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PubMed1998

Retroperitoneal Castleman's disease of the hyaline vascular type presenting arborizing calcification.

Castleman's disease (CD) usually manifests as a solitary mediastinal tumor and only rarely as an isolated retroperitoneal mass. In the latter instances it is difficult to distinguish radiographically from other retroperitoneal masses. We report a 22-year-old female patient with retroperitoneal CD of the hyaline vascular type presenting with arborizing calcification. This characteristic calcification pattern is considered unique to CD, and is useful in diagnosis when present.

Adult↗
PubMed2005

Proliferation potential of spinal meningiomas.

OBJECTIVES: The goal of the present study was to quantitatively assess the proliferation index and progesterone receptor status of spinal versus intracranial meningiomas and to determine if these biological indicators can describe the clinical behavior of these tumors. This information could provide the spinal surgeon with important additional information concerning surgical management and follow-up recommendations for the individual patient. METHODS: The study group consisted of 26 patients with spinal and 241 patients with intracranial meningiomas. Patients with atypical or anaplastic tumors as well as with neurofibromatosis type II were excluded from the study. Furthermore both groups were matched according to age, sex and resection grade (total resection according the Simpson classification). Proliferation index (Ki-67 Labelling index [LI]) and progesterone-receptor (PR) status of spinal and intracranial meningiomas were compared. Clinical charts including surgical and histological records and imaging studies were reviewed. Correlations with histological subtype, intratumoral calcifications, tumor vascularity and recurrence-free survival were analyzed. RESULTS: Compared to the spinal group with a mean Ki-67 LI of 2.48% and a positive PR-status of 46%, proliferation rates of intracranial meningiomas were significant higher (Ki-67 LI 3.6%; P-value 0.041). No significant difference in PR status was seen (spinal PR-status 46%, P-value 0.261). Furthermore spinal meningiomas were less vascularized and showed less intratumoral calcifications. Time to recurrence was similar in spinal and intracranial tumors. CONCLUSION: Spinal and intracranial meningiomas differ in their proliferation activity but not in their PR status. However, despite lower proliferation rates, time to recurrence in spinal and cranial meningiomas is comparable in totally excised tumors. Further studies are needed to determine the role of other biological indicators in spinal meningioma growth and response to therapy.

Adult↗
PubMed2004

Secondary hyperparathyroidism: review of the disease and its treatment.

BACKGROUND: Most patients with chronic kidney disease (CKD) stage 5 develop secondary hyperparathyroidism (SHPT). SHPT is an adaptive response to CKD and its associated disruptions in the homeostatic control of serum phosphorus, calcium, and vitamin D. The poor control of mineral and parathyroid hormone (PTH) levels characteristic of SHPT is associated with serious clinical consequences. OBJECTIVE: This review discusses the pathophysiology and consequences of SHPT, as well as the efficacy and limitations of current treatment modalities. METHODS: Literature searches were conducted using the MEDLINE, EMBASE, and BIOSIS databases. Additional information was obtained from Internet web sites, textbooks, and nephrology congress abstracts. RESULTS: Patients with uncontrolled SHPT are at higher risk for cardiovascular morbidity and mortality, hospitalization, bone disease, vascular and soft-tissue calcification, and vascular access failure than patients whose mineral and PTH levels are well managed. New National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI) targets for calcium, phosphorus, calcium-phosphorus product, and PTH control have recently been published with the aim of improving the management of mineral metabolism in CKD patients. Data from observational studies suggest that the majority of patients currently have PTH and mineral levels outside these target ranges. CONCLUSIONS: Given the inadequacies of current therapies, novel agents are being developed that may help improve the management of SHPT.

Calcium↗
PubMed2006

Calcium deposition and associated chronic diseases (atherosclerosis, diffuse idiopathic skeletal hyperostosis, and others).

Extracellular matrix mineralization or calcification occurs in many pathologic conditions, including atherosclerosis, medial wall calcification, diffuse idiopathic skeletal hyperostosis, and chondrocalcinosis. Vascular wall calcification is the most common and involves two mechanisms: passive calcification resulting from breakdown of the protection system and active calcification resulting from transdifferentiation of mesenchymal cells in the vascular wall to bone. Although reports are conflicting, several matrix proteins are identified as protective factors against dystrophic calcification in nonosseous tissues. Serum matrix Gla protein may be a marker of osteometabolic syndromes that cause hyperostosis and plays a role in Milwaukee shoulder syndrome.

Atherosclerosis↗
PubMed2001

Mitral annulus calcification--a window to diffuse atherosclerosis of the vascular system.

Mitral annulus calcification (MAC) is a chronic, non-inflammatory, degenerative process of the fibrous support structure of the mitral valve. It occurs more often in women and the elderly. MAC is associated with known atherosclerotic risk factors such as diabetes mellitus, hypertension and hypercholesterolemia. It is also known that patient with MAC have higher prevalence of left atrial and left ventricular enlargement, hypertrophic cardiomyopathy, atrial fibrillation, aortic valve calcification and stenosis, various cardiac conduction defects, bacterial endocarditis, cardiovascular events and stroke, though the etiological basis is unknown. Pathological studies from the 80s present a theory that MAC is a form of atherosclerosis. In order to test this theory we conducted during the last years a few clinical studies to examine the association of MAC and known atherosclerotic phenomena. We found higher prevalence of aortic atheroma in patients with MAC and atheroma thickness. We also found in MAC patients higher prevalence of carotid artery stenosis, coronary artery stenosis, peripheral artery stenosis and higher levels of beta2-Glycoprotein I antibodies in patients with MAC thickness equal or greater than 5 mm. These studies support the theory that MAC is a form of atherosclerosis and define a group of patients with higher prevalence of atherosclerotic disease in multiple blood vessels. The purpose of this review is to summarize the data concerning MAC and atherosclerotic processes, emphasizing that MAC in itself may be an atherosclerotic process.

Arteriosclerosis↗
PubMed1989

Calcification of the ductus venosus: a cause of right upper quadrant calcification in the newborn.

The authors report three cases of ductus venosus calcification as an additional cause of vascular liver calcification in the newborn. All three infants had umbilical venous catheters. The calcification may be caused by extravasated fluids given through the catheter or by local trauma due to catheter insertion. An obliquely oriented, paravertebral "tram-track" calcification in the right upper quadrant, particularly in a premature infant with a history of umbilical venous catheterization, should suggest the diagnosis of calcified ductus venosus.

Calcinosis↗
PubMed2004

Breast arterial calcifications as an indicator of systemic vascular disease.

PURPOSE: To evaluate the association between mammographically detected arterial calcifications and systemic vascular disease. MATERIAL AND METHODS: The medical records of 77 women who had either breast arterial calcifications or underwent surgery for carotid stenosis, abdominal aortic aneurysm, or femoropopliteal bypass (study groups A and B) were evaluated and compared with 33 women without breast arterial calcifications (group C). Patients in both arms of the study underwent additional vascular tests or mammography. RESULTS: Currently available data indicate that there is a statistically significant correlation between the presence of arterial calcifications on the mammogram and atheromatosis of the carotid or femoral arteries. CONCLUSION: Screening mammograms might be useful in the detection of women at risk for systemic vascular disease.

Adult↗
PubMed2001

Oxidative stress modulates osteoblastic differentiation of vascular and bone cells.

Oxidative stress may regulate cellular function in multiple pathological conditions, including atherosclerosis. One feature of the atherosclerotic plaque is calcium mineral deposition, which appears to result from the differentiation of vascular osteoblastic cells, calcifying vascular cells (CVC). To determine the role of oxidative stress in regulating the activity of CVC, we treated these cells with hydrogen peroxide (H(2)O(2)) or xanthine/xanthine oxidase (XXO) and assessed their effects on intracellular oxidative stress, differentiation, and mineralization. These agents increased intracellular oxidative stress as determined by 2,7 dichlorofluorescein fluorescence, and enhanced osteoblastic differentiation of vascular cells, based on alkaline phosphatase activity and mineralization. In contrast, H(2)O(2) and XXO resulted in inhibition of differentiation markers in bone osteoblastic cells, MC3T3-E1, and marrow stromal cells, M2-10B4, while increasing oxidative stress. In addition, minimally oxidized low-density lipoprotein (MM-LDL), previously shown to enhance vascular cell and inhibit bone cell differentiation, also increased intracellular oxidative stress in the three cell types. These effects of XXO and MM-LDL were counteracted by the antioxidants Trolox and pyrrolidinedithiocarbamate. These results suggest that oxidative stress modulates differentiation of vascular and bone cells oppositely, which may explain the parallel buildup and loss of calcification, seen in vascular calcification and osteoporosis, respectively.

Alkaline Phosphatase↗
PubMed2006

Impact of treatment with calcimimetics on hyperparathyroidism and vascular mineralization.

Soft tissue calcification that involves primarily the medial portion of the arterial vasculature is a widely recognized and common complication of chronic kidney disease Vascular calcification (VC) causes increased arterial stiffness and contributes to the high cardiovascular mortality and morbidity in dialysis patients. The pathogenesis of VC is complex and includes factors that promote calcification and others that inhibit calcification. Studies in dialysis patients have shown a correlation between VC and a number of uremia-related factors. Overall, abnormalities in calcium and phosphate metabolism, such as hyperphosphatemia and a raised serum calcium-phosphorus product traditionally have been thought of as important determinants in patients with chronic renal failure. Common therapeutic interventions in secondary hyperparathyroidism have come under scrutiny for associations with the development of VC. Calcimimetics provide a means of controlling serum levels of parathyroid hormone in secondary hyperparathyroidism without increasing the calcium-phosphorus product and, more important, may lower the risk for VC in these patients.

Calcinosis↗
PubMed2005

Comparison of surgically removed cardiac valves of patients with ESRD with those of the general population.

BACKGROUND: Patients with end-stage renal disease (ESRD) have increased vascular and valvular calcification compared with the general population. Recently, 44% of renal transplant recipients were found to have vascular calcification of the medial layer of the inferior epigastric artery that was associated with deposition of bone matrix proteins. Similar findings have been reported for native and bioprosthetic cardiac valves surgically removed from patients without ESRD. METHODS: To determine whether valvular calcification in patients with ESRD is similar to that in patients without ESRD, we retrospectively examined surgically excised native cardiac valves of all hemodialysis patients and compared them pathologically with those of matched controls without renal failure. Valves were examined by using routine stains and immunohistochemistry for markers to endothelial cells, macrophages, B and T lymphocytes, alkaline phosphatase, osteopontin, and bone morphogenic protein 4. RESULTS: Histologically, 7 of 10 valves from patients with ESRD had moderate to severe inflammation compared with 1 of 10 valves from control patients. Patients with ESRD had more endothelial cells/vascularity (P = 0.002) and macrophages (P = 0.069). There was no difference between the 2 groups with respect to B and T lymphocytes, alkaline phosphatase, osteopontin, or bone morphogenic protein 4. CONCLUSION: The noncollagenous proteins bone morphogenic protein and osteopontin have been shown in surgically removed cardiac valves of patients with ESRD and the general population. However, valvular calcification in patients with ESRD is associated with enhanced inflammation, consistent with the previously reported greater C-reactive protein levels in this patient population and their increased risk for death.

Alkaline Phosphatase↗
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↗
PubMed2001

Calcification comparison of polymers for vascular graft.

Polytetrafluoroethylene (PTFE), polyurethane (PU) and silicone are widely known biocompatible polymers which are commonly used for vascular grafts. However, in vitro and in vivo calcifications of these polymers have been found to seriously compromise their quality as biomaterials. In consideration of this problem, the present study compared the calcification rate and extent of PTFE, PU and silicone. Using the in vitro flow-type method, PTFE, PU and silicone films were tested for 1, 4, 7, 10, 14 and 21 days. After 21 days of in vitro calcification test, the calcium levels on PTFE, PU and silicone were 35.89 +/- 5.01 microg/cm2, 23.73 +/- 0.68 microg/cm2 and 19.86 +/- 5.28 microg/cm2, respectively. The higher observed calcium level for PTFE may be due to the effect of the rough surface of PTFE in accumulating calcium ions on the polymer surface. From the 7th day of test, the [Ca]/[P] molar ratio started to decrease over time, and PTFE showed a faster calcification process. This decreasing [Ca]/[P] molar ratio demonstrated the typical calcification mechanism consisting of phosphorus ion accumulation following calcium ion accumulation. This study concluded that PU and silicone are less calcified than PTFE film, a finding in good agreement with previously published studies.

Biocompatible Materials↗
PubMed2000

Expression of osteopontin in calcified coronary atherosclerotic plaques.

Advanced atherosclerosis is often associated with dystrophic calcification and remodeling of extracellular matrix of vascular wall. Recently many studies have documented a general relationship between calcification and severity of coronary disease, and discussed the feasibility of electron beam computed tomography for detecting and quantifying the coronary artery calcification in the patients. The present study investigated the expression and the localization of osteopontin, one of noncollagenous bone matrix protein, within the calcified coronary arteries. Autopsy-derived coronary artery specimens were scanned and reconstructed to visualize the pattern of coronary calcification using a novel microscopic computed tomography technique. The localization of the osteopontin were evaluated by immunohistochemial stain with LF7. The present study showed that the pattern of coronary calcification is variable and the expression of osteopontin is localized mainly to calcified lesion. The smooth muscle cells in addition to macrophage expressed osteopontin protein in human coronary atherosclerotic plaques. Soluble osteopontin released near to the sites of vascular calcification may represent an adaptive mechanism aimed at regulating the process of vascular calcification.

Aged↗
PubMed2003

Musculoskeletal manifestations of chronic renal failure.

Musculoskeletal problems remain among the main limitations of the quality of life of renal failure patients, in particular of those treated with long-term maintenance dialysis. Renal osteodystrophy continues to receive great attention. The mechanisms of uremic skeletal resistance to parathormone (PTH) are further investigated. The assay used for the dosage of "intact PTH" has been found to detect 7-84 fragments with an inhibitory effect on the action of the whole hormone. A decrease in the density of PTH receptor on osteoblasts is another recently evidenced factor. Investigations of the recently described RANK-RANKL system have demonstrated an increase in serum osteprotegerin levels, which, together with the two above-mentioned abnormalities, may explain bone resistance to PTH. These are important advances in the understanding of renal osteodystrophy as skeletal resistance to PTH appears to play an important part in the pathophysiology of secondary hyperparathyroidism and of adynamic bone disease. Because of this skeletal resistance, it has been recommended for several years that serum PTH level be monitored and kept twofold to threefold above the upper value of the normal level to maintain normal bone turnover in dialysis patients. Relative hypoparathyroidism has recently been found to be associated with increased spontaneous fracture rate and mortality, so this recommendation appears to hold adequate, despite the demonstration that serum PTH levels in this range are a poor predictor of bone turnover and that chronic parathyroid gland hyperplasia is likely to favor parathyroid gland autonomization. Recent publications have insisted on the role that hyperphosphatemia plays not only in the development of secondary hyperparathyroidism, but also of vascular, especially coronary, calcification and as a predictor of mortality. This "silent killer" of uremic patients is one of the main targets for therapeutic intervention. Extensive use of calcium-containing phosphate binders has been recently criticized as calcium overload appears to favor vascular calcification. Sevelaner (RenaGel) is a calcium- and aluminum-free phosphate binder that is an important advance in the management of renal osteodystrophy, especially in patients with extraskeletal calcification and hypercalcemia. The use of vitamin D derivatives has also raised concern because they enhance calcium and phosphorus absorption and reduce bone turnover. New metabolites with fewer hypercalcemic effects have been developed. Calcium-sensing receptor agonists are stimulating interest and are likely to take an important place in the future management of renal osteodystrophy. Uremic myopathy has received recent attention. Impaired muscle capillary oxygen transfer has been identified as a pathophysiologic factor, and progressive resistance training has been shown to improve the condition. Finally, a new entity, nephrogenic fibrosing dermopathy, has been described, which must be distinguished from calciphylaxis and scleromyxedema.

Clinical Trials as Topic↗
PubMed2004

Autoimmune pancreatitis: imaging features.

PURPOSE: To retrospectively determine imaging findings in patients with autoimmune pancreatitis. MATERIALS AND METHODS: Twenty-nine patients (25 male and four female; mean age, 56 years; range, 15-82 years) with histopathologic diagnosis of autoimmune pancreatitis were examined. Data were reviewed by two radiologists in consensus. Imaging findings for review included those from helical computed tomography (CT), 25 patients; magnetic resonance (MR) imaging with MR cholangiopancreatography (MRCP), four patients; endoscopic ultrasonography (US), 21 patients; endoscopic retrograde cholangiopancreatography (ERCP), 19 patients; and percutaneous transhepatic cholangiography, one patient. Images were analyzed for appearances of pancreas, biliary and pancreatic ducts, and other findings, such as peripancreatic inflammation, encasement of vessels, mass effect, pancreatic calcification, peripancreatic nodes, and peripancreatic fluid collection. Follow-up images were available in nine patients. Serologic markers such as serum immunoglobulin G (IgG) and antinuclear antibody levels were available in 12 patients. RESULTS: CT showed diffuse (n = 14) and focal (n = 7) enlargement of pancreas. Seven patients had minimal peripancreatic stranding, with lack of vascular encasement, calcification, or peripancreatic fluid collection. Nine patients had enlarged peripancreatic lymph nodes. MR imaging showed focal (n = 2) and diffuse (n = 2) enlargement with rimlike enhancement in one. MRCP revealed pancreatic duct strictures in two and sclerosing cholangitis-like appearance in one. Endoscopic US showed diffuse enlargement of pancreas with altered echotexture in 13 patients and focal mass in the head in six. ERCP showed stricture of distal common bile duct in 12 patients, irregular narrowing of intrahepatic ducts in six, diffuse irregular narrowing of pancreatic duct in nine, and focal stricture of proximal pancreatic duct in six. Serologic markers showed increased IgG and antinuclear antibody levels in seven of 12 patients. At follow-up, CT abnormalities and common bile duct strictures resolved after steroid therapy in three patients. CONCLUSION: Features that suggest autoimmune pancreatitis include focal or diffuse pancreatic enlargement, with minimal peripancreatic inflammation and absence of vascular encasement or calcification at CT and endoscopic US, and diffuse irregular narrowing of main pancreatic duct, with associated multiple biliary strictures at ERCP.

Adolescent↗