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PubMedDate not supplied

Renal calcification: a complication of dexamethasone therapy in preterm infants with bronchopulmonary dysplasia.

We have previously reported a case study in which renal calcification formation may have been a complication of dexamethasone exposure in an infant with bronchopulmonary dsyplasia. To determine whether dexamethasone is associated with renal calcification formation, we conducted a prospective, nonrandomized study of 36 infants < 30 weeks' gestation and weighing < 1250 gm treated with dexamethasone because of bronchopulmonary dysplasia and compared them with a group not receiving dexamethasone. We identified seven infants in the dexamethasone group (n = 19) but no infant in the comparison group (n = 17) with renal calcifications at 2 months of age (p = 0.008). The urinary calcium excretion tended to be increased (15.5 +/- 16.6 vs 6.9 +/- 6.7 mg/kg/day ¿p = 0.05¿) and the calcium/creatinine ratio was significantly greater in the dexamethasone group (1.2 +/- 1.0 vs 0.6 +/- 0.4 ¿p = 0.02¿). Infants who received dexamethasone were significantly smaller 819.1 +/- 141.1 vs 954.6 +/- 141 gm ¿p = 0.008¿), were younger (26.2 +/- 1.7 vs 27.7 +/- 1.2 weeks ¿p = 0.004¿), received ventilator support longer (33.3 +/- 14.7 vs 12.1 +/- 14.7 days ¿p = 0.0001¿), and required more days of supplemental oxygen (54.3 +/- 9.7 vs 36.4 +/- 23.8 days ¿p = 0.009¿). We conclude that smaller, younger, and sicker infants are at the highest risk for the development of renal calcifications and that dexamethasone may be associated with increased urinary calcium excretion, which contributes to renal calcification formation.

Bronchopulmonary Dysplasia↗
PubMed1996

Non-invasive visualization of coronary arteries with and without calcification by electron beam computed tomography.

Coronary artery disease (CAD) is one of the leading causes of mortality and morbidity in the western industrialized countries. Recent studies demonstrate the feasability of successful primary and secondary prevention. However, the detection of early stages of coronary artery disease is an unresolved issue. Whereas sensitivity and specificity of traditional risk factor assessment and stress tests are limited, the analysis of coronary calcification allows to obtain a direct sign of coronary atherosclerosis. This concept has been applied using fluoroscopy and conventional computed tomography (CT). However, the exact localization and quantification of coronary calcification only became possible with the advent of electron beam CT (EBCT). This new method showed a high prevalence of coronary calcification in the asymptomatic population. With the definition of a standardized "calcium score" the normal age-specific distribution and amount of coronary calcification was investigated. EBCT proved to be more sensitive in the diagnosis of both non-obstructive and obstructive coronary artery disease than risk factor analysis and stress testing, respectively. Obstructive coronary artery disease, however, cannot yet be predicted with high enough accuracy. A close correlation of EBCT coronary calcification was found to a) the total coronary plaque volume defined by histo-pathology, b) intracoronary ultrasound findings, c) the number of coronary risk factors, d) the coronary prognosis. Using EBCT, a reliable non-invasive identification of persons at risk was obtained for the first time. Guidelines for the use of EBCT in the early diagnosis and treatment of coronary artery disease are being developed.

Adult↗
PubMed1996

[Renal cell carcinoma associated with circumferential "ring-like" calcification].

A 37-year-old man was found to have large calcification in the left kidney in a health check. This calcification has not changed in size during 3 years with computerized tomographic (CT) studies. However, a suspicious lesion for a malignant tumor with the calcification was suggested by a magnetic resonance image (MRI) study. Thus, the patient underwent tumor enucleation and the histology showed the mixed typed renal cell carcinoma. Although it remains controversial, partial nephrectomy or tumor enucleation would be considered in a case of renal cell carcinoma with calcification, which is usually considered to have a favorable prognosis compared to that of a tumor without a calcification.

Adult↗
PubMed1996

Impact of glutaraldehyde on calcification of pericardial bioprosthetic heart valve material.

BACKGROUND: This study was conducted to investigate the impact of the preservation method of bioprosthetic heart valve materials on calcification rates and biocompatibility of the biologic tissue. METHODS: In subcutaneous rat implants, conventionally preserved bioprosthetic heart valve material was compared with bovine pericardium that was treated with L-glutamic acid to reduce residual glutaraldehyde released from the fixed tissue. Both these methods were compared with bovine pericardium that was stabilized by a dye-mediated photooxidation reaction without glutaraldehyde. Biocompatibility of these biomaterials was tested in vitro using human endothelial cell cultures. RESULTS: Conventionally preserved bovine pericardium with a high amount of glutaraldehyde incorporated into the tissue resulted in severe calcification 63 days after subcutaneous implantation in rats (165.4 +/- 20 mg Ca2+/g dry weight). Postfixation treatment with L-glutamic acid, which reduces free, unbound aldehyde groups, showed a significant decrease in calcification (89.6 +/- 14 mg Ca2+/g dry weight). Glutaraldehyde-free preservation by dye-mediated photooxidation showed no calcification after 63 days of subcutaneous implantation (1.0 +/- 0.4 mg Ca2+/g dry weight). Regular endothelial cell proliferation was observed on photooxidized and L-glutamic acid-treated tissue, whereas conventionally treated tissue caused endothelial cell death. CONCLUSIONS: This study underlines the detrimental role of glutaraldehyde in the calcification process of bioprosthetic heart valve materials and emphasizes alternative preservation methods that reduce or avoid the use of glutaraldehyde.

Animals↗
PubMed1996

Proteins and bioprosthetic calcification in the rat model.

BACKGROUND AND AIM OF THE STUDY: The mechanism of valvular bioprostheses calcification is still unknown, but early studies showed increased Gla-protein content in calcified valves. Using an experimental model, which reproduces the clinical process, we therefore analyzed the role of minerals and proteins in bioprosthetic valvular calcification. METHODS: Glutaraldehyde pretreated porcine valves were studied before and after implantation in rats by X-ray, calcium (Ca) and phosphorus (P) measurement, Fourier Transform Infrared (FTIR) spectroscopy, SDS-PAGE and 45Ca ligand blotting of the extracted proteins. RESULTS: Before implantation, there was no X-ray calcification with very little Ca and P content. After implantation, X-ray calcifications appeared on day seven with increased Ca and P up to day 35 (p < 0.05, ANOVA). FTIR revealed structural proteins alone before implantation, plus minor proportions of lipids on day two, which always preceded Ca and P appearance. Ca and P increased up to day 35, first as amorphous and changed in carbapatite over time. SDS-PAGE before implantation revealed two proteins (66-kD and 54-kD) alone, which were sustained up to day 35. The 66-kD had 45Ca affinity. On day two, many other proteins appeared on SDS-PAGE, four of which (52, 45, 14 and below 14-kD) with 45Ca affinity. Protein pattern did not change from day two to 35. CONCLUSIONS: Valvular bioprosthesis calcification is associated with progressive increase in Ca and P content and at least five calcium-binding proteins: one intrinsic valvular protein, pre-existing to implantation, plus four other, extrinsic valvular proteins adsorbed within the tissue after implantation.

Animals↗
PubMed1997

In vivo and in vitro models of calcification in porcine aortic valve cusps.

Both in vivo and in vitro models have been developed to study the initiation and progression of dystrophic calcification of bioprosthetic heart valves. Circulatory in vivo models have proven to be the most predictive of the success of a new valve designs or anticalcification schemes; however, these experiments are time consuming and expensive. An appealing alternative to circulatory implantation is the sub-cutaneous rat implantation model. This model is inexpensive and calcification occurs rapidly. Recent studies have shown, however, that some anticalcification methods work well in the subcutaneous model but are ineffective in the circulatory model. In vitro models would provide the most convenient method for testing new anticalcification strategies but, to date, no in vitro test system has been developed which produces calcification of rates and with morphology comparable with that in vivo models. We have also studied the effects of collagen damage and cell extraction on the calcification of porcine aortic valve cusps both in vitro and in the subcutaneous rat model, and found significant differences in the patterns of mineralization. The objectives of this paper therefore are to compare and contrast the different experimental protocols and procedures reported in the literature to better define the effects of different model systems on the calcification process.

Animals↗
PubMed1997

A new in vitro test method for calcification of bioprosthetic heart valves.

To investigate the calcification behavior of different bioprosthetic heart valves and verify possible hypotheses of the etiology of valve calcification, an accelerated pulse tester for bioprostheses was developed, whereby up to ten valves can be tested under identical test conditions. Each valve was mounted in a separate compartment on a piston and cyclically moved through a calcifying solution at frequencies of up to 800/min at 37 degrees C: An appropriate calcifying solution was evaluated by incubation tests of bovine and porcine tissue. Calcification was confirmed by measuring Ca and phosphate depletion by atomic absorption spectroscopy, von Kossa staining, EDAX, and microradiography. The first tests were successfully carried out on porcine valves that had been nondestructively assessed for tissue/stress anomalies by holographic interferometry prior to the calcification test. The tests showed that 75% of irregular fringe pattern areas corresponded to the calcification areas.

Animals↗
PubMed1997

[Sturge-Weber syndrome with atypical calcifications].

INTRODUCTION: The syndrome, or disease, or Sturge Weber (SSW) is a neuro-ectodermic disorder of unknown incidence, sporadic presentation and specific sex incidence. It is characterized by the presence of a flat, facial angioma which affects at least the first branch of the trigeminal nerve, association with ipsilateral leptomeningeal vascular anomalies, one or more symptoms (epilepsy, hemiparesia, hemiplegia or mental retardation) and ipsilateral vascular lesions of the choroid which lead to glaucoma. As a consequence of lepto-meningeal involvement, homolateral cerebral hemi-atrophy develops together with cortico-subcortical calcifications with a characteristic "railway line" appearance. CLINICAL CASE: We present the case of a six month old girl with a flat port wine angioma on the left half of her face, including three branches of the trigeminal nerve and the left half of her body. She had partial motor crises of the right leg. On the cranial CT there were left periventricular calcifications and calcifications of the choroid plexus. Gadolinium-MR showed signs of left cerebral hemi-atrophy, which was confirmed on the cerebral SPECT (left temporal hypoperfusion). CONCLUSION: This case is interesting on account of the presence of atypical calcifications, both with regard to the sites and age of presentation. We emphasize the need for cranial CT to rule out the presence of calcifications, (as in this case) not seen on Xray of the skull or on MR. We favour the use of cerebral SPECT as a complementary diagnostic technique.

Brain Diseases↗
PubMedDate not supplied

[Hemodynamic significance of fluoroscopic diagnosis of coronary artery calcification].

The onset of coronary arterial calcification is an active, organized, metabolically regulated process that occurs only when the initial changes of atherosclerosis are present. Coronary arterial calcification may represent an attempt to protect the arterial wall mechanically. Determination of hemodynamic significance in detecting coronary heart disease was the aim of the study. 110 patients with suspected angina pectoris were performed fluoroscopy and coronary angiography after-wards. In 77 patients (70%) was determined coronary arteriosclerosis using coronary angiography, and in 33 (30%), finding was normal. Out of 77 (70%) patients with positive funding in 44 patients (57.14%) calcifications were detect using fluoroscopy, while in 33 (42.86%) were not. Out of 33 (30%) patients without arteriosclerosis calcifications were detected in 5 (15.15%) patients, and in 28 (84.85%) were not. According to our results and literature review, the calcification finding confirms the presence of already existing significant stenosis on the coronary artery or a high risk for hemodynamic disorder within the next two to five years.

Calcinosis↗
PubMed1978

Treatment of ectopic calcification in uremia.

Nine uremic patients on maintenance hemodialysis who showed wide arterial and/or stable periarticular calcifications in spite of a well controlled hyperphosphatemia were treated with the diphosphonate disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) in doses of 7.5 to 10 mg/kg of body wt/per day for 5 to 9 months. No clinical or biochemical side-effects were noted. A significant reduction of the extent of periarticular calcifications was observed in five patients: two of them had a complete regression of soft-tissue calcifications, and one patient showed a reduction of arterial calcification. EHDP (7.5 to 10 mg/kg of body wt/per day) induced a significant increase of the osteoid volume and osteoid surface without significant modification of the calcification front. No evident effect on bone resorption and on the mineral content of the radius has been observed.

Adult↗
PubMed1952

The effect of dyes on the calcification of hypertrophic rachitic cartilage in vitro.

The calcification of rat hypertrophic cartilage slices in vitro is markedly inhibited by preliminary exposure to metachromatic and other basic dyes. The dyes are effective at 10(-3) to 10(-4)M in the absence of calcium and phosphate. This inhibition does not occur at the same low dye concentration if calcium and phosphate are present. Neither ion alone is effective in preventing the inhibition. The inhibitory action can be removed by placing slices which have been treated with basic dye in a solution which contains calcium and phosphate ions, plus an acid dye, Orange G. Most acid dyes do not inhibit calcification, except at very high concentrations. Alizarin and quinalizarin are exceptional, and produce marked inhibition at 10(-3)M, an effect which is perhaps attributable to the tendency of these dyes to form lakes with calcium. Rachitic cartilage slices which no longer calcify in inorganic phosphate as a result of treatment with basic dyes show normal calcification in the presence of organic phosphate esters. These results are discussed in terms of the possibility that chondroitin sulfate ester participates in normal calcification.

Animals↗
PubMed1996

Viable cells are a requirement for in vitro cartilage calcification.

It is a common belief that chondrocyte death must precede calcification in the growth plate. To challenge this dogma, cell devitalization was induced in an in vitro model that mimics in situ cartilage calcification. Chick limb-bud mesenchymal cells, plated in micromass culture, differentiate to form a cartilaginous matrix which mineralizes in the presence of inorganic or organic phosphate. The mineral formed resembles physiologic mineral in crystal size, composition, and distribution. Killing cells by water lysis, ethanol fixation, freeze-thawing, trypsinization, or impairing their function by oligomycin treatment prior to the time at which mineralization commenced, prevented mineral deposition. In contrast, devitalizing cells by any of these techniques after mineralization commenced resulted in dystrophic calcification (excessive, randomly distributed mineral of larger than physiologic crystal size). Based on analyses of 45Ca uptake, FT-IR microscopy, X-ray diffraction, and transmission electron microscopy, it is concluded that the presence of viable cells is obligatory for physiologic cartilage calcification in the differentiating chick limb-bud mesenchymal cell culture system.

Animals↗
PubMed1988

A synthetic polypentapeptide of elastin for initiating calcification.

A polypentapeptide (PPP) of tropoelastin having a repeating amino acid sequence of (Val-Pro-Gly-Val-Gly)n was evaluated for its potential to initiate in vivo calcification and to enhance bone formation in nonhealing calvarial wounds (8.0 mm) in 396 adult Walter Reed rats. There were four configurations of the PPP (molecular weight range of 50-100K dalton) consisting of 1-dry PPP; 2-coacervate PPP; 3-gamma irradiated, cross-linked PPP; 4-calcified, gamma irradiated, cross-linked PPP. These four iterations plus a control group of animals constituted the five treatment classes that were evaluated at days 1, 3, 7, 21, 42, and 147. Seventy two rats were used for each treatment and 36 rats for the control. Following euthanatization, specimens were placed into 70% ethanol, embedded in polymethyl methacrylate, sectioned at 3.5 micrometers, and alternating sections were stained with Masson-Goldner trichrome and von Kossa stains. Histomorphometric analysis was accomplished using a Zeiss Universal microscope (250 X) and Videoplan Image Analysis System to evaluate five random histologic fields from margin to margin of the craniotomy. Trabecular bony volume and area of calcification islands were quantitated. A Student's t test for unpaired data to determine treatment differences (within the same temporal groups) revealed that there was no significant difference between treatments and control for trabecular bony volume; however, there was a significant difference between experimentals and control for calcification islands (P less than 0.05) such that calcifications islands for the experimentals were greater than the control. There was not a significant difference between experimental treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2025

Genetic background of neurological disorders with basal ganglia calcification.

BACKGROUND: Bilateral basal ganglia calcifications (BGCs), if severe, are known hallmarks for idiopathic BGC disease (IBGC), but if milder, are often considered radiological findings of unknown significance. In previous studies, only a minority of patients with BGC had monogenic forms of IBGC. METHODS: We studied consecutive patients from a tertiary neurology clinic with bilateral BGCs of variable severity, and their families. We analyzed known IBGC genes, and an extended panel of genes linked to monogenic stroke and metabolic conditions. Clinical, radiological, and genetic data were collected, including vascular risk factors, cerebrovascular events, imaging findings (total calcification score, white matter hyperintensities, ischemic/hemorrhagic lesions), and relevant family history. RESULTS: Twenty-four families with BGCs and neurological symptoms were analyzed. Disease-causing variants were identified in 14 families (58.3%). Eight patients had IBGC (variants in SLC20A2, PDGFB, MYORG), 4 had mitochondrial disease (MT-TL1), and 2 had monogenic vascular conditions (GAL, MAP3K6). Three variants were novel. BGC severity was highest in IBGC cases, while vascular and mitochondrial cases had milder calcifications. White matter hyperintensities were seen in 94.7% of cases and correlated highly with the total calcification score. Clinical vascular events had occurred in 41.7% cases. No monogenic cause was found in 10 patients, although many of these showed clinical or radiological features suggestive of monogenic disease. CONCLUSIONS: Bilateral BGCs can occur in many neurogenetic disorders apart from IBGCs, and a broader genetic search increases the diagnostic yield. Patients with BGCs frequently had clinical cerebrovascular events, which emphasizes the role of cerebrovascular pathology in BGCs.

Humans↗
PubMed2005

Reversible metastatic visceral calcification detected by 99mTc-methylene diphosphonate bone scanning in breast cancer.

Diffuse metastatic visceral calcification is rare in breast cancer. We report on a 57-year-old woman with breast cancer and hypercalcemia who had diffuse metastatic visceral calcifications on lungs, myocardium, stomach, and thyroid on a (99m)Tc-methylene diphosphonate bone scan. Visceral calcifications were completely resolved 6 months after successful anticancer and zoledronic acid treatments. Bone scanning offers a useful diagnostic tool for both identifying visceral calcification and assessing the response to therapy in chemosensitive malignities with hypercalcemia such as breast cancer.

Antineoplastic Agents↗
PubMed2006

In-vitro study of the spontaneous calcification of PHEMA-based hydrogels in simulated body fluid.

In-vitro calcification of poly(2-hydroxyethyl methacrylate) (PHEMA)-based hydrogels in simulated body fluid (SBF) under a steady/batch system without agitation or stirring the solutions has been investigated. It was noted that the formation of calcium phosphate (CaP) deposits primarily proceeded through spontaneous precipitation. The CaP deposits were found both on the surface and inside the hydrogels. It appears that the effect of chemical structure or reducing the relative number of oxygen atoms in the copolymers on the degree of calcification was only important at the early stage of calcification. The morphology of the CaP deposits was observed to be spherical aggregates with a thickness of the CaP layer less than 0.5 microm. Additionally, the CaP deposits were found to be poorly crystalline or to have nano-size crystals, or to exist mostly as an amorphous phase. Characterization of the CaP phases in the deposits revealed that the deposits were comprised mainly of whitlockite [Ca(9)MgH(PO(4))7] type apatite and DCPD (CaHPO4.2H2O) as the precursors of hydroxyapatite [Ca(10)(PO(4))6(OH)2]. The presence of carbonate in the deposits was also detected during the calcification of PHEMA based hydrogels in SBF solution.

Biocompatible Materials↗
PubMed1989

Prostaglandin D2 stimulates calcification of human osteoblastic cells.

Studies on prostaglandin (PG) regulation of bone formation and resorption metabolism have been complicated by the heterogeneity of the tissue, which involves the interaction between and the activities of two bone cell types, osteoblasts and osteoclasts. In a simplified assay system using a cultured human osteoblastic cell line which has the capacity to form calcified tissue, we determined the effects of PGs on calcification. Of the PGs tested, PGD2 has a remarkable stimulatory activity on osteoblast calcification, but that the effective form is probably a metabolite, delta 12-PGJ2. This calcification function is not cAMP-mediated. PGD2 acts directly on osteoblast to cause stimulation of calcification.

Calcification, Physiologic↗
PubMed1992

Regulation of growth plate cartilage degradation in vitro: effects of calcification and a low molecular weight angiogenic factor (ESAF).

Endothelial cell stimulating angiogenic factor (ESAF) is an activator of matrix metalloproteinases, including latent collagenase, and is released by chondrocytes during calcification. ESAF, added to cultured growth plate chondrocytes, elicited a time-dependent, 2.4-fold increase in matrix lysis (compared with 30% for IL-1). Matrix breakdown was suppressed by addition of tissue inhibitor of metalloproteinase (TIMP). Although calcification has been previously reported to stimulate ESAF production, no corresponding increase in cartilage lysis was seen in the present study. However, the level of ESAF that cultures produce during calcification is many times less than that added to the cultures in this series of experiments. We conclude that ESAF can produce dramatic increases in cartilage breakdown (apparently by activation of latent enzymes), but only at levels in excess of those stimulated by calcification. This indicates that ESAF may operate in concert with other initiators, perhaps from the invading endothelial cells.

Angiogenesis Inducing Agents↗