of wide research in evaluating atherosclerotic progression. The study aimed to determine whether an association exists between the presence of aortic valve calcium (a-CS) and coronary calcium (ca-CS) in patients with aortic valve stenosis as detected by multislice computed tomography (MSCT). METHOD: We examined 45 patients (27M; 18F); aged 67 (SD 9.5) with the aortic valve stenosis mean grad. 47.8 mmHg; max. grad. 75.3 mmHg; mean aortic valve area 1.02 cm2. The quantitative evaluation of calcifications on the aortic valve (a-CS) and in the coronary arteries (ca-CS) was performed in all patients with the use of MSCT and conventional coronary angiography (CCA). Aortic valve and total coronary artery calcium score were analysed. U-Mann-Whitney test and Pearson's correlation were used in the statistical analysis. The correlation coefficients between a-CS and ca-CS and between the lesions in coronarography and ca-CS were calculated. RESULTS: There was a weak correlation between aortic valve calcifications and coronary artery calcifications p=0.05, r=0.1. In 18 patients no coronary calcifications were found, none of the patients had lesions in CCA. In all patients with ca-CS > 400 there were significant stenoses in coronary arteries. A correlation between significant stenoses in CCA and ca-CS was established (p<0.01). CONCLUSIONS: Aortic valve calcium score (a-CS) may indicate the advancement of coronary artery calcifications in the patients with aortic valve stenosis. In this particular group ca-CS correlates well with stenoses in coronary arteries, as identified by CCA. Patients with the ca-CS > 400 are at high risk of coronary arteries stenoses, which is significant information in operation procedure qualification and time to surgery.

Aged↗
PubMed2003

[Diabetic angiopathy and the progression of vascular calcification].

The frequency of atherosclerotic diseases in diabetes is very high. In the occurrence of atherosclerosis the severity of diabetes is not so important. The mild diabetic condition with obesity will be a strong factor to relate with atherogenesis. As mentioned above the atherogenesis in diabetes is slightly complicated, because multiple risk factors accumulate in diabetes mellitus. These factors are hyperglycemia, hyperlipidemia, hypertension, smoking, and obesity, It has been clarified that the mechanism of arterial calcification will be same as in bone calcification process which is regulated by the various bone metabolic factors. In diabetes mellitus the characteristic vascular changes is that there is multiple calcification in the various arteries including aorta, coronary artery, and peripheral arterioles. It is considered that the necrosis and apoptosis of vascular smooth muscle cells and the transforming of vascular cells to bone cell or cartilage cell are induced and related to arterial calcification. The other factor of calcification would be inflammatory changes related to atheroma formation.

English Abstract↗
PubMed2003

[Assessment of coronary calcification by computed tomography inclusive of 3DCT].

Coronary artheroclerosis in diabetes patients can be divided into 2 phases, one is seen in the early phase of diabetes or insulin resistance syndrome as unstable plaque with lipid-rich core, thinner fibrous caps and small dose or a lack of calcification and the other in the late or advanced stage of diabetes is hard and stable plaque with much fibrous protein and calcification which extends from truncal to peripheral areas. In diabetic patients in the late stage, coronary accidents occur as the chronic multiple vessel diseases with a lot of calcification, while in the early stage of diabetes vasospastic angina and acute coronary syndrome with less calcification tends to occur. We can find out the coronary calcification by EBCT or 3DCT easily which is characteristic in patients of diabetes complicated with coronary artery disease and in the early stage the stenosis of left truncal artery or large vessels of LAD can be detectable by 3DCT.

English Abstract↗
PubMed2002

[Ectopic calcification in dialysis patients].

Vascular calcification is the most important type of the ectopic calcinosis in dialysis patients. Hyperphosphatemia is an independent risk factor for the vascular calcification. A sodium-dependent phosphate co-transporter is associated with an increase in the intracellular phosphate concentration in vascular cells. After degeneration and/or apoptosis of smooth muscle cells in the vascular walls, macrophage infiltration into the calcified tissues followed by production of bone matrix protein leads to the vascular calcification. Uremic conditions such as hyperphosphatemia may enhance the vascular calcification. Therefore, we should treat the vascular calcification in association with bone remodeling in dialysis patients.

English Abstract↗
PubMed2002

[Vascular calcification in end stage renal disease].

Vascular calcification is thought to play a crucial role in the excessive cardiovascular mortality and morbidity in patients with end-stage renal disease (ESRD). Recent evidence suggests that uremic vascular calcification is an active cell-mediated process resembling osteogenesis in bone, rather than passive precipitation of calcium and phosphorus in the setting of deranged mineral metabolism. To date, several bone-associated proteins (osteopontin, bone sialoprotein, alkaline phosphatase, type I collagen) have been demonstrated in histological sections of vessels obtained from patients with ESRD or calcific uremic arteriolopathy. In in vitro experiments, addition of uremic serum upregulates osteopontin expression by cultured vascular smooth muscle cells. We are only beginning to understand the process by which vascular smooth muscle cells transform into osteoblast-like cells, although phosphorus may play a key role. Additional factors mediating or modulating development of vascular calcification in ESRD remain to be identified. Further understanding of the pathophysiology of uremic vascular calcification is needed to design effective therapeutic strategies to intervene with this devastating condition in ESRD population.

Journal Article↗
PubMed2005

Contribution of selected serum inflammatory mediators to the progression of chronic rheumatic valve disease, subsequent valve calcification and NYHA functional class.

BACKGROUND AND AIM OF THE STUDY: The mechanism of the underlying principle of the progression of chronic rheumatic valve disease (RVD) and subsequent valve calcification are yet not clearly understood. The study aim was to determine whether serum markers of inflammation impact on the severity of chronic RVD, subsequent valve calcification and NYHA functional class. METHODS: The study group comprised 92 patients (27 males, 65 females; mean age 40 +/- 14 years) with RVD; the control group included 50 age- and gender-matched subjects without echocardiographic signs of RVD. All patients underwent echocardiographic of rheumatic valve severity, valve calcification and NYHA functional class. Levels of cytokines (interleukin-6 (IL-6), interleukin-2 receptor (IL-2R), interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha)) and serum inflammatory markers (fibrinogen, high-sensitive C-reactive protein (hs-CRP)) were measured in all subjects. RESULTS: Plasma levels of IL-6, IL-8, IL-2R, TNF-alpha and hs-CRP were significantly higher in patients with RVD than in controls (p < 0.001). Significant correlations were identified between mitral score and fibrinogen (p = 0.002), IL-6 (p = 0.007), TNF-alpha (p < 0.001) and hs-CRP levels (p < 0.001). Fibrinogen, hs-CRP, IL-6, TNF-alpha and IL-2R levels correlated with functional class severity, while IL-6 and TNF-a levels correlated strongly with valve calcification (p < 0.001). CONCLUSION: The chronic phase of RVD is associated with ongoing serum inflammatory mediators which correlate strongly with the severity of valve involvement, valve scarring, subsequent valve calcification and decreasing functional status. Future research in this area should focus on whether anti-inflammatory drugs might reduce progression, morbidity and mortality in patients with chronic RVD.

Adult↗
PubMedDate not supplied

The echo-guided treatment of calcific tendinitis of the shoulder.

The authors report the results of percutaneous mini-invasive treatment of chronic calcific tendinitis of the rotator cuffs. A total of 39 patients have been treated by echo-guided injection under local anaesthesia since June 2000 with a follow-up of about 2 years. Considerable reduction in symptoms was obtained in 34 patients within a few days of treatment; improvement was moderate in 5 cases, there were no complications in any of the cases. Complete regression of calcification was observed in 21 patients, there was a more than 60% reduction in calcific deposits in 11 patients, there was little reduction in 5, and the calcification remained unchanged in 2. The method, based on our experience, proved to be simple to execute, low-cost and easily repeatable, offering good results from a symptomatological point of view as well. It is the purpose of this study to determine and maximize mini-invasive treatment that will allow for the elimination or reduction of calcifications by means of percutaneous and echo-guided access.

Calcinosis↗