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Histogram-based selective deblurring to improve computed tomography imaging of calcifications.

OBJECTIVES: Computed tomography (CT) imaging of small high-density structures, eg, calcifications, is hampered by image blur. This study aims to deconvolve calcifications in the transverse and longitudinal directions while avoiding noise amplification and edge-ringing artifacts in the surrounding low-density structures. MATERIALS AND METHODS: A method referred to as histogram-based selective deblurring (HiSD) has been developed to generate a restored image by combining the low-intensity (ie, Hounsfield Units) information of the original image with the high-intensity information of the deconvolved image. HiSD is evaluated on phantom and in vitro atherosclerotic plaque CT images by comparing the original and restored images with their corresponding reference micro-CT images both qualitatively and quantitatively. RESULTS: HiSD reduces calcification blur in the transverse and longitudinal directions without introducing noise and ringing-artifacts in the surrounding tissues. Calcification area and volume measurements are significantly improved in the restored images (reducing on average overestimation by 32% and 83%, respectively). CONCLUSIONS: HiSD significantly improves CT visualization and quantification of small high-density structures imaged in vitro.

Algorithms↗

Unusual manifestations of metastatic pulmonary calcification: high-resolution CT and pathological findings.

The aim of this report is to describe the high-resolution CT and pathologic findings of 3 patients with unusual manifestations of metastatic pulmonary calcification. These include a case that presented with extensive dense consolidation, a case of metastatic calcification that improved spontaneously, and a case of metastatic calcification in a patient with no demonstrable biochemical abnormality or underlying disease. We conclude that metastatic calcification may present with dense bilateral consolidation, may improve spontaneously, and may rarely present in patients with no apparent underlying biochemical abnormality.

Adult↗

Mechanisms of bioprosthetic heart valve calcification.

BACKGROUND: Cryopreserved human heart valves are used in approximately 20% of the tissue heart valve procedures performed annually. The pathophysiology of allograft failure is not fully understood. The authors proposed the hypothesis that the rapid deterioration observed in some allograft heart valve recipients is caused by disruptive interstitial ice damage that occurs during cryopreservation and subsequently leads to accelerated valve degeneration on implantation. METHODS: This hypothesis was tested by comparison of the standard commercial heart valve freezing method of cryopreservation and an ice-free, vitrification method of cryopreservation with fresh controls in a subcutaneous, juvenile rat implant model of calcification. Calcium concentration in explants was determined by atomic absorption spectroscopy. RESULTS: Statistically significant calcification (P<0.05) was observed in both syngeneic and allogeneic cryopreserved valves relative to fresh valves. The ice-free cryopreservation method demonstrated significant reduction of allogeneic heart valve calcification (P<0.01). Comparison of fresh syngeneic and allogeneic grafts at the 3-week time point demonstrated significantly higher calcium content in allograft valve explants (P<0.005). CONCLUSIONS: These findings demonstrate that allogeneic valve calcification is influenced by two factors, the cryopreservation method used and immunogenicity. Alternative cryopreservation methods that avoid ice formation may improve the in vivo performance of cryopreserved allogeneic heart valves.

Animals↗

The future of the carbon cycle: review, calcification response, ballast and feedback on atmospheric CO2.

The operation of the carbon cycle forms an important part of the processes relevant to future changes in atmospheric carbon dioxide. The balance of carbon between terrestrial and oceanic reservoirs is an important factor and here we focus in particular on the oceans. Future changes in the carbon cycle that may affect air-sea partitioning of CO(2) are difficult to quantify but the palaeoceanographic record and modern observational studies provide important evidence of what variations might occur. These include changes in surface nutrient use, the oceanic inventory of nutrients, and the elemental composition and rain-rate ratio of marine particles. Recent work has identified two inter-linked processes of potential importance that we consider in some detail: the response of marine calcification to changes in surface water CO(2) and the association of particulate organic carbon with ballast minerals, in particular biogenic calcite. We review evidence from corals, coccolithophores and foraminifera, which suggests that the response of reduced calcification provides a negative feedback on rising atmospheric CO(2). We then use a box model to demonstrate how the calcification response may affect the organic carbon rain rate through the ballast effect. The ballast effect on export fluxes of organic and inorganic carbon acts to counteract the negative calcification response to increased CO(2). Thus, two oceanic buffers exert a significant control on ocean-atmosphere carbonate chemistry: the thermodynamic CO(2) buffer; and the ballast/calcification buffer. Just how tightly coupled the rain-rate ratio of CaCO(3)/C(org) is to fluxes of ballast minerals is an important question for future research.

Atmosphere↗

Skeletal lesions and arterial calcifications of the feet in diabetics.

A radiological study of the feet was performed in 162 unselected diabetic patients with gangrene. They were compared with 59 diabetic patients without gangrene, 45 patients with familial amyloidosis and polyneuropathy and 30 healthy controls. The patients with familial amyloidosis had severe distal neuropathy but normal oral glucose tolerance test curves. Radiographic findings, e.g. skeletal destructions (diabetic osteopathy) and arterial calcification of the medial type were classified without knowledge of the clinical findings. Osteopathy was more common in diabetic patients with gangrene than in the other groups of patients. Medial arterial calcification was more common among diabetics with gangrene compared to patients with amyloidosis and to controls. There were no differences between diabetics without gangrene and patients with amyloidosis, but both of these groups had more calcifications than the controls. Our study suggests that diabetic osteopathy is not caused by peripheral neuropathy per se. The skeletal and skin lesions in diabetic patients are probably equivalent lesions localized to different tissues in the feet. It has been suggested that medial degeneration in the arterial wall is due to neuropathy. In agreement with this suggestion, the patients with familial amyloidosis and neuropathy had medial calcification. However, in diabetic patients this does not exclude other etiological agents.

Aged↗

Calcification of eccrine poroma.

Two cases of eccrine poroma with calcification were described, both of which were those of the Winkelmann-MacLeod type. They occurred on the face and lower leg. We supposed that calcification in both cases was dystrophic in nature due to minor pressure or injury. The feature of calcification within the nests of eccrine poroma has rarely been reported. However, it seemed to be physiologically consistant that calcification occurs in eccrine poroma which originates from eccrine sweat glands.

Acrospiroma↗

Calcification in the human choroid plexus, meningiomas and pineal gland.

Calcification in the stroma of adult telencephalic choroid plexus was studied of 20 postmortem brains and one biopsy by light microscopy, transmission and scanning electron microscopy and compared with calcification in psammoma bodies in normal arachnoid, five spinal meningiomas and in calcospherites of six pineal glands. Fifteen fetal and newborn choroid plexuses were also examined by light microscopy. Calcium deposition was observed in the subepithelial regions of the adult choroid plexus, in the walls of blood vessels but was mostly seen in spherical psammoma bodies. Collagen whorls 20-60 microns in diameter and surrounded by arachnoid cells, were observed in the stroma of the choroid plexus; calcium, phosphorous and iron were deposited in the collagen whorls to form psammoma bodies. Matrix vesicles and spicules resembling hydroxyapatite were associated with the arachnoid cells surrounding the collagen whorls and with the collagen fibres within the whorls. The dense amorphous calcified core of each psammoma body was surrounded by an outer coating of entwined collagen fibres readily visible by scanning electron microscopy. Similar psammoma bodies were occasionally observed in normal arachnoid. Psammoma bodies in meningiomas resembled those in the choroid plexus stroma. Calcospherites in the pineal differed from psammoma bodies; they were lobulated, more irregular in shape and did not have a collagen base. The results of this study suggest that psammoma bodies in the choroid plexus, as in meningiomas, form by a process of dystrophic calcification associated with arachnoid cells and collagen fibres. The presence of iron in the choroid plexus psammoma bodies may be a result of haemorrhage into the stroma. The mechanism of calcification in pineal remains unclear.

Adult↗

Spontaneous calcific cerebral embolus.

Spontaneous calcific cerebral embolus is a rare complication of calcific vascular disease such as calcified aortic plaques, and calcific aortic and mitral stenosis. Fewer than 10 case reports are described in the literature. Cerebral ischaemic symptoms may provide the indication for surgical replacement, even in the absence of valvular insufficiency or stenotic symptoms. We report a case of stroke in a young man with a known bicuspid calcific aortic valve.

Adult↗

Intracranial calcification and tumoural calcinosis during vitamin D therapy.

Extraskeletal calcifications are frequently observed in patients with chronic renal failure. However, clinically, they usually remain silent. In this report, we describe two patients with massive extraskeletal calcifications that caused significant morbidity. The first patient had tumoural calcification located on the shoulder and the second patient had severe neurological symptoms caused by intracranial calcifications. High calcium phosphorus product and severe secondary hyperparathyroidism were present in both patients. Furthermore, they both received inappropriately high doses of active vitamin D, even though they failed to respond to this therapy. We suggest to monitor closely the calcium, phosphorus and parathyroid hormone levels during calcitriol therapy and to perform parathyroidectomy, without delay, in patients who were resistant to calcitriol.

Adolescent↗

Vascular calcification, autonomic neuropathy, and peripheral blood flow in patients with diabetic nephropathy.

The possibility that digital gangrene in patients with diabetic nephropathy might be due to abnormalities of peripheral blood flow secondary to vascular calcification has been investigated. Twenty patients with renal failure due to diabetic nephropathy were studied. Peripheral blood flow was measured using venous occlusion plethysmography, together with an assessment of medial arterial calcification on plain radiographs of the hands and feet, and transcutaneous oxygen tension (TcPO2). Hallux blood flow was markedly raised (median 22.5, range 11.5-56.5, ml min-1 100-ml-1) compared with non-diabetic control subjects (4.7, 1.1-10.5, ml min-1 100-ml-1; p less than 0.01) and similar to that in diabetic patients with autonomic neuropathy (29.5, 16.7-49.6, ml min-1 100-ml-1). Although vascular calcification was common and extensive in the patients with diabetic nephropathy, TcPO2 measurements in the supine foot were normal and did not indicate tissue ischaemia. We conclude that despite extensive vascular calcification high peripheral blood flow occurs in the feet of these patients at rest together with normal transcutaneous oxygen tension.

Adult↗

The role of abnormal phosphorus metabolism in the progression of chronic kidney disease and metastatic calcification.

The role of abnormal phosphorus metabolism in the progression of renal disease and metastatic calcification. Hyperphosphatemia is a common biochemical abnormality in advanced renal failure. The resulting increase serum calcium x phosphorus product results in the deposition of hydroxyapatite crystals. The crystalline properties of these deposits incite an inflammatory response manifested by encapsulated tumoral deposits around joints, acute inflammatory arthritis, and irritative conjunctivitis. These deposits occur in association with marked elevation of serum phosphorus levels, and are prevented and eradicated by normalizing serum phosphorus levels. The calcium-phosphate deposits which occur in heart and lungs are nonapatitic. These deposits were never clearly related to hyperphosphatemia. They are mainly of historic interest because currently they are rarely seen. Their eradication appears to be more of a result of improved dialytic techniques than correction of serum phosphorus levels. The presence, persistence, and progression of vascular calcification are more closely related to patient age and duration of dialysis than hyperphosphatemia. This suggests that these deposits are a result of dystrophic calcification occurring de novo in a diseased or damaged vessel wall. Phosphorous restriction has also been shown to be protective of renal functional deterioration in experimental renal disease. It is unclear whether the protective effect is mediated through phosphate restriction or phosphate depletion. In conclusion, control of serum phosphorus levels in dialyzed uremic patients has clearly decreased morbidity associated with periarticular, articular, and conjunctiva hydroxyapatite deposits. In contrast, phosphorous control has had little effect on the presence or severity of vascular calcification.

Calcinosis↗

Cardiovascular calcification in Hispanic Americans (HA) with chronic kidney disease (CKD) due to type 2 diabetes.

BACKGROUND: Cardiovascular calcification (CVC) is common and severe in patients with end-stage renal disease on dialysis. However, the prevalence and severity of CVC is less well documented in patients with chronic kidney disease (CKD) not yet on dialysis. METHODS: Fifty-eight nondialyzed HA with type 2 diabetes and CKD were enrolled. They comprise 29 patients with stages 1 and 2 CKD (early CKD group) and 26 patients with stages 4 and 5 CKD (advanced CKD group). Coronary artery calcification (CAC) was measured by ultrafast spiral computed tomography, while peripheral artery calcification (PAC) was evaluated by plain x-ray of the chest, pelvis, thighs, and lower extremities. RESULTS: The prevalence of CAC and PAC were significantly higher in the advanced CKD group compared to the early CKD group (73% vs. 38%; P < 0.01 and 85% vs. 35%; P < 0.0001, respectively). The median CAC scores were 18-fold greater in the advanced CKD group (138.9 vs. 7.8, respectively). By linear regression analysis, a strong association was found between the level of renal function and ln total volume of CAC. CONCLUSION: Our data indicate that CAC and PAC are common and severe in HA diabetic patients with CKD not previously treated with dialysis, calcium-based phosphate binders, or vitamin D analogues. Lower level of renal function is associated with increased burden of vascular calcification in predialysis patients with CKD.

Adolescent↗

Caseous calcification of the mitral annulus: unusual case of spontaneous resolution.

Mitral annular calcification (MAC) is a common echocardiographic finding. Caseous calcification is a rare variant appearing as a round, tumor-like mass with central echolucent area located in the periannular region. Although occasionally misdiagnosed as a tumor and submitted to exploratory cardiotomy, this lesion appears to carry a benign prognosis. The true significance of caseous calcification is unknown; it might be an early and reversible stage of MAC or an atheroma-like lesion. We describe a case of caseous calcification with spontaneous resolution in a 60-year-old woman-such a finding should be considered in the differential diagnosis of intracardiac masses.

Calcinosis↗

Metastatic pulmonary calcification in a dialysis patient: case report and a review.

A 19-year-old male presented with chest pain and dyspnea. He was anephric following nephrectomy for focal segmental glomerulosclerosis, had a subsequent failed transplant, and had been dialysis dependent for 3 years. Workup revealed hyperparathyroidism and an abnormal chest X-ray and computed tomography scan, significant for massive extra-skeletal pulmonary calcification. A markedly abnormal Technitium99 methylene diphosphonate (Tc99m-MDP) bone scan confirmed the clinical suspicion of metastatic pulmonary calcification. Metastatic pulmonary calcification (MPC) is common, occurring in 60% to 80% of dialysis patients on autopsy and bone scan series. It may lead to impaired oxygenation and restrictive lung disease. Typically, the calcium crystal is whitlockite rather than hydroxyapatite, which occurs in vascular calcification. Four major predisposing factors may contribute to MPC in dialysis patients. First, chronic acidosis leaches calcium from bone. Second, intermittent alkalosis favors deposition of calcium salts. Third, hyperparathyroidism tends to cause bone resorption and intracellular hypercalcemia. Finally, low glomerular filtration rate can cause hyperphosphatemia and an elevated calcium-phosphorus product. There may be other factors. Some authors suggest that the incidence of MPC in recent years may be lower due to improved dialysis techniques. The diagnosis is confirmed by biopsy, but can be suspected by typical findings on a Tc99m-MDP bone scan. Therapy is limited to ensuring adequate dialysis, correcting calcium-phosphorus product, and hyperparathyroidism; discontinuing vitamin D analogues may help. Conflicting reports show that transplantation may either improve or worsen the situation. MPC should be considered in dialysis patients who have characteristic abnormal chest radiography and/or pulmonary symptoms.

Adult↗

Amygdalae calcifications associated with disease duration in lipoid proteinosis.

OBJECTIVES: To describe imaging findings of central nervous system involvement in patients with lipoid proteinosis. METHODS: Patients with lipoid proteinosis followed in the dermatology and neurology departments of the State University of Campinas between 2002 and 2004 were evaluated using high-resolution MRI and computerized tomography (CT). RESULTS: We reviewed the charts of three patients (two women) with lipoid proteinosis with, ages ranging from 5 to 44 years. Symptomatic disease duration ranged from 2 to 39 years. MRI scans showed hypointense signal in FLAIR and T2 images in the amygdalae in two of three patients. Brain CT scans from two patients showed that MRI findings were calcifications. The calcification was more evident in patients with longer disease duration. Epilepsy was identified in one patient with longer disease duration. No other epileptogenic lesion was identified on MRI in this patient. CONCLUSION: Lipoid proteinosis is associated with bilateral amygdalae calcification. These findings were more evident in patients with longer disease duration. Epilepsy, when present, may be related to these calcifications. Patients with lipoid proteinosis should be followed with MRI/CT in order to identify these abnormalities.

Adult↗

Calcification in a pineal tumour studied by transmission electron microscopy, electron diffraction and x-ray microanalysis.

The calcification in a totally calcified pineal tumour was studied. Transmission electron microscopy indicated that the tumour was a pinealoma. The type of calcification was investigated by bright-field and dark-field transmission electron microscopy in addition to electron diffraction and electron-induced x-ray fluorescence. The calcified material consisted predominantly of amorphous calcium phosphate. The type of calcification differs from the normal calcification present in pineal acervuli which consists of crystalline hydroxypatite.

Brain Neoplasms↗

Coeliac disease, unilateral occipital calcifications, and drug-resistant epilepsy: successful lesionectomy.

PURPOSE: To draw attention to the triad of coeliac disease (CD), occipital calcifications, and drug-resistant epilepsy, with focus on the outcome of epilepsy surgery. METHODS: We describe a male patient who despite a diagnosis of CD from the age of 9 did not comply with the gluten-free diet. At the age of 11 he developed simple and complex partial seizures with visual symptoms, anxiety, and ambulatory automatisms. His epilepsy appeared to be drug resistant, and after having tried nine antiepileptic drugs (AEDs), alone or in combinations, he underwent a presurgical evaluation at the age of 30. Interictal standard electroencephalograms (EEGs) disclosed frequent biparieto-occipital epileptiform discharges. Computed tomography showed cortical-subcortical punctate calcifications in the right parieto-occipital region, where his seizures seemed to start, according to ictal EEG registrations from intracranial strip electrodes. RESULTS: At the age of 31 he underwent epilepsy surgery. A 5 x 6 cm large area of the right parieto-occipital region was resected, including the area with calcifications. Except for a few short-lasting episodes of anxiety (simple partial seizures?) he has now been seizure-free for 12 years. AEDs were withdrawn 5 years ago. Postoperatively he was left with an upper left-sided quadrant anopsia, which is not bothering him. CONCLUSIONS: In patients with CD, unilateral occipital calcifications, and drug-resistant epilepsy, epilepsy surgery should be considered, as a lesionectomy might be very successful.

Adult↗

Scrotal calcinosis: origin from dystrophic calcification of eccrine duct milia.

Scrotal calcinosis is a rare benign disorder considered idiopathic by most recent authors, although an origin from dystrophic calcification of epidermoid cysts has been proposed. In 3 of 4 cases which were otherwise typical of scrotal calcinosis, there was calcification of the contents of small cysts lined by stratified squamous epithelium. These structures were identified as eccrine duct milia because some of them communicated with eccrine ducts and there were ultrastructural features of eccrine duct differentiation in one case. The eccrine nature of the milia was confirmed using the immunoperoxidase technique for the demonstration of carcinoembryonic antigen (CEA) which serves as a marker of eccrine sweat glands. Since a transition could be seen between degenerating calcified milia and typical nodules, it appeared that the calcific deposits of scrotal calcinosis result from the breakdown of such lesions. Staining of deposits unassociated with cyst walls with the technique for the demonstration of CEA supported this conclusion. An advanced stage of evolution of the disease could account for the absence of visible cysts in many cases. We propose the term "hidrocalcinosis of the scrotum" for this distinctive form of cutaneous calcification.

Adult↗