Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CALCIFICATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,189 records · Page 66Linked to original sources
PubMed2005

Atorvastatin inhibits hypercholesterolemia-induced calcification in the aortic valves via the Lrp5 receptor pathway.

BACKGROUND: Calcific aortic valve disease is the most common indication for surgical valve replacement in the United States. The cellular mechanisms of valve calcification are not well understood. We have previously shown that cellular proliferation and osteoblastogenesis are important in the development of valvular heart disease. Lrp5, a known low-density receptor-related protein, plays an essential role in cellular proliferation and osteoblastogenesis via the beta-catenin signaling pathway. We hypothesize that Lrp5 also plays a role in aortic valve (AV) calcification in experimental hypercholesterolemia. METHODS AND RESULTS: We examined the effects of cholesterol and atorvastatin in Watanabe rabbits (n=54). Group I (n=18) received a normal diet, group II (n=18) a 0.25% cholesterol diet, and group III (n=18) a 0.25% (w/w) cholesterol diet with atorvastatin for the development of calcification. The AVs were examined for cellular proliferation, Lrp5/beta-catenin, and bone matrix markers. Bone formation was assessed by micro-computed tomography, calcein injection, and osteopontin expression. Low-density lipoprotein with and without atorvastatin was also tested in AV myofibroblasts for cellular proliferation and regulation of the Lrp5/beta-catenin pathway. Our results demonstrate that the cholesterol diet induced complex bone formations in the calcified AVs with an increase in the Lrp5 receptors, osteopontin, and p42/44 expression. Atorvastatin reduced bone formation, cellular proliferation, and Lrp5/beta-catenin protein levels in the AVs. In vitro analysis confirmed the Lrp5/beta-catenin expression in myofibroblast cell proliferation. CONCLUSIONS: Hypercholesterolemic AV calcification is attenuated by atorvastatin and is mediated in part by the Lrp5/beta-catenin pathway. This developmental pathway may be important in the signaling pathway of this disease.

Animals↗
PubMed2004

Pulse pressure is an independent predictor for the progression of aortic wall calcification in patients with controlled hyperlipidemia.

Recent epidemiological studies suggested that calcifications of the aorta and the coronary arteries are important predictors for cardiovascular morbidity and mortality. However, the relation between blood pressure components and the progression of vascular wall calcification has remained unclear. We quantified calcium deposits in the abdominal aorta as the percentage of aortic calcification volume (%ACV) using computed tomography in patients with hyperlipidemia. Those who had aortic calcification were treated with lipid-lowering agents and followed-up for >2 years (6.3+/-3.2 years). The relationship between the components of blood pressure and the increase in %ACV per year (Delta%ACV/year) was assessed in subjects in whom serum lipid levels were well controlled during the follow-up periods. An age- and sex-adjusted correlation analysis showed that Delta%ACV/year was significantly correlated to body mass index (r=0.229, P=0.015), systolic blood pressure (r=0.244, P=0.009), and pulse pressure (r=0.359, P<0.001). A multivariate regression analysis revealed that pulse pressure is an independent and the most sensitive predictor for Delta%ACV/year (beta=0.389, P<0.001) among the blood pressure components. These results suggested that increase in pulse pressure promotes the progression of vascular calcification.

Aortic Diseases↗
PubMed2004

Pathophysiology of vascular calcification in chronic kidney disease.

Patients with chronic kidney disease (CKD) on dialysis have 2- to 5-fold more coronary artery calcification than age-matched individuals with angiographically proven coronary artery disease. In addition to increased traditional risk factors, CKD patients also have a number of nontraditional cardiovascular risk factors that may play a prominent role in the pathogenesis of arterial calcification, including duration of dialysis and disorders of mineral metabolism. In histological specimens from the inferior epigastric artery of dialysis patients, we have found expression of the osteoblast differentiation factor core binding factor alpha-1 (Cbfa1) and several bone-associated proteins (osteopontin, bone sialoprotein, alkaline phosphatase, type I collagen) in both the intima and medial layers when calcification was present. In cultured vascular smooth muscle cells, the addition of pooled serum from dialysis patients (versus normal healthy controls) accelerated mineralization and increased expression of Cbfa1, osteopontin, and alkaline phosphatase to a similar magnitude as does beta-glycerophosphate alone. However, a lack of inhibitors of calcification may also be important. Dialysis patients with low levels of serum fetuin-A, a circulating inhibitor of mineralization, have increased coronary artery calcification and fetuin-A can inhibit mineralization of vascular smooth muscle cells in vitro. These data support that elevated levels of phosphorus and/or other potential uremic toxins may play an important role by transforming vascular smooth muscle cells into osteoblast-like cells, which can produce a matrix of bone collagen and noncollagenous proteins. This nidus can then mineralize if the balance of pro-mineralizing factors outweighs inhibitory factors.

Animals↗
PubMed1996

Risk of stroke in a cohort of 815 patients with calcification of the aortic valve with or without stenosis.

BACKGROUND AND PURPOSE: We sought to establish the possible role of calcification of the aortic valve with or without stenosis as a risk factor for stroke. METHODS: Occurrences of stroke, stroke subtypes, and concomitant cardiovascular risk factors were prospectively analyzed in 300 patients with echocardiographic evidence of aortic valve calcification, 515 patients with calcified aortic valve stenosis, and 562 control subjects. RESULTS: Twenty-four patients with aortic valve calcification, 24 patients with calcified aortic valve stenosis, and 27 control subjects had a stroke during follow-up. Using Cox proportional hazards models, we found that strokes were not significantly associated with aortic valve calcification with or without stenosis, but hypertension and any carotid stenosis were associated. On multiple logistic regression analysis, we did not find any association between one of the two valve lesions and indirect possible indications of cardiogenic embolism such as territorial as opposed to small deep brain infarcts or the presence of silent brain infarcts. CONCLUSIONS: Aortic valve calcification with or without stenosis is not a risk factor for stroke.

Age Factors↗
PubMed1999

Intracerebral calcification in systemic sclerosis.

BACKGROUND AND PURPOSE: Advanced cerebrovascular wall calcification was recently observed at autopsy in 2 patients with systemic sclerosis. To further investigate this issue, we conducted a prospective CT study of scleroderma patients to detect intracerebral calcification. METHODS: Thirty-seven consecutive patients with systemic sclerosis underwent unenhanced brain CT. Images were blindly interpreted, together with those of 2 age-matched (+/-1 year) and sex-matched control subjects per patient. RESULTS: Intracerebral calcification was found in 12 patients (32.4%) and 7 controls (9.5%) (P=0.006). Among the patients, intracerebral calcification was associated with the duration of Raynaud's phenomenon (P=0.005) and not with age (P=0.086). CONCLUSIONS: Intracerebral calcification is closely associated with scleroderma, which suggests that scleroderma causes primary cerebrovascular changes.

Adult↗
PubMed2001

Leptin enhances the calcification of vascular cells: artery wall as a target of leptin.

Leptin, the product of the ob gene, regulates food intake, energy expenditure, and other physiological functions of the peripheral tissues. Leptin receptors have been identified in the hypothalamus and in extrahypothalamic tissues. Increased circulating leptin levels have been correlated with cardiovascular disease, obesity, aging, infection with bacterial lipopolysaccharide, and high-fat diets. All these conditions have also been correlated with increased vascular calcification, a hallmark of atherosclerotic and age-related vascular disease. In addition, the differentiation of marrow osteoprogenitor cells is regulated by leptin. Thus, we hypothesized that leptin may regulate the calcification of vascular cells. In this report, we tested the effects of leptin on a previously characterized subpopulation of vascular cells that undergo osteoblastic differentiation and calcification in vitro. When treated with leptin, these calcifying vascular cells had a significant 5- to 10-fold increase in alkaline phosphatase activity, a marker of osteogenic differentiation of osteoblastic cells. Prolonged treatment with leptin enhanced the calcification of these cells, further supporting the pro-osteogenic differentiation effects of leptin. Furthermore, the presence of the leptin receptor on calcifying vascular cells was demonstrated using reverse transcriptase polymerase chain reaction, immunocytochemistry, and Western blot analysis. We also identified the presence of leptin receptor in the mouse artery wall, localized to subpopulations of medial and adventitial cells, and the expression of leptin by artery wall cells and atherosclerotic lesions in mice. Taken together, these results suggest that leptin regulates the osteoblastic differentiation and calcification of vascular cells and that the artery wall may be an important peripheral tissue target of leptin action.

Alkaline Phosphatase↗
PubMed2001

Smooth muscle cell phenotypic transition associated with calcification: upregulation of Cbfa1 and downregulation of smooth muscle lineage markers.

Bovine aortic smooth muscle cell (BASMC) cultures undergo mineralization on addition of the organic phosphate donor, beta-glycerophosphate (betaGP). Mineralization is characterized by apatite deposition on collagen fibrils and the presence of matrix vesicles, as has been described in calcified vascular lesions in vivo as well as in bone and teeth. In the present study, we used this model to investigate the molecular mechanisms driving vascular calcification. We found that BASMCs lost their lineage markers, SM22alpha and smooth muscle alpha-actin, within 10 days of being placed under calcifying conditions. Conversely, the cells gained an osteogenic phenotype as indicated by an increase in expression and DNA-binding activity of the transcription factor, core binding factor alpha1 (Cbfa1). Moreover, genes containing the Cbfa1 binding site, OSE2, including osteopontin, osteocalcin, and alkaline phosphatase were elevated. The relevance of these in vitro findings to vascular calcification in vivo was further studied in matrix GLA protein null (MGP(-/-)) mice whose arteries spontaneously calcify. We found that arterial calcification was associated with a similar loss in smooth muscle markers and a gain of osteopontin and Cbfa1 expression. These data demonstrate a novel association of vascular calcification with smooth muscle cell phenotypic transition, in which several osteogenic proteins including osteopontin, osteocalcin, and the bone determining factor Cbfa1 are gained. The findings suggest a positive role for SMCs in promoting vascular calcification.

Animals↗
PubMed2000

Calcification of poly(2-hydroxyethyl methacrylate) hydrogel sponges implanted in the rabbit cornea: a 3-month study.

Poly(2-hydroxyethyl methacrylate) (PHEMA) hydrogels have been used in the past as ocular implants. In a recent development, PHEMA sponges have shown suitable properties as materials for the peripheral component of an artificial cornea (keratoprosthesis). However, the propensity of PHEMA to calcify could threaten the long-term stability of the implanted devices. In an attempt to improve the understanding of the calcification mechanism, the dynamics, extent, and nature of calcified deposits within PHEMA sponges implanted in the cornea were investigated in this study, and the possible correlation between necrosis of cells and calcification was critically examined. Samples of a PHEMA sponge were implanted in rabbit corneas and explanted at predetermined time points (2, 4, and 12 weeks). The samples were examined by microscopy (light, transmission, scanning) and energy dispersive analysis of X-rays. Histological assessment and semiquantitative analysis of the amount of calcium deposited was performed using image analysis. An in vitro experiment was also performed by incubating sponge samples for 2 weeks in a solution of calcium and phosphate ions at a ratio similar to that in hydroxyapatite, in the absence of cells. Calcification was not seen in the 2- and 4-week explants, however, small deposits were detected in two of the 12-week explants, both within and on the sponge's constituent polymer particles. The deposit volumes represented 0.094% and 0.21%, respectively, of the total sponge volumes. Calcium deposits were present in large amounts both within the constituent polymer particles and on the surface of the sponges incubated in the abiotic calcifying solution. Cooperative mechanisms are suggested for the calcification of PHEMA sponges in vivo. The initial event may occur at a molecular level, when plasma proteins are adsorbed onto the polymer surface and bound through chelation to the calcium ions present in the medium. After their natural degradation, these structures may act as nucleation sites for calcium phosphate crystallization. Concurrently, the calcium ions can diffuse into the hydrogel particles and then the spontaneous precipitation of calcium phosphate may be caused by supersaturation due to the lower content of water in polymer, an effect which is likely predominant in vitro. The second event is the recruitment of phagocytic cells to clear calcium debris. Degeneration of these cells may then form nucleation sites for secondary calcification.

Animals↗
PubMed2006

Matrix GLA protein function in human trabecular meshwork cells: inhibition of BMP2-induced calcification process.

PURPOSE: The matrix GLA (MGP) gene has been found to be among the 10 most highly expressed genes in the human trabecular meshwork (TM), and its expression is affected by conditions associated with glaucoma. Because MGP protein has been shown to play a key role in inhibiting calcification in cartilage and arterial vessels, MGP's function in human TM was investigated. METHODS: Perfused TM tissue and primary human TM (HTM) cells originated from donors of nonglaucomatous eyes. MGP mRNA was assayed by relative quantitative and real-time PCR. AdhMGP recombinant adenovirus was generated by bacterial transposition. Western blot analyses were cross-reacted with MGP N-terminal- and conformational-specific antibodies. MGP/BMP2 colocalization was analyzed by confocal microscopy. gamma-Carboxylation activity was measured by incorporation of 14CO2 into FLEEL synthetic peptide. Alkaline phosphatase (ALP) activity was used as a marker of osteogenic differentiation and a calcification precursor. Calcification was assessed by measuring direct calcium (o-cresolphthalein). Normalization was conducted with a telomerase probe (genomic DNA). RESULTS: HTM cells contained high levels of gamma-carboxylase activity and were able to convert MGP to its active conformation. Overexpression of MGP in HTM cells reduced ALP activity in a model of BMP2-induced osteogenesis. MGP colocalized intracellularly with BMP2. HTM cells aged in culture exhibited increased calcium content, increased ALP, decreased normalized MGP expression and lower gamma-carboxylase activity. CONCLUSIONS: MGP protein is active and functions as an inhibitor of BMP2-induced ALP activity in the HTM cells. The human TM may undergo a calcification process with age. Inhibition of the calcification mechanism mediated by MGP could be used to regulate resistance and elevated IOP.

Adenoviridae↗
PubMed1976

Bone pyrophosphate in uremia and its association with extraosseous calcification.

The mean bone pyrophosphate was 0.360 +/- 0.15 mg/g in 8 controls and 1.22 +/- 1.39 mg/g bone in 27 uremic patients (P less than 0.0025). 13 of the 27 uremic patients had bone pyrophosphate levels greater than 2 SD above control values. The ash content of uremic bones with increased pyrophosphate levels (group II) was 56 +/- 9% as compared to 64 +/- 2% in control bones (P less than 0.01) and 60 +/- 7% in uremic bones having normal pyrophosphate levels (P less than 0.1) (group I). The magnesium content of bones in group II was 338 +/- 47 as compared to 211 +/- 13 (P less than 0.0005) in the controls and 294 +/- 73 mmol/kg ash (P less than 0.05) in group I. In group II, but not group I, there was a significant inverse correlation between duration of dialysis and percent bone ash (r = -0.59) (P less than 0.05). A definite relationship existed between elevated bone pyrophosphate levels and soft tissue calcification. In group II the mean pulmonary calcium content was 530 +/- 459 as compared to 32 +/- 26 mmol/kg/ash in group I (P less than 0.0025). All patients with a bone pyrophosphate level greater than 1.4 mg/g bone had extensive pulmonary calcification. It is concluded that the excess bone pyrophosphate present in some uremic patients is either deposited in the apatite crystal in the transphosphorylated form or else as the magnesium salt since the pyrophosphate is resistant to pyrophosphatase and surface adsorption of pyrophosphate is not altered by the increased bone pyrophosphate levels. The excess bone pyrophosphate could disturb bone calcification mechanisms in uremic patients. The association between increased bone pyrophosphate and soft tissue calcification suggests that the disordered pyrophosphate metabolism may be important in the pathogenesis of extraosseous calcification.

Binding Sites↗
PubMed1980

Vitamin K-dependent calcium binding proteins in aortic valve calcification.

The pathogenesis of valvar calcification, which complicates the course of cardiac valve disease and also affects tissue valve prostheses, is incompletely understood. The present work explores the possible role of the vitamin K-dependent, calcium-binding amino acid, gamma-carboxyglutamic acid (Gla) in valve mineralization. Gla is normally found in the vitamin K-dependent clotting factor proteins, and is also present in unique calcium binding proteins in bone, kidney, and lung. Unique Gla-containing proteins have also been isolated from pathologic calcifications including calcium containing renal stones and calcified atherosclerotic plaque. Calcified valves including specimens with calcific aortic stenosis, calcified porcine xenograft valves, and a calcified aortic homograft valve were analyzed for Gla content, complete amino acid analysis, and tissue calcium and phosphorus levels. Normal porcine valves contained protein-bound Gla (2.0-10.6 Gla/10(4) amino acids): no Gla was present in normal valve leaflets. Furthermore, Gla levels paralleled tissue calcium content in the calcified valves. In addition, complete amino acid analysis indicated a decline in valvar collagen content plus increased acidic proteins in conjunction with valvar calcification and the presence of Gla-containing proteins. These results suggest that calcific valvar disease may result in part from vitamin K-dependent processes.

1-Carboxyglutamic Acid↗
PubMed2003

The serum protein alpha 2-Heremans-Schmid glycoprotein/fetuin-A is a systemically acting inhibitor of ectopic calcification.

Ectopic calcification is a frequent complication of many degenerative diseases. Here we identify the serum protein alpha2-Heremans-Schmid glycoprotein (Ahsg, also known as fetuin-A) as an important inhibitor of ectopic calcification acting on the systemic level. Ahsg-deficient mice are phenotypically normal, but develop severe calcification of various organs on a mineral and vitamin D-rich diet and on a normal diet when the deficiency is combined with a DBA/2 genetic background. This phenotype is not associated with apparent changes in calcium and phosphate homeostasis, but with a decreased inhibitory activity of the Ahsg-deficient extracellular fluid on mineral formation. The same underlying principle may contribute to many calcifying disorders including calciphylaxis, a syndrome of severe systemic calcification in patients with chronic renal failure. Taken together, our data demonstrate a critical role of Ahsg as an inhibitor of unwanted mineralization and provide a novel therapeutic concept to prevent ectopic calcification accompanying various diseases.

Animals↗
PubMed2005

Msx2 promotes cardiovascular calcification by activating paracrine Wnt signals.

In diabetic LDLR-/- mice, an ectopic BMP2-Msx2 gene regulatory program is upregulated in association with vascular calcification. We verified the procalcific actions of aortic Msx2 expression in vivo. CMV-Msx2 transgenic (CMV-Msx2Tg(+)) mice expressed 3-fold higher levels of aortic Msx2 than nontransgenic littermates. On high-fat diets, CMV-Msx2Tg(+) mice exhibited marked cardiovascular calcification involving aortic and coronary tunica media. This corresponded to regions of Msx2 immunoreactivity in adjacent adventitial myofibroblasts, suggesting a potential paracrine osteogenic signal. To better understand Msx2-regulated calcification, we studied actions in 10T1/2 cells. We found that conditioned media from Msx2-transduced 10T1/2 cells (Msx2-CM) is both pro-osteogenic and adipostatic; these features are characteristic of Wnt signaling. Msx2-CM stimulated Wnt-dependent TCF/LEF transcription, and Msx2-transduced cells exhibited increased nuclear beta-catenin localization with concomitant alkaline phosphatase induction. Msx2 upregulated Wnt3a and Wnt7a but downregulated expression of the canonical inhibitor Dkk1. Dkk1 treatment reversed osteogenic and adipostatic actions of Msx2. Teriparatide, a PTH1R agonist that inhibits murine vascular calcification, suppressed vascular BMP2-Msx2-Wnt signaling. Analyses of CMV-Msx2Tg(+) mice confirmed that Msx2 suppresses aortic Dkk1 and upregulates vascular Wnts; moreover, TOPGAL(+) (Wnt reporter); CMV-Msx2Tg(+) mice exhibited augmented aortic LacZ expression. Thus, Msx2-expressing cells elaborated an osteogenic milieu that promotes vascular calcification in part via paracrine Wnt signals.

Alkaline Phosphatase↗
PubMed1988

Idiopathic basal ganglia calcification and organic mood disorder.

Idiopathic basal ganglia calcification is a syndrome consisting of bilateral basal ganglia calcifications, neuropsychiatric abnormalities, disturbances of movement, and normal calcium and phosphorus metabolism. The best described neuropsychiatric alterations are dementia and an organic psychosis. Organic mood disorder has been reported less often, and mania secondary to idiopathic basal ganglia calcification has not been noted previously. The authors describe five patients with idiopathic basal ganglia calcification and organic mood changes, including one patient with secondary mania. Symptoms of idiopathic basal ganglia calcification resemble those of other disorders affecting subcortical structures and support an association between mood, affect, cognition, and the extrapyramidal nuclear system. Treatment may ameliorate the mood disorder.

Adult↗
PubMedDate not supplied

The presence of a calcific plaque in the common carotid artery as a predictor of coronary atherosclerosis.

Many contradictory reports have been published investigating the relationship between coronary artery disease (CAD) and the increased intima-media thickness (IMT) in the common carotid artery (CCA). However, only a limited number of studies evaluate the relationship between CAD and CCA disease as reflected by both the plaque morphology (fibrous and calcific plaques) and IMT. We have studied the associations between CAD and the wall morphology of CCA by B-mode ultrasound (US). One hundred and forty-four subjects, whose angiography was planned on the basis of suspected CAD, were included into the study. The patients were divided into 4 groups on the basis of B-mode US findings; Group I: normal, Group II: increased IMT (IMT >/= 0.8 mm and plaque absent), Group III: fibrous plaque, Group IV: calcific plaque. Coronary artery disease was diagnosed in 63 patients. A statistically significant correlation was found between CAD and CCA wall morphology (r =0.42, CI (95%) = 0.30-0.51, p<0.001). Positive predictive values were 45.0%, 48.4%, and 75.0% in patients with increased IMT, fibrous plaque, and calcific plaque, respectively. None of the women with normal CCA wall morphology had significant coronary artery lesion. With respect to the normal group, the risk for CAD increased by 4.3 fold with the existence of fibrous plaque (p=0.02) and by 9.9 fold with the existence of calcific plaque (p<0.001). It has been shown that the CCA wall morphology determined by B-mode US is correlated with CAD in patients with chest pain, and the presence of calcific plaque is a better predictor for CAD than that of fibrous plaque and increased IMT. Women with chest pain and normal CCA wall morphology may not need coronary angiography.

Carotid Artery Diseases↗
PubMedDate not supplied

Calcific insertional Achilles tendinopathy: reattachment with bone anchors.

BACKGROUND: Recalcitrant calcific insertional Achilles tendinopathy is difficult to treat. HYPOTHESIS: Bursectomy, excision of the distal paratenon, disinsertion of the tendon, removal of the calcific deposit, and reinsertion of the Achilles tendon with bone anchors is safe and effective. STUDY DESIGN: Longitudinal study. METHODS: Twenty-one patients (six women) (21 feet) (average age 46.9 +/- 6.4 years) with recalcitrant calcific insertional Achilles tendinopathy were treated surgically with removal of the calcific deposit; the Achilles tendon was reinserted with bone anchors. RESULTS: At an average follow-up of 48.4 months, one patient necessitated a further operation. Eleven patients reported an excellent result, and five a good result. The remaining five patients could not return to their normal levels of sporting activity and kept fit by alternative means. The results of the VISA-A questionnaire were markedly improved in all patients, from an average of 62.4% to 88.1%. CONCLUSIONS: We recommend disinsertion of the Achilles tendon to excise the calcific deposit fully and reinsertion of the Achilles tendon in the calcaneus with suture anchors. No patient experienced a traumatic disinsertion of the reattached tendon. However, five patients were not able to return to their original level of physical activity.

Achilles Tendon↗
PubMed2002

Epilepsy, occipital calcifications, and oligosymptomatic celiac disease in childhood.

The association of epilepsy, occipital calcifications, and celiac disease has been recognized as a distinct syndrome. The objective of this study was to present the clinical, electrophysiologic, and neuroradiologic features in a series of patients with this syndrome. Thirty-two patients with the constellation of epilepsy, occipital calcifications, and celiac disease were identified in our epilepsy clinic. The mean age was 11 years and the mean length of follow-up was 7.4 years. The 1990 criteria of the European Society of Pediatric Gastroenterology and Nutrition were used to diagnose celiac disease. The Kruskal-Wallis statistics test was employed with a signficance of P < .05. Thirty-one patients had partial seizures, 21 of them with symptoms related to the occipital lobe. In most patients, the epilepsy was controlled or the seizures were sporadic. Three developed severe epilepsy. Occipital calcifications were present in all cases. Computed tomography in 7 patients showed hypodense areas in the white matter around calcifications, which decreased or disappeared after a period of gluten-free diet in 3 patients. A favorable outcome of epilepsy was detected in patients with the earliest dietary therapy. This study presents the largest series of children with this syndrome outside Italy. White-matter hypodensities surrounding calcifications are rarely reported. A prompt diagnosis of celiac disease might improve the evolution of the epilepsy and may improve cognitive status.

Adolescent↗
PubMed2001

Coronary calcification and cardiac events after percutaneous intervention in dialysis patients.

BACKGROUND: Previous studies have described increased vascular calcification in renal dialysis patients. The clinical significance of this finding with respect to outcomes after percutaneous coronary intervention in this population is unknown. METHODS: We analysed a prospective interventional database at a single tertiary center and identified 41 dialysis patients who underwent coronary angioplasty. All studies were reviewed for the presence of coronary calcium in the target and reference vessels and compared with respect to baseline clinical factors and cardiovascular outcomes. RESULTS: The mean ages for those with and without coronary calcification were 63.6 +/- 11.0 and 67.3 +/- 11.0, respectively, P = 0.30. The groups were similar in years on dialysis, diabetes, hypertension, smoking, and measures of calcium and phosphate balance. The total cholesterol, LDL-C, HDL-C, and triglycerides were 162.5 +/- 42.3 and 202.0 +/- 54.5, P = 0.02; 94.9 +/- 39.6 and 121.2 +/- 48.1, P = 0.18; 39.3 +/- 12.4 and 47.3 +/- 12.2, P = 0.15; 157.4 +/- 100.4 and 181.3 +/- 187.4, P = 0.15, for those with and without calcification, respectively. The composite of target vessel revascularization, myocardial infarction, or death was 47.4% and 77.3% for those with and without calcification, respectively, P = 0.06. The Cox proportional hazards model, controlling for years on dialysis, showed a significant, event-free survival in those with coronary calcium seen fluoroscopically, P = 0.05. CONCLUSIONS: In dialysis patients, coronary calcification identified in the target or reference vessels is associated with lower total cholesterol and favourable interventional outcomes.

Adult↗