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At least 55 records · Page 3Linked to original sources

PubMed2006

Lower-extremity arterial calcification as a correlate of coronary artery calcification.

Coronary artery calcification (CAC) has been used as a testing modality for coronary atherosclerosis burden. In diabetes, arterial calcification in the tunica media is common and predicts renal and cardiovascular mortality. It is unknown whether the 2 calcification processes are related. We identified risk factors associated with lower-extremity arterial calcification (LEAC) and determined its relationship to the presence of CAC 6 years later and the incidence of complications in type 1 diabetes mellitus. A random sample of 190 participants from the Pittsburgh Epidemiology of Diabetes Complications Study, a prospective cohort of childhood-onset type 1 diabetes mellitus, received radiographs of their ankles and feet at the 4-year follow-up examination (1990-1992) and was followed up for approximately 6 years. At the 10-year examination, 121 of these individuals received an electron beam tomography scan. Male sex (odds ratio [OR] = 12.72, P < .0001), diabetes duration (OR = 4.53, P < .0001), and autonomic neuropathy (AN; OR = 5.92, P = .007) independently increased the odds of LEAC. Controlling for other known risk factors (duration and high-density lipoprotein cholesterol), we found that LEAC correlated with the presence of CAC 6 years later (OR = 1.12, P = .03), although adjusting for neuropathy attenuated this relationship (P = .08). LEAC also independently predicted AN but not the onset of other diabetes complications. Although arterial calcification in the lower extremities and the heart share many of the same risk factors, LEAC is an independent correlate of the later presence of CAC and AN. Thus, factors related to the calcification process in addition to vascular risk factors may play a role in determining the extent of CAC.

Adult↗

PubMed2002

Coronary calcification detected by electron-beam computed tomography and myocardial infarction. The Rotterdam Coronary Calcification Study.

AIMS: Available data are insufficient to determine the relation between coronary calcification and coronary events in the general population. We cross-sectionally examined the association between coronary calcification and myocardial infarction in the prospective Rotterdam Coronary Calcification Study. METHODS AND RESULTS: From 1997 onwards, subjects were invited for electron-beam computed tomography scanning to detect coronary calcification. The study was embedded in the population-based Rotterdam Study. Calcifications were quantified in a calcium score according to Agatston's method. Calcium scores were available for 2,013 participants with a mean age of 71 years (standard deviation, 5.7 years). A history of myocardial infarction prior to scanning was present in 229 subjects. Compared to subjects in the lowest calcium score category (0-100), the age-adjusted odds ratio for myocardial infarction in subjects in the highest calcium score category (above 2,000) was 7.7 (95% confidence interval, 4.1-14.5) for men, and 6.7 (95% confidence interval, 2.4-19.1) for women. Additional adjustment for cardiovascular risk factors only slightly altered the estimates. The association was observed across all age subgroups, i.e. also in subjects of 70 years and older. CONCLUSION: A strong and graded association was found between coronary calcification and myocardial infarction. The association remained at high ages.

Calcinosis↗

PubMed1991

[The demonstration of calcifications in magnetic resonance tomography (MRT). The effect of different parameters on the MRT imaging of cerebral calcifications].

The effect of various factors on the demonstration of calcified lesions was studied in 131 areas of calcification which had been demonstrated by CT. By means of MRI (SE 400/30 or GE315/14, 90 degrees and SE 1600/30 + 70; 0.5T) 117 of the 131 calcified lesions (89%) produced a signal difference. Of these 117 lesions, 80 (61%) were recognised as calcification by MRI. Large areas of calcification (more than 5 mm) and high density calcification (more than 100 Hu) were recognised significantly more often than small or low density calcifications. T2-weighted images demonstrated calcification more often than other sequences. With conventional pulse sequences, calcified lesions were frequently recognised as abnormalities on MRI, but their recognition as calcified lesions is unreliable.

Brain↗

PubMed2002

Inactivation of the osteopontin gene enhances vascular calcification of matrix Gla protein-deficient mice: evidence for osteopontin as an inducible inhibitor of vascular calcification in vivo.

Osteopontin (OPN) is abundantly expressed in human calcified arteries. To examine the role of OPN in vascular calcification, OPN mutant mice were crossed with matrix Gla protein (MGP) mutant mice. Mice deficient in MGP alone (MGP(-/-) OPN(+/+)) showed calcification of their arteries as early as 2 weeks (wk) after birth (0.33 +/- 0.01 mmol/g dry weight), and the expression of OPN in the calcified arteries was greatly up-regulated compared with MGP wild-types. OPN accumulated adjacent to the mineral and colocalized to surrounding cells in the calcified media. Cells synthesizing OPN lacked smooth muscle (SM) lineage markers, SM alpha-actin and SM22alpha. However, most of them were not macrophages. Importantly, mice deficient in both MGP and OPN had twice as much arterial calcification as MGP(-/-) OPN(+/+) at 2 wk, and over 3 times as much at 4 wk, suggesting an inhibitory effect of OPN in vascular calcification. Moreover, these mice died significantly earlier (4.4 +/- 0.2 wk) than MGP(-/-) OPN(+/+) counterparts (6.6 +/- 1.0 wk). The cause of death in these animals was found to be vascular rupture followed by hemorrhage, most likely due to enhanced calcification. These studies are the first to demonstrate a role for OPN as an inducible inhibitor of ectopic calcification in vivo.

Animals↗

PubMed2002

Calcific trochanteric bursitis: resolution of calcifications and clinical remission with non-invasive treatment. A case report.

Calcific trochanteric bursitis, a common regional pain syndrome, is characterized by chronic, intermittent aching pain over the lateral aspect of the hip and limitation of function. Effective treatment is invasive, including infiltration therapy and surgical intervention. The therapeutic effects of conservative treatment modalities have not been proven. A 59-year-old woman presented at the department of physical medicine and rehabilitation with a 2-year history of pain in the right hip. She had been treated with several agents such as glucocorticoids and local anesthetics (via injection) for two years, but without success. Physical examination revealed the clinical diagnosis of bursitis trochanterica. Radiographic findings showed calcified rounded masses measuring about 1.5 cm in diameter around the greater trochanter; a calcific bursitis trochanterica was diagnosed. The patient presented for conservative treatment in order to avoid surgical intervention for removing the calcification and the bursal sac. A non-invasive treatment regimen including intensive pulsed ultrasound therapy, physiotherapy and iontophoresis was started. The conservative treatment led to a remission of both, symptoms as well as radiographic findings, which revealed complete resolution of calcifications. This case report shows that, in cases of calcific trochanteric bursitis (including those with extensive calcifications), a non-invasive conservative treatment regimen including intensive high-dosed pulsed ultrasound therapy should be attempted before more invasive treatment (injections, surgery) is considered.

Bursitis↗

PubMed1975

[Calcification in gliomas: first report with special reference to roentgenological calcification (author's transl)].

The mechanism and the clinical significance of calcium deposits in glioma have been still obscure. Excluding pinealomas, 221 histologically proven intracranial gliomas were studied. The presence of roentgenological calcification in 27 of the authers' series represented an incidence of 12 percent. The incidence of roentgenological calcification in various types of glioma were as follows: astrocytoma grades 1 & 2-15%, astrocytoma grades 3 & 4-7%, medulloblastoma-5%, ependymoma-17%, oligodendrogioma-60%, and choroid plexus papilloma-25%. There was no characteristic relationship between the incidence of calcification and the age distribution. One exception was noted that in astrocytoma grades 1 & 2 the incidence of roentgenological calcification tended to be higher in younger patients than in older patients. The percentage of calcified tumors in both sexes was the same. In astrocytoma and ependymoma the incidence of roentgenological calcification was far greater in the supratentorial tumor than in the infratentorial tumor. According to their roentgenological appearance, calcified tumors were separated into four groups, but any specific appearance could not be claimed for any particular type of glial tumors. Only in astrocytoma both the duration of symptoms and the postoperative survival time of the calcified cases were longer than those of the uncalcified. But in other types of glioma there were no significant differences in the postoperative survival time between the calcified cases and the uncalcified ones. In 5 cases of astrocytomas the calcium deposits did not exist on preoperative radiographs, which were found postoperatively after chemotherapy and/or radiotherapy. In conclusion, it is not the histological type but the duration of the clinical course that plays more important role in calcification of gliomas.

Adolescent↗

PubMed2003

Association of breast arterial calcifications detected by mammography and coronary artery calcifications quantified by multislice CT in a population of post-menopausal women.

PURPOSE: To assess the correlation between the presence and extent of breast arterial calcifications (BAC) detected at mammography and the extent of coronary atherosclerosis, as evaluated by multislice computed tomography (MSCT) coronary calcium quantification in a population of post-menopausal women. MATERIALS AND METHODS: Seventy-four post-menopausal women aged under 65 years who had undergone mammography at our Department were studied by MSCT for coronary calcium quantification. The mammograms were screened for vascular calcifications which were graded according to severity and extension. The presence of coronary artery calcifications was assessed by MSCT using the < > cardiac reconstruction software. The data obtained were analyzed using the statistical package SPSS (version 10.1) for Windows. RESULTS: The presence and severity of breast arterial calcifications showed a strong correlation with coronary calcifications in both models. DISCUSSION AND CONCLUSIONS: The study demonstrated that the presence of BAC is strongly correlated with the amount of coronary calcium detected by MSCT and therefore with the extent of coronary atherosclerosis. Moreover, there is a linear correlation between BAC severity and coronary calcium content, each incremental increase in BAC severity being associated with an average increase in coronary calcium content. Therefore, the presence and severity of BAC may provide indirect qualitative and quantitative information on the calcium present in the coronaries. As mammography is increasingly used as a screening test for breast carcinoma, breast arterial calcifications may represent an important sign with epidemiological and clinical significance for primary prevention.

Breast↗

PubMed2005

[Breast arterial calcifications and coronary calcifications: a common link with atherosclerotic subclinical disease?].

Coronary artery calcifications seem to be correlated with a high risk of coronary heart disease. Computed tomography has been shown to be capable of providing accurate, non-invasive measurements of coronary artery calcifications. Coronary calcium is a recognized marker of atherosclerosis. Atherosclerotic burden of coronary arteries correlates strongly with the amount of coronary artery calcifications measured by computed tomography. The presence and extent of breast arterial calcifications detected at mammography has been associated with diabetes and hypertension and it seems to be correlated with the extent of coronary atherosclerosis. This review analyzes the relationship between coronary artery calcifications, breast arterial calcifications and the increased risk of subsequent cardiovascular events.

Adult↗

PubMed1978

Effect of hydrochlorothiazide on urine saturation with brushite, in vitro collagen calcification by urine, and urinary inhibitors of collagen calcification.

To clarify further the beneficial effect of thiazide diuretics on recurrent calcium nephrolithiasis, the effect of short-term hydrochlorothiazide therapy on urine saturation with brushite (CaHPO(4).2H(2)O), in vitro collagen calcification by urine, and urinary inhibitors of calcification was studied.In 22 patients with idiopathic calcium oxalate/phosphate stones the urine calcium excretion decreased, the urine magnesium excretion increased and the urine magnesium/calcium ratio increased significantly (P < 0.001) during hydrochlorothiazide therapy. Supersaturation of the urine with brushite, which was present in 19 of the 22 patients, was reduced significantly (P < 0.001) in all during thiazide therapy, and to the undersaturated range in 16. The ability of urine to calcify collagen in vitro also decreased significantly (P < 0.001) during thiazide therapy, a change that correlated significantly (r = 0.4513, P < 0.05) with the decrease in brushite saturation. The concentration of urinary inhibitors of calcification, as determined with an in vitro collagen calcification system, was decreased significantly (P < 0.01) by thiazide therapy.It was concluded that, in addition to decreasing urine calcium excretion and increasing urine magnesium excretion, thiazide diuretics decrease the urinary brushite saturation and thus may prevent spontaneous nucleation or crystal growth, or both, of calcium phosphate. The ability of thiazides to decrease collagen calcification in vitro suggests that they may also prevent crystal growth on a nidus of organic matrix. Thiazides do not appear to act by increasing the excretion of urinary inhibitors of calcification.

Adult↗

PubMed1992

Prevention of tissue calcification on bioprosthetic heart valve by using epoxy compounds: a study of calcification tests in vitro and in vivo.

Calcification is the principal cause of the clinical failures of the bioprosthetic heart valves fabricated from glutaraldehyde pretreated porcine aortic valves or bovine pericardium. In this paper, we compared the calcification on various types of bovine pericardiums pretreated with two hydrophilic epoxy compounds adding GA post-treatment (EP 1 and EP 2), glutaraldehyde (GA)- and nontreated pericardium (Fresh), respectively, by in vitro and in vivo tests. Significant decrease of calcification was found by pretreatment with both epoxy compounds rather than with glutaraldehyde: 0.250 +/- 0.001 (Fresh), 0.276 +/- 0.058 (EP 1), 0.302 +/- 0.071 (EP 2), and 0.478 +/- 0.172 (GA) micrograms (Ca)/mg (dried tissue), respectively, after 20 days dipping in a simulating serum solution in vitro; 115.13 +/- 60.11 (Fresh), 129.84 +/- 51.08 (EP 1), 167.39 +/- 20.81 (EP 2), and 205.19 +/- 16.86 (GA) micrograms/mg, respectively, after 3 months subcutaneous implantation in rabbits. The in vitro method for evaluating calcification designed by us gave the similar order among four samples with that obtained by in vivo test. Because the bovine pericardium pretreated with the epoxy compounds adding GA post-treatment possesses the greater tenacity than that pretreated only with epoxy compounds or GA, meanwhile the calcification is also significantly decreased with this pretreatment, it may be expected that the bovine pericardium with this pretreatment will have the greater anticalcification and durability in dynamic stress.

Animals↗

PubMed2004

Risk factors for coronary calcification in older subjects. The Rotterdam Coronary Calcification Study.

AIMS: We examined associations between cardiovascular risk factors and coronary calcification assessed by electron-beam tomography (EBT) in an unselected population of older subjects. METHODS AND RESULTS: The Rotterdam Coronary Calcification Study is a population-based study in subjects > =55 years. Participants underwent EBT scanning. Coronary calcification was quantified according to the Agatston score. Cardiovascular risk factors were assessed 7 years before and concurrently to scanning. We used the first 2013 participants for the present analyses. Risk factors assessed 7 years before scanning were strongly associated with calcium score. Associations with blood pressure and cholesterol attenuated when measured concurrently to scanning. Although the number of risk factors was strongly associated with a high calcium score in asymptomatic subjects, 29% of the men and 15% of the women without risk factors had a high calcium score. CONCLUSIONS: This population-based study in older subjects shows that cardiovascular risk factors are associated with coronary calcification. Associations were stronger for risk factors measured at earlier age. Almost 30% of the men and 15% of the women without risk factors had extensive coronary calcification.

Age Distribution↗

PubMed1984

Calcific pancreatitis: calcification patterns and pancreatogram correlations.

The abdominal radiographs of 74 patients with calcific pancreatitis were reviewed to assess the distribution, density and patterns of calcification. These characteristics were compared with the results of endoscopic retrograde cholangiopancreatography and ultrasonography. There was a decreasing gradient of calcification from head to tail in most patients. Foci of calcification greater than 5 mm in diameter were almost always associated with pancreatic duct obstruction. Endoscopic retrograde cholangiopancreatography did not provide additional diagnostic information and is unnecessary in calcific pancreatitis except when a precise map is required before operation.

Adolescent↗

PubMed2006

Dexamethasone downregulates calcification-inhibitor molecules and accelerates osteogenic differentiation of vascular pericytes: implications for vascular calcification.

Vascular calcification is present in many pathological conditions and is recognized as a strong predictor of future cardiovascular events. Current evidence suggests that it is a regulated process involving inducing and inhibitory molecules. Glucocorticoids have great clinical importance as antiinflammatory drugs and can act as potent inducers of osteogenic differentiation in vitro. The effect of glucocorticoids on vascular cells in vivo remains obscure. Pericytes are pluripotent cells that can differentiate into osteoblasts, and recent evidence suggests that they could participate in vascular calcification. We hypothesized that the synthetic glucocorticoid dexamethasone would enhance the rate of pericyte differentiation and mineralization in vitro with a concomitant suppression of calcification-inhibitory molecules. Three weeks of dexamethasone treatment induced a 2-fold increase in (1) alkaline phosphatase activity, (2) calcium deposition, and (3) the number of nodules formed in vitro; and a reduction in the expression of matrix Gla protein (MGP), osteopontin (OPN), and vascular calcification-associated factor (VCAF) mRNAs. The glucocorticoid receptor antagonist Org 34116 abolished dexamethasone-accelerated pericyte differentiation, nodule formation, and mineralization. Data obtained using Org 34116, the transcription inhibitor actinomycin D, and the protein synthesis inhibitor cyclohexamide suggest that MGP, OPN, and VCAF mRNA abundance are controlled at different and multiple levels by dexamethasone. This is the first report showing that dexamethasone enhances the osteogenic differentiation of pericytes and downregulates genes associated with inhibition of mineralization. Our study highlights the need for further investigation into the long-term consequences of prolonged glucocorticoid therapy on vascular calcification.

Animals↗

PubMed2006

The role of the irritative zone and of the number and distribution of calcifications in the severity of epilepsy associated with intracranial calcifications.

OBJECTIVE: To determine the influence of the location of the irritative zone, and the number and the distribution of the intracranial calcifications in the severity of epilepsy associated with intracranial calcifications. METHOD: We studied 47 patients with epilepsy and intracranial calcifications, 24 with normal (Group A) and 23 with abnormal interictal EEGs (Group B), a control group (n=21) with abnormal interictal EEGs and normal CT-scans (Group C). Clinical, electroencephalographic and neuroradiological features were compared among groups. RESULTS: Temporal lobe interictal EEG abnormalities were found in 23/24 Group B patients, and in all Group C patients. Most Group B and Group C patients presented temporal lobe seizure symptomatology, whereas in most Group A patients symptomatology was rolandic (p=0.0001). Epilepsy was more severe in Group B and Group C patients than in Group A patients (p=0.0001 and p=0.0054). No relationship was found between the number of calcifications and epilepsy severity. CONCLUSION: An irritative zone at the temporal lobe is more relevant in determining the severity, symptomatology and frequency of seizures than the number and location of calcifications.

Adolescent↗

PubMed2002

Cerebral, myocardial and cutaneous ischemic necrosis associated with calcific emboli from aortic and mitral valve calcification in a patient with end-stage renal disease.

We report the case of a 57-year-old diabetic male with chronic renal failure who developed secondary hyperparathyroidism and calcification of mitral and aortic valves and interatrial septum. Multiple ischemic lesions developed in the skin of hands, feet and penis, and in the brain, and these were presumed to be due to septic emboli from cardiac valvular infective endocarditis. Multiple blood cultures were negative, however, and despite antibiotic therapy the patient expired. Autopsy (limited to trunk) demonstrated multiple calcific emboli in the heart and spleen, apparently derived from the prominent calcific deformities in the aortic and mitral valves. These were associated with acute and organizing myocardial infarcts and acute splenic infarcts, suggesting that the multiple ischemic lesions in the brain were also due to calcific emboli. A possible contributory component of infective endocarditis, however, was indicated by postmortem cultures of aortic and mitral valves positive for Enterococcus faecium. Calcific embolism is a rarely recognized but potentially lethal complication of end-stage renal disease, and the clinical diagnosis and the preventive therapeutic options for the control of the product of calcium and phosphate and/or parathyroidectomy should be considered.

Aortic Valve↗

PubMed2001

Localizational alterations of calcium, phosphorus, and calcification-related organics such as proteoglycans and alkaline phosphatase during bone calcification.

To further approach the mechanisms of bone calcification, embryonic rat calvariae were observed at electron microscopic level by the means of fine structures and various cytochemical localizations, including nonspecific proteoglycan (PG) stained by cuprolinic blue (CB), decorin, chondroitin sulfate, hyaluronan, and alkaline phosphatase (ALP), as well as the elemental mapping of calcium (Ca) and phosphorus (P) by energy-filtering transmission electron microscopy (EFTEM). In the calvariae, calcification advanced as the distance from osteoblasts increased. Closer to the osteoblasts, the osteoid was marked by an abundance of CB-positive PGs around collagen fibrils. After crystallization within matrix vesicles, calcified nodules formed and expanded, creating a coherent calcified matrix. The sizes of CB-positive PG-like structures diminished as calcification proceeded. Although small CB-positive structures were accumulated in early stage-calcified nodules, they were localized along the periphery of larger calcified nodules. Cytochemical tests for decorin, chondroitin sulfate, and hyaluronan determined their presence in the areas around collagen fibrils of the osteoid, as well as in and around calcified nodules, whereas ALP was found in the matrix vesicles, as well as in and around the calcified nodules. Ca tended to localize at the PG sites, while P often mapped to the collagen fibril structures, in the uncalcified matrix. In contrast, Ca/P colocalization was visible in and around the calcified nodules, where ALP and smaller CB-positive structures were observed. The difference in the localization patterns of Ca and P in uncalcified areas may limit the local [Ca2+][PO4(3-)] product, leading to the general inhibition of hydroxyapatite crystallization. The downsizing of CB-positive structures suggested enzymatic fragmentation of PGs. Such structural alterations would contribute to the preservation and transport of calcium. ALP possesses the ability to boost local phosphate anion concentration. Therefore, structurally altered PGs and ALP may cooperate in Ca/P colocalization, thus promoting bone calcification.

Alkaline Phosphatase↗

PubMed1996

Calcific tenosynovitis associated with calcific myonecrosis of the leg: imaging features.

The findings with histologically proven calcific tenosynovitis of the tibialis anterior tendon associated with calcific myonecrosis are described. This case emphasizes the typical appearance of this unusual relationship such as peripheral plaque-like calcifications of the tendon sheath, fluid-calcium levels, presentation as painless mass, and calcification and liquefaction of muscle bundles.

Aged↗

PubMed2004

Calcification of intraocular hydrogel lens: evidence of dystrophic calcification.

PURPOSE: To report and describe the surface calcification of three cases of implanted intraocular hydrogel lens. METHODS: Three surgically extracted hydrogel intraocular lenses were studied by light and transmission electron microscopy as well as by energy dispersion X-ray microanalysis. RESULTS: The lens surfaces were covered by granular deposits of calcium phosphate, clearly delineated by von Kossa and alizarin stains for calcium. Transmission electron microscopy showed the deposits to be located within the superficial lens material to a depth of 7 microm and to be associated with what appear to be traces of cellular material including basement membrane and plasmalemma. To the authors' knowledge there has been only one other transmission electron microscopic study. Energy dispersion X-ray microanalysis showed the deposits to contain calcium and phosphorous in all cases. CONCLUSIONS: This study confirms and extends the previous reports of five cases of calcification of hydrogel intraocular lenses. The exact mechanism of calcification remains obscure but evidence suggesting cell-mediated dystrophic calcification of the lens surface is presented. Further study is required to monitor the incidence and development of this phenomenon.

Aged↗