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PubMed1986

Age-related change in calcifications in the thoracic aorta: a study with computed tomography.

Calcifications in the thoracic aorta at the level of the 11th and the 12th thoracic vertebrae in 592 men and 333 women were studied using computed tomography. The ages ranged from 40 to 88 years. Incidence of calcification increased proportionally to the advancing age from the forties to the eighties in men, and from the fifties to the seventies in women: incidence of calcification (%) = 2.41 X age (years)-113 in men (p less than 0.01); incidence of calcification (%) = 3.16 X age (years)-160 in women (p less than 0.01). Calcification index (CI) was calculated as an indicator of calcification in the thoracic aorta: (calcified portion along the entire circumference of the aorta) X 80. The CI in the subjects with calcifications increased with the advancing age both in men and women: CI = 0.200 X age (years)-4.47 in men (p less than 0.01); CI = 0.312 X age (years)-12.7 in women (p less than 0.01).

Adult↗
PubMed2006

Vascular calcifications: pathogenesis, management, and impact on clinical outcomes.

The predisposition to vascular calcifications in patients with chronic kidney disease (CKD) has gained great interest in recent years as many studies have described its likely impact on morbidity and mortality. The mechanism by which the process of vascular calcification is produced is complex, and it does not consist in a simple precipitation of calcium and phosphate but is instead an active and modifiable process. Several "modifiable and nonmodifiable" factors that are able to promote vascular calcification are extremely frequent in patients with CKD. Most of the present strategies to decrease vascular calcifications are based in the control of the more prevalent modifiable risk factors. Unfortunately, the extremely important nonmodifiable risk factors, which are highly prevalent, such as older age, time on dialysis, and diabetes, are not under one's control. Recent studies also have shown that vascular calcifications in some localizations were associated with increased osteoporotic fractures not only in dialysis patients but also in the general population, and interestingly, mortality also was associated significantly and positively with vascular calcifications and nontraumatic bone fractures. Despite that new strategies may improve the management of vascular diseases and specifically have a positive impact on the high prevalence of vascular calcifications, still the best possible control of the bone metabolic and inflammatory parameters are in the primary line. The horizon of the coming decade looks promising, but solid clinical and epidemiologic data are needed to manage better the bone- and cardiovascular-related disorders in patients with CKD.

Bone Density↗
PubMed2005

Optical measurement of age-related calcification in human blood vessels.

Vascular calcification is commonly associated with aging. Quantification of calcium accumulation in vessel walls is important in understanding the mechanisms of vascular calcification. To elucidate age-related change of calcification, site dependence of calcification, and the effect of hemodynamic stress on calcification, we measured calcium contents in various blood vessels with atomic emission spectrometry and simulated blood flow in the vessels by computational fluid dynamics. The content of calcium in the arteries increased progressively with aging while there is no change in the veins. The higher accumulation of calcium occurred in the arteries of the lower limb in comparison to the arteries of the upper limb. In the arterial bifurcation, there was the correlation at hemodynamic stress distribution and calcium content. The results of this study quantitatively support clinical findings of nonuniform calcification, and suggest that hemodynamic stress affects vascular calcification.

Age Factors↗
PubMed1977

Calcifications and the therapeutically irradiated breast.

Mammograms of 81 patients who received radiation therapy to the breast were analyzed for patterns of pre- and postirradiation calcifications. Malignant calcifications may remain stable, diminish, or completely disappear following irradiation. The persistence of calcifications need not indicate residual cancer. Calcifications can develop following irradiation which are similar to either intraductal or secretory calcifications. Unusual calcifications may develop at the site of an irradiated cancer. It is important to recognize that benign calcifications can develop so that they will not be confused with recurrent malignancy.

Breast Neoplasms↗
PubMed1985

Vascular calcification in types II and IV hyperlipoproteinemia: radiographic appearance and clinical significance.

Nearly 90% of patients with clear-cut hyperlipidemia seen in clinical practice have type II or IV hyperlipoproteinemia. Previous studies have shown that these syndromes have different distributions of coronary artery atherosclerosis and different outcomes after coronary bypass grafting. A characteristic pattern of vascular calcification on chest films might have some prognostic value. Therefore, to determine the location and extent of aortic root and coronary artery calcification seen on chest films, 33 consecutive patients with type II and 17 with type IV hyperlipoproteinemia were studied who were admitted for coronary arteriography between 1970 and 1982. Among the 33 patients with type II disease, 21 women and 12 men, 22 had radiographically visible calcification that was different in distribution from that usually found in atherosclerotic disease. The ascending aorta was involved in 21 and the arch in 12. In eight patients, the calcium outlined a distinctive narrowing of the ascending aorta. Six patients had significant left ventricular obstruction; in five it was from aortic valve stenosis. Of the 17 type IV patients, 16 men and one woman, none had aortic calcification or left ventricular outflow obstruction, and only one had coronary artery calcification. These data demonstrate that patients with type II hyperlipoproteinemia have severe calcific atherosclerosis of the aortic root that often is visible on chest films. Such calcification may alert physicians to the presence of type II hyperlipoproteinemia and the high probability of severe coronary artery disease.

Adolescent↗
PubMed1989

Calcific tendinitis of the long head of the biceps brachii distal to the glenohumeral joint: plain film radiographic findings.

Calcific tendinitis is a painful condition related to deposition of hydroxyapatite crystals; it favors large joints. The shoulder, specifically the tendons of the rotator cuff and the insertion of the long head of the biceps on the superior glenoid rim, is a well-recognized location for this abnormality. The purpose of this article is to describe a second site of calcific tendinitis of the biceps, distal to the joint and corresponding to the junction of the tendon and muscle. Radiographs in 119 cases of calcific tendinitis of the shoulder, obtained between 1980 and 1988, were reviewed. Twenty had calcific tendinitis in the region of the tendon of the long head of the biceps (nine at the glenoid insertion and 11 adjacent to the humeral shaft). All 11 patients with calcific tendinitis at the more distal site had a small, homogeneous deposit adjacent to the proximal humeral shaft. The densities in these 11 cases followed the normal course of the tendon of the long head of the biceps and were therefore medial to the proximal humeral shaft on the internal rotation view, lateral to the proximal humeral shaft on the external rotation view, and anterior to the proximal humeral shaft on the axillary projection. The major differential diagnosis of calcific tendinitis of the tendon of the long head of the biceps is loose bodies trapped in the biceps tendon sheath. Although the position of the soft-tissue densities in these two entities is similar, loose bodies have an appearance of bone, and their source (degenerative arthritis or recurrent dislocations) is usually apparent. A site of calcific tendinitis distal to the glenohumeral joint that is detectable on plain films is reviewed. Accurate diagnosis depends on understanding the anatomy of the tendon of the long head of the biceps brachii. The clinical charts of the 11 patients also are summarized, with emphasis on the association between the roentgen finding and bicipital tendinitis and impingement syndrome.

Adult↗
PubMed1993

Renal calcifications in patients with autosomal recessive polycystic kidney disease: prevalence and cause.

OBJECTIVE: We investigated the prevalence of renal calcifications in children with autosomal recessive polycystic kidney disease and studied the metabolic changes that could cause this complication. SUBJECTS AND METHODS: Nine patients with known autosomal recessive polycystic kidney disease were examined with sonography and CT and screened for biochemical evidence of metabolic causes of nephrocalcinosis. RESULTS: CT showed bilateral renal calcifications in seven of the nine patients. The two patients without renal calcifications were less than 1 year old. Four patients had only a few calcifications and three patients had many. The severity of the renal calcifications correlated with the degree of kidney failure. All patients with kidney failure were found to have urine acidification defects. Hypocitraturia was present in all patients. CONCLUSION: Our results show that renal calcifications are common in older children with autosomal recessive polycystic kidney disease. Hypocitraturia and the urine acidification defect resulting from kidney failure are the leading factors in the pathogenesis of the calcifications.

Adolescent↗
PubMed1999

The spectrum of benign and malignant etiologies of cervical node calcification.

OBJECTIVE: The purpose of this study was to determine if the presence and pattern of lymph node calcification can be used to make a limited differential diagnosis and differentiate benign from malignant disease. MATERIALS AND METHODS: Two radiologists reviewed each of 2300 neck CT scans obtained at our institution between January 1996 and July 1998 for the presence of nodal calcifications. The scans were obtained as 3-mm contiguous axial sections, and most were obtained with IV contrast material. Twenty-six scans revealed nodal calcification, which was classified as being within the node itself or along the periphery of the node. The diagnosis was established from surgical specimens for 20 patients and from CT-guided thin-needle biopsy for four patients. For two patients, the diagnosis was inferred from a previously well-documented case of the disease. RESULTS: Of the 2300 scans, 26 (1%) showed nodal calcification. Of these 26, eight (31%) were from patients with benign disease; six (23%) from patients with treated diseases, including four lymphomas and one infection; and 12 (46%) from patients with malignancies, including nine cases of head and neck primary tumors and three cases of metastatic adenocarcinoma from breast and lung primary tumors. CONCLUSION: Cervical node calcification is rare. On the basis of our limited number of cases, nodal calcification, regardless of its location within the node, is not a reliable predictor of either benign or malignant disease. However, nodal calcification does suggest a limited differential diagnosis that most commonly includes tuberculosis, treated lymphoma, and metastatic thyroid carcinoma, adenocarcinoma, or squamous carcinoma.

Adult↗
PubMed2001

Calcifications of lobular carcinoma in situ of the breast: radiologic-pathologic correlation.

OBJECTIVE: Because lobular carcinoma in situ is thought to be an incidental finding at breast pathology, the finding of lobular carcinoma in situ at core biopsy poses a diagnostic dilemma of radiologic-pathologic concordance. The purpose of this article is to describe the radiologic-pathologic correlation of calcifications associated with lobular carcinoma in situ of the breast. MATERIALS AND METHODS: Between July 1999 and July 2000, seven excisional biopsies resulted in findings of lobular carcinoma in situ of mammographic calcifications. The radiographic features of the calcifications were characterized by the Breast Imaging Reporting and Data System lexicon, and pathologic features were reviewed. RESULTS: Two forms of lobular carcinoma in situ were associated with calcifications: the classic form with small, uniform cells, and the pleomorphic form with larger cells frequently associated with central necrosis. On mammography, all calcifications were clustered, punctate, high density, and smaller than or equal to 0.5 mm, although mammographically visible calcifications found in the pleomorphic type tended to be larger and more dense. Additionally, infiltrating lobular carcinoma was found after surgical excision in two (40%) of five patients with pleomorphic lobular carcinoma in situ. CONCLUSION: Calcifications can be associated with lobular carcinoma in situ and therefore concordant at stereotactic core biopsy. The classic form may be incidental and clinically innocuous. The pleomorphic form is morphologically similar to ductal carcinoma in situ and may have a greater tendency for invasion.

Adult↗
PubMed2002

Calcification in lymphoma occurring before therapy: CT features and clinical correlation.

OBJECTIVE: Calcification in lymphoma occurring before therapy is rare. We assessed the prevalence, CT features, and clinical significance of calcification in nodes and masses in patients with lymphoma occurring before therapy. SUBJECTS AND METHODS: CT of the chest, abdomen, and pelvis of 956 newly diagnosed patients with lymphoma was evaluated prospectively for calcifications in enlarged lymph nodes and lymphoma masses. Findings were correlated with histologic type of disease, tissue parameters, and clinical course. Calcifications were further evaluated on follow-up CT. RESULTS: Of 956 patients with lymphoma (704 with non-Hodgkin's lymphoma and 252 with Hodgkin's lymphoma), eight patients (0.84%) showed calcifications in involved sites, seven of whom had non-Hodgkin's lymphoma and one of whom had Hodgkin's lymphoma. Calcifications were present in lymph nodes and masses in the mediastinum in five patients, in the retroperitoneum in two patients, and in the adrenal in one patient. All eight patients had the aggressive type of lymphoma. Four patients later relapsed, one of whom died. A fifth patient died after only minimal response to treatment. CONCLUSION: Calcification in patients with lymphoma occurring before therapy is rare as opposed to that in lymphoma after therapy. It occurred in our patients more often in the mediastinum, in patients with non-Hodgkin's lymphoma rather than in patients with Hodgkin's lymphoma, and only in patients with the aggressive type of disease.

Adult↗
PubMedDate not supplied

[Calcifications from cardiac etiology in chest radiography]

OBJECTIVE: Children s chest X-ray calcification images can be related to pulmonary, mediastinal and rarely cardiac parenchymatous pathology. This report describes cases of cardio thoracic calcifications. We emphasize the importance of chest X-ray to track thoracic calcifications. In spite of the fact that it is rare, the cardiac etiology must be considered due to the possibility of surgical treatment.METHODS: Regarding the period from 1988 to 1997 the authors reviewed the chest X-rays of 2108 patients. In 3 of them thoracic calcifications of cardiac etiology were observed.RESULTS: Of these three patients, two were 7 years old and the third was 3 years old. Case 1 presented a calcification in the right atrium topography caused by a heart tumor of Fibroma type. In case 2 the calcification was in the pulmonary trunk, presenting as a calcified aneurysm of the ductus arteriosus. In case 3 the child had pulmonary stenosis and the chest X-ray showed a calcified image on the left cardiac boards caused by a thrombo in the right ventricle wall.CONCLUSION: The authors emphasize the importance of chest X-ray in the diagnosis of thoracic calcifications, and comment that in spite of the being rare, the cardiac causes should be considered due to the possibility of surgical treatment.

Journal Article↗
PubMed2006

Role of osteoprotegerin and its ligands and competing receptors in atherosclerotic calcification.

Vascular calcification significantly impairs cardiovascular physiology, and its mechanism is under investigation. Many of the same factors that modulate bone osteogenesis, including cytokines, hormones, and lipids, also modulate vascular calcification, acting through many of the same transcription factors. In some cases, such as for lipids and cytokines, the net effect on calcification is positive in the artery wall and negative in bone. The mechanism for this reciprocal relation is not established. A recent series of reports points to the possibility that two bone regulatory factors, receptor activator of NF-kappaB ligand (RANKL) and its soluble decoy receptor, osteoprotegerin (OPG), govern vascular calcification and may explain the phenomenon. Both RANKL and OPG are widely accepted as the final common pathway for most factors and processes affecting bone resorption. Binding of RANKL to its cognate receptor RANK induces NF-kappaB signaling, which stimulates osteoclastic differentiation in preosteoclasts and induces bone morphogenetic protein (BMP-2) expression in chondrocytes. A role for RANKL and its receptors in vascular calcification is spported by several findings: a vascular calcification phenotype in mice genetically deficient in OPG; an increase in expression of RANKL, and a decrease in expression of OPG, in calcified arteries; clinical associations between coronary disease and serum OPG and RANKL levels; and RANKL induction of calcification and osteoblastic differentiation in valvular myofibroblasts.

Animals↗
PubMed1978

Selective calcification of pancreatic islets of Langerhans. An unusual association with hypercalcemia and diabetes mellitus.

An unusual and extensive calcification of islets of Langerhans was found at autopsy in a man, 58 years old, who developed myeloma and, subsequently, hypercalcemia and diabetes. Although the islet cell calcification appears to be related to the hypercalcemia, the pathogenesis of the calcification is not clear, as primary metastatic calcification of pancreatic islets due to hypercalcemia does not occur. In support of this, a retrospective study of pancreatic tissue from 52 hypercalcemic patients with parathyroid adenoma and 34 patients with multiple myeloma, who frequently have hypercalcemia, did not reveal islet calcification. The islet calcification is ascribed to primary islet cell degeneration and necrosis, with hypercalcemia playing an augmenting but crucial role. It is considered that the combination of islet degeneration and calcification resulted in the diabetic state.

Calcinosis↗
PubMed2006

Elastin calcification in the rat subdermal model is accompanied by up-regulation of degradative and osteogenic cellular responses.

Calcification of vascular elastin occurs in patients with arteriosclerosis, renal failure, diabetes, and vascular graft implants. We hypothesized that pathological elastin calcification is related to degenerative and osteogenic mechanisms. To test this hypothesis, the temporal expression of genes and proteins associated with elastin degradation and osteogenesis was examined in the rat subdermal calcification model by quantitative real-time reverse transcription-polymerase chain reaction and specific protein assays. Purified elastin implanted subdermally in juvenile rats exhibited progressive calcification in a time-dependent manner along with fibroblast and macrophage infiltration. Reverse transcription-polymerase chain reaction analysis showed that relative gene expression levels of matrix metalloproteinases (MMP-2 and MMP-9) and transforming growth factor-beta1 were increased in parallel with calcification. Gelatin zymography showed strong MMP activities at early time points, which were associated with high levels of soluble elastin peptides. Gene expression of core binding factor alpha-1, an osteoblast-specific transcription factor, increased in parallel with elastin calcification and attained approximately 9.5-fold higher expression at 21 days compared to 3 days after implantation. Similarly, mRNA levels of the bone markers osteopontin and alkaline phosphatase also increased progressively, but osteocalcin levels remained unchanged. We conclude that degenerative and osteogenic processes may be involved in elastin calcification.

Alkaline Phosphatase↗
PubMed1990

The relationship of pineal calcification to subtypes of tardive dyskinesia in bipolar patients.

Recent studies have suggested that bipolar patients may be at high risk for developing tardive dyskinesia (TD) if exposed to chronic neuroleptic therapy. It has been suggested that reduced melatonin secretion may favor the development of TD in bipolar and schizoaffective patients. Since pinealectomized rats have been reported to develop increased incidence and severity of abnormal chewing movements, and as depression is associated with reduced melatonin secretion, the increased risk of TD in bipolar patients may be associated with diminished melatonin secretion. Evidence suggestive of an inverse correlation between pineal calcification and reduced melatonin secretion, led me to study the relationship between pineal calcification on CT scan and the severity of axial (truncal) and limb and orofacial dyskinesias in bipolar patients with TD. The incidence of pathologically enlarged pineal calcifications (i.e., greater than 1 cm in diameter) in the bipolar patients was 25 times greater than the reported incidence in the literature among nonpsychiatric patients. In addition, there was a significant difference in scores of axial dyskinesias between patients with pineal calcification of less than 1 cm in diameter compared to those with pineal calcification of greater than 1 cm in diameter (F = 3.24; p = .04, one-way ANOVA). There was no significant association between scores of limb and orofacial dyskinesias and pineal calcification. These findings suggest a meaningful association between the presence of enlarged pineal calcification, and axial dyskinesias in bipolar patients. Further studies using direct plasma melatonin measurements are required to more precisely define the association between TD and melatonin secretion in bipolar patients.

Adult↗
PubMed1985

Hepatocellular calcification.

A rare example of hepatocellular calcification is described. The lesion is characterized by the presence of granular calcific deposits within the cytoplasm of hepatocytes. In this instance the calcification was dystrophic, developing on the basis of centrilobular necrosis secondary to cor pulmonale. A transient hyperphosphatemia probably augmented the calcification process. Intracellular calcification was also observed in occasional cardiac myocytes. The intracytoplasmic calcific granules represent mineral-laden mitochondria. Sequestration of calcium by mitochondria is a common biochemical mechanism mediating various forms of toxic cell death. Pathological cellular calcification can be viewed as an uncommon morphological expression of this biochemical process.

Aged↗
PubMed1976

Tissue degradation of calcific Schistosoma haematobium eggs.

Calcific eggs of Schistosoma haematobium were separated from an inactive sandy patch in a cystectomy specimen from an Egyptian farmer; the purified egg suspension was injected into tail veins of inbred mice, some of which were killed immediately and some at intervals of 1, 2, 11, 14, 30, 90, 120, 180, and 365 days. Lungs were examined by tissue digestion and histologic analysis. Calific egg burdens decayed in an exponential manner (eggs/g of lung tissue = 284.9e-0.001x where e = natural log and x = time in days), with a loss of 5,610 eggs/g of lung tissue, i.e., 98% reduction over the year of the experiment. Histologic examination revealed that calcific S. haematobium eggs incited a typical granulomatous reaction as they decalcified. Compared with viable egg granulomata, the response to calcific eggs was accelerated in onset, of lesser magnitude but persisted longer. Small numbers of calcific eggs persisted for at least 1 year after injection of either viable or calcific eggs. It is concluded that despite the apparent lack of tissue reaction to calcific eggs in chronic bladder lesions, these eggs are not antigenically exhausted foreign bodies. Moreover, it is shown that calcific eggs are degraded in significant numbers by mammalian tissue.

Animals↗
PubMed2001

Association of mild hyperhomocysteinemia with aortic calcification in hypercholesterolemic patients.

Homocysteine is considered to be an independent risk factor for atherosclerosis. Experimental animal models of hyperhomocysteinemia show aortic calcification, suggesting that this disorder is associated with aortic calcification in humans. A total of 28 patients with hyperlipidemia were enrolled into this study. The degree of aortic calcification at the level of the bifurcation and 1 cm proximal to the bifurcation was assessed by computed tomography of the aorta and the association between calcification of the aorta and the plasma level of homocysteine was then analyzed. The mean plasma homocysteine level in 28 patients was 8.7 microM. They were divided into 2 groups, high homocysteine level group (HHL; homocysteine level >8.7 microM) and low homocysteine level group (LHL; homocysteine level < = 8.7 microM). The degree of aortic calcification at the level of the bifurcation differed significantly between the two groups (19.1% vs. 10.5%; p < 0.01). We found that mild hyperhomocysteinemia was associated with aortic calcification, which suggests that interventions to reduce the plasma level of homocysteine may also reduce the severity of aortic calcification.

Aged↗