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1
Gade, Piyusha S., Riikka Tulamo, Kee-won Lee, Fernando Mut, Eliisa Ollikainen, Chih-Yuan Chuang, Bong Jae Chung, et al. "Calcification in Human Intracranial Aneurysms Is Highly Prevalent and Displays Both Atherosclerotic and Nonatherosclerotic Types." Arteriosclerosis, Thrombosis, and Vascular Biology 39, no. 10 (October 2019): 2157–67. http://dx.doi.org/10.1161/atvbaha.119.312922.
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Objective: Although the clinical and biological importance of calcification is well recognized for the extracerebral vasculature, its role in cerebral vascular disease, particularly, intracranial aneurysms (IAs), remains poorly understood. Extracerebrally, 2 distinct mechanisms drive calcification, a nonatherosclerotic, rapid mineralization in the media and a slower, inflammation driven, atherosclerotic mechanism in the intima. This study aims to determine the prevalence, distribution, and type (atherosclerotic, nonatherosclerotic) of calcification in IAs and assess differences in occurrence between ruptured and unruptured IAs. Approach and Results: Sixty-five 65 IA specimens (48 unruptured, 17 ruptured) were resected perioperatively. Calcification and lipid pools were analyzed nondestructively in intact samples using high resolution (0.35 μm) microcomputed tomography. Calcification is highly prevalent (78%) appearing as micro (<500 µm), meso (500 µm–1 mm), and macro (>1 mm) calcifications. Calcification manifests in IAs as both nonatherosclerotic (calcification distinct from lipid pools) and atherosclerotic (calcification in the presence of lipid pools) with 3 wall types: Type I—only calcification, no lipid pools (20/51, 39%), Type II—calcification and lipid pools, not colocalized (19/51, 37%), Type III—calcification colocalized with lipid pools (12/51, 24%). Ruptured IAs either had no calcifications or had nonatherosclerotic micro- or meso-calcifications (Type I or II), without macro-calcifications. Conclusions: Calcification in IAs is substantially more prevalent than previously reported and presents as both nonatherosclerotic and atherosclerotic types. Notably, ruptured aneurysms had only nonatherosclerotic calcification, had significantly lower calcification fraction, and did not contain macrocalcifications. Improved understanding of the role of calcification in IA pathology should lead to new therapeutic targets.
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Li, Yuan, Changqiu Wang, Anhuai Lu, Kang Li, Xiao Cheng, Chongqing Yang, Yanzhang Li, Yan Li, and Hongrui Ding. "A Comparative Study of Pathological Nanomineral Aggregates with Distinct Morphology in Human Aortic Atherosclerotic Plaques." Journal of Nanoscience and Nanotechnology 21, no. 1 (January 1, 2021): 547–54. http://dx.doi.org/10.1166/jnn.2021.18449.
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Calcification exists in atherosclerotic plaques in the form of nanomineral aggregates and is closely related to the development of atherosclerosis. Spheroidal and massive calcification are two major types of calcification found in atherosclerotic tissue. However, the exact difference between these two types of calcification is still not clear. Samples composed entirely of spheroidal calcifications and massive calcifications were isolated from aortic atherosclerotic plaques and tested using both bulk and microscopic analysis techniques. Scanning electron microscopy and transmission electron microscopy showed that spheroidal calcifications had a core–shell structure. Massive calcifications were composed of randomly arranged nanocrystals. Synchrotron radiation X-ray diffraction, Raman spectroscopy and selected area electron diffraction showed amorphous calcium phosphate, whitlockite and carbonate hydroxyapatite all existing in spheroidal calcification, while massive calcification only consisted of carbonate hydroxyapatite. We conclude that amorphous calcium phosphate may act as a precursor phase of spheroidal calcifications that eventually transforms into a crystalline phase, while whitlockite in lesions could aggravate the progression of atherosclerosis.
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Golüke, Nienke M. S., Enrico Meijer, Emiel A. van Maren, Annemarieke de Jonghe, Mariëlle H. Emmelot-Vonk, Evelien van Valen, Pim A. de Jong, and Huiberdina L. Koek. "Amount and Distribution of Intracranial Calcification in Symptomatic and Asymptomatic Primary Familial Brain Calcification." Neurology: Clinical Practice 13, no. 4 (May 9, 2023): e200163. http://dx.doi.org/10.1212/cpj.0000000000200163.
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Background and ObjectivesIn clinical practice, it can be difficult to differentiate between intracranial calcifications related to primary familial brain calcification (PFBC) or aging. Also, little is known about the consequences of the amount of intracranial calcifications in patients with PFBC. Therefore, we aimed to compare the amount and distribution of intracranial calcifications in persons with PFBC with controls and between asymptomatic and symptomatic PFBC cases.MethodsThis was a case-control study including patients with PFBC and controls. Controls received a CT of the brain because of a trauma and had at least some basal ganglia calcification. The Nicolas score and volume of calcification were used to quantify intracranial calcifications on the CT scans. Receiver operating characteristic curves were obtained to calculate optimal cutoff points to discriminate between cases and controls. Mann-WhitneyUtests and logistic regression, adjusted for age and sex, were used to compare the amount of calcification.ResultsTwenty-eight cases (median age 65 years, 50.0% male) and 90 controls (median age 74 years, 46.1% male) were included. Calcification scores were higher in cases (median volume: 4.91 cm3against 0.03 cm3,p< 0.001, median Nicolas score: 26.5 against 2.0,p< 0.001) than controls. Calcifications were also more diffusely distributed in cases. To differentiate between cases and controls, optimal cutoff points were ≥0.2 cm3for the calcification volume and ≥6.0 for the Nicolas score. Calcification was higher for symptomatic than asymptomatic cases (calcification volume: 13.62 cm3against 1.61 cm3,p= 0.01, Nicolas score: 39.0 against 15.5,p= 0.02). After adjustment for age and sex, the Nicolas score remained significantly higher in symptomatic patients, and the calcification volume did not.DiscussionPatients with PFBC had more severe intracranial calcifications, and these calcifications were more diffusely distributed through the brain compared with controls. Symptomatic patients with PFBC might have more intracranial calcifications than asymptomatic persons.
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Vos, Annelotte, Aryan Vink, Remko Kockelkoren, Richard A. P. Takx, Csilla Celeng, Willem P. T. M. Mali, Ivana Isgum, Ronald L. A. W. Bleys, and Pim A. de Jong. "Radiography and Computed Tomography Detection of Intimal and Medial Calcifications in Leg Arteries in Comparison to Histology." Journal of Personalized Medicine 12, no. 5 (April 29, 2022): 711. http://dx.doi.org/10.3390/jpm12050711.
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Calcifications are common in the tunica intima and tunica media of leg arteries. There is growing interest in medial arterial calcifications, as they may be modifiable with treatment. We aimed to investigate radiography and computed tomography (CT) for the detection and characterization of both types of arterial calcification in leg arteries in relation to histology. In a postmortem study we therefore investigated 24 popliteal and 24 tibial arteries. The reference standard was presence of arterial calcification and the dominance of intimal or medial calcification on histology. Radiographs and CT scans were scored for presence of calcification and for dominant intimal or medial pattern based on prespecified criteria (annularity, thickness, continuity). Both radiography and CT detected 87% of histologically proven calcifications but missed mild calcifications in 13%. When only the arteries with detected calcifications were included, a moderate agreement was observed on intimal/medial location of calcifications between histology and radiography (correct in 19/24 arteries (79%); Kappa 0.58) or CT (correct in 33/46 arterial segments (72%); Kappa 0.48). With both modalities there was a slight tendency to classify intimal calcifications as being located in the media and to miss media calcification. Our study demonstrates the potential and limitations of both radiography and CT to detect and classify arterial calcifications in leg arteries.
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Wu, Baijian, Xuan Pei, and Zhi-Yong Li. "How Does Calcification Influence Plaque Vulnerability? Insights from Fatigue Analysis." Scientific World Journal 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/417324.
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Background.Calcification is commonly believed to be associated with cardiovascular disease burden. But whether or not the calcifications have a negative effect on plaque vulnerability is still under debate.Methods and Results.Fatigue rupture analysis and the fatigue life were used to evaluate the rupture risk. An idealized baseline model containing no calcification was first built. Based on the baseline model, we investigated the influence of calcification on rupture path and fatigue life by adding a circular calcification and changing its location within the fibrous cap area. Results show that 84.0% of calcified cases increase the fatigue life up to 11.4%. For rupture paths 10Dfar from the calcification, the life change is negligible. Calcifications close to lumen increase more fatigue life than those close to the lipid pool. Also, calcifications in the middle area of fibrous cap increase more fatigue life than those in the shoulder area.Conclusion.Calcifications may play a positive role in the plaque stability. The influence of the calcification only exists in a local area. Calcifications close to lumen may be influenced more than those close to lipid pool. And calcifications in the middle area of fibrous cap are seemly influenced more than those in the shoulder area.
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Sekimoto, Teruo, Takamasa Tanaka, Tatsuya Shiraki, Renu Virmani, and Aloke V. Finn. "How does atherosclerotic plaque become calcified, and why?" AIMS Medical Science 11, no. 4 (2024): 421–38. http://dx.doi.org/10.3934/medsci.2024029.
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<p>Vascular calcification involves the crystallization of calcium/phosphate in the form of hydroxyapatoite in the extracellular matrix of the arterial wall. Vascular calcification is categorized into 3 main etiologies: (1) inflammatory/atherosclerotic (mostly intimal), (2) metabolic (mostly medial), and (3) genetic background (mostly medial). Several overlapping mechanisms trigger all three types of calcifications. Intimal coronary artery calcification simultaneously develops with the progression of atherosclerosis and has been recognized as a surrogate marker of atherosclerotic inflammatory vascular disease. Pathologically, atherosclerotic calcification initially occurs as microcalcifications (0.5 to 15 µm) and results in larger dense calcification, eventually forming sheet calcifications (>3 mm). Among the plaque types, the degree of calcification is the highest in fibrocalcific plaques, followed by healed plaque ruptures, and is the lowest in pathologic intimal thickening. Recent pathologic and imaging-based studies suggest that massive dense calcifications are usually associated with stable plaques, whereas microcalcifications are indicative of vulnerable plaques which may cause acute thrombotic events. Although the mechanisms of calcification are not fully elucidated, apoptotic inflammatory cells and smooth muscle cells, along with the induction of bone formation, play crucial roles in its initiation and progression. A deeper understanding of vascular calcification will improve the risk stratification and patient outcomes through the development of new therapies.</p>
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Sridhar, Sucheta, Yingyue Zhou, Adiljan Ibrahim, Sergio Bertazzo, Tania Wyss, Amanda Swain, Upasana Maheshwari, Sheng-Fu Huang, Marco Colonna, and Annika Keller. "Targeting TREM2 signaling shows limited impact on cerebrovascular calcification." Life Science Alliance 8, no. 1 (October 28, 2024): e202402796. http://dx.doi.org/10.26508/lsa.202402796.
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Brain calcification, the ectopic mineral deposits of calcium phosphate, is a frequent radiological finding and a diagnostic criterion for primary familial brain calcification. We previously showed that microglia curtail the growth of small vessel calcification via the triggering receptor expressed in myeloid 2 (TREM2) in thePdgfbret/retmouse model of primary familial brain calcification. Because boosting TREM2 function using activating antibodies has been shown to be beneficial in other disease conditions by aiding in microglial clearance of diverse pathologies, we investigated whether administration of a TREM2-activating antibody could mitigate vascular calcification inPdgfbret/retmice. Single-nucleus RNA-sequencing analysis showed that calcification-associated microglia share transcriptional similarities to disease-associated microglia and exhibited activated TREM2 and TGFβ signaling. Administration of a TREM2-activating antibody increased TREM2-dependent microglial deposition of cathepsin K, a collagen-degrading protease, onto calcifications. However, this did not ameliorate the calcification load or alter the mineral composition and the microglial phenotype around calcification. We therefore conclude that targeting microglia with TREM2 agonistic antibodies is insufficient to demineralize and clear vascular calcifications.
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Speelman, Lambert, Ajay Bohra, E. Marielle H. Bosboom, Geert Willem H. Schurink, Frans N. van de Vosse, Michel S. Makaroun, and David A. Vorp. "Effects of Wall Calcifications in Patient-Specific Wall Stress Analyses of Abdominal Aortic Aneurysms." Journal of Biomechanical Engineering 129, no. 1 (July 27, 2006): 105–9. http://dx.doi.org/10.1115/1.2401189.
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It is generally acknowledged that rupture of an abdominal aortic aneurysm (AAA) occurs when the stress acting on the wall over the cardiac cycle exceeds the strength of the wall. Peak wall stress computations appear to give a more accurate rupture risk assessment than AAA diameter, which is currently used for a diagnose. Despite the numerous studies utilizing patient-specific wall stress modeling of AAAs, none investigated the effect of wall calcifications on wall stress. The objective of this study was to evaluate the influence of calcifications on patient-specific finite element stress computations. In addition, we assessed whether the effect of calcifications could be predicted directly from the CT-scans by relating the effect to the amount of calcification present in the AAA wall. For 6 AAAs, the location and extent of calcification was identified from CT-scans. A finite element model was created for each AAA and the areas of calcification were defined node-wise in the mesh of the model. Comparisons are made between maximum principal stress distributions, computed without calcifications and with calcifications with varying material properties. Peak stresses are determined from the stress results and related to a calcification index (CI), a quantification of the amount of calcification in the AAA wall. At calcification sites, local stresses increased, leading to a peak stress increase of 22% in the most severe case. Our results displayed a weak correlation between the CI and the increase in peak stress. Additionally, the results showed a marked influence of the calcification elastic modulus on computed stresses. Inclusion of calcifications in finite element analysis of AAAs resulted in a marked alteration of the stress distributions and should therefore be included in rupture risk assessment. The results also suggest that the location and shape of the calcified regions—not only the relative amount—are considerations that influence the effect on AAA wall stress. The dependency of the effect of the wall stress on the calcification elastic modulus points out the importance of determination of the material properties of calcified AAA wall.
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Wen, Jirui, Yali Miao, Shichao Wang, Ruijie Tong, Zhiwei Zhao, and Jiang Wu. "Calcification: A Disregarded or Ignored Issue in the Gynecologic Tumor Microenvironments." International Journal of Gynecologic Cancer 28, no. 3 (March 2018): 486–92. http://dx.doi.org/10.1097/igc.0000000000001185.
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AbstractAlthough calcification in the gynecologic tumor microenvironments is a common phenomenon, doctors and researchers still disregard or ignore the issue. In fact, this change in the gynecologic tumor microenvironments is clinically significant and a number of studies have reported an association between calcification and gynecological tumor progression. In ovarian cancer, calcification is predominantly psammomatous and largely occurs in serous papillary ovarian tumors. In addition, calcification in ovarian cancer correlated with lower histologic grade and may indicate a poorer survival rate. In uterine fibroids, calcification occurs as a degenerative change and is predictive of a good prognosis. As for endometrial cancer and cervical cancer, calcification rarely occurs in these cancers. The mechanism of calcification in the gynecologic tumor microenvironments is not currently clear. One theory is that calcification occurs due to degeneration of the tumor cells; another theory is that calcification occurs in response to secretions from cells in the tumor microenvironment. Although previous studies have revealed a direct association between calcifications and gynecological tumors, this association has not been fully clarified. To better clarify the significance of calcification in terms of diagnosing and treating gynecological tumors, the associations between calcification and the different histologic stages and prognosis in gynecological tumors should be further studied. In particular, more attention should be paid to the morphological characteristics, chemical nature, and mechanism of calcifications in the gynecological tumor microenvironments.
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Zhou, Yuwen, and Qiu Meng. "Bevacizumab associated calcifications might be a prognostic marker in patients with metastatic colorectal cancer." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e16108-e16108. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e16108.
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e16108 Background: Cetuximab associated calcifications is a positive predictive factor in metastatic colorectal cancer (mCRC). In patients with glioblastoma, bevacizumab-induced calcifications are also related to a better prognosis. However, tumor calcifications are rarely recognized in mCRC patients treated with bevacizumab. This study was to investigate the correlation between clinical outcome and calcification in mCRC who received bevacizumab and chemotherapy as the first-line treatment. Methods: A single retrospective cohort study was conducted with all diagnosed mCRC cases who received bevacizumab and chemotherapy as the first-line therapy in our hospital from January 2016 to January 2019. Clinical variables were retrieved from medical records and tumor calcification were evaluated independently by radiologists on the basis of computed tomography scans. A univariate and multivariate COX regression analysis was performed to evaluate the association between calcification and outcome. Results: 159 patients with an average age of 59.0 years were included. Median follow-up was 29.6 months. Among all enrolled patients, 31 had tumor calcification [31/159 (19.5%)]. The median overall survival (OS) and progression-free survival (PFS) was significantly better in patients with calcification than those without calcification (28.0 vs. 24.9 months, p= 0.024; 12.0 vs. 10.0 months, p= 0.026). A higher objective response rate (61.3% vs. 50.0%) was also observed in calcification group. On multivariate analysis, tumor calcification was independently associated with OS (hazard ratio 1.799, 95% CI 1.002–3.230) and PFS (hazard ratio 1.609, 95% CI 1.013–2.557). Conclusions: Tumor calcification was independently associated with improved prognosis in colorectal cancer. It might be a potential prognostic marker.
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Saba, Luca, Valentina Nardi, Riccardo Cau, Ajay Gupta, Hooman Kamel, Jasjit S. Suri, Antonella Balestrieri, et al. "Carotid Artery Plaque Calcifications: Lessons From Histopathology to Diagnostic Imaging." Stroke 53, no. 1 (January 2022): 290–97. http://dx.doi.org/10.1161/strokeaha.121.035692.
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The role of calcium in atherosclerosis is controversial and the relationship between vascular calcification and plaque vulnerability is not fully understood. Although calcifications are present in ≈50% to 60% of carotid plaques, their association with cerebrovascular ischemic events remains unclear. In this review, we summarize current understanding of carotid plaque calcification. We outline the role of calcium in atherosclerotic carotid disease by analyzing laboratory studies and histopathologic studies, as well as imaging findings to understand clinical implications of carotid artery calcifications. Differences in mechanism of calcium deposition express themselves into a wide range of calcification phenotypes in carotid plaques. Some patterns, such as rim calcification, are suggestive of plaques with inflammatory activity with leakage of the vasa vasourm and intraplaque hemorrhage. Other patterns such as dense, nodular calcifications may confer greater mechanical stability to the plaque and reduce the risk of embolization for a given degree of plaque size and luminal stenosis. Various distributions and patterns of carotid plaque calcification, often influenced by the underlying systemic pathological condition, have a different role in affecting plaque stability. Modern imaging techniques afford multiple approaches to assess geometry, pattern of distribution, size, and composition of carotid artery calcifications. Future investigations with these novel technologies will further improve our understanding of carotid artery calcification and will play an important role in understanding and minimizing stroke risk in patients with carotid plaques.
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Schurgers, Leon J., Hermann Aebert, Cees Vermeer, Burkhard Bültmann, and Jan Janzen. "Oral anticoagulant treatment: friend or foe in cardiovascular disease?" Blood 104, no. 10 (November 15, 2004): 3231–32. http://dx.doi.org/10.1182/blood-2004-04-1277.
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Abstract Calcification is a common complication in cardiovascular disease and may affect both arteries and heart valves. Matrix γ-carboxyglutamic acid (Gla) protein (MGP) is a potent inhibitor of vascular calcification, the activity of which is regulated by vitamin K. In animal models, vitamin K antagonists (oral anticoagulants [OACs]) were shown to induce arterial calcification. To investigate whether long-term OAC treatment may induce calcification in humans also, we have measured the grade of aortic valve calcification in patients with and without preoperative OAC treatment. OAC-treated subjects were matched with nontreated ones for age, sex, and disease. Calcifications in patients receiving preoperative OAC treatment were significantly (2-fold) larger than in nontreated patients. These observations suggest that OACs, which are widely used for antithrombotic therapy, may induce cardiovascular calcifications as an adverse side effect.
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Olesen, Ping, Kirsten Nguyen, Lise Wogensen, Thomas Ledet, and Lars Melholt Rasmussen. "Calcification of human vascular smooth muscle cells: associations with osteoprotegerin expression and acceleration by high-dose insulin." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 2 (February 2007): H1058—H1064. http://dx.doi.org/10.1152/ajpheart.00047.2006.
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Arterial medial calcifications occur often in diabetic individuals as part of the diabetic macroangiopathy. The pathogenesis is unknown, but the presence of calcifications predicts risk of cardiovascular events. We examined the effects of insulin on calcifying smooth muscle cells in vitro and measured the expression of the bone-related molecule osteoprotegerin (OPG). Human vascular smooth muscle cells (VSMCs) were grown from aorta from kidney donors. Induction of calcification was performed with β-glycerophosphate. The influence of insulin (200 μU/ml or 1,000 μU/ml) on calcification was judged by measuring calcium content in the cell layer and by von Kossa staining. OPG was measured in the medium by ELISA. Histochemistry was used for determination of alkaline phosphatase (ALP). Bone sialoprotein (BSP) and OPG mRNA expressions were done by RT-PCR. β-Glycerophosphate was able to induce calcification in human smooth muscle cells from a series of donors after variable time in culture. Decreased OPG amounts were observed from the cells during the accelerated calcification phase. High dose of insulin (1,000 μU/ml) accelerated the calcification, whereas lower concentrations (200 μU/ml) did not. Calcified cells expressed ALP and BSP activity in high levels. In conclusion, high concentration of insulin enhances in vitro-induced calcification in VSMCs. Altered OPG levels during the calcification raise the possibility that OPG may have a potent function in regulating the calcification process or it may represent a consequence of mineralization. Effects of insulin and modulations by OPG on the calcification process in arterial cells may play a role in the development of calcifications as part of the diabetic macroangiopathy.
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Vieceli Dalla Sega, Francesco, Francesca Fortini, Paolo Severi, Paola Rizzo, Iija Gardi, Paolo Cimaglia, Claudio Rapezzi, Luigi Tavazzi, and Roberto Ferrari. "Cardiac Calcifications: Phenotypes, Mechanisms, Clinical and Prognostic Implications." Biology 11, no. 3 (March 9, 2022): 414. http://dx.doi.org/10.3390/biology11030414.
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There is a growing interest in arterial and heart valve calcifications, as these contribute to cardiovascular outcome, and are leading predictors of cardiovascular and kidney diseases. Cardiovascular calcifications are often considered as one disease, but, in effect, they represent multifaced disorders, occurring in different milieus and biological phenotypes, following different pathways. Herein, we explore each different molecular process, its relative link with the specific clinical condition, and the current therapeutic approaches to counteract calcifications. Thus, first, we explore the peculiarities between vascular and valvular calcium deposition, as this occurs in different tissues, responds differently to shear stress, has specific etiology and time courses to calcification. Then, we differentiate the mechanisms and pathways leading to hyperphosphatemic calcification, typical of the media layer of the vessel and mainly related to chronic kidney diseases, to those of inflammation, typical of the intima vascular calcification, which predominantly occur in atherosclerotic vascular diseases. Finally, we examine calcifications secondary to rheumatic valve disease or other bacterial lesions and those occurring in autoimmune diseases. The underlying clinical conditions of each of the biological calcification phenotypes and the specific opportunities of therapeutic intervention are also considered and discussed.
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Museedi, Abdulrahman S., and Thierry H. Le Jemtel. "Mitral Annular Calcification-Related Valvular Disease: A Challenging Entity." Journal of Clinical Medicine 13, no. 3 (February 3, 2024): 896. http://dx.doi.org/10.3390/jcm13030896.
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Mitral valve annular calcification-related valvular disease is increasingly common due to the rising prevalence of age-related mitral annular calcifications. Mitral annular calcification alters the structure and function of the mitral valve annulus, which in turn causes mitral valve regurgitation, stenosis, or both. As it frequently coexists with comorbid conditions and overlapping symptoms, mitral annular calcification-related valvular disease poses significant diagnostic and therapeutic challenges. For instance, left ventricular diastolic dysfunction hinders the assessment of mitral valvular disease. Detection of mitral annular calcifications and assessment of related mitral valve disease hinge on two-dimensional echocardiography. Comprehensive assessment of mitral annular calcifications and related mitral valve disease may require multidetector computed tomography and three-dimensional echocardiography. Invasive hemodynamic testing with exercise helps identify the cause of symptoms in patients with comorbid conditions, and transcatheter interventions have emerged as a viable therapeutic option for older patients. After an outline of the normal mitral annulus, we examine how mitral annular calcifications lead to mitral valve disease and how to accurately assess mitral regurgitation and stenosis. Lastly, we review surgical and transcatheter approaches to the management of mitral annular calcification-related mitral valve regurgitation, stenosis, or both.
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Firincioglulari, Mujgan, Secil Aksoy, Kaan Orhan, and Finn Rasmussen. "Comparison of Intracranial and Extracranial Carotid Artery Calcifications between Obstructive Sleep Apnea Patients and Healthy Individuals: A Combined Cone-Beam Computed Tomography and Polysomnographic Study." Radiology Research and Practice 2022 (July 9, 2022): 1–8. http://dx.doi.org/10.1155/2022/1625779.
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Purpose. This study aimed to compare the presence and grades of intra- and extracranial carotid artery calcifications between obstructive sleep apnea (OSA) and non-OSA patients. Methods. CBCT records of 190 patients (95 OSA patients and 95 non-OSA patients) were retrospectively collected and analyzed. Patient demographic data, including age and gender for both study groups and body mass index (BMI), and apnea-hypopnea index (AHI) for OSA patients were recorded. The presence of intra- and extracranial carotid artery calcifications and the number of calcifications were noted according to the grading scale. Results. There was a significant difference in carotid artery calcifications between OSA patients and healthy individuals. A total of 56.8% of the OSA patients showed at least one carotid artery calcification, whereas 13.8% of healthy individuals showed at least one carotid artery calcification ( p < 0.05 ). For intracranial calcifications, OSA patients showed a significantly higher prevalence than healthy individuals ( p < 0.05 ). The results showed that as the apnea-hypopnea index increases in OSA patients, the incidence of carotid artery calcification increases simultaneously. AHI > 30 patients showed the highest percentage of calcifications. Conclusion. In conclusion, OSA patients showed a higher prevalence of calcified carotid artery calcifications than healthy individuals. The results can be interpreted as the higher AHI, the more carotid artery calcification occurs. As these lesions can be a precursor of future strokes, 3D MDCT/CBCT images should evaluate meticulously not only extracranial but also intracranially, especially in OSA patients.
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Wu, Jian-Hui, Wei Zeng, Ren-Guo Wu, Mei Wang, Fei Ye, and Min-Yi Fu. "Comparison of Ultrasonography and CT for Determining the Preoperative Benign or Malignant Nature of Thyroid Nodules: Diagnostic Performance According to Calcification." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382094818. http://dx.doi.org/10.1177/1533033820948183.
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Background: The present study was designed to investigate the presence or absence of calcification and whether calcification size affect the diagnostic accuracy of ultrasonography (US) and computed tomography (CT) in predicting the benign or malignant nature of thyroid nodules. Material and Methods: From May 2014 to April 2019, 445 patients underwent thyroid US and neck CT before thyroid surgery. In each case, US and CT were retrospectively examined by radiologists. We divided the patients into 3 groups according to the type of calcification: no calcification, microcalcification, and macrocalcification. And macrocalcification group divided into rim calcifications and non-rim calcifications groups. We evaluated the diagnostic accuracy of US and CT for differentiating malignant from benign thyroid nodules using histopathological results as a reference standard. Results: In the overall population, adding CT to US resulted in greater sensitivity, lower specificity, and lower accuracy in the prediction of the benign or malignant nature of nodules. In the group with no calcification, US had a significantly greater accuracy than CT and combined US/CT. In the group with macrocalcification, especially in rim calcifications, adding CT to US resulted in greater sensitivity than US, and CT exhibited greater sensitivity and accuracy than US. Conclusion: US is superior to CT for the prediction of the benign or malignant nature of nodules in thyroid lesions according to calcification and CT is also currently not recommended as a routine imaging tool for thyroid nodules. However, the superior sensitivity and accuracy of CT in lesions with macrocalcification especially in rim calcifications may enable CT to play a complementary role in identifying benign and malignant nodules.
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Ferreira, Luciana Bueno, Etel Gimba, João Vinagre, Manuel Sobrinho-Simões, and Paula Soares. "Molecular Aspects of Thyroid Calcification." International Journal of Molecular Sciences 21, no. 20 (October 19, 2020): 7718. http://dx.doi.org/10.3390/ijms21207718.
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In thyroid cancer, calcification is mainly present in classical papillary thyroid carcinoma (PTC) and in medullary thyroid carcinoma (MTC), despite being described in benign lesions and in other subtypes of thyroid carcinomas. Thyroid calcifications are classified according to their diameter and location. At ultrasonography, microcalcifications appear as hyperechoic spots ≤ 1 mm in diameter and can be named as stromal calcification, bone formation, or psammoma bodies (PBs), whereas calcifications > 1 mm are macrocalcifications. The mechanism of their formation is still poorly understood. Microcalcifications are generally accepted as a reliable indicator of malignancy as they mostly represent PBs. In order to progress in terms of the understanding of the mechanisms behind calcification occurring in thyroid tumors in general, and in PTC in particular, we decided to use histopathology as the basis of the possible cellular and molecular mechanisms of calcification formation in thyroid cancer. We explored the involvement of molecules such as runt-related transcription factor-2 (Runx-2), osteonectin/secreted protein acidic and rich in cysteine (SPARC), alkaline phosphatase (ALP), bone sialoprotein (BSP), and osteopontin (OPN) in the formation of calcification. The present review offers a novel insight into the mechanisms underlying the development of calcification in thyroid cancer.
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Pagare, Jaishri, and Anza N.S. "SOFT TISSUE CALCIFICATIONS : ASERIES OF FOUR CASES." International Journal of Advanced Research 11, no. 01 (January 31, 2023): 401–6. http://dx.doi.org/10.21474/ijar01/16029.
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Heterotrophic calcificationsare pathologic calcifications of the soft tissue regiondue to any chronic inflammatory cause(dystrophic calcification) or by hypercalcemic states in the body(metastatic calcification) or due to any idiopathic cause. It is usually detected as an incidental finding and rarely appears symptomatic. Here we are presenting fewcase reports of patients with soft tissue calcifications that reported to the department of Oral Medicine andRadiology.
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Djuric, Petar, Nada Dimkovic, Georg Schlieper, Zivka Djuric, Milan Pantelic, Milica Mitrovic, Aleksandar Jankovic, Marko Milanov, Jovana Kuzmanovic Pficer, and Jürgen Floege. "Sodium thiosulphate and progression of vascular calcification in end-stage renal disease patients: a double-blind, randomized, placebo-controlled study." Nephrology Dialysis Transplantation 35, no. 1 (November 25, 2019): 162–69. http://dx.doi.org/10.1093/ndt/gfz204.
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Abstract Background Sodium thiosulphate (NaTS) is mostly used in haemodialysis (HD) patients with calcific uraemic arteriolopathy. This double-blind, randomized, placebo-controlled study assessed the effect of NaTS on progression of cardiovascular calcifications in HD patients. Methods From 65 screened patients, we recruited 60 patients with an abdominal aorta Agatston calcification score ≥100. Thirty patients were randomized to receive NaTS 25 g/1.73 m2 and 30 patients to receive 100 mL of 0.9% sodium chloride intravenously during the last 15 min of HD over a period of 6 months. The primary endpoint was the absolute change of the abdominal aortic calcification score. Results The abdominal aortic calcification score and calcification volume of the abdominal aorta increased similarly in both treatment groups during the trial. As compared with the saline group, patients receiving NaTS exhibited a reduction of their iliac artery calcification score (−137 ± 641 versus 245 ± 755; P = 0.049), reduced pulse wave velocity (9.6 ± 2.7 versus 11.4 ± 3.6; P = 0.000) and a lower carotid intima-media thickness (0.77 ± 0.1 versus 0.83 ± 00.17; P = 0.033) and had better preservation of echocardiographic parameters of left ventricular hypertrophy. No patient of the NaTS group developed new cardiac valve calcifications during the trial as compared with 8 of 29 patients in the saline group. By univariate analysis, NaTS therapy was the only predictor of not developing new valvular calcifications. No adverse events possibly related to NaTS infusion were noted. Conclusions While NaTS failed to retard abdominal aortic calcification progress, it positively affected calcification progress in iliac arteries and heart valves as well as several other cardiovascular functional parameters.
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Oh, Eunhye, Jeesu Min, Seon Hee Lim, Ji Hyun Kim, Il-Soo Ha, Hee Gyung Kang, and Yo Han Ahn. "Extraskeletal Calcifications in Children with Maintenance Peritoneal Dialysis." Childhood Kidney Diseases 25, no. 2 (December 31, 2021): 117–21. http://dx.doi.org/10.3339/jkspn.2021.25.2.117.
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Chronic kidney disease (CKD)-mineral and bone disorder (CKD-MBD) is a common complication of CKD, often accompanied by extra-skeletal calcification in adult patients. As increased vascular calcification is predicted to increase cardiovascular mortality and morbidity, the revised Kidney Disease: Improving Global Outcomes guidelines recommend avoiding calcium-containing phosphate chelators. However, extra-skeletal calcification is less commonly noticed in pediatric patients. Here, we report our experience of such a complication in pediatric patients receiving maintenance peritoneal dialysis. Extra-skeletal calcification was noticed at the corneas, pelvic cavity, and soft tissues of the lower leg in 4 out of 32 patients on maintenance peritoneal dialysis. These patients experienced the aggravation of extra-skeletal calcifications during peritoneal dialysis, and 2 of them underwent excisional operations. It is required to monitor extra-skeletal calcifications in children on kidney replacement therapy.
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Wang, Zhihong, Hao Zhang, Ping Zhang, Liang He, and Wenwu Dong. "Diagnostic Value of Ultrasound-detected Calcification in Thyroid Nodules." Annals of the Academy of Medicine, Singapore 43, no. 2 (February 15, 2014): 102–6. http://dx.doi.org/10.47102/annals-acadmedsg.v43n2p102.
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Introduction: This study analyses the diagnostic value of ultrasonography (US) detection for calcification in thyroid nodules. Materials and Methods: We analysed the preoperative US findings and clinical characteristics of 577 malignant and 3434 benign thyroid patients who underwent surgery in our hospital. Results: The malignant rate in patients with microcalcification hyperechoic and tiny calcification foci ≤2 mm in diameter was significantly higher than the non-calcification and other calcification group (P <0.001). The malignant rate in single calcification nodule was significantly higher than that in multiple nodule group (P <0.01). Most of the patients (37/39) with lymph node calcification were malignant. The malignant rate of calcification and microcalcification was significantly higher in patients <45 years old than in older patients (P <0.05). Conclusion: Compared with other calcifications, microcalcification should be a better predictor of thyroid carcinoma. Malignancy should be highly suspected in patients with single calcification nodule, especially with lymph node calcification. Patients younger than 45 years of age with calcification or microcalcification have a greater risk for thyroid carcinoma. Key words: Age, Single nodule, Thyroid carcinoma, Ultrasonography
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Bazhenova, D. A., O. S. Puchkova, E. A. Mershina, and V. E. Sinitsyn. "Evaluation of Breast Vascular Calcifications as a Predictor for Coronary Artery Calcification." Journal of radiology and nuclear medicine 102, no. 3 (July 23, 2021): 196–202. http://dx.doi.org/10.20862/0042-4676-2021-102-3-196-202.
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Background. Cardiovascular diseases are one of the main causes of death among women, and current prevention paradigms may not be sufficient in this group. In this context, it has been suggested that the detection of breast vascular calcifications can improve the screening and assessment of the risk of cardiovascular diseases in apparently healthy women.Objective: to study the role of breast vascular calcifications as a potential predictor for coronary artery calcification. Material and methods. Examinations were made in 123 patients who underwent digital mammography and cardiac computed tomography to estimate a coronary artery calcium score.Results. The use of the Wilcoxon-Mann-Whitney W-test for abnormal distribution showed a relationship between the presence of breast vascular calcifications and calcium score (p< 0.001), and that between aortic wall calcification and calcium score (p< 0.001).Conclusion. Breast vascular calcifications detected by mammography are an indicator of a higher frequency of coronary artery calcification and, apparently, a predictor for the increased risk of cardiovascular disease.
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Yatzidis, Hippocrates, and Basil Agroyannis. "Sodium Thiosulfate Treatment of Soft -Tissue Calcifications in Patients with End-Stage Renal Disease." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 7, no. 4 (October 1987): 250–52. http://dx.doi.org/10.1177/089686088700700411.
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Five patients on maintenance hemo dialysis for more than five years, who had tumoral calcifications, were treated by sodium thiosulfate for three to IS months. Four patients with periarticular and soft-tissue calcifications achieved regression of varying degrees and the motion of the adjacent joints was considerably improved. The fifth patient had calcification of penis; sodium thiosulfate produced early relief of symptoms and later complete disappearance of the calcification.
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Freise, Christian, Ki Young Kim, and Uwe Querfeld. "ALindera obtusilobaExtract Blocks Calcium-/Phosphate-Induced Transdifferentiation and Calcification of Vascular Smooth Muscle Cells and Interferes with Matrix Metalloproteinase-2 and Metalloproteinase-9 and NF-κB." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/679238.
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Vascular calcifications bear the risk for cardiovascular complications and have a high prevalence among patients with chronic kidney disease. Central mediators of vascular calcifications are vascular smooth muscle cells (VSMC). They transdifferentiate into a synthetic/osteoblast-like phenotype, which is induced, for example, by elevated levels of calcium and phosphate (Ca/P) due to a disturbed mineral balance. An aqueous extract fromLindera obtusiloba(LOE) is known to exert antifibrotic and antitumor effects or to interfere with the differentiation of preadipocytes. Using murine and rat VSMC cell lines, we here investigated whether LOE also protects VSMC from Ca/P-induced calcification. Indeed, LOE effectively blocked Ca/P-induced calcification of VSMC as shown by decreased VSMC mineralization and secretion of alkaline phosphatase. In parallel, mRNA expression of the calcification markers osterix and osteocalcin was reduced. Vice versa, the Ca/P-induced loss of the VSMC differentiation markers alpha smooth muscle actin and smooth muscle protein 22-alpha was rescued by LOE. Further, LOE blocked Ca/P-induced mRNA expressions and secretions of matrix metalloproteinases-2/-9 and activation of NF-κB, which are known contributors to vascular calcification. In conclusion, LOE interferes with the Ca/P-induced transdifferentiation/calcification of VSMC. Thus, LOE should be further analysed regarding a potential complementary treatment option for cardiovascular diseases including vascular calcifications.
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Bhatt, Bhupendra Prasad. "Evaluation of intracranial physiological calcifications in Computed Tomography." Radiography Open 9, no. 1 in progress (October 27, 2023): 50–59. http://dx.doi.org/10.7577/radopen.5205.
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Introduction: Intracranial physiological calcifications are not related to any pathological conditions, rather they are due to the normal deposition of calcium or iron in the different parts of the brain. Computed Tomography (CT) scan is superior to all other modalities in terms of sensitivity in the detection of intracranial physiological calcifications. The objective of the study was to evaluate the frequency and location of intracranial physiological calcifications and also study them according to age and gender.
Methods: A prospective cross-sectional study with a purposive sampling technique was conducted from November 2020 to February 2021 at the Department of Radiology and Imaging. CT scan images of every age group were reviewed from the base of the skull to the vertex excluding images with intracranial pathologies, injuries, artifacts, contrast enhancement and the patients with follow-up scans. Data were analyzed using SPSS version 25. Descriptive analysis was primarily preferred accompanied by inferential statistics.
Results: Out of 412 patients, 60.7% were male and the mean age was 41.16 ±19.915 years. The total number of calcifications was 795. 92.8% of patients showed calcifications. Males had a higher number of calcifications. The highest number of calcifications was seen in the age group 20-30. The highest calcification was seen in the pineal gland (76%) followed by the choroid plexus (70.4%) and the lowest in the caudate nucleus (0.38%). The earliest age of calcification was 8 years. There was a significant relationship between the increase in age and the increase in calcification (p<0.05). There was also a significant difference between male and female calcifications (p<0.05).
Conclusion: This study can be useful for clinicians to differentiate normal physiological intracranial calcifications from pathological calcification which will reduce misinterpretation of the calcifications.
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Babu, Bincy, R. J. Hemalatha, A. Josephin Arockia Dhivya, T. R. Thamizhvani, and R. Chandrasekaran. "A comparative study on segmentation methods of micro calcification in mammogram." International Journal of Engineering & Technology 7, no. 2.25 (May 3, 2018): 113. http://dx.doi.org/10.14419/ijet.v7i2.25.16571.
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The primary indication of breast cancer is the presence of calcification clusters. It is challenging and lengthy process for radiologists to identify and classify micro calcifications as non-cancerous or cancerous. In this proposed work, a novel method for the detection of micro calcification clusters in mammograms is explained that consists of two main sections. First, mammogram preprocessing is done. Second, micro calcification are segmented out. In preprocessing noise and label are removed as well as contrast is enhanced. Then various segmentation methods are used for comparison of calcification region. Watershed segmentation, Marker controlled watershed segmentation (MCWS), Texture segmentation and Level set segmentation methods are applied to Digital Database for Screening Mammography (DDSM) database. Results show that the MCWS provides quite acceptable detection performance. The major advantage of this method is its capability to detect micro calcifications perfectly even in case of very dense mammograms. The performance of different methods is evaluated by comparing the obtained segmented image with expert radiologist data. The comparison study aptly shows that the micro calcifications can be exactly segment and can avoid over segmentation problem of existing method.
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Goo, Hyung mo, Sang-Youl Yoon, and Seong-Hyun Park. "Fahr disease presenting with multiple cerebral calcifications." Journal of the Korean Society of Stereotactic and Functional Neurosurgery 19, no. 1 (June 30, 2023): 22–25. http://dx.doi.org/10.52662/jksfn.2023.00038.
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Fahr disease, also known as idiopathic basal ganglion calcification, is a rare and genetically heterogeneous neurological disorder. Herein, we report a rare case of Fahr disease presenting with multiple cerebral calcifications. A 63-year-old woman presented with dizziness to a local clinic. Brain computed tomography performed on admission revealed multiple high-intensity lesions in both basal ganglia, both cerebellar hemispheres, and the left frontal lobe. In contrast, brain magnetic resonance imaging (MRI) showed no prominent lesions on T2- and T1-weighted images, and there was no contrast enhancement after gadolinium injection. However, multiple dark signals were detected on gradient echo MRI. The location and radiological appearance of the lesion resembled those of a physiological intracranial calcification, except for asymmetric calcification in both cerebellar hemispheres and the left frontal subcortical white matter. The patient was diagnosed with basal ganglion calcification with multiple cerebral cavernous malformations or, less likely, brain tumors. Through a careful radiological and clinical review, the calcifications were diagnosed as Fahr disease. Follow-up was planned. It is important to consider the presence of multiple intracranial calcifications in the basal ganglia, cerebellum, or deep subcortical white matter as a warning sign for Fahr disease.
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Sabau, Monica, Alexandra Comanescu, Teodor Maghiar, and Daniela Dinulescu. "Hypoparathyroidism diagnosed by neurological signs and widespread intracerebral calcifications." Romanian Journal of Neurology 9, no. 1 (March 31, 2010): 44–50. http://dx.doi.org/10.37897/rjn.2010.1.8.
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Neurological signs associated with intracerebral calcifications require a complex management of calcium, phosphate and parathormone levels and search of a series of general and cerebral disease too. The mechanisms of intracerebral calcification in hypoparathyroidism are not completely known. Neurological signs associated with intracerebral calcification are very rarely the presenting symptoms of hypoparathyroidism. We present 2 cases in which the diagnosis of hypoparathyroidism was brought on by several neurological signs and widespread intracerebral calcification.
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Sio, Maria Christina D., Jacqueline Austine U. Uy, and Ronaldo G. Soriano. "Calcifications in Thyroid Ultrasonography and Thyroid Carcinoma." Philippine Journal of Otolaryngology-Head and Neck Surgery 29, no. 2 (December 2, 2014): 15–18. http://dx.doi.org/10.32412/pjohns.v29i2.413.
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Background: Thyroid nodules are a common disease entity occurring in 5-10% of the general population and increasing with age. Their detection on ultrasonography ranges from 13% to 67%. Calcifications on ultrasound may occur in both benign and malignant diseases, but have been cited for increased risk of thyroid carcinoma.
Objective: To determine the association of calcifications found on thyroid ultrasonography and the different types of calcifications with thyroid carcinoma.
Method:
Study Design: Retrospective Study
Setting: Tertiary Private Hospital
Participants: 126 patients with pre-operative thyroid or neck ultrasonography who subsequently underwent thyroidectomy (total or subtotal, with or without frozen section) were selected from a database covering a one-year period from January to December 2012. The presence and type of calcification on ultrasonography was correlated with the final histopathologic report for a diagnosis of thyroid carcinoma. Sensitivity, specificity, positive and negative predictive values were obtained.
Results: 51 out of 126 studies (40%) were observed to have calcifications of any description, in both histologically benign (41%) and malignant (59%) nodules. Calcifications seen in malignancy arose from papillary carcinoma (86%). Follicular carcinoma and others (Plasmacytoma and Lymphoma) accounted for 7% each. The peripheral type of calcification was most prevalent accounting for 37% (11 out of 30). The sensitivity of detecting calcifications on ultrasonography is 58.82%, specificity 81.33%, positive predictive value 68.18% and negative predictive value 74.38%. Chi square test computed was 21.54 (P <0.05).
Conclusion: There was an association between calcification found on ultrasonography and thyroid carcinoma and 86% of the calcifications were peripheral patterns, mostly found in papillary thyroid carcinomas. Ultrasonography alone is not sufficient in diagnosing thyroid carcinoma, but may increase the suspicion of malignancy depending on the type of calcification.
Keywords: Thyroid carcinoma, papillary carcinoma, calcifications, ultrasonography
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Hagar, Abdullah, Yijian Li, Xin Wei, Yong Peng, Yuanning Xu, Yuanweixiang Ou, Zijie Wang, et al. "Incidence, Predictors, and Outcome of Paravalvular Leak after Transcatheter Aortic Valve Implantation." Journal of Interventional Cardiology 2020 (May 22, 2020): 1–11. http://dx.doi.org/10.1155/2020/8249497.
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Background. Paravalvular leak (PVL) is common after transcatheter aortic valve implantation (TAVI) and has been linked with worse survival. This study aimed to investigate the determinants and outcome of PVL after TAVI and determine the role of aortic valve calcification (AVC) distribution in predicting PVL. Methods and Results. This was a retrospective cohort study of 270 consecutive patients who underwent TAVI. Determinants and outcomes of ≥mild PVL were assessed. Matching rates of PVL jet with AVC distribution were calculated. AVC volume, larger annulus dimensions, and transvalvular peak velocity were risk factors for ≥mild PVL after TAVI. AVC volume was an independent predictor of ≥mild PVL. On the other hand, annulus ellipticity, left ventricular outflow tract nontubularity, and diameter-derived prosthesis mismatch were not found to predict PVL after TAVI. PVL jet matched, in varying proportions, with calcification at all aortic root regions, and the highest matching rate was with calcifications at body of leaflets. Moreover, matching rates were less with commissure compared to cusp calcifications. Mild or greater PVL was not associated with all-cause and cardiovascular mortality up to 1-year follow-up. Conclusion. ≥mild PVL after TAVI is common and can be predicted by aortic root calcification volume, larger annulus dimensions, and pre-TAVI transvalvular peak velocity, with calcification volume being an independent predictor for PVL. However, annulus ellipticity, left ventricular outflow tract nontubularity, and diameter-derived prosthesis mismatch had no role in predicting PVL. Importantly, body of leaflet calcifications (versus annulus and tip of leaflet) and cusp calcifications (versus commissure calcification) are more important in predicting PVL. No association between ≥mild PVL and increased risk of all-cause and cardiovascular mortality at 1-year follow-up.
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Patil, Karthikeya, CJ Sanjay, Eswari Solayappan, and Namrata Suresh. "Facial, lingual, and infraorbital artery calcification: A rare incidental radiographic finding." European Journal of Anatomy 27, no. 3 (May 2023): 361–66. http://dx.doi.org/10.52083/iyau7211.
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Identifying calcification of arteries in the head and neck region may aid in the diagnosis of advanced systemic conditions. In contrast, failure to recognize them can result in incorrect diagnoses and ineffective treatments. Radiographic analyses can be used to detect such calcifications. This report focuses on calcifications discovered in the facial, lingual, and infraorbital arteries following a routine dental care panoramic radiograph. This report is particularly notable because it is the second in the literature to highlight the calcification of all three arteries.
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Masoud, Mirzaie, Josefina Kusnirova, Johann Philipp Addicks, and Sheila Fatehpur. "Matrix-GLA-Protein and Vascular Calcification: Can Diet Influence the Consequences of Matrix GLA Protein Inactivation? A Review." International Journal of Innovative Research in Medical Science 6, no. 10 (October 5, 2021): 678–86. http://dx.doi.org/10.23958/ijirms/vol06-i10/1235.
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In vascular calcification, as a physiological process, intimal arterial calcification (IAC) associated with increased cardiovascular risk is distinguished from medial arterial calcification (MAC) localized mainly in the lamina elatica interna, which are not only based on different pathophysiological mechanisms. They also lead to different cardiovascular diseases. While intimal arterial calcification involves inflammation and lipid accumulation, a calcification process similar to desmal ossification plays the main role in medial arterial calcification. In this context, the phenotype change of smooth muscle cells from muscular type to synthesizing form in the tunica media is considered to be of great importance, which puts the matrix GLA protein, mainly involved in bone metabolism, in the center of interest. The present review work elucidates the molecular biological basis of interaction of matrix GLA protein subunits in the pathogenesis of vascular calcifications and the influence of diet on the consequences of underactivation of matrix GLA protein.
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Yamamoto, Ko, Masahiro Natsuaki, Takeshi Serikawa, Masanori Okabe, and Yusuke Yamamoto. "Nodular Calcification in Saphenous Vein Graft Successfully Treated by Percutaneous Coronary Intervention." Case Reports in Cardiology 2018 (November 8, 2018): 1–4. http://dx.doi.org/10.1155/2018/5138705.
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Nodular calcification is sometimes detected in the native coronary artery. However, it is very rare to find in a saphenous vein graft (SVG). We herein report a rare case of stable angina pectoris (AP) due to nodular calcification. A 75-year-old man who had previously undergone coronary artery bypass grafting was admitted to our hospital due to stable AP. On angiography, significant stenosis was detected in the proximal SVG. Based on the findings of coronary angiography and optical coherence tomography, a red thrombus was suspected at the culprit lesion. However, nodular calcification was also suspected, as there were calcifications around the lesion. As intravascular ultrasound showed the protruding calcification, which we judged to be a nodular calcification, the calcified SVG lesion was successfully treated by percutaneous coronary intervention without any complications. Nodular calcification should be considered as a potential cause of AP, even when located in a SVG.
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MINAMI, A., K. SUDA, K. KANEDA, and M. KUMAKIRI. "Extensive Subcutaneous Calcification of the Forearm in Systemic Lupus Erythematosus." Journal of Hand Surgery 19, no. 5 (October 1994): 638–41. http://dx.doi.org/10.1016/0266-7681(94)90134-1.
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We report two cases with long-standing systemic lupus erythematosus (SLE) who developed widespread calcification in subcutaneous tissue and peri-articular structures. To our knowledge only 26 case reports have appeared concerning this abnormality in SLE. However, there has been no report of calcification in an SLE patient in the literature of orthopaedic surgery. The calcifications of the forearm were marginally removed because of pain surrounding them. X-ray analysis revealed that the calcification was made of pure calcium phosphate.
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Pasynkov, D. V., E. А. Romanycheva, I. A. Egoshin, A. А. Kolchev, S. N. Merinov, O. V. Busygina, and M. A. Mikhaltsova. "Automated differentiation of calcifications and their clusters on the mammography image: the outcomes of the computer aided diagnosis system module." Diagnostic radiology and radiotherapy 15, no. 3 (October 11, 2024): 72–81. http://dx.doi.org/10.22328/2079-5343-2024-15-3-72-81.
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INTRODUCTION: Previously we developed the computer aided detection system (CAD) for mammography MammCheck II that increased the detection rate of small and difficult to detect breast carcinomas (BC). However this system was not specifically designed for calcification detection and discrimination. On the other hand, the calcifications had no influence on the CAD capability to detect BCs that appeared as a focal lesions.OBJECTIVE: To develop the approach for automated differentiation of benign and suspicious calcifications on the mammography images and assess its clinical value.MATERIALS AND METHODS: For the developed software testing we used a set of 390 mammography images with calcifications of all possible types (278 images with benign and 112 images with suspicious calcifications). For classification we used linear support vector machine (SVM) model, that was trained on the set of 126 images (70 — benign and 56 — suspicious). We developed two SVM models: with no vascular calcification analysis and with it. Statistics: for comparison between the normally distributed samples we used the Student’s T-test, for non-normally distributed — Wilcoxon signed-rank or Chi-square tests. For correlation testing of normally distributed samples the Paerson coefficient was calculated, for non-normally distributed samples — the Spearman or Kendall correlation coefficients. The statistical significance corresponded to Р-values <0,05.RESULTS: During the testing of the first model version with no vascular calcification analysis we discovered the similarity of small early vascular calcifications and the suspicious ones. As a result this model falsely classified 14 of 23 (60.87%) vascular calcification clusters as suspicious. Therefore the model was improved. The final discrimination results for all calcification types (both benign and suspicious) obtained with the help of improved model were the following: true positive conclusions — 375/390 (96.15%), false positive conclusions — 15/390 (3.84%). In both cases when suspicious calcifications were classified as benign the wrong results were een only on one mammography view. At the same time, on another view the suspicious calcifications were correctly classified.DISCUSSION: During the CAD development it seems important not only mark the suspicious areas but also suppress false positive markings corresponding to the obviously benign lesions. However it is important during this operation not to suppress the true positive markings. Therefore such systems are inevitably characterized by a certain shift to decreased prognostic value of suspicious markings at the expense of the highest possible prognostic value of benign markings. In our viewpoint, the developed approach meets this requirement. Moreover, its integration into the CAD allows to suppress the markings of soft tissue lesions associated with typical benign calcifications, appeared on the previous processing steps. This capability may decrease the false positive rate of the main CAD module.CONCLUSION: The developed approach to benign and suspicious calcification discrimination (version with vascular calcification analysis) on the mammography image provided the sensitivity — 98.21%, specificity — 95.32%, negative predictive value (benign marking) — 99.25%, positive predictive value (suspicious marking) — 89.43%.
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Wasim Ijaz, Asim Qureshi, Naveed Iqbal, Eizza Niaz, Abid Hussain, and Ifham Khan Jadoon. "Frequency of posterior teeth that presented with pulpal calcifications after orthodontic treatment; a retrospective radiographic assessment." Professional Medical Journal 31, no. 05 (May 4, 2024): 800–805. http://dx.doi.org/10.29309/tpmj/2024.31.05.8013.
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Objective: To assess the pulpal calcification that was presented on radiographs after the completion of orthodontic treatment. Study Design: Retrospective Observational study. Setting: Department of Orthodontic, Ayub Medical College Abbottabad. Period: October 2023 to November 2023. Methods: Following the inclusion and exclusion criteria, the current study was carried out on patients who had reported and registered for orthodontic intervention within the previous five years and had case records from the orthodontics department available. A total of 670 case records were assessed for selecting 191 cases as per sample size. Results: Among 191 patients, 30.4% were male and 69.6% were female. The highest percentage belonged to the 14-16 age group (32%), followed by 20-22 (28.3%), 17-19 (26.2%), and 23-25 (12.6%) age groups. Pre-treatment calcification was 17.8% (n=34), rising to 28.3% (n=54) post-treatment. Pulp calcification significantly increased after orthodontic treatment (p<0.05). No significant differences were found between gender and age groups regarding pulp calcification (p>0.05). However, a significant association existed between pulp calcification and treatment duration (p<0.05). The 25-30 months treatment duration had the highest occurrence (n=27), followed by 31-36 months (n=19). Mandibular teeth had a higher prevalence of pulp calcification (53.7%) than maxillary teeth (46.3%), with tooth number 36 having the highest prevalence (25.9%). A significant relationship was observed between the left and right sides of the dental arches, with the left side exhibiting greater tooth calcification (68.5%) than the right side (31.5%). Conclusions: The present study concluded that there was an increase in the frequency of pulpal calcifications in the observed posterior teeth after orthodontic treatment. Pulpal calcifications were significantly more prevalent in the posterior teeth of the mandibular arch compared to the maxillary arch. Moreover, the likelihood of pulpal calcification increased over the duration of orthodontic treatment.
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Alcantara, Ethel H., Jae-Hee Kwon, Min-Kyung Kang, Young-Eun Cho, and In-Sook Kwun. "Zinc Deficiency Promotes Calcification in Vascular Smooth Muscle Cells Independent of Alkaline Phosphatase Action and Partly Impacted by Pit1 Upregulation." Nutrients 16, no. 2 (January 18, 2024): 291. http://dx.doi.org/10.3390/nu16020291.
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Inorganic phosphate (Pi) is a critical determinant of calcification, and its concentration is regulated by alkaline phosphatase (ALP) and Pit1. ALP is a key regulator of osteogenic calcification and acts by modulating local inorganic phosphate (Pi) concentrations through hydrolyzing pyrophosphate in the extracellular matrix (ECM). Pit1, a sodium-dependent phosphate transporter, regulates calcification via facilitating phosphate uptake within the cells. To investigate whether zinc differentially regulates osteoblastic and vascular calcifications, we examined ALP activity and Pit1 in osteoblastic and vascular smooth muscle cells (VSMCs). Our findings demonstrate that calcification in osteoblastic MC3T3-E1 cells is decreased via diminished ALP action under zinc deficiency. In contrast, zinc-deficiency-induced calcification in VSMCs is independent of ALP action, as demonstrated by very weak ALP activity and expression in calcified VSMCs. In zinc-deficient A7r5 VSMC, P accumulation increased with increasing Na phosphate concentration (3–7 mM) but not with β-GP treatment, which requires ALP activity to generate Pi. Ca deposition also increased with Na phosphate in a dose-dependent manner; in contrast, β-GP did not affect Ca deposition. In osteoblastic cells, Pit1 expression was not affected by zinc treatments. In contrast, Pit1 expression is highly upregulated in A7r5 VSMC under zinc deficiency. Using phosphonoformic acid, a competitive inhibitor of Pit1, we showed that calcification is inhibited in both A7r5 and MC3T3-E1 cells, indicating a requirement for Pit1 in both calcifications. Moreover, the downregulation of VSMC markers under zinc deficiency was restored by blocking Pit1. Taken together, our results imply that zinc-deficiency-induced calcification in VSMC is independent of ALP action in contrast to osteoblastic calcification. Moreover, Pit1 expression in VSMCs is a target for zinc deficiency and may mediate the inhibition of VSMC marker expression under zinc deficiency.
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Seime, Till, Asim Cengiz Akbulut, Moritz Lindquist Liljeqvist, Antti Siika, Hong Jin, Greg Winski, Rick H. van Gorp, et al. "Proteoglycan 4 Modulates Osteogenic Smooth Muscle Cell Differentiation during Vascular Remodeling and Intimal Calcification." Cells 10, no. 6 (May 21, 2021): 1276. http://dx.doi.org/10.3390/cells10061276.
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Calcification is a prominent feature of late-stage atherosclerosis, but the mechanisms driving this process are unclear. Using a biobank of carotid endarterectomies, we recently showed that Proteoglycan 4 (PRG4) is a key molecular signature of calcified plaques, expressed in smooth muscle cell (SMC) rich regions. Here, we aimed to unravel the PRG4 role in vascular remodeling and intimal calcification. PRG4 expression in human carotid endarterectomies correlated with calcification assessed by preoperative computed tomographies. PRG4 localized to SMCs in early intimal thickening, while in advanced lesions it was found in the extracellular matrix, surrounding macro-calcifications. In experimental models, Prg4 was upregulated in SMCs from partially ligated ApoE−/− mice and rat carotid intimal hyperplasia, correlating with osteogenic markers and TGFb1. Furthermore, PRG4 was enriched in cells positive for chondrogenic marker SOX9 and around plaque calcifications in ApoE−/− mice on warfarin. In vitro, PRG4 was induced in SMCs by IFNg, TGFb1 and calcifying medium, while SMC markers were repressed under calcifying conditions. Silencing experiments showed that PRG4 expression was driven by transcription factors SMAD3 and SOX9. Functionally, the addition of recombinant human PRG4 increased ectopic SMC calcification, while arresting cell migration and proliferation. Mechanistically, it suppressed endogenous PRG4, SMAD3 and SOX9, and restored SMC markers’ expression. PRG4 modulates SMC function and osteogenic phenotype during intimal remodeling and macro-calcification in response to TGFb1 signaling, SMAD3 and SOX9 activation. The effects of PRG4 on SMC phenotype and calcification suggest its role in atherosclerotic plaque stability, warranting further investigations.
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Nissrin, Bassim, Rezki Basma, and Sakout Majid. "Association between Periodontitis and Pulp Calcifications: Radiological Study." International Journal of Dentistry 2022 (August 22, 2022): 1–8. http://dx.doi.org/10.1155/2022/9599554.
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Objective. The presence of intrapulpal calcifications is one of the effects reported as a consequence of periodontal pathology. Although the impact of the pulp pathology on the periodontium is obvious, the contrary remains unclear and controversial. This study was conducted in order to better understand this fact and establish a potential association between periodontitis and intrapulpal calcifications and then to determine the factors associated with their occurrence. Materials and Methods. To investigate the issue, a retrospective radiological study using periapical preoperative radiographics assessed 332 teeth taken from the records of 79 patients who received treatment for periodontitis. In the second part of the study, 81 of the sample with intact dental crowns presenting an attachment loss were compared to their contralateral with intact dental crowns without any attachment loss. The study of the association between periodontitis and intrapulpal calcifications and the factors associated with their occurrence was performed by the Chi squared and Fisher’s exact tests. The significance level was set at 0.05. Results. The results indicated that 251 (75.6%) teeth had an attachment loss while 102 (30.7%) had intrapulpal calcification. Among the 206 (62%) teeth with intact crown, only 6 (1.8%) showed calcification in the pulp cavity and 20 (6%) showed calcification in the root canals, with a statistically significant difference ( p < 0.005 ) compared to teeth with restorations and caries. For the 32 (19.7%) teeth with coronary calcification, 18 (22.2%) presented an attachment loss versus 14 (17.2%) without attachment loss; the difference was not statistically significant ( p = 0.6 ). Similarly, only 13 (16%) of a total of 22 (13.5%) teeth with root canal calcification had attachment loss versus 9 (11.1%) without attachment loss. This difference was not statistically significant ( p = 0.5 ). Conclusion. This radiographic study revealed no association between the presence of periodontitis and the occurrence of intrapulpal calcifications. Although intrapulpal calcifications were present in some teeth with loss of attachment, they were not necessarily the consequence of periodontal disease.
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Rennenberg, Roger J. M. W., Bernard J. van Varik, Leon J. Schurgers, Karly Hamulyak, Hugo ten Cate, Tim Leiner, Cees Vermeer, Peter W. de Leeuw, and Abraham A. Kroon. "Chronic coumarin treatment is associated with increased extracoronary arterial calcification in humans." Blood 115, no. 24 (June 17, 2010): 5121–23. http://dx.doi.org/10.1182/blood-2010-01-264598.
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Abstract Vascular calcification is a marker of increased cardiovascular risk. Vitamin K–dependent matrix Gla protein (MGP) is important in inhibiting calcification. Because MGP activation is vitamin K dependent, we performed a cross-sectional study investigating the relationship between the use of vitamin K antagonists and extracoronary vascular calcification. From the Dutch thrombosis services we selected 19 patients younger than 55 years who had no other cardiovascular risk factors and who had used coumarins for more than 10 years, and compared these to 18 matched healthy controls. MGP was measured, and a plain x-ray of the thighs was taken to assess femoral arterial calcifications. The odds ratio for calcification in patients versus controls was 8.5 (95% confidence interval [CI] 2.01-35.95). Coumarin use and MGP were associated with calcification, even after adjusting for other risk factors. We conclude that long-term use of coumarins is associated with enhanced extracoronary vascular calcification, possibly through the inhibition of MGP carboxylation.
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Som, Panchali, Rajarshi Roy, Sumit Datta, Asis Kumar Ghosal, Anubha Saha, and Subhajit Halder. "Physiological Intracranial Calcification in Eastern Indian Population-A CT Scan Study." National Journal of Clinical Anatomy 06, no. 01 (January 2017): 059–70. http://dx.doi.org/10.1055/s-0039-1700723.
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Abstract Background and Aims:Knowledge of physiological calcification in brain parenchyma is essential to avoid misinterpretation during radiological evaluation. The calcifications are commonly seen in pineal gland, falx cerebri, tentorium cerebelli and choroid plexus. Objective:To determine the incidence of physiological intracranial calcification and its relationship to age and sex in eastern Indian population. Materials and Method: A cross sectional descriptive study of CT scan brain was performed in age group between 20-80 yrs in eastern India. The study was conducted on 64 Slice MDCT PHILIPS Brilliance. Bulk of our patients was of road traffic accidents and routine CT scan study revealed these physiological calcifications and did not possess any morphological abnormality. Results: 852 patients of which 503 male and 349 female were studied and overall 1429 separate calcified areas were identified due to co-existent calcifications in most of the patients. The incidence of calcification was in pineal gland (62%), choroid plexus (53%), dura mater (26%), basal ganglia (2.8%), dentate nucleus (1.4%) and Habenular nuclei (6%). Incidence is more in male than in female. Conclusion: Physiological calcifications in some of the intracranial structures are not a very uncommon finding and it should not be confused with a pathological one.
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Sultanova, M. J., V. A. Azizov, and T. A. Sadigova. "Possibilities of digital radiography in the coronary arteries calcification diagnosis in patients with rheumatoid arthritis." Kazan medical journal 97, no. 2 (April 15, 2016): 236–39. http://dx.doi.org/10.17750/kmj2016-236.
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AIM. To assess coronary calcification nature in patients with rheumatoid arthritis using digital radiography.METHODS. Chest and distal upper extremities X-ray examination results of the 60 patients with rheumatoid arthritis were retrospectively analyzed. The patients mean age was 54.3±7.8 years, mean disease duration - 8.34±0.3 years. The correlation closeness assessment of qualitative features in the observed group was performed by Pearson correlation coefficient.RESULTS. When performing distal upper extremities X-ray examination, in 9 (15.0±4.6%) patients stage I, in 16 (26.7±5.7%) - II, in 21 (35.0±6.2 %) - III, in 14 (23.3±5.5%) patients - stage IV rheumatoid arthritis was found. In 19 (31.7±6.0%) patients coronary calcifications were visualized in the anterior interventricular branch of the left coronary artery, in 14 (23.3±5.5%) patients - in the circumflex branch of the left coronary artery, in 10 (16.7±4.8%) - in the right coronary artery, in 10 (16.7±4.8%) patients - the main trunk of the left coronary artery. In 7 (11.7±4.1%) patients aortic arch calcifications were found. It was found that the coronary calcifications incidence was higher in more prolonged disease course. Correlation relationship between coronary calcifications and rheumatoid arthritis stage was determined: in 7 (77.8±4.1%) patients with stage I, 14 (87.5±4.8%) patients with stage II and in all patients with stage III and IV coronary and aortic calcifications of various nature were identified. The coronary calcification incidence and prevalence had a direct correlation with the patient’s age: in most cases (66.7±10.3%) patients aged 55-60 years had multivessel calcification (≥3).CONCLUSION. There is a close correlation relationship between coronary calcifications and rheumatoid arthritis stages; coronary calcification incidence and prevalence in patients with rheumatoid arthritis depends on age, as well as the disease duration and stage, which is particularly important in the treatment strategy determination.
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Stoyukhina, Alevtina S. "Focal ossification as one of the reasons for erroneous diagnosis of chorioretinal lesions." Ophthalmology journal 12, no. 3 (December 16, 2019): 31–39. http://dx.doi.org/10.17816/ov15931.
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Focal calcifications of the retina and choroid occur usually in such well-known tumors as: retinoblastoma, choroidal osteoma, choroidal hemangioma, retinal astrocytoma. In addition, cases of idiopathic or secondary calcification are known, the most common of them is sclerochoroidal calcification. The article provides a detailed analysis of the clinical and tomographic pictures of ossifying conditions occurring in adults. It is shown that, in addition to a different ophthalmoscopic picture, these conditions are characterized by a different level of localization of the pathological calcification zone and a different stage of retinal damage.
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Kei, Olivia C. Y., Walter J. Duncan, and Derek G. Human. "Pulmonary arterial and intracranial calcification in the recipient of a twin–twin transfusion." Cardiology in the Young 12, no. 5 (October 2002): 488–90. http://dx.doi.org/10.1017/s1047951102000859.
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Pulmonary arterial and intracranial calcifications are rarely found in children. A female infant, the recipient of a twin–twin transfusion syndrome was found, by ultrasound and computed tomography, to have both pulmonary arterial and intracerebral calcification. A rare condition, termed idiopathic arterial calcification of infancy, is the likely cause. This condition carries a poor prognosis and is usually fatal.
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Nicolas, Gaël, Monica Sanchez-Contreras, Eliana Marisa Ramos, Roberta R. Lemos, Joana Ferreira, Denis Moura, Maria J. Sobrido, et al. "Brain calcifications and PCDH12 variants." Neurology Genetics 3, no. 4 (July 26, 2017): e166. http://dx.doi.org/10.1212/nxg.0000000000000166.
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Objective:To assess the potential connection between PCDH12 and brain calcifications in a patient carrying a homozygous nonsense variant in PCDH12 and in adult patients with brain calcifications.Methods:We performed a CT scan in 1 child with a homozygous PCDH12 nonsense variant. We screened DNA samples from 53 patients with primary familial brain calcification (PFBC) and 26 patients with brain calcification of unknown cause (BCUC).Results:We identified brain calcifications in subcortical and perithalamic regions in the patient with a homozygous PCDH12 nonsense variant. The calcification pattern was different from what has been observed in PFBC and more similar to what is described in in utero infections. In patients with PFBC or BCUC, we found no protein-truncating variant and 3 rare (minor allele frequency <0.001) PCDH12 predicted damaging missense heterozygous variants in 3 unrelated patients, albeit with no segregation data available.Conclusions:Brain calcifications should be added to the phenotypic spectrum associated with PCDH12 biallelic loss of function, in the context of severe cerebral developmental abnormalities. A putative role for PCDH12 variants remains to be determined in PFBC.
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Lee, Kyoung Min, Jee Eun Lee, Eun Suk Cha, Jin Chung, Jeoung Hyun Kim, and Byung In Moon. "Dystrophic Calcifications in the Breast from Secondary Hyperparathyroidism." Breast Care 13, no. 1 (January 12, 2017): 44–46. http://dx.doi.org/10.1159/000484198.
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Background: Soft tissue calcification is common in patients with secondary hyperparathyroidism who have received long-term treatment with hemodialysis. However, calcifications in the breast parenchyma are not common. We report a case of a woman with dystrophic breast calcifications from secondary hyperparathyroidism. Case Report: A 65-year-old woman presented with a palpable mass in her right breast which she had discovered 1 month ago. She had a medical history of end-stage renal disease. Mammography and ultrasound revealed large dystrophic calcifications in both breasts. Core needle biopsy was performed for calcifications in the right breast, and the pathologic diagnosis was dystrophic calcification in the stroma from secondary hyperparathyroidism. Conclusion: Reviewing our case will contribute to a fast and correct diagnosis in patients with dystrophic breast calcifications and lab results indicating secondary hyperparathyroidism, and will help discriminate these benign lesions from malignancies.
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Serindere, Mehmet, and Gokhan Polat. "Intracranial physiological calcifications: A computed tomography study." Imaging, April 13, 2023. http://dx.doi.org/10.1556/1647.2023.00114.
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AbstractBackground and aimIntracranial calcifications (ICs) occur when metals such as calcium or iron accumulate in blood vessels, glands or other structures related to the brain. They can be physiological or pathological. Currently, the most sensitive method for imaging IC is cranial computed tomography (CT). The aim of this retrospective study was to evaluate physiological ICs and the co-existence of them by CT.Patients and methods1,000 cranial CT scans of patients were retrospectively evaluated. Pineal calcification, choroid plexus calcification, habenular calcification, petroclinoid ligament calcification, basal ganglia calcification, falx cerebri and tentorium cerebelli calcification were evaluated and recorded.ResultsOf 1,000 patients, 65.7% had IC. The incidence of ICs in different sites were as follows: pineal calcification (37.7%), choroid plexus calcification (52.1%), habenular calcification (33.5%), petroclinoid calcification (21.8%), basal ganglia calcification (0.6%), falx cerebri calcification (6.2%) and tentorium cerebelli calcification (0.2%). The incidence and co-existence of calcifications were significantly higher in females than in males (P < 0.05). Pineal, choroid plexus, petroclinoid ligament calcifications were significantly higher in females than in males (P < 0.05). The incidence and co-existence of calcifications increased with age. Tentorium Cerebelli calcification did not differ significantly between age groups (P > 0.05).ConclusionsICs may be a common finding and encountered incidentally on CT scans which is gold standard to evaluate them. It is important to distinguish physiological calcifications from pathological ones, in the differentiation of pathological lesions with calcifications.
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Imanaka, Takahiro, Kenichi FUJII, Rin Hoshina, Hirokazu Tanaka, Nagataka Yoshihara, Toshio Kimura, Kojiro Miki, et al. "Abstract 12487: Ex Vivo Assessments of Human Nodular Calcification: Optical Frequency Domain Imaging and Histopathology." Circulation 146, Suppl_1 (November 8, 2022). http://dx.doi.org/10.1161/circ.146.suppl_1.12487.
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Introduction: It has been reported that a nodular calcification is associated with a calcified nodule and the reappearance of in-stent failure after percutaneous coronary intervention. Hypothesis: This study evaluated characteristics of nodular calcification on optical frequency domain imaging (OFDI) image in comparison to histopathology. Methods: One hundred and seven matched OFDI and histopathological cross-sections from 13 coronary arteries of 5 human autopsy hearts were evaluated. In histopathological assessment, a nodular calcification was defined as a fragmented calcification with accumulated fibrin. In OFDI analysis, calcification arc, shape of luminal surface, lumen side shape of calcification, irregularity of lumen surface, and irregularity of calcification surface of lumen side were analyzed in each OFDI image. Results: There were 10 nodular calcifications and 97 non-nodular calcifications in histopathological slices. The calcification arc was significantly smaller in nodular calcification than in non-nodular calcification [89.5° (56.4-108) vs. 126° (82.0-190), p =0.02]. OFDI features of a nodular calcification were characterized by a convex shape of the luminal surface (90.0% in nodular calcifications vs. 6.2% in non-nodular calcifications, p <0.01), a convex shape of calcification (90.0% vs 18.6%, p <0.01), an irregular luminal surface (50.0% vs 0%, p <0.01), and an irregular calcification surface of lumen side (60.0% vs 3.1%, p <0.01). Conclusion: This study suggests that OFDI has a potential capability to distinguish between nodular calcification and non-nodular calcification based on angle of calcification, shape and irregularity of luminal surface and those of calcification.
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El-Sharkawy, Magdy Mohamed Saeed, Ahmed Hassan Mohamed El Thakaby, Reem Mohsen El Sharabasy, and Mahmoud Fathy Mohamed ElBahrawy. "Relation Between Matrix Gla Protein and Cardiac Vavular Calcifications in Haemodialysis Patients." QJM: An International Journal of Medicine 114, Supplement_1 (October 1, 2021). http://dx.doi.org/10.1093/qjmed/hcab100.080.
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Abstract Background Heart valve calcification was first described a century ago. Its pathologic features were first described by Dewitsky in 1910. Valvular heart disease is common in end-stage renal disease patients. The incidence of valvular heart disease is 5 times greater in dialysis patients than in the general population MGP plays a key role in the inhibition of tissue calcification, which was demonstrated in MGP-deficient mice Objective To detect the prevalence of cardiac valvular calcifications among end stage renal disease patients on prevalent haemodialysis and its relation to Matirx Gla protein. Patients and Methods Enrolled patients were recruited from Ain shams hospitals, divided into two groups according to the presence/absence of valvular calcifications on echocardiographic examination as follows: Group A: included patients with valvular calcifications. Group B: included patients without valvular calcifications. Results In current study, 19 (23.8%) patients showed mitral calcification, 30 (37.5%) showed aortic calcification and 44 (55.0%) had calcification in general as 5 patients had both mitral and aortic calcifications. In current study, the patient who had calcification were significantly older, heavier in weight and BMI and were had HD for longer than those who didn’t have calcification. Patient who had calcification had lower levels of both platelets and urea than those who didn’t have calcification. In current study, the mean ucMGP was 549.5 ± 160.1 and the patient who had calcification had higher levels of ucMGP than those who did not have calcification. There was a significant positive correlation between age, weight, BMI, duration of HD and ucMGP. And there was a significant negative correlation between platelet count, serum albumin and ucMGP. Conclusion In current study, MGP was able to significantly differentiate between patients with and without calcification at a cutoff point (>564 pg/mlv) with sensitivity 86.36%, specificity 97.22. Our study confirmed that older age, hypertension, diabetes mellitus low platelet, higher ucMGP and blood urea are the most predictive parameters of valvular calcifications in hemodialysis patients. Other markers were not associated with valvular calcifications. ucMGP serum levels can significantly differentiate between HD cases with valvular calcifications and those not and those who had findings in CXR.