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PubMed1995

Calcification of breast implant capsules: incidence, diagnosis, and contributing factors.

From January 1990 to August 1994, more than 6000 patients with silicone-gel breast implants were clinically assessed regarding their implant status. Of these, 82 patients requested removal of their implants (150 implants). Of the 150 implants that were removed, 24 (16%) demonstrated calcified capsules. All 12 patients with calcification demonstrated this finding bilaterally. All calcified capsules demonstrated discrete calcified plaques on their inner surface. All 12 patients presented with Baker class IV contractures, with pain as their chief complaint. One patient demonstrated calcification on a routine chest radiograph. One patient demonstrated a stippled appearance on xeromammogram. Capsular calcification was related to the duration of implantation. All 6 implants that had been in place for 23 to 26 years were associated with calcification. These implants were all of the thick-walled Dacron-backed type. All thick-walled Dacron-backed implants that were removed in this study were associated with calcification. Of the 69 implants that had been inserted for 11 to 20 years, 18 (26.1%) were associated with calcification. Fifteen of these 16 implants were ruptured. None of the implants that had been in place for 10 years or less demonstrated calcification.

Breast Implants↗
PubMedDate not supplied

Correlation of radiographic and histologic findings in arterial calcification.

Intimal calcific atherosclerosis may lead to diminished organ perfusion, whereas medial calcification (Mönckeberg type) is of no physiologic significance. Thirty-nine excised arteries were studied by correlating specimen radiographs with transverse histologic sections to determine whether intimal and medial calcification could be reliably distinguished by radiographic criteria. The calcification was correctly localized in 92% of the arteries studied. Intimal calcification was usually irregular and patchy, whereas medial calcification was regular and diffuse. In one case, extensive medial calcification obscured intimal disease. Plain radiographs may be a useful way to follow progression, regression and the effects of therapy on vaso-occlusive disease in certain high-risk patients.

Aorta↗
PubMed2000

Cigarette smoking increases the risk of pancreatic calcification in late-onset but not early-onset idiopathic chronic pancreatitis.

An association exists between cigarette smoking and pancreatitis owing to alcohol. We determined whether cigarette smoking affected the course of pancreatic calcification and insufficiency in idiopathic chronic pancreatitis. Medical records were analyzed of 24 persons with early- and 42 with late-onset idiopathic chronic pancreatitis who were diagnosed between 1976 and 1982 and then followed prospectively until 1985. Smoking equaled >5 pack-years before calcification or insufficiency or last follow-up. Mean follow-up after onset of chronic pancreatitis was 27 and 13 years in early- and late-onset idiopathic chronic pancreatitis, respectively. Incidence of calcification in the two groups was 58 and 43%, respectively. In early-onset idiopathic chronic pancreatitis, smokers and nonsmokers developed calcification at a similar rate and frequency (58%). In late-onset idiopathic chronic pancreatitis, smokers developed pancreatic calcifications faster (p < 0.001) and more frequently (83 vs. 13%, p < 0.001) than nonsmokers. The association between smoking and pancreatic calcification was independent of gender, body mass index, and exocrine or endocrine insufficiency. Smoking did not affect development of exocrine or endocrine insufficiency. Cigarette smoking increases the risk of pancreatic calcification of late- but not of early-onset idiopathic chronic pancreatitis. These data support encouraging cessation of smoking in chronic pancreatitis.

Adult↗
PubMedDate not supplied

Educational attainment and coronary and aortic calcification in postmenopausal women.

OBJECTIVE: Low socioeconomic status is a risk factor for clinical coronary heart disease, a relatively crude outcome associated with important biases. By avoiding these biases, subclinical assessments could facilitate efforts to understand the association between socioeconomic status and coronary disease. The current study 1) evaluated the nature of the associations between educational attainment and subclinical atherosclerosis and 2) examined if biologic, behavioral, and psychosocial factors mediated these associations. METHODS: Participants were 308 women from the Healthy Women Study who underwent a clinic examination of risk factors either 5 (N = 32) or 8 (N = 276) years after the menopausal transition. Aortic and coronary calcification were measured using electron beam tomography. RESULTS: Logistic regression analysis with orthogonal polynomials revealed a marginally significant linear trend for coronary calcification, with the more educated groups showing lower calcification than the less educated groups. A significant linear trend was also observed for aortic calcification. In addition, a marginally significant quadratic trend was observed for aortic calcification so that the effect began to reverse at the highest level of education. Measured risk factors were associated with education and with the calcification outcomes, but they explained little of the associations between educational attainment and coronary or aortic calcification. None of the factors tested met the minimum criterion for mediation. CONCLUSIONS: The findings show that lower education is associated with greater early stage atherosclerosis. Subclinical assessments, such as electron beam tomography, represent useful alternatives for studies of socioeconomic status and coronary artery disease.

Aorta↗
PubMed1997

Calcification of lumbar ligamentum flavum and facet joints capsule.

STUDY DESIGN: The incidence of calcification in ligamentum flavum and posterior capsule demonstrated by computed tomography was reviewed in a series of 147 patients in whom 419 lumbar levels were studied. OBJECTIVES: To find a relationship between mechanical lumbar pathology and the calcification of the ligamentum flavum and posterior capsule. SUMMARY OF BACKGROUND DATA: Calcification of the ligamentum flavum and posterior capsule has been found in diffuse idiopathic skeletal hyperostosis and in metabolic disorders. Although this fact is considered a manifestation of degenerative disease of the spine, it barely has been studied, and many questions remain unresolved. METHODS: Calcifications were classified according to location as follows: 1) ligamentum flavum: upper attachment, lateral or capsular extension, caudal attachment, interlaminar portion or 2) posterior capsule. RESULTS: The following statistical associations were found: 1) degenerative facet joint disease with posterior capsule and lateral or capsular extension calcifications, 2) lumbarized vertebra with lateral or capsular extension and upper attachment calcifications, and 3) isthmic spondylolisthesis with lateral or capsular extension calcification.

Adult↗
PubMed2005

Vitamin K1 intake and coronary calcification.

OBJECTIVES: The activity of matrix Gla-protein (MGP), a potent inhibitor of vascular calcification, is dependent on carboxylation using vitamin K as a co-factor. In animals, low intake of total vitamin K has been shown to accelerate vascular calcification via the MGP mechanism. This has led to the hypothesis that low levels of dietary vitamin K intake may be a risk factor for accelerated vascular calcification in humans due to decreased MGP activity. Additionally, some authors have suggested that current recommended daily intake values for vitamin K might be insufficient to fully inhibit vascular calcification via the MGP mechanism. The aim of this study was to examine the relationship between dietary vitamin K1 (the most prevalent dietary form of vitamin K) intake and premature coronary artery calcification (CAC) in an asymptomatic screening population. METHODS: We conducted a prospective study of 807 consecutive active-duty US Army personnel, 39-45 years of age, without known coronary heart disease. Vitamin K1 intake was measured with the Block Dietary Questionnaire and CAC was identified using electron-beam computed tomography (EBCT). RESULTS: We found no significant correlation between CAC score and vitamin K1 intake (r = 0.132, P = 0.106). Multivariate analysis with adjustment for cardiac risk factors showed no association between dietary vitamin K1 intake and CAC. CONCLUSIONS: Dietary vitamin K1 (phylloquinone) intake appears to be unrelated to premature coronary calcification in a screening population. Further investigation into the relationship of vascular calcification and other forms of vitamin K1 (menaquinones) is indicated.

Adult↗
PubMed2001

Recent advances in multifactorial regulation of vascular calcification.

Calcification presents important clinical implications in cardiovascular diseases, especially in coronary arteries. Epidemiological evidence has shown the coexistence of vascular calcification with both atherosclerosis and osteoporosis, and increasing evidence has shown the role of hyperlipidemia and atherogenic phospholipids in vascular calcification. The etiology of vascular calcification is also increasingly recognized as an active process. Vascular calcification initiates with matrix vesicle formation and mineralization following a process similar to that in bone. In addition, many bone regulatory factors have been shown to be present in calcified atherosclerotic lesions. In this review, we focus on the new developments emerging during the past year in regulation of vascular calcification. Regulatory factors include matrix GLA protein, the phosphate cotransporter Pit-1, a calcium-sensing receptor related factor, osteoprotegerin, leptin, bisphosphonates and oxidized lipids. Some of these, including oxidized lipids, osteoprotegerin, and bisphosphonates, appear to regulate mineralization in both bone and vasculature and may account for the co-existence of osteoporosis and atherosclerotic calcification that is independent of age.

Animals↗
PubMed2002

Novel mechanisms in accelerated vascular calcification in renal disease patients.

PURPOSE OF REVIEW: Vascular calcification occurs more often and earlier in patients with end-stage renal disease than in normal controls. It is a regulated biological process following many of the cellular and molecular programs in osteogenesis. This review summarizes some of the regulatory mechanisms that may explain its severity in renal patients. RECENT FINDINGS: A subpopulation of cells from arteries and cardiac valves produce a mineralizing matrix and undergo osteoblastic differentiation. Osteogenic differentiation regulators are found in calcified but not normal arteries. Phosphate levels have dramatic effects on vascular calcification in vitro, through a sodium phosphate transporter signaling molecular changes. Atherogenic oxidized lipids promote osteoblastic differentiation of vascular cells and inhibit bone mineralization. In uremic patients, the severity of dyslipidemia corresponds with the progression of vascular calcification. Oxidative stress and inflammatory mediators may underlie the effects of oxidized lipids. In dialysis patients, the degree of cardiac valvular calcification corresponds with levels of C-reactive protein. Genetic factors may also contribute. Polymorphisms of the inflammatory adhesion molecule, E-selectin, associate with coronary calcification in young women. Mice deficient in matrix GLA protein, which inhibits bone morphogenetic protein activity, develop complete ossification of the aorta, presumably as a result of unopposed osteogenic activity on vascular mesenchyme. Since matrix GLA protein function requires gamma-carboxylation of its glutamate residues by a vitamin K dependent carboxylase, warfarin treatment may affect vascular calcification by blocking vitamin K and hence matrix GLA protein activity. SUMMARY: These findings indicate that vascular calcification is regulated both positively and negatively by a wide variety of mechanisms affecting patients with renal disease.

Animals↗
PubMed2004

Vascular calcification mechanisms.

Vascular calcification is highly correlated with cardiovascular disease mortality, especially in patients with ESRD or diabetes. In addition to the devastating effects of inappropriate biomineralization seen in cardiac valvulopathies, calciphylaxis, and idiopathic arterial calcification, vascular calcification is now recognized as a marker of atherosclerotic plaque burden as well as a major contributor to loss of arterial compliance and increased pulse pressure seen with age, diabetes, and renal insufficiency. In recent years, several mechanisms to explain vascular calcification have been identified including (1) loss of inhibition, (2) induction of bone formation, (3) circulating nucleational complexes, and (4) cell death. Alterations in calcium (Ca) and phosphorus (P) balance as seen in patients with ESRD promotes vascular calcification via multiple mechanisms and may explain the alarmingly high levels of cardiovascular disease deaths in these patients. Strategies to control Ca and P levels in patients with ESRD have met with early success in preventing progression of vascular calcification. Whether or not vascular calcification can be reversed is not yet known, but exciting new studies suggest that this may be possible in the future.

Calcinosis↗
PubMed2005

Fetuin-A and extraosseous calcification in uremia.

PURPOSE OF REVIEW: It has become increasingly clear that vascular calcification, as part of accelerated uremic atherosclerosis, may powerfully predict mortality in the dialysis population. Secondary hyperparathyroidism and its consequences explain part of this phenomenon; however, serum concentrations of calcium and phosphate ions exceed their solubility product in an aqueous solution and must be prevented from precipitation by additional mechanisms. Fetuin-A is an inflammation-related calcium-regulatory glycoprotein acting as a systemic calcification inhibitor. The emerging role of fetuin-A deficiency as a risk factor in dialysis patients was documented in a cross-sectional study demonstrating a significant correlation with all-cause and cardiovascular mortality. RECENT FINDINGS: In-vitro studies in vascular smooth muscle cells revealed that fetuin-A interacts directly with matrix vesicle release and may thus modulate vascular calcification processes locally and at early stages. Accordingly, prominent fetuin-A staining of calcified vessel segments obtained from uremic patients, in the absence of local expression, emphasizes its potential role as a circulating defense against overwhelming calcification. While increased fetuin-A levels positively correlated with vascular calcification in patients with diabetes and mild to moderate renal impairment, an inverse relationship was observed in dialysis patients. Both chronic inflammation and uremia may thus contribute to exhausting fetuin-A release in the late stages of kidney disease. Specific polymorphisms of the fetuin-A gene may be additional determinants of fetuin-A deficiency. SUMMARY: Deficiencies of calcification inhibitors such as fetuin-A are relevant pathomechanisms in the progression of uncontrolled vascular calcification and may offer potential for future therapeutic approaches.

Blood Proteins↗
PubMed2004

Calciphylaxis and metastatic calcification associated with nephrogenic fibrosing dermopathy.

BACKGROUND: Calciphylaxis and metastatic calcification are known complications of chronic renal failure. Recently, a sclerosing condition of the skin termed nephrogenic fibrosing dermopathy (NFD) has been described in patients with renal disease, many of whom have undergone hemodialysis and/or renal transplantation. To our knowledge, the simultaneous occurrence of both conditions in the same patient, in the same lesion, has not been previously reported. CASE REPORT: We report the clinical, microscopic, and immunohistochemical features of two patients with chronic renal failure whose lesional skin biopsies showed both subcutaneous calcification and NFD. We consider the possible mechanisms that might explain the coexistence of these two disorders. RESULTS: Both patients presented with erythematous, indurated skin over the lower extremities. Purpuric, reticulated patches, necrosis, or ulceration were not observed. Microscopic examination showed the characteristic changes of NFD involving dermis and subcutaneous septa. In addition, biopsies of both individuals showed subcutaneous calcification, one in a diffuse distribution and the other involving the walls of subcutaneous vessels, as seen in calciphylaxis. Calcification was not suspected clinically in either case. CONCLUSIONS: Metastatic calcification or calciphylaxis and NFD can occur simultaneously in patients with chronic renal failure and may be found together in the same lesion. Because subcutaneous calcification may not be suspected clinically in these cases, and in view of the adverse outcomes frequently associated with calciphylaxis, we recommend deep incisional biopsy of patients presenting with the clinical features of NFD. Both the fibrosis and the calcification of chronic renal failure may be related to the activity of transforming growth factor-beta/Smad signaling cascades.

Adult↗
PubMed1994

Effect of degenerative spinal and aortic calcification on bone density measurements in post-menopausal women: links between osteoporosis and cardiovascular disease?

The effect of spinal degenerative changes and aortic calcification on bone mineral density measurements was studied in 115 healthy early post-menopausal women. Lateral lumbar spine radiographs and quantitative computer tomography images were used to determine the presence and severity of aortic calcification and degenerative changes in the lumbar spine. Women with spinal degenerative calcification had higher spine bone density when measured by dual photon absorptiometry compared to those without calcification (P < 0.01), but this was not reflected by the quantitative computer tomography or the proximal femur bone densities, suggesting that spinal calcification artefactually increases spinal bone density when measured by dual photon techniques. Women with aortic calcification had significantly lower quantitative computer tomography and proximal femur bone density compared to those without calcification (both P < 0.05). These women may be at increased risk for both osteoporosis and cardiovascular disease, suggesting a common aetiological factor such as oestrogen deficiency.

Aortic Diseases↗
PubMed1989

Coronary artery calcification identified by CT in patients over forty years of age.

In a study of 100 unselected patients forty years of age or older, routine CT of the thorax demonstrated coronary artery calcification in 41%. Calcification of the left anterior descending was most common, occurring in 34%. For patients 60 years of age and over, clinical evidence of coronary artery disease was 1.7 times more common in those with calcification compared to those without; however, for patients under 60, coronary artery disease was 5.5 times more common in those with calcification than those without. Because of the strong relationship that is known to exist between coronary artery calcification and coronary arteriosclerosis, we believe that the incidental discovery of coronary artery calcification on routine CT of the thorax has significance. All patients under 60 with coronary artery calcification discovered on CT should be investigated for hyperlipidemia if this has not been done, and, if they are not known to have a history of coronary artery disease, they should have a stress test and, if positive, arteriography may be warranted.

Adult↗
PubMed2005

Modeling the implications of changes in vascular calcification in patients on hemodialysis.

BACKGROUND: The Treat-to-Goal Study found that sevelamer slowed the progression of coronary calcification in patients on hemodialysis compared to calcium-based phosphate binders. To understand the implications of this effect for cardiovascular events, risk equations are needed. METHODS: Data on 179 patients on hemodialysis treated at one center in France included biochemical values during the year prior to study entry, patient characteristics, and cardiovascular events over an average of 4 years. As arterial calcification was evaluated ultrasonographically and quantified using a 0 to 4 score, an equation relating this to the electron-beam tomography (EBT)-based calcification score used in the trial was developed and applied to all patients. The estimated scores were then used in survival and Cox proportional hazards analyses of cardiovascular events in relation to the degree of calcification, controlling for other characteristics. RESULTS: Mean age at inclusion was 54 years, dialysis vintage 70 months, average follow-up 49 months; 32% suffered an event. The calcification score, diabetes, C-reactive protein (CRP), diastolic blood pressure, gender, smoking and hypertension are independent predictors of cardiovascular risk. The resulting equation indicates that, relative to a calcification score below 400, the risk of an initial event increases 44% for a score of 600, and more than doubles for a score of 1000. CONCLUSION: In the absence of long-term follow-up studies, these equations permit quantification of the expected long-term clinical consequences of the impact of various phosphate binders on vascular calcification. Together with resource use and cost information, these equations are key inputs for formal cost-effectiveness analyses.

Blood Pressure↗
PubMedDate not supplied

The role of vitamin D in vascular calcification in chronic kidney disease.

Vascular calcification is a significant cause of morbidity and mortality in patients with chronic kidney disease (CKD). Disorders of mineral metabolism are likely involved in the pathogenesis of vascular calcification. Calcitriol and its analogs are effective in suppressing parathyroid hormone levels in patients with secondary hyperparathyroidism and CKD, but experimental studies demonstrate that these drugs can act directly on vascular smooth muscle cells. In some in vitro studies and in animal models of CKD, calcitriol has induced vascular calcification. Newer analogs of vitamin D appear to be less likely to induce vascular calcification, although published data are scarce. However, there is really no clear evidence in dialysis patients that calcitriol or analog administration is directly responsible for the induction of vascular calcification. However, indirectly, by oversuppression of parathyroid hormone (PTH) and induction of a low-turnover bone disease state, or by increased calcium-phosphorus product, the administration of calcitriol or its analogs may contribute to vascular calcification in patients with CKD. However, prospective randomized trials in CKD patients are necessary to fully understand the impact of calcitriol and analog therapy on vascular calcification.

Animals↗
PubMed2000

Transesophageal echocardiographic spectrum of calcific mitral abnormalities in patients with end-stage renal disease.

This report provides a morphological description of atypical and unusual mitral and submitral calcifications in patients with end-stage renal disease. The use of transesophageal echocardiography (TEE) with enhanced image quality and resolution has made possible a detailed evaluation of the distribution and echocardiographic morphology of mitral calcification in end-stage renal disease. To our knowledge, there has been no such prior report with TEE. Our TEE observations reveal that in addition to the common well known posterior mitral annulus calcification, the following varieties of calcification also exist: basal calcification of both mitral leaflets with sparing of free edges, calcification in the intervalvular fibrosa region, and small calcific excrescences at the bases of both mitral leaflets. These abnormalities have previously received little or no attention.

Adult↗
PubMed2006

Role of phosphorus and vitamin D analogs in the pathogenesis of vascular calcification.

Vascular calcification is a mortality risk factor for stage 5 chronic kidney disease patients. We investigated the role of phosphorus and vitamin D analogs in the pathogenesis of vascular calcification using in vivo, ex vivo, and in vitro models. Our results demonstrate that uremic rats receiving a hyperphosphatemia-inducing diet did not exhibit aortic calcification despite elevated levels of serum phosphorus and calcium-phosphorus (CaxP) product. The vitamin D analog 1alpha-hydroxyvitamin-D2 [1alpha(OH)D2] at 0.17 microg/kg raised serum calcium, phosphorus, CaxP product, and aortic calcification in the uremic rats, but 19-nor-1alpha,25(OH)2D2 (19-nor) at the same dose had no significant effect. At 0.67 microg/kg, both 1alpha(OH)D2 and 19-nor had similar effects on serum calcium, phosphorus, and CaxP product, but only 1alpha(OH)D2 induced significant aortic calcification. Only aortic rings from 1alpha(OH)D2-treated uremic rats exhibited a significant increase in 45Ca uptake ex vivo. When aortic rings from normal rats or a primary culture of human coronary artery smooth muscle cells were treated with phosphorus or vitamin D analogs in vitro, high phosphorus induced calcium accumulation and/or 45Ca uptake in a dose- or time-dependent manner, whereas vitamin D analogs including 1alpha(OH)D2 up to 100 nM had no significant effect despite the presence of a functional vitamin D receptor. However, serum from 1alpha(OH)D2-treated uremic rats induced 45Ca uptake into smooth muscle cells cultured in high phosphorus. These results suggest that the regulation of vascular calcification in vivo cannot be easily replicated in the ex vivo or in vitro models, and high phosphorus and some vitamin D analogs such as 1alpha(OH)D2 exert interactive effects on modulating vascular calcification.

Animals↗
PubMed2003

Corneal calcification after amniotic membrane transplantation.

BACKGROUND: /aims: Amniotic membrane transplantation (AMT) has become well established as a treatment for chronic epithelial defects, conjunctival reconstruction, and partial limbal cell deficiency. The aim of this study was to describe cases of corneal calcification following AMT and to search for risk factors that might predispose to this unusual finding. METHODS: Details of 117 AMTs on 93 corneas of 91 patients with a follow up period of at least 1 month performed since 1999 were collected prospectively. In those with calcification clinical photographs were studied and the medical records retrospectively examined. RESULTS: 15 calcifications in 117 AMTs (12.8%) were identified, occurring 3-17 (median 6.1) weeks after AMT, during a follow up period of 4-151 (median 25) weeks. Overall epithelial healing rate was 83%. Calcification covered a surface area between 0.7-40.5 mm(2) maximum size with varied morphology. The primary diagnosis was diverse. Risk factors included the use of phosphate eye drops and pre-existing calcification in the operative or other eye. No patient with a "patch" AMT developed calcification. CONCLUSIONS: Corneal calcification occurs after some cases of AMT. A common risk factor was the postoperative use of phosphate containing eye drops.

Adolescent↗