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PubMed2004

Giant intracerebral choroid plexus calcification.

While small calcifications of the choroid plexus are frequent, a large, single intracerebral calcification originating from the choroid plexus is rare. This report presents a 27-year-old woman who was admitted because of right temporal headache which had persisted for months. There was no neurological deficit. Computed tomography demonstrated a mass of calcium density measuring approximately 3 x 3 x 4 cm in the right temporal region, extending to the temporal skull base and to the rostral edge of the petrous bone. At surgery a very hard, poorly vascularised tumour originating from the choroid plexus of the temporal horn of the right lateral ventricle was completely removed. Histological workup yielded the diagnosis of a markedly calcified choroid plexus with no indication of neoplasia or inflammation. Physiological intracranial calcifications resulting from local tissue dystrophy are usually incidental. In the case presented here, a large intracerebral choroid plexus calcification was detected in a patient presenting with episodes of severe headache. The potential pathogenetic mechanism is discussed.

Adult↗
PubMed2006

Genetic and enzymatic analysis for two Japanese patients with idiopathic infantile arterial calcification.

Idiopathic infantile arterial calcification (IIAC) is a life-threatening disorder in young infants. Cardiovascular symptoms are usually apparent within the first month of life. The symptoms are caused by calcification of large and medium-sized arteries, including the aorta, coronary arteries, and renal arteries. Most of the patients die by 6 months of age because of heart failure. Recently, homozygous or compound heterozygous mutations for the ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) gene were reported as causative for the disorder. ENPP1 regulates extracellular inorganic pyrophosphate (PPi), a major inhibiter of extracellular matrix calcification. Two Japanese patients with IIAC were studied. One, from first-cousin parents, showed a typical clinical course. The onset in the second patient was late. Both of the patients were clinically compatible for IIAC; arterial calcification was shown, and hypertension was prominent. We sequenced all the exons and exon-intron boundaries of the gene and measured nucleotide pyrophosphohydrolase (NPPH) activity of ENPP1. Homozygous Arg730Stop was detected in the typical IIAC patient. The mutation was a novel nonsense mutation and not detected in 60 healthy controls. His NPPH activity was 4% of normal. On the other hand, the late-onset patient was not shown to have any mutations. NPPH activity in this patient was 70% of normal. We confirmed that ENPP1 was also responsible for the Japanese patient with IIAC. The atypical late-onset phenotype may not be associated with ENPP1 abnormalities. IIAC is considered to be a clinically and genetically heterogeneous disorder.

Arteries↗
PubMed2006

Myofibroblasts in the stroma of metastatic pulmonary calcification in a patient with chronic renal failure.

We present a case of metastatic pulmonary calcification. Histologically, deposition of hematoxyphilic materials was seen along the alveolar and vessel walls. Fibrous tissues were also seen within the alveolar lumens, resulting in intra-alveolar fibrous pneumonia. Immunohistochemically, CD34-positive perivascular adventitial fibroblasts were seen in normal alveolar septa, whereas no myofibroblasts were observed. In contrast, perivascular adventitial fibroblasts were absent in the alveolar septa of the lesion of metastatic calcification, whereas many myofibroblasts were present in the fibrous tissue within alveolar lumens. No positive cells for TGF-(beta1) were observed in the lesion of metastatic calcification, but positive cells for PDGF-BB were focally seen in adveolar epithelial cells. Finally, many myofibroblasts appear in the alveolar lumens of metastatic pulmonary calcification, and we suggest that these myofibroblasts may be derived from CD34-positive perivascular adventitial fibroblasts and PDGF-BB may be involved in the pathogenesis of surrounding fibrosis.

Becaplermin↗
PubMed2006

Soft tissue calcifications in the lower extremities of severely diabetic patients simulating venous stasis or collagen vascular disease.

The purpose of this work is to report soft tissue calcifications in severely diabetic patients that simulate venous stasis or scleroderma, without other stigmata of these diseases. Findings from lower extremity radiographs were reviewed on two patients with severe diabetes mellitus and abnormal soft tissue calcifications. Findings were correlated with clinical history, physical exam findings, and laboratory values. Both patients in this study demonstrate radiographic findings of lower extremity soft tissue calcifications similar to those seen in venous stasis or scleroderma. Clinical history, physical examination, and laboratory values support severe diabetes mellitus, with no evidence of these other disease entities. Patients with severe diabetes mellitus may exhibit soft tissue calcifications of their lower extremities that may simulate the changes of venous stasis or scleroderma. This association has not been previously described.

Adult↗
PubMed2004

Impact of high coronary artery calcification score (CACS) on survival in patients on chronic hemodialysis.

BACKGROUND: Electron-beam computed tomography (EBCT) is a noninvasive measure of coronary artery calcification and, therefore, could be a marker of developing cardiovascular disease. Whether the coronary artery calcification score (CACS) is a prognostic marker in chronic dialysis patients is not known. METHODS: In the present study, the mortality rate was observed in relation to the baseline CACS. EBCT was performed in 104 chronic hemodialysis patients (62 men and 42 women) in one dialysis unit. The mean (SD) duration of hemodialysis was 48.7 (62.6) months at the time of EBCT. The mean (SD) age at EBCT was 55.9 (13.6) years, ranging from 23 to 88 years. The duration of follow-up was 43.8 (19.3) months after the EBCT. Cox proportional hazard analysis was performed to examine the impact of CACS on survival after adjusting for age, sex, duration of dialysis, diabetes mellitus, hypertension, serum albumin, and dyslipidemia. RESULTS: The CACS was distributed from zero to 5896, with a median of 200. During the study period, 24 patients (15 men and 9 women) died, 7 in the low CACS group (<200) and 17 in the high CACS group (> or =200). The 5-year cumulative survival rate was 84.2% in the low CACS group and 67.9% in the high CACS group. The adjusted relative risk (95% confidence interval) of death was 1.001 (1.000-1.002); P = 0.0003, for the absolute value of CACS. CONCLUSIONS: The present study suggested that CACS was an independent predictor of death in patients on chronic hemodialysis. Patients with a high CACS should be carefully monitored and evaluated for reversible prognostic factors such as dyslipidemia and, probably, hyperphosphatemia and a high value for the calcium x phosphate product.Electron-beam computed tomography (EBCT) is a noninvasive measure of coronary artery calcification and, therefore, could be a marker of developing cardiovascular disease. Whether the coronary artery calcification score (CACS) is a prognostic marker in chronic dialysis patients is not known.

Adult↗
PubMed2006

Osteoprotegerin is not associated with angiographic coronary calcification.

UNLABELLED: Coronary artery calcification may play a significant role in the pathophysiology of plaque progression and healing. We hypothesized that osteoprotegerin, an inhibitor of osteoclastogenesis, may participate in the calcification of coronary plaques or the response to injury after coronary stenting. A prospective registry was performed in 2004. Blood samples from 100 patients undergoing percutaneous coronary intervention (PCI) were obtained before PCI and 24 h after PCI. The concentrations of osteoprotegerin (OPG), C-reactive protein, interleukin-6, and soluble CD40 ligand (sCD40L) were determined by ELISA. Quantitative coronary angiography was performed to define the presence of culprit lesion calcification (CLC). Comparisons among markers of inflammation and tertiles of OPG were stratified with respect to CLC. Patients with CLC (n = 28) compared with no CLC (n = 71) were older (P < 0.01), had lower creatinine clearance (P < 0.01), lower hemoglobin (P = 0.02), and were less likely to smoke (P = 0.04). Patients without CLC were over twice as likely to present with a marker-positive acute coronary syndrome. CLC was associated with less pre-PCI platelet-mediated inflammation as measured by sCD40L (4.65 vs. 7.15 pg/ml, P = 0.05), but not with lower levels of OPG. Inflammatory cytokines increased significantly after PCI for patients with and without CLC. For patients in the highest tertile of OPG at baseline, there was a reduction in OPG after PCI. Systemic osteoprotegerin levels are not associated with angiographic calcification of culprit plaques. For patients with elevated levels of OPG prior to PCI, there is a significant reduction after PCI consistent with a counterregulatory role for OPG. CONDENSED ABSTRACT: Both calcified and non-calcified culprit plaques exhibited a similar inflammatory response to stent-mediated injury. After PCI, osteoprotegerin decreased while proinflammatory cytokines increased, which may be consistent with a counterregulatory role for osteoprotegerin.

Aged↗
PubMed2004

Mediastinal cyst with rim calcification.

A 58-year-old man who had been undergoing treatment for chronic pericarditis for 15 months was found to have a calcified mediastinal mass shadow on a chest X-ray and was referred to us for further study and treatment. Chest computed tomography and magnetic resonance imaging showed an anterior mediastinal multilocular tumor with rim calcification. Tumor markers were within normal limits. The patient was preoperatively diagnosed as having a calcified mediastinal cyst, and median sternotomy was performed to remove the cystic tumor and the surrounding thymic tissues. Histological examination revealed that the cyst wall consisted of dense fibrous tissue and calcification without epithelial cell lining on the inner surface. Thymic tissue was present around the cyst wall. Although we suspected a thymic cyst from the intraoperative findings, the final diagnosis was made as mediastinal cyst with rim calcification. We herein present a rare case of mediastinal cyst with rim calcification.

Calcinosis↗
PubMed2003

Arterial calcification in diabetes.

Diabetes is associated with an increased prevalence of atherosclerotic vascular disease and cardiovascular mortality. In diabetic patients, medial calcification appears to be a strong independent predictor of cardiovascular mortality, it occurs particularly in those with neuropathy. Recent evidence suggests that medial calcification in diabetes is an active, cell-mediated process, similar to that observed in patients with end-stage renal disease (ESRD), in which vascular smooth muscle cells (VSMCs) express a number of bone matrix proteins that act to either facilitate or regulate the calcification process. Several bone-associated proteins (e.g., osteopontin, bone sialoprotein, alkaline phosphatase, type 1 collagen, osteocalcin) have been demonstrated in histologic sections of vessels obtained from patients with diabetes or ESRD. In in vitro experiments, high glucose induced cell proliferation and expression of osteopontin in cultured VSMCs. Hypoxia had additive effects of hyperglycemia on VSMCs. In addition, uremic serum upregulates osteoblast transcription factor Cbfa 1 and osteopontin expression in cultured VSMCs. The pathogenesis of vascular calcification in diabetes is not completely understood, although high glucose and other potential factors may play an important role by transforming VSMCs into osteoblast-like cells. Further understanding of the mechanism by which diabetes induces this complication is needed to design effective therapeutic strategies to intervene with this process.

Arteries↗
PubMed1979

Sensitivity and specificity of echocardiography in the assessment of valve calcification in mitral stenosis.

Eighty-seven patients (64 females and 23 males) with mitral stenosis were studied by M-mode echocardiography to assess the sensitivity and the specificity of the echocardiographic technique in the identification of valve calcification. The mitral valves were examined at operation, and the amounts of calcium were graded as heavy, light, or absent. We compared this with the amount of calcification assessed by radiographic, previously accepted echocardiographic, and newly derived echocardiographic criteria. In identifying the presence or absence of valve calcification, radiography was the least sensitive (53.7 per cent), but the most specific (90.9 per cent) technique, and has the highest predictive accuracy (90.6 per cent). Previously accepted echocardiographic criteria had the highest sensitivity (92.6 per cent), but the lowest specificity (12.1 per cent), and the lowest predictive accuracy (63.3 per cent). The newly derived echocardiographic parameter MT/ST (ratio between the maximal thickness of the left ventricular margin of the interventricular septum) was both sensitive (75.9 per cent) and specific (81.8 per cent) and also had a predictive accuracy (87.2 per cent) similar to that of radiographic techniques. The MT/ST ratio is demonstrated to be the most useful non-invasive method for assessing valve calcification in mitral stenosis.

Adolescent↗
PubMed1984

Calcification of the tricuspid anulus diagnosed by two-dimensional echocardiography.

An 84-year-old female who previously underwent repair of an atrial septal defect had evidence of increased reflectiveness of the posterior tricuspid anulus in the apical four-chamber view and the right ventricular two-chamber view. In addition, the inferior vena cava was dilated and during contrast echocardiography, contrast echoes appeared during systole suggesting tricuspid regurgitation. Tricuspid annular calcification was confirmed by fluoroscopic examination. Tricuspid annular calcification is extremely rare and in the present series occurred in 1 of 80 patients with mitral annular calcification. Lateral resolution echoes from a calcified aortic valve and echoes originating from a calcified right coronary artery have to be distinguished from tricuspid annular calcification.

Aged↗
PubMed1976

Echocardiographic and clinical spectrum of mitral anular calcification.

To establish the reliability of echocardiography in making the diagnosis of mitral anular calcification 10 consecutive patients with dense echoes at the mitral anular area were examined fluoroscopically, using an image intensifier. Nine of these had distinct mitral anular calcification. The echocardiographic reliability thus confirmed, 30 cases with similar findings were reviewed and the total group of 40 cases were used to define the echocardiographic spectrum of mitral anular calcification. This lesion extended variably from the anulus to involve the posterior left ventricular wall, mitral valve leaflets, aortic root, aortic valve and interventricular septum. The pleomorphic echocardiographic findings introduce difficulties in the diagnosis of pericardial effusion and mitral stenosis. Echocardiography is a reliable method of diagnosing mitral anular calcification, but care must be taken to avoid confusing this condition with others it resembles.

Aged↗
PubMed1979

Coronary calcification in the diagnosis of coronary artery disease.

Clinical, postmortem and angiographic studies of coronary calcification are reviewed to define the value of fluoroscopy in the diagnosis and management of coronary artery disease. Autopsy studies consistently show a unique association between calcification of the coronary arteries and atherosclerosis. The relation of coronary calcification to the presence of major stenosis is more variable but is strong enough to be of clinical value, particularly in the younger subject. The diagnostic value of fluoroscopy can be improved by attention to the detailed features of calcification observed with the technique. Combined use of fluoroscopy and exercise testing appears to be a valid and as yet unexploited approach to the noninvasive diagnosis of coronary stenosis. Fluoroscopy has been a neglected method of noninvasive diagnosis and is sufficiently promising to warrant greater clinical use.

Calcinosis↗
PubMed1995

Prevention of calcification of heart valve bioprostheses: an experimental study in rat.

To eliminate highly antigenic substances, bovine pericardium was washed in 5% sodium chloride (NaCl) for 24 hours, followed by incubation in trypsin for 40 minutes. To achieve adequate fixation, NaCl-trypsin-treated pericardium was preserved in glutaraldehyde (GA) solution with gradually increasing concentrations from 0.1% to 0.25%. To inactivate the free aldehyde groups and residual GA on the surface of the implant, NaCl-trypsin-GA-treated pericardial samples were posttreated separately with 1% lysine, 8% monosodium glutamate, and 4% chitosan. Fresh (untreated) and 0.1%, 0.2%, and 0.625% GA-treated and NaCl-trypsin-GA-treated pericardial specimens were prepared for comparative study. All samples were implanted subdermally in rats for 2, 4, 8, and 12 weeks for calcification studies. Morphologic and chemical analyses showed mild calcification in fresh pericardia (Ca, 10.5 +/- 1.25 micrograms/mg, von Kossa +) and in glutamate-posttreated pericardia (Ca, 11.5 +/- 3.45 micrograms/mg, von Kossa +). Calcium was practically undetectable in chitosan-posttreated implants (Ca, 1.1 +/- 0.27 micrograms/mg, von Kossa 0), whereas severe calcification was noticed in the rest of the samples (mean Ca greater than 200.0 micrograms/mg, von Kossa ) at 12 weeks. This study suggests that posttreatment with an amino compound such as chitosan would prevent the calcification of GA-treated bioprostheses at an early implantation stage, but elimination of antigenic factors and adequate GA fixation would prevent tissue degeneration, thus enabling the prosthesis to function over a long period.

Animals↗
PubMed1996

Calcification of bovine pericardium: glutaraldehyde versus No-React biomodification.

BACKGROUND: Calcific degeneration is the most frequent cause of clinical dysfunction of glutaraldehyde (GA)-pretreated bioprosthetic heart valves. The No-React (NR) process has been shown to be a promising anticalcification treatment. In this comparative study, our objective was to delineate the advantages of the NR treatment over GA. METHODS: Bovine pericardial strips pretreated with GA and NR were individually incubated in calcium phosphate solution for 21 days at 37 degrees C. The pretreated bovine pericardium then was implanted subcutaneously in rats and retrieved at 14, 21, and 35 days after-implantation. Mineral and morphologic analyses were performed on each specimen. RESULTS: The NR-treated pericardium revealed significantly reduced in vitro calcification compared with the GA-treated tissue (mean tissue calcium content 1.3 +/- 0.2 versus 5.9 +/- 0.7 micrograms/mg; p < 0.001). Mineral analysis showed progressive calcification of the GA-pretreated pericardium over the period of implantation (calcium content increasing from 49.6 +/- 9.6 micrograms/mg after 2 weeks to 134.3 +/- 9.1 micrograms/mg at 5 weeks after-implantation). The NR-treated implants had calcified significantly less (p < 0.05) at each corresponding interval. Moreover, morphologic examinations demonstrated a protracted inflammatory response in the form of giant cell and mononuclear cell infiltration associated with intrinsic collagen disruption in the GA-treated tissue; the NR-treated pericardium maintained morphologic integrity with a mild inflammatory response. CONCLUSIONS: The NR biochemical process appears not only to attenuate pericardial calcification, but also to abort the host's destructive inflammatory response to the xenograft.

Animals↗
PubMed1989

Covalent binding of aminopropanehydroxydiphosphonate to glutaraldehyde residues in pericardial bioprosthetic tissue: stability and calcification inhibition studies.

Calcification has limited the clinical utility of bioprosthetic heart valves fabricated from either glutaraldehyde-pretreated bovine pericardium or porcine aortic valves. Aminopropanehydroxydiphosphonate (APDP), covalently bound to residual aldehyde groups in glutaraldehyde-treated pericardial bioprosthetic tissue, has been shown to inhibit cardiovascular calcification in the rat subdermal model. Using 3H-labeled glutaraldehyde (GLUT) at a concentration of 0.02 M and 0.14 M 14C-labeled APDP, we assessed the effects of GLUT incubation temperature (4 degrees or 25 degrees C) and pH of the GLUT incubation solution (pH 4.0, 7.4, or 10.0) on the GLUT incorporation step and subsequent APDP binding (24 hr 25 degrees C) into bioprosthetic valve (BPV) tissue (bovine pericardium). Increased incorporation of GLUT and APDP occurred at lower GLUT incubation temperature (GLUT, 346.05 +/- 1.9 nM/mg, 4 degrees C vs 259.76 +/- 1.39 nM/mg, 25 degrees C; APDP, 57.56 +/- 4.43 nM/mg, 4 degrees C vs 36.36 +/- 0.46 nM/mg, mean +/- standard error, at 25 degrees C). There also was a greater incorporation of GLUT but not APDP at the higher glutaraldehyde pretreatment pH (GLUT, pH 10.0, 213.73 +/- 73 nM/mg vs pH 4, 132.08 +/- 43 nM/mg; APDP, pH 10.0, 51.41 +/- 12 nM/mg vs pH 4.0, 49.97 +/- 6 nM/mg). In vivo studies revealed that all groups with treated BPV implanted for 21 days in male 3-week-old CD rats demonstrated a loss of both GLUT (12-50%) and APDP (48-64%) compared to preimplant content. BPV implant calcification was significantly inhibited in all groups treated with APDP compared to control Ca2+ (5.54 +/- 2.1-9.64 + 1.2 micrograms/mg, APDP pretreated, vs 93.64 +/- 11.65 micrograms/mg, control; P less than or equal to 0.001) despite the progressive loss of both GLUT and APDP with time. It is concluded that preincubation of BPV tissue in GLUT at lower temperature (4 degrees C) and higher pH (10.0) enhanced BPV GLUT uptake and subsequent APDP covalent binding. In addition, in the rat subdermal model, BPV tissue calcification was markedly inhibited by APDP, despite a significant loss of bound drug.

Aldehydes↗
PubMed1986

Human and experimental lens repair and calcification.

Lens repair and calcification have been studied in an experimental rabbit model of anterior segment necrosis. Findings were compared with those in a human senile cataractous lens with subcapsular calcification. Rabbit lenses subjected to anterior segment ischemia underwent a repair process similar to that observed in perforating lens injuries. Cellular response included the formation of fibroblast-like cells that covered epithelial defects of the anterior pole. These observations suggest that the lens epithelium can transform into fibroblast-like cells. The calcification process was a non-cell-induced, and the observed mineral was probably nucleating on organic molecules. Elemental analysis demonstrated that crystals contained calcium and phosphorus with a ratio of 2:1. The mineral was probably hydroxyapatite. Since morphological findings in rabbit lenses closely resemble those of the studied cataractous human lens, the rabbit model appears to simulate one type of lens calcification in senile cataract.

Aged↗
PubMed1985

Diffuse hepatic calcification as a sequela to shock liver.

A 31-yr-old Japanese woman who was on chronic hemodialysis for 3 yr died of intractable congestive heart failure. Three years before death, the patient was in a state of shock for 48 h due to ventricular tachycardia and gastrointestinal bleeding, which was followed by marked elevation of serum transaminase. Four months later, abdominal plain radiography demonstrated diffuse hepatic calcification. At autopsy, microscopic examination of the liver revealed parenchymal necrosis and tiny calcifications in the central to midzonal area of the lobule. Calcification in the degenerative area of the hepatic lobule occurred subsequent to parenchymal ischemia after overt shock that lasted for 2 days. Although a definitive explanation for the calcification was not obtained, it may be related to the disturbances of intracellular Ca2+ homeostasis as a result of ischemic liver injury or it may be related to an elevated calcium-phosphorus product in the uremic state.

Adult↗
PubMed1994

Myocardial calcification: a predictor of poor outcome for myocarditis treated with extracorporeal life support.

Myocarditis is an inflammatory disease of the myocardium with a variety of causes. It is potentially reversible, and has been treated successfully with extracorporeal life support (ECLS). With increasing severity, myocarditis results in significant damage to myocardial cells. Dystrophic calcification of the myocardium may occur, serving as a marker of severe damage. At the authors' institution, from July 1990 to January 1992, five patients (four neonates, one 5 year old) with severe myocarditis refractory to medical management were treated with venoarterial ECLS. Three survived (60%) and two died. All patients were female, and their age range was 2 weeks to 5 years. Nonsurvivors had significant myocardial calcification, which was detected by a chest roentgenogram as well as a two-dimensional echocardiogram; the three survivors had no evidence of calcification. The nonsurvivors had minimal recovery of myocardial function and subsequently had their ECLS discontinued at 83 and 169 hours, respectively. The authors conclude that the development of progressive myocardial calcification in conjunction with a lack of recovery of cardiac function is a sign of severe myocardial damage and poor prognosis. Continuation of ECLS in this setting may not be warranted.

Calcinosis↗