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PubMed2000

Warfarin-induced artery calcification is accelerated by growth and vitamin D.

The present studies demonstrate that growth and vitamin D treatment enhance the extent of artery calcification in rats given sufficient doses of Warfarin to inhibit gamma-carboxylation of matrix Gla protein, a calcification inhibitor known to be expressed by smooth muscle cells and macrophages in the artery wall. The first series of experiments examined the influence of age and growth status on artery calcification in Warfarin-treated rats. Treatment for 2 weeks with Warfarin caused massive focal calcification of the artery media in 20-day-old rats and less extensive focal calcification in 42-day-old rats. In contrast, no artery calcification could be detected in 10-month-old adult rats even after 4 weeks of Warfarin treatment. To directly examine the importance of growth to Warfarin-induced artery calcification in animals of the same age, 20-day-old rats were fed for 2 weeks either an ad libitum diet or a 6-g/d restricted diet that maintains weight but prevents growth. Concurrent treatment of both dietary groups with Warfarin produced massive focal calcification of the artery media in the ad libitum-fed rats but no detectable artery calcification in the restricted-diet, growth-inhibited group. Although the explanation for the association between artery calcification and growth status cannot be determined from the present study, there was a relationship between higher serum phosphate and susceptibility to artery calcification, with 30% higher levels of serum phosphate in young, ad libitum-fed rats compared with either of the groups that was resistant to Warfarin-induced artery calcification, ie, the 10-month-old rats and the restricted-diet, growth-inhibited young rats. This observation suggests that increased susceptibility to Warfarin-induced artery calcification could be related to higher serum phosphate levels. The second set of experiments examined the possible synergy between vitamin D and Warfarin in artery calcification. High doses of vitamin D are known to cause calcification of the artery media in as little as 3 to 4 days. High doses of the vitamin K antagonist Warfarin are also known to cause calcification of the artery media, but at treatment times of 2 weeks or longer yet not at 1 week. In the current study, we investigated the synergy between these 2 treatments and found that concurrent Warfarin administration dramatically increased the extent of calcification in the media of vitamin D-treated rats at 3 and 4 days. There was a close parallel between the effect of vitamin D dose on artery calcification and the effect of vitamin D dose on the elevation of serum calcium, which suggests that vitamin D may induce artery calcification through its effect on serum calcium. Because Warfarin treatment had no effect on the elevation in serum calcium produced by vitamin D, the synergy between Warfarin and vitamin D is probably best explained by the hypothesis that Warfarin inhibits the activity of matrix Gla protein as a calcification inhibitor. High levels of matrix Gla protein are found at sites of artery calcification in rats treated with vitamin D plus Warfarin, and chemical analysis showed that the protein that accumulated was indeed not gamma-carboxylated. These observations indicate that although the gamma-carboxyglutamate residues of matrix Gla protein are apparently required for its function as a calcification inhibitor, they are not required for its accumulation at calcification sites.

Aging↗
PubMedDate not supplied

Calcification of the ligamentum arteriosum in adults: CT features.

OBJECTIVE: The present study describes the frequency and pattern of ligamentum arteriosum calcification seen on chest CT in adults. MATERIALS AND METHODS: We retrospectively reviewed 402 sequential unenhanced chest CT studies for ligamentum arteriosum calcification, atherosclerotic cardiac or aortic calcification, and granulomatous calcification. The pattern of calcification was characterized as curvilinear, punctate, or clumped. RESULTS: Mean patient age was 60 (+/- 18, range 18-97) years with 214 women (53%) and 188 men (47%). Of these patients 194 (48%) had calcification in the ligamentum arteriosum including 26 (6%) with calcification in the ligamentum arteriosum alone, 108 (27%) with atherosclerotic calcification, 11 (3%) with granulomatous calcification, and 49 (12%) with both. A total of 100 patients (25%) had no calcifications. In the study population 169 patients (42%) had atherosclerotic calcification, 32 (8%) had granulomatous calcification, and 75 (19%) had both. The patterns of calcification for the 26 patients with calcification of the ligamentum arteriosum alone were curvilinear (7 patients, 27%), punctate (17 patients, 65%), and clumped (2 patients, 8%). The pattern of ligamentum arteriosum calcification for the 108 patients with only atherosclerotic and ligamentum arteriosum calcification was curvilinear (28 patients, 26%), punctate (32 patients, 30%), and clumped (48 patients, 44%). The patients without any calcifications and the patients with ligamentum arteriosum calcification formed one group (based on their similarity in age, mean 47 years) with a prevalence of ligamentum arteriosum calcification of 21%. The patients with atherosclerotic and ligamentum arteriosum calcification formed a second group (mean age 71 years) with a prevalence of ligamentum arteriosum calcification of 65%. CONCLUSION: On unenhanced chest CT calcification of the ligamentum arteriosum is a common finding in adults and increases in prevalence with increasing age and atherosclerosis.

Adolescent↗
PubMed2006

Association of sonographically detected calcification with thyroid carcinoma.

BACKGROUND: Calcification can be detected in both benign and malignant nodules and is often neglected by clinical physicians. The purpose of this study was to investigate the association of thyroid nodule calcification detected on ultrasound with thyroid carcinoma. METHODS: One hundred seven cases of thyroid carcinoma and 215 cases of benign thyroid nodules were selected from the records of inpatients of our hospital who had high-resolution ultrasonography preoperatively and pathologic diagnosis postoperatively between 2001 and 2004. The case numbers and percentage of calcification, fine stippled psammomatous (FSP), and non-FSP calcification in benign nodules and thyroid carcinoma, sex, and age groups (<45 years and >or=45 years) were retrospectively reviewed. Statistical analysis was performed using chi-square test and odds ratio. Sensitivity and specificity of calcification and FSP calcification on ultrasonography were also calculated. RESULTS: The incidence of calcification, non-FSP calcification, and FSP calcification were significantly higher in thyroid carcinoma than in the benign group (p < .001, p = .03, and p < .001, respectively). However, FSP calcification was more significant than the non-FSP calcification (p = .001) for predicting thyroid cancer. The incidence of non-FSP calcification and FSP calcification did not differ significantly between the sexes (p = .50 and p = .83, respectively). The relative risk of malignancy incidence was significantly higher in those younger than 45 years old with FSP calcification (p < .001). The incidence of non-FSP calcification was significantly higher in the older group (p = .03). The sensitivity of calcification and FSP calcification for the detection of malignancy was 63.55% and 24.30%, respectively; the specificity was 69.77% and 96.77%, respectively. CONCLUSIONS: The detection of calcification on ultrasonography should increase the clinical index of suspicion for thyroid carcinoma and alert the physician. FSP calcification is valuable and has a very high specificity for predicting thyroid carcinoma, particularly for those younger than 45 years old or with calcified regional lymph nodes. To increase the sensitivity for the diagnosis of thyroid carcinoma, tests such as fine-needle aspiration cytology should also be performed. The use of these modalities could result in earlier detection of thyroid carcinoma. The use of ultrasound to detect calcification and FSP calcification is as efficient as thyroid papillary macrocarcinoma in predicting microcarcinoma.

Adolescent↗
PubMed2006

Vascular calcification in chronic kidney disease.

Vascular calcification is often encountered in advanced atherosclerotic lesions and is a common consequence of aging. Calcification of the coronary arteries has been positively correlated with coronary atherosclerotic plaque burden, increased risk of myocardial infarction, and plaque instability. Chronic kidney disease (CKD) patients have two to five times more coronary artery calcification than healthy age-matched individuals. Vascular calcification is a strong prognostic marker of cardiovascular disease mortality in CKD patients. Vascular calcification has long been considered to be a passive, degenerative, and end-stage process of atherosclerosis and inflammation. However, recent evidence indicates that bone matrix proteins such as osteopontin, matrix Gla protein (MGP), and osteocalcin are expressed in calcified atherosclerotic lesions, and that calcium-regulating hormones such as vitamin D3 and parathyroid hormone-related protein regulate vascular calcification in in vitro vascular calcification models based on cultured aortic smooth muscle cells. These findings suggest that vascular calcification is an actively regulated process similar to osteogenesis, and that bone-associated proteins may be involved in the development of vascular calcification. The pathogenesis of vascular calcification in CKD is not well understood and is almost multifactorial. In CKD patients, several studies have found associations of both traditional risk factors, such as hypertension, hyperlipidemia, and diabetes, and uremic-specific risk factors with vascular calcification. Most patients with progressive CKD develop hyperphosphatemia. An elevated phosphate level is an important risk factor for the development of calcification and cardiovascular mortality in CKD patients. Thus, it is hypothesized that an important regulator of vascular calcification is the level of inorganic phosphate. In order to test this hypothesis, we characterized the response of human smooth muscle cell (HSMC) cultures to inorganic phosphate levels. Our findings indicate that inorganic phosphate directly regulates HSMC calcification through a sodium-dependent phosphate transporter mechanism. After treatment with elevated phosphate, there is a loss of smooth muscle lineage markers, such as alpha-actin and SM-22alpha, and a simultaneous gain of osteogenic markers such as cbfa-1 and osteocalcin. Elevated phosphate may directly stimulate HSMC to undergo phenotypic changes that predispose to calcification, and offer a novel explanation of the phenomenon of vascular calcification under hyperphosphatemic conditions. Furthermore, putative calcification inhibitory molecules have been identified using mouse mutational analyses, including MGP, beta-glucosidase, fetuin-A, and osteoprotegerin. Mutant mice deficient in these molecules present with enhanced cardiovascular calcification, demonstrating that specific molecules are normally important in suppressing vascular calcification. These findings suggest that the balance of inducers, such as phosphate, and inhibitors, such as MGP, fetuin-A, and others, are likely to control whether or not calcification occurs under pathological conditions.

Alkaline Phosphatase↗
PubMed2002

Mitral inflow and mitral annular motion velocities in patients with mitral annular calcification: evaluation by pulsed Doppler echocardiography and pulsed Doppler tissue imaging.

AIMS: We evaluated the relationship between the mitral inflow velocities by pulsed Doppler echocardiography and mitral annular motion velocities by pulsed Doppler tissue imaging in patients with mitral annular calcification. METHODS AND RESULTS: Fifty-three patients with mitral annular calcification were divided into two groups: severe mitral annular calcification (n=15, mitral annular calcification bigger than or equal 5mm in width) and mild mitral annular calcification (n=38, mitral annular calcification <5mm in width). In addition, 20 patients with hypertensive heart disease (HHD group) and mild left ventricular hypertrophy but no mitral annular calcification and 30 normal individuals (normal group) were studied. The early diastolic mitral inflow velocity (E) was higher in the severe mitral annular calcification group (0.75+/-0.26 m/s) than in the HHD and normal groups (mild mitral annular calcification, 0.65+/-0.21; HHD, 0.57+/-0.24; normal, 0.55+/-0.15m/s), and the late diastolic mitral inflow velocity (A) was higher in the severe mitral annular calcification group (1.24+/-0.23 m/s) than in the other three groups (mild mitral annular calcification, 0.96+/-0.20; HHD, 0.84+/-0.23; normal, 0.75+/-0.13 m/s). In contrast, the early and late diastolic annular velocities (Ea, Aa) were lower in the severe mitral annular calcification group (Ea: 5.7+/-2.2; Aa: 11.9+/-4.4 cm/s) than in the other three groups (Ea: mild mitral annular calcification, 8.3+/-2.5; HHD, 7.7+/-2.2; normal, 9.0+/-1.8 cm/s; Aa: mild mitral annular calcification, 14.2+/-4.1; HHD, 14.3+/-2.8; normal, 14.2+/-2.1cm/s). Mitral valve area was smaller in the severe mitral annular calcification group (2.6+/-1.0 cm(2)) than in the other three groups (mild mitral annular calcification, 3.1+/-0.7; HHD, 4.1+/-0.7; normal, 4.2+/-0.9 cm(2)). In the mitral annular calcification and normal groups, the A correlated inversely with mitral valve area (r=-0.67, P<0.01) and directly with severity of mitral annular calcification (r=0.65, P<0.01), and the Ea correlated inversely with left ventricular wall thickness (r=-0.37, P<0.01) and severity of mitral annular calcification (r=-0.45, P<0.01). CONCLUSION: Patients with severe mitral annular calcification have higher mitral inflow velocities due to mitral annular restriction and lower mitral annular velocities caused by decreased mitral annular motion and abnormal left ventricular relaxation.

Aged↗
PubMed1993

Mammographic calcifications and risk of subsequent breast cancer.

BACKGROUND: Women with proliferative benign breast lesions are at increased risk of breast cancer, and some studies have provided evidence that microscopic calcifications in such lesions enhance the risk. PURPOSE: This study was performed to determine whether calcifications on mammograms are predictive of subsequent breast cancer. METHODS: Data for this study were collected on women enrolled at four of the clinics that participated in the Breast Cancer Detection and Demonstration Project (BCDDP). The presence, morphology, and distribution of calcifications visualized on baseline mammograms for 686 women who developed breast cancer over a 7- to 10-year period of follow-up were compared with those for 1357 controls who remained cancer free. We also compared presence and types of calcifications in breasts in which cancer subsequently developed with those in the contralateral breast. RESULTS: Calcifications were evident at baseline in at least one breast in 381 (55.5%) of 686 cases and in 606 (44.7%) of 1357 controls. The estimated relative risk (RR) of breast cancer was 1.68 in women with calcifications, compared with those having none. There was a statistically significant trend of increasing risk with number of breasts with calcifications; RR increased from 1.28 to 2.14 in women with calcifications in one and both breasts, respectively. In women with unilateral calcifications, RR was greater for the breast in which the calcification occurred (1.48) than for the opposite breast (1.08). The elevated risk persisted for more than 6 years from identification of the calcification, suggesting that these lesions were not indicative of existing carcinomas detected later. Risk was greatest in women with clustered calcifications of any morphology or linearly distributed punctate calcifications (RR = 3.64), and the cancer in women with such calcifications was 4.65 times more likely to occur in the involved breast than in the contralateral breast. Multiple and scattered punctate calcifications, and those of any number or distribution that were ring-shaped or linear, were also associated with subsequent risk of breast cancer (RR = 2.09 and 1.76, respectively) but were not strongly predictive of the side on which the breast cancer occurred. Risk was not altered in women with single punctate or large conglomerate calcifications, although the cancers that subsequently occurred in women with the latter lesions were over three times more likely to develop in the breast with the calcification than in the opposite breast. CONCLUSIONS: These findings are consistent with previously reported relationships between breast cancer and specific histologic types of noninvasive breast lesions. Some types of mammographic calcifications appear to be independent risk factors for breast cancer. IMPLICATIONS: If these results are confirmed by other investigators, mammographic calcifications could serve as an additional indicator of women at high risk for breast cancer who may benefit from intensified follow-up.

Breast Diseases↗
PubMed1998

Capsular calcification associated with silicone breast implants: incidence, determinants, and characterization.

Capsular calcification was present clinically in 64 of 404 silicone gel breast implant capsules (15.8%) analyzed from 1981 to 1996. It presented as white-gray plaques on the inner surface of capsules in 62 of 64 capsules, and as massive heterotopic ossification in 2 capsules. Chi-squared analysis confirmed that calcification was related to the generation of the implant (i.e., year of manufacture; p < 0.001). All 28 first-generation implants (1963-1972, with Dacron patches) were clinically intact and all demonstrated extensive calcification. Their mean duration in situ was 17.6 years (range, 14-28 years). Thirty-four of the 348 second-generation implants (9.8%; 1973-1987) were associated with capsular calcification. Their mean duration in situ was 16.0 years (range, 13-22 years). Because all first-generation implants demonstrated calcification, they were compared with the second-generation implants that had been in place for the same duration (>14 years). Only 42% of these 81 second-generation implants demonstrated calcification, compared with 100% of the first-generation implants (p < 0.001). Thus, thicker first-generation implants with Dacron patches are more likely to calcify and the effect is not entirely due to their longevity. None of the 28 third-generation implants (1987-1991) demonstrated calcification. Their mean duration in situ was 4.2 years (range, 2-7 years). For second-generation implants, calcification was related to duration in situ (p < 0.001). None of the 294 implants in place for less than 11 years were associated with significant clinical calcification. The percentages of capsules with calcification were 13 to 14 years, 33%; 15 to 16 years, 45%; and 17 to 22 years, 57%. Calcification with second-generation implants was not associated with patches on the envelopes. Of the 34 second-generation implants with calcification, only two had patches (composed of silicone, not Dacron). Among second-generation implants, calcification was related to implant integrity. Of implants in place for more than 12 years, 52.5% of those implants that were ruptured showed calcification, but only 10.0% of intact implants demonstrated calcification (p < 0.001). Seventeen of the 64 calcified capsules were examined histologically. In all of these specimens, calcification existed in two forms: globular aggregates on the surface of the capsule (adjacent to the implant) and actual bone formation within the fibrous tissue of the capsule. All calcified capsules demonstrated both globular aggregates and true bone formation regardless of the implant generation, duration in situ, or integrity. Ultrastructural analysis was performed on four capsules from 2 women who had received first-generation Dow Corning gel implants 24 and 28 years previously, and on 2 capsules from one woman who had received Heyer-Schulte gel implants 21 years previously. These capsules were analyzed according to distribution, density, mineral nature, crystal phases, and elements within crystals by electron microscopy, energy-dispersive X-ray spectrometry, and electron diffraction. These analyses confirmed two types of calcification, each with hydroxyapatite crystals. In areas of heterotopic bone, crystals 40 x 10 nm were deposited in an orderly fashion on collagen fibers. In contrast, in areas of globular aggregates, spherulitic aggregates of much larger crystals were present, without any relationship to the collagen. Titanium was demonstrated in capsules of first-generation implants at areas of attachment of the Dacron patches. The calcification associated with saline implants revealed only one form of crystal: agglomerates, which were adherent to the elastomeric shell of the implants. A hypothesis is presented to explain the differences in calcification deposition properties between silicone gel-filled and saline-filled breast implants.

Adult↗
PubMed1999

[Echo-guided percutaneous treatment of chronic calcific tendinitis of the shoulder].

PURPOSE: We report on our personal technique and the results of US-guided percutaneous treatment of chronic calcific tendinitis. MATERIAL AND METHODS: January 1997 to March 1999, seventy patients with known chronic calcific supraspinatus tendinitis were submitted to the US-guided treatment. All patients had undergone plain radiography, US, and physical and psychiatric examination. Plain radiography and aspiration biopsy demonstrated hard and radiopaque calcification in 59 patients and soft and faintly milky calcification in 11 cases; calcification diameter ranged 6-30 mm. US showed tendon thickening, with bulging of the outer tendon surface; 10 patients also had moderate dilatation of the subacromial bursa. Psychiatric examination revealed chronic pain exacerbated at night, which was always associated with motion impairment. The selection criteria for treatment were calcification diameter > 6 mm, integrity of the tendon, and chronic pain. After superficial planes were anesthetized, a 16 G needle was positioned inside the calcification under US guidance and the calcific deposits were fragmented and aspirated. Then, 0.5-1 mL triamcinolone acetonide (40 mg) was injected in the soft tissues or subacromial bursa. RESULTS: Pain resolution and recovery of the full range of motion were seen in 42 patients (60%), and mild functional impairment was seen in 7 cases (10%), while 2 patients (2%) were unchanged. Post-treatment plain radiography showed calcification disappearance in 41 patients (58.5%) and debulking in 29 (41.5%); the calcifications were significantly debulked (> 60%) in 27 patients (38.5%). However, calcification diameter was substantially unchanged in 2 patients (3%) and there remained tendon bulging; in these patients clinical symptoms did not improve. No rotator cuff tears or new tendon calcifications were found in any of our patients even at 19-28 months' follow-up. DISCUSSION: The US-guided technique always allowed easy location of calcific deposits and complete aspiration of all soft calcifications. Splintering of hard calcifications helped migration of residual deposits to vascularized soft tissues, which accelerated the--frequently complete--resorption process. We privileged extensive and prolonged fragmentation of the calcifications using a single needle, versus the technique using a second needle, saline lavage and aspiration of residual deposits. CONCLUSION: US-guided percutaneous treatment with aspiration and splintering of chronic calcific supraspinatus tendinitis is a conservative, simple, well-tolerated procedure which can be considered the method of choice after the failure of medical treatment.

Adult↗