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At least 811 records · Page 45Linked to original sources
PubMed2002

Calcification of homograft valves in the pulmonary circulation -- is it device or donation related?

OBJECTIVE: Homograft valved conduits are used in the reconstruction of right ventricular outflow tract (RVOT), and calcification is a recognised phenomenon in these devices. The purpose of this study was to assess the effect of type (pulmonary and aortic) and mode of harvest of these cryopreserved homografts (cadaveric and beating heart) on the incidence of calcification of these conduits when used in the pulmonary circulation. METHODS: A retrospective study was carried out on 60 patients with congenital heart defects who underwent reconstruction of RVOT using cryopreserved homograft valved conduits. The homografts were harvested from two different groups of donors; beating heart donors and cadaveric donors. The period of study was from 1st January 1990 to 31st December 2000. There were 34 males and 26 females, and the median age was 75 months. The 30-day mortality was 10 (16.7%). The 50 survivors were followed-up 3-108 months (median 36 months). Twenty-four had aortic homografts and 26 pulmonary homografts. Twenty-four devices were from cadaveric donors and 26 from beating heart donors. RESULTS: There were 10 (20%) calcified devices, all aortic in origin. In a logistic regression analysis, aortic homografts were significant risk factor for calcification (P=0.0006). However, source of harvest was not significantly related to the incidence of calcification (P=0.6). CONCLUSION: Cryopreserved pulmonary homografts placed in the right side of the heart are less likely to undergo calcification. Homografts harvested from beating heart donors do not appear to reduce the incidence of calcification.

Adult↗
PubMedDate not supplied

Arthroscopic treatment of calcific tendinitis of the shoulder.

We evaluated 48 patients arthroscopically treated for calcific tendinitis. All patients' were treated by removal of the calcific deposit whenever possible and resection of the coracoacromial ligament. Those cases showing evidence of subacromial stenosis by x-ray evaluation or intraoperative findings were treated with an arthroscopic arcromioplasty during the same procedure. For postoperative functional assessment we used the Constant score. After surgery the Constant score significantly improved. All patients who were treated by acromioplasty showed significant flattening of the bony configuration of the acromion. The x-ray review showed that none of the blurred calcific deposits regained sharper borders after operation and also that no transparent deposit was converted into a denser appearance after the procedure. Those patients with postoperative elimination or reduction of the calcific deposits had significantly better outcomes than those who had no radiographic change. Acromioplasty did not improve the results. The aim of arthroscopic treatment in calcific tendinitis is to remove the calcific deposit.

Acromion↗
PubMed2001

Mammographic finding as predictor of survival in 1-9 mm invasive breast cancers. worse prognosis for cases presenting as calcifications alone.

PURPOSE: To investigate breast cancer survival in small invasive breast cancers in relation to mammographic findings. MATERIALS AND METHODS: We investigated a consecutive series of 96 cases of 1-9mm small invasive breast cancers diagnosed 1988-1994. Median follow-up of the survivors was 7 years (range: 4.5-10.5). Mammographic findings were classified into rounded masses, spiculated masses, calcifications (casting or pleomorphic) and masses combined with calcifications. Lymph node status and histological malignancy grade were also evaluated. Eight year survival rate in breast cancer was estimated with the Kaplan-Meier method and risk of death with proportional-hazards regression. RESULTS: 6/96 women died from breast cancer. 3/14 had calcifications alone, 2/56 with spiculated masses, 1/12 with rounded masses. 5/78 who died were node-negative cancers and 1/4 was node-positive. The survival rate for the whole group was 93%: 77% for the calcifications alone group, 95% for spiculated masses and 91% for rounded masses. The survival rate for the node-negative cancers was 92% compared to 75% for node-positive cancers. Calcifications alone (p = 0.01) and node positivity (p =0.03) had each independent significant higher risk of death taking finding, node status and grade into account. CONCLUSION: Small invasive breast cancers mammographically presenting as casting or pleomorphic calcifications alone have a significantly worse prognosis than other types.

Adult↗
PubMed2001

Severe valvular and aortic arch calcification in a patient with Gaucher's disease homozygous for the D409H mutation.

Gaucher's disease is an autosomal recessive inherited defect of the lysosomal enzyme glucocerebrosidase, which leads to glucocerebroside accumulation in the reticuloendothelial system. Homozygosity for the D409H mutation has been associated with cardiovascular valvular disease. We present a case of a 17-year-old Palestinian patient who presented with severe aortic and mitral valvular calcification, as well as calcification of the ascending aorta, the aortic arch and the ostia of his coronary arteries. The patient was confirmed to be homozygous for the D409H mutation in the glucocerebrosidase gene. The patient's enzyme assay for glucocerebrosidase activity was 5 nm/h/mg protein (normal 13-22 nm/h/mg). The patient presented with symptoms of dyspnea and chest pain. He had a 6-year history of documented aortic valve calcification by echocardiogram after two of his older brothers died of congestive heart failure and severe valvular calcification. Cardiac catheterization showed a severely calcified aorta with almost no motion of the aortic valve leaflets and severe calcification of the mitral valve and the mitral valvular apparatus. The patient underwent extensive cardiac surgery with aortic and mitral valve replacements and intraoperative findings confirmed calcification of the entire aortic root. Electron microscopy of the valves confirmed the presence of Gaucher's cells. Enzyme therapy with imiglucerase was initiated. The patient is in stable condition, 20 months post-operatively.

Adolescent↗
PubMed1990

Soft tissue calcification in pediatric patients with end-stage renal disease.

Soft tissue calcification is a recognized complication of uremia in adult patients and has been implicated as a cause of ischemic necrosis, cardiac arrhythmias, and respiratory failure. However, soft tissue calcification has been regarded as rare in pediatric renal patients. Following a sudden death due to pulmonary calcinosis in an adolescent after renal transplantation, we retrospectively reviewed clinical, biochemical and autopsy data of 120 patients with uremia, on dialysis, or following renal transplantation cared for at Childrens Hospital of Los Angeles from 1960 to 1983. Soft tissue calcification was found in 72 of 120 patients (60 percent). Forty-three patients (36 percent) had systemic calcinosis (Group A): the most frequent sites of mineral deposition were blood vessels, lung, kidney, myocardium, coronary artery, central nervous system, and gastric mucosa. Vascular calcification was uniformly accompanied by deposits in other organs. Twenty-nine patients had small amounts of focal calcification (Group B) and 48 patients had no soft tissue calcification (Group C). By multiple logistic regression analysis, the use of vitamin D or its analogues, the form of vitamin D medication prescribed, the peak calcium x phosphorus product, the age at onset of renal failure, and male sex were jointly associated with calcinosis (Group A). Vitamin D therapy showed the strongest independent association with calcinosis and the probability of calcinosis was greater in patients receiving calcitriol when compared with dihydrotachysterol and vitamin D2 or D3. The duration of renal failure, peak serum calcium, serum calcium at death, serum phosphorus at death, and primary renal diagnosis, were not statistically associated with calcinosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcinosis↗
PubMed2001

Diffuse calcification of the airways.

Airway calcification is usually restricted to the cartilaginous conducting portion of the bronchial tree. Alternatively, calcification of the alveoli is a relatively common consequence of calcium and phosphate imbalance. We wish to report an unusual case in which diffuse calcification of the entire bronchial tree, absent alveolar calcification, was identified in a patient with renal dysfunction. Pathologists should not exclude metastatic calcification when considering the etiology of bronchial calcification.

Adult↗
PubMed2006

Novel insights into vascular calcification.

Vascular calcification is not just a hallmark of uremic arterio- and atherosclerosis, but also a significant cardiovascular risk factor in patients with chronic kidney disease. In contrast to the previous assumption that vascular calcification predominantly occurs by passive precipitation of calcium and phosphate ions, recent research led to the insight that extraosseous calcification is a highly regulated process. High serum phosphate and calcium levels may induce a process of osteogenic 'bone-like' differentiation of vascular smooth muscle cells, while deficiencies of calcification inhibitors or a disturbed balance towards calcification inducers may have a relevant pathophysiological influence on the initiation and progression of calcified lesions. This overview summarizes some of the best explored novel risk factors for disturbances of calcium and phosphate homeostasis and points to the integral role of hyperphosphatemia as a modifiable key trigger in calcification processes.

Atherosclerosis↗
PubMed2001

Pathophysiological mechanisms of vascular calcification in end-stage renal disease.

Vascular calcification has been clearly defined as a risk factor for cardiovascular mortality in the general population and is highly prevalent in end-stage renal disease (ESRD), where it is associated with a number of markers of increased mortality such as left ventricular hypertrophy. The pattern of calcification in ESRD is characterized by mineral deposition in the tunica media, in contrast to non-ESRD populations, where calcification of atheromatous plaque predominates. This difference may have important clinical implications. The pathophysiological mechanisms underlying both types of vascular calcification remain to be clarified; however, current evidence suggests that they are active processes rather than passive mineral precipitation, and the presence in the vasculature of cells expressing an osteoblastic phenotype may be of central importance. In ESRD, the presence of secondary and tertiary hyperparathyroidism, disordered calcium and phosphate homeostasis, and the use of vitamin D- and calcium-based treatments in its therapy may all contribute to vascular calcification. These issues and the impact on other current and future therapies have great importance for clinical nephrology, and a better understanding of vascular calcification through a focused research effort is essential.

Calcinosis↗
PubMed2002

Cardiovascular calcification in patients with end-stage renal disease: a century-old phenomenon.

The mortality risk from cardiovascular disease is increased in patients with end-stage renal disease (ESRD). This is due to both traditional and dialysis-specific factors. Recently, a number of the dialysis-specific risk factors have been implicated in the pathogenesis of cardiovascular calcification. These include: hyperphosphatemia, high calcium-phosphate (Ca x P) product, elevated parathyroid hormone levels, duration of dialysis, and treatment with calcium-containing phosphate binders and vitamin D analogs. The recent availability of electron beam computed tomography (EBCT) has triggered increased awareness of the occurrence of cardiovascular calcification in ESRD patients. Given the development of transient hypercalcemia with calcium-containing binders, a link between calcium load from use of calcium-containing phosphate binders and development coronary calcification has been proposed. However, a causal relationship between use of these agents and cardiovascular calcification has not been established. Moreover, this phenomenon had been recognized over a century ago, long before these phosphate binders became available. Although its pathogenesis is likely to be multifactorial, available data strongly implicate elevated serum phosphorus as the primary culprit. Furthermore, the risk of calcification may be aggravated by vitamin D therapy, particularly in patients with severe secondary hyperparathyroidism. Therefore, achieving vigorous control of serum phosphorus, Ca x P product and parathyroid hormone level might decrease cardiovascular calcification and improve survival of patients on maintenance hemodialysis. Since calcium acetate is the most cost-effective phosphate binder available, we recommend that it should remain the first line treatment of hyperphosphatemia in patients with ESRD.

Calcinosis↗
PubMed2000

A novel in vitro assessment of tissue valve calcification by a continuous flow type method.

A dynamic flow type testing to study calcification was self-designed to investigate calcification in bioprosthetic heart valves. The apparatus consists of a container into which leaflets from a porcine aortic valve are placed, a chamber that contains calcium solution, and a peristaltic pump that provides a continuous supply of the solution toward the container. Efficacy of the apparatus was compared with the conventional batch type calcification testing at 37 degrees C through measuring the amount of calcium and phosphate deposited by inductively coupled plasma (ICP) and scanning electron microscope (SEM). After 14 days, calcium levels detected from the calcified deposit on leaflets were 470.4 +/- 37.0 microg/cm3 in the flow type testing whereas in the batch type testing levels were 81.0 +/- 6.7 microg/cm3. Though the calcium level on the leaflet increased as the exposure time to calcium solution increased in both testings, the rate and the tendency of calcification could be assessed very rapidly by flow type testing in comparison with batch type testing. [Ca]/[P] molar ratio decreased over time, and after 14 days, the ratio was close to 1.83 +/- 0.18 in the flow type testing. The ratio could not be determined in the batch type testing because the deposit was too small to assess. The descending rate of [Ca]/[P] molar ratio demonstrates that deposited calcium-complex at the earliest stage may interact with inorganic phosphate ions to create a calcified deposit mineral precursor. This in vitro dynamic flow type calcification testing was a favorable tool for rapid investigation of calcification.

Aortic Valve↗
PubMed2001

Vascular calcification and inorganic phosphate.

Vascular calcification is highly correlated with elevated serum phosphate levels in uremic patients. To shed light on this process, we examined the ability of extracellular inorganic phosphate (Pi) levels to regulate human aortic smooth muscle cell (HSMC) culture mineralization in vitro. When cultured in media containing normal physiological levels of Pi (1.4 mmol/L Pi), HSMC grew in monolayers and did not mineralize. In contrast, HSMC cultured in media containing Pi levels comparable to those seen in hyperphosphatemic individuals (>1.4 mmol/L), showed dose-dependent increases in cell culture calcium deposition. Mechanistic studies showed that elevated Pi treatment of HSMC also enhanced the expression of the osteogenic markers, osteocalcin and Cbfa-1. The effects of elevated Pi on HSMC were mediated by a sodium-dependent phosphate cotransporter (NPC), as indicated by the ability of the specific NPC inhibitor, phosphonoformic acid (PFA), to dose-dependently inhibit Pi-induced calcium deposition as well as osteocalcin and Cbfa-1 gene expression. Using polymerase chain reaction and Northern blot analyses, the NPC in HSMC was identified as Pit-1 (Glvr-1), a member of the type III NPCs. Interestingly, platelet-derived growth factor-BB (PDGF-BB), a potent atherogenic stimulus, increased the maximum velocity (Vmax) but not the affinity (Km) of phosphate uptake, enhanced the expression of Pit-1 mRNA, and induced HSMC culture calcification in a time- and dose-dependent manner. Importantly, in the presence of PDGF, HSMC culture calcification occurred under normophosphatemic conditions. These data suggest that elevated Pi may directly stimulate HSMC to undergo phenotypic changes that predispose to calcification and may help explain both the phenomena of human metastatic calcification under hyperphosphatemic conditions as well as increased calcification in PDGF-rich atherosclerotic lesions.

Actins↗
PubMed2002

Conjunctival and corneal calcification and bone metabolism in hemodialysis patients.

Conjunctival and corneal calcification is well recognized as a metastatic calcification in patients undergoing hemodialysis. In 44 male hemodialysis patients, we examined the relationship between the severity of conjunctival and corneal calcification and age; duration of hemodialysis; serum levels of calcium (Ca), phosphorus (P), intact parathyroid hormone (iPTH), alkaline phosphatase (ALP), and osteocalcin; and bone mineral density (BMD). The mean age was 58.3 years (range, 33-79 yr), and the mean duration of hemodialysis was 94.3 months (range, 25-258 mo). The serum level of Ca was 9.6 +/- 0.1 mg/dL, P was 5.9 +/- 0.1 mg/dL, Ca x P was 57.5 +/- 1.2, iPTH was 204.0 +/- 34.6 pg/mL, ALP was 173.8 +/- 11.8 U/L, and osteocalcin was 62.8 +/- 9.5 ng/mL. Lumbar BMD was 0.997 +/- 0.022 g/cm2 and radial BMD was 0.642 +/- 0.015 g/cm2. There was a significant positive correlation between the severity of conjunctival and corneal calcification and the duration of hemodialysis (P < 0.0001), the serum levels of P (P = 0.0035), the Ca x P (P = 0.0034), the iPTH (P = 0.0154), the ALP (P < 0.0001), and the osteocalcin (P = 0.0010), and was negatively correlated with radial BMD (P = 0.0008). However, the severity of conjunctival and corneal calcification was not significantly correlated with age (P = 0.986), serum Ca levels (P = 0.138), or lumbar BMD (P = 0.449). Based on these findings, we suggest that the conjunctival and corneal calcification developed by excessive serum levels of Ca and P associated with abnormal bone and mineral metabolism. This resulted in an increased bone turnover and decreased BDM after prolonged hemodialysis even though efforts were made to maintain the homeostasis of Ca and P metabolism in hemodialysis patients by using various therapeutic approaches.

Adult↗
PubMed2002

Eliciting a terminology for mammographic calcifications.

AIM: Two studies were carried out to establish, validate and assess descriptors for use in the differential diagnosis for mammographic calcifications. METHODS: In Study 1, eleven radiologists were asked to 'think out loud' as they interpreted 20 sets of calcifications. Participants used 159 terms to describe calcifications. We used this data to design a scheme with 50 descriptors. In Study 2, ten radiologists used the scheme to describe 40 sets of calcifications. We assessed the capacity of the terms to discriminate between benign and malignant calcifications, testing them against radiologists' assessments of malignancy and follow-up data. RESULTS: All descriptors were used by at least 5 radiologists. Five additional descriptors were required. With some exceptions, properties that discriminated between benign and malignant outcomes were highly correlated with radiologists' assessment of risk. Many descriptors have a fairly low sensitivity but high specificity. CONCLUSIONS: Our data suggest that radiologists consider a wide range of features than is included in existing reporting schemes. Our scheme allows a richer characterization of calcifications, potentially improving the reporting and understanding of these abnormalities.

Breast Diseases↗
PubMed2005

Changes in cardiovascular calcification after parathyroidectomy in patients with ESRD.

BACKGROUND: The effect of parathyroidectomy on vascular calcification in patients with end-stage renal disease has been a subject of interest for many years, although studies in this area have not been definitive. The purpose of this investigation is to determine changes in vascular calcification after subtotal parathyroidectomy by using fast-gated helical computed axial tomographic imaging to measure coronary and carotid artery calcification. METHODS: Computed tomographic imaging was performed at baseline and in follow-up on 10 patients who had undergone subtotal parathyroidectomy and 10 reference patients who had not undergone parathyroidectomy. RESULTS: Patients who underwent subtotal parathyroidectomy had a mean change in coronary calcification of -92.3 +/- 469/y, and reference patients had a mean change of +479 +/- 630/y (P = 0.03). The 2 parathyroidectomy patients with the highest baseline scores had significant declines in both coronary and carotid calcification. CONCLUSION: In this study, subtotal parathyroidectomy is associated with a significant decrease in vascular calcification in 2 of 10 dialysis patients with high coronary artery calcium scores and stabilization in 7 of 10 patients with low baseline scores.

Adult↗
PubMed2006

Fulminant pulmonary calciphylaxis and metastatic calcification causing acute respiratory failure in a uremic patient.

Calciphylaxis is a rare and life-threatening disorder characterized by small-vessel mural calcification with intimal proliferation, fibrosis, and thrombosis, resulting in tissue ischemic necrosis. Although it has been viewed as a systemic disease involving mainly the dermis, subcutaneous fat, or muscle, calciphylaxis of other organs rarely is reported. We describe the case of a 25-year-old uremic woman who rapidly developed massive pulmonary calcification that led to acute respiratory failure after the initiation of hemodialysis therapy. Chest radiography and high-resolution computed tomography showed typical pulmonary calcification. Pulmonary calciphylaxis and metastatic calcification were confirmed further by lung tissue biopsy. No skin or muscle calciphylaxis was discovered. Despite multiple factors precipitating pulmonary calciphylaxis in this patient, we speculate that hemodialysis was the main culprit in accelerating the development of fulminant pulmonary calciphylaxis and metastatic calcification. Alteration in the local environment from an acid to an alkaline condition and a relatively high dialysate calcium level in the presence of systemic hyperphosphatemia are believed to have facilitated the deposition of calcification. This case highlights the importance of "visceral calciphylaxis" and early identification of its causes.

Acute Disease↗
PubMed2006

A case report comparing various radiological tests in the diagnosis of calcific uremic arteriolopathy.

BACKGROUND: Calcific uremic arteriolopathy (CUA) is a rare necrotizing skin condition characterized by calcification in arterioles, leading to ischemia and skin ulcerations. This disease affects 1% to 4% of patients with chronic kidney disease and has a reported mortality rate up to 80%. The diagnosis of CUA is based on clinical judgment suggested by the characteristic skin lesions. Although skin biopsy is the gold standard for establishing the diagnosis, it is performed infrequently because of poor healing and risk for secondary infections. METHODS: In this case report, we compare the ability of various radiological tests to show arteriolar calcifications of patients with CUA. Our patient had biopsy-proven CUA manifesting as chronic nonhealing ulcers of the calves. She underwent soft-tissue x-ray of the affected extremities and high-resolution (0.5-mm slice) computed tomographic (CT) scanning with 3-dimensional image reconstruction. We also used a dedicated mammography machine to obtain images of the patient's calves. Images were compared based on the ability to show small-vessel calcification. RESULTS: Plain soft-tissue x-ray showed mildly increased soft-tissue density and very few calcified vessels, whereas CT showed few calcified small- and medium-sized arterioles. Diffuse calcification of small arterioles in a mesh-like pattern was shown by means of the mammography technique. CONCLUSION: Simple, safe, and inexpensive x-ray imaging using the mammography technique was superior to plain soft-tissue x-ray and 3-dimensional CT in showing the hallmark arteriolar calcifications of patients with CUA. Thus, we propose a possible role for this technique in diagnosing CUA.

Aged↗
PubMed1977

[Intracranial calcification on computer tomography a comparison with radiography (author's transl)].

It is possible to demonstrate extremely fine calcification by computer tomography which cannot be shown by skull radiographs. A value of + 70 CT units was found to be the limit below which calcification visible on the CT could no longer be demonstrated radiographically. The incidence of calcification of the falx and of the choroid plexus is considerably greater on the CT than on radiographs, although no difference was found for calcification of the pineal body. Since it is possible to demonstrate cerebral substance and CSF pathways simultaneously, it is possible to obtain an exact anatomical localisation of any calcification. CT is the method of choice for the demonstration and investigation of intracranial calcification.

Brain Diseases↗
PubMed2000

[Detection and quantification of coronary calcification: an update].

The demonstration of calcification of the coronary arterial wall indicates the presence of coronary heart disease (CHD). The prevalence of coronary calcifications increases with age. The extent of the calcifications correlates with the total coronary plaque burden and with the probability of a future myocardial infarction in symptomatic patients. In asymptomatic subjects with risk factors for a myocardial event demonstration of coronary calcifications is diagnostic for coronary atherosclerotic disease before clinical manifestation of the disease. Exact quantification of coronary arterial calcifications (calcium scoring) has become possible with electron beam computed tomography (EBCT) or ECG triggered subsecond CT scanners. Further improvements in the detection of coronary calcifications can be expected with the introduction of multi-slice CT. The prognostic relevance of coronary calcium scoring in asymptomatic high-risk patients is not yet clearly defined. It remains to be clarified whether newer, volume based methods of calcium quantification will be superior to the classic calcium score (Agatston-Score) for risk assessment and follow-up in this patient group.

Calcinosis↗