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At least 1,711 records · Page 95Linked to original sources
PubMed2004

[Association of brain computed tomography images of intracranial calcifications in three different cases of hypoparathyroidism].

The problem of intracranial calcifications in children has not been widely discussed in the literature yet. The aim of this study is to emphasise different clinical aspects of intracranial calcifications found in subcortical nuclei and cerebellum in children with disturbed calcium metabolism. We report three different cases of hypoparathyroidism in children in whom similar radiological changes on computed tomography (CT) of the brain were found. An 11-year-old boy was referred to us after episode of tetany. We confirmed the diagnosis of idiopatic hypoparathyroidism (presence of Chvostek and Trousseau signs, hypocalcemia, hyperphosphatemia, low parathormone serum concentration). On brain CT small, symmetric calcifications in the subcortical nuclei and frontal lobes were imaged. A diagnosis of pseudohypoparathyroidism type Ib in 10-year-old girl was established on the basis of clinical symptoms (syncope with seizures, recurrent carpopedal spasms in the past) and laboratory investigations (hypocalcemia, hyperphosphatemia, high parathormone serum concentration). In 11-year-old girl autoimmune polyglandular syndrome type I was diagnosed (hypoparathyroidism with chronic mucocutaneous candidiasis and nail dystrophy from the age of 2). CT of the brain showed multiple irregular symmetric calcifications in cerebellar hemispheres, internal capsula and subcortical nuclei on the border of white and grey matter in both frontal lobes.

Brain Diseases↗
PubMed2004

Severe calcification in left main stem coronary artery stenosis visible on routine chest radiograph.

Coronary calcification is a strong predictor of significant coronary stenosis in symptomatic patients. While discrete calcification within coronary arteries is only detected by sensitive methods such as computed tomography, severe calcification can already be seen on the plain chest radiograph. In this article, we describe a patient with a high grade left main stem coronary artery stenosis who presented with a severe focal calcification on the plain chest radiograph in projection of the offspring of the left coronary artery.

Aged↗
PubMed2004

Diagnosis of non-dental conditions. Carotid artery calcifications on panoramic radiographs identify patients at risk for stroke.

BACKGROUND: The oral and maxillofacial manifestations of some occult systemic disorders may be identified during the provision of dental care. Medical conditions so identified should be referred to a physician for confirmation by appropriate test and indicated therapy. Atherosclerosis at the bifurcation of the carotid artery is a common cause of stroke, and, when such lesions are calcified, they may easily be identified on a panoramic radiograph since the carotid bifurcation lies within the field of a properly performed X-ray. LITERATURE REVIEWED: To examine the degree to which this finding is recognized by the dental community, the authors conducted a PubMed review to find publications that detailed the identification of carotid artery calcifications on panoramic radiographs. RESULTS: Between 1981-2003, there were 39 peer-reviewed dental manuscripts and 29 pertinent abstracts reporting the observation of incidental carotid calcifications visible on routine panoramic radiographs. These studies documented a 3% to 5% prevalence of carotid artery calcifications in the general dental population, with higher percentages occurring in patients having medical illnesses associated with advanced atherosclerosis. PRACTICE IMPLICATIONS: The widespread recognition that calcifications seen in the region of the carotid bifurcation can identify a population at increased risk of stroke supports the practice of routinely examining this area during review of panoramic radiographs. Since a panoramic radiograph is often obtained for dental reasons, in many instances, further examination of the area of the carotid bifurcation is essentially cost-free, and can serve to prolong lives and bring significant savings in overall health care costs by assisting in the prevention of critical events such as strokes.

Arteriosclerosis↗
PubMed2003

[Significance of vascular calcification in diabetic patients with increased risks of cardiovascular disease and stroke].

Patients with diabetes have greatly elevated risks of atherosclerotic diseases such as coronary artery disease (CAD) and stroke. Vascular calcification in advanced atherosclerosis is a common feature in diabetic patients. In vitro and in vivo studies suggest that apoptosis and chondro/osteogenic differentiation of vascular wall cells such as smooth muscle cells may play important roles in the progression of vascular calcification. Diabetes may promote vascular calcification through the action of various factors including hyperglycemia, oxidative stress, tumor necrosis factor-alpha, and advanced glycation end products. Detection of coronary calcium by electron-beam computed tomography (EBCT) revealed clinical significance of vascular calcification and this technique may be a useful method to identify diabetic patients with increased risks of cardiovascular disease and stroke.

English Abstract↗
PubMed2002

[Molecular mechanism of vascular calcification in renal failure].

Vascular calcification is the most frequent cause of death in chronic renal failure. In recent studies molecular mechanism for regulation of vascular calcification is becoming to clear. An important regulator of vascular calcification is the extracellular levels of inorganic phosphate. Also, various bone matrix proteins and factors regulates vascular calcification in ESRD patients.

English Abstract↗
PubMed2002

[Inhibitory effects of bisphosphonate on vascular calcification].

Recently, it has been hypothesized that vascular calcification is an actively regulated process in which vascular smooth muscle cells (VSMCs) acquire osteoblast-like functions. Bisphosphonates prevent in vitro calcification of VSMCs and probably inhibit phosphate transport by sodium dependent phosphate transporter which plays a key role in VSMCs calcification. The effects of bisphosphonate on VSMCs have important implications for the future management of patients with vascular calcification.

English Abstract↗
PubMed2002

[Hormonal regulation of vascular calcification].

Recent evidence suggests that vascular calcification is a controlled process and involves the altered differentiation of mesenchymal cells. For example, vitamin D(3) was reported to enhance vascular calcification by suppressing PTHrP action that is an inhibitor of calcification. Quite recently, leptin has been shown to enhance the osteoblastic differentiation of stromal cells and calcification of vascular cells. These results suggest the intimate relationship between bone and lipid or adipose tissue.

English Abstract↗
PubMed2002

[Vitamin K and vascular calcification].

Until recently, vitamin K has been exclusively related to blood coagulation. During the last decade, a second function for vitamin K-dependent proteins has become apparent : the regulation of tissue calcification. One of them is the function of Matrix Gla Protein (MGP) : potent inhibitors of vascular calcification. The function of MGP became clear from transgenic mice (MGP-deficient mice). Further research on MGP will resolve the complicated mechanism of atherosclerosis, especially of the arterial calcification. The recommended daily allowance for vitamin K to prevent vascular calcification should be evaluated.

English Abstract↗
PubMed2002

[Suppressive effects of bisphosphonates on the vascular calcification in ESRD patients].

The progress of aortic calcification is associated with the incidence of cardiac and cerebrovascular diseases in hemodialysis patients. The present study was designed to determine whether etidronate can affect the development of aortic calcification in hemodialysis patients. Etidronate was given orally just before sleep on the day of dialysis, which was performed 2 or 3 sessions per week. Aortic calcification area (ACA), bone mineral density (BMD), and biochemical parameters were measured 6 months after the start of etidronate treatment to them compare with control. ACA in the control group showed a statistically significant increase after 6 months. However, the patients who received etidronate had no significant changes in ACA. Clinical and biochemical parameters and BMD were not influenced by etidronate treatment except serum alkaline phosphatase. These results suggest that etidronate has a potential ability to inhibit the progression of vascular calcification in hemodialysis patients, and that this beneficial effect of etidronate may prevent cardiovascular and cerebrovascular diseases that are major causes of death in hemodialysis patients.

English Abstract↗
PubMed2001

[Molecular mechanism for regulation of vascular calcification].

Until recently, vascular calcification was considered to be a passive, degenerative, and end-stage process of vascular disease. However, the observation of bone matrix proteins in calcified vascular tissues has changed this paradigm. Vascular calcification is an actively regulated process in which vascular cells may acquire osteoblast-like function. An important regulator of vascular calcification is the levels of Inorganic Phosphate (Pi). Pi directly regulates calcification through a sodium-dependent phosphate transporter system.

English Abstract↗
PubMed2001

[Renal dysfunction and hyperphosphatemia--role of hyperphosphatemia on vascular calcification].

Coronary-artery calcification was present in 14 of 16 hemodialysis patients who were 20 to 30 years old by electron-beam computed tomography. Bone matrix protein, such as osteopontin produced by infiltrating macrophages into the atherosclerotic arterial lesions, is thought to be associated with vascular calcification. Therefore, it is required to recognize the interaction between abnormal bone metabolism and vascular calcification. Control of serum phosphorus levels is likely to be most important for the prevention and treatment of vascular calcification in patients with end-stage renal diseases.

English Abstract↗
PubMedDate not supplied

[Prevention of extraskeletal calcifications in uremia].

Secondary hyperparathyroidism (HPTH) is a common feature in end-stage renal disease (ESRD) patients. The three main factors involved in secondary HPTH pathogenesis are high phosphate levels, hypocalcemia and vitamin D deficiency. Recently, many studies demonstrated a strong association between bone disease and cardiovascular events in chronic kidney disease patients. In addition, cardiovascular events are the most frequent cause of death in patients with chronic renal failure. Increased levels of serum phosphorus and calcium-phosphate product are directly involved in the pathogenesis of extraskeletal calcifications (blood vessels, soft tissues, etc) in dialyzed patients compared to the non-uremic population. Recent studies suggested that vascular calcification is due not only to a passive calcium-phosphate deposition on atherosclerotic arteries, but also to active mechanisms regulated by bone-associated genes. In particular, fetuin and matrix Gla-protein are two 'protective' proteins associated with reduced vascular calcification and could be the regulatory keys in preventing this process in renal failure. The limitations of calcium salts as phosphate-binders in patients with advanced renal failure have been thoroughly evaluated in the last 5 yrs. New phosphate binders, which do not contain aluminum or calcium, have been developed to reduce the risk of extraskeletal calcifications in ESRD.

Animals↗
PubMedDate not supplied

Left atrial, pulmonary vein and dural calcification in a patient with arrhythmia and chronic renal failure.

Left atrial and dural calcification in chronic renal failure is very rare. Massive atrial calcification can lead to arrhythmia and diagnosis of this condition is important to take prophylactic measures in dialysis patients. Noninvasive diagnosis of left atrial calcification is also important as it can complicate valvular surgery. We report on a patient with chronic renal failure presenting with arrhythmia in whom left atrial calcification involving interatrial septum is diagnosed by thorax CT examination.

Adult↗
PubMed2005

Influence of angiotensin-converting enzyme gene insertion/deletion polymorphism on rheumatic valve involvement, valve severity and subsequent valve calcification.

BACKGROUND AND AIM OF THE STUDY: The relationship between the severity of chronic rheumatic heart disease (RHD) and predisposing factors is unknown, and genetic predictors for severe scarring and calcification of the mitral valve are not well defined. A high angiotensin-converting enzyme (ACE) activity has been demonstrated in valve tissue. Thus, a case-control study was conducted to investigate any possible relationship between ACE gene polymorphisms and chronic mitral valve disease severity and calcification. METHODS: This case-control study included 82 patients (24 males, 58 females; mean age 40.3 +/- 14.7 years) with chronic rheumatic mitral valve, and 154 control subjects (53 males, 101 females; mean age 43.4 +/- 13.4 years). ACE gene insertion/deletion (I/D) polymorphisms were identified using polymerase chain reaction methods. RESULTS: Among RHD subjects, 31 (30.6%) were D/D, 25 (32.7%) were I/D, and 26 (18.8%) were I/I. Among controls, 57 (57.4%) were D/D, 69 (61.3%) were I/D, and 28 (35.2%) were I/I. The frequency of ACE I/I genotype was higher in RHD subjects than in controls (chi2 = 7.4, df = 2, p < 0.030; D/D versus I/D versus I/I), or (chi2 = 5.5, df = 1, p < 0.019; DD + ID versus II). Predisposition to RHD was significantly less frequent in the D/D genotype. There was no statistically significant difference in the genetic analysis of RHD with respect to mitral valve score, severity of mitral regurgitation and left atrial diameter. Mitral valve calcification was significantly associated with a higher frequency of I/I genotype and I/D genotype than D/D genotype alone (chi2 = 6.2, df = 2, p = 0.043). The ACE I/I genotype was associated with a predisposition to a greater risk of severe calcific valve disease. CONCLUSION: The ACE I/I genotype is more common in patients with rheumatic valve disease than in the normal population. This suggests that the ACE gene polymorphism may be involved in the pathogenesis of rheumatic heart disease.

Adolescent↗
PubMedDate not supplied

[Differential diagnosis of intracranial calcifications].

INTRODUCTION: Intracranial calcifications are a frequent chance finding in many neuroimaging tests. We report two clinical cases with intracranial calcifications as a common feature, but which had very different aetiologies and presenting symptoms. CASE REPORTS: The first case involved a 51-year-old male with a single tonic-clonic convulsive seizure associated to hypocalcemia secondary to hypoparathyroidism who presented extensive brain calcifications affecting the dentate nuclei, pons, periependymal and basal ganglia, and whose convulsive attacks remitted once normal Ca2+ values were restored. The second case was a 25-year-old female patient whose convulsive seizures were yet another symptom of Fahr's syndrome, which was associated to spastic paralysis, athetosis, mental retardation and occasionally hypoplasia of the optic nerve; the calcifications were located in the grey nuclei of the cerebrum and cerebellum. CONCLUSIONS: A correct history and physical and neurological examination must be carried out, and a detailed study of Ca2+/ P+ and hormonal metabolism is also required. A CAT scan is the preferred neuroimaging technique to achieve a proper differential diagnosis and to decide on the therapeutic approach that is best suited to the pathophysiological mechanisms that lead to the formation of these calcium deposits.

Adult↗
PubMed1992

[Pathology of the placenta. X. Syncytial proliferation, calcification, cysts, pigments and metabolic disorders].

Part X of this review is devoted to the remaining pathologico-anatomic patterns which are associated with regressive alterations. Increased syncytial proliferation is the most important aspect within that complex, since it may be a consequence of intervillous and intravillous hypoxia and may thus provide a clue to effects of that kind. Placental calcification may be subdivided by two major groups. The first is relating to "dystrophic" calcification following the same rules in the placenta as it does in other places, in other words, it is calcification of necrotic tissue portions or acidotic areas of decreased circulation. Calcification may just as well occur to particular structures of the placenta, such as the epithelial basal membrane, syncytial proliferations or in walls of vessels. Placental cysts usually are localized at the placental base (in septa), their development being owed to hypoxic events during ontogenesis. They actually are pseudocysts. Placental icterus (along with severe maternal icterus) is macroscopically identifiable with unambiguity. The biliary pigment, histologically, is localized in HOFBAUER cells. Additional reference is made to melanin deposits (in concomitance with congenital giant naevus) and placental alterations in conjunction with rare metabolic disorders.

Calcinosis↗
PubMedDate not supplied

Bone metabolism, vascular calcifications and mortality: associations beyond mere coincidence.

Bone and cardiovascular disorders are common age-related disorders in the general population and also in patients suffering from chronic kidney disease (CKD). Recent studies have shown an association between these two disorders and the rate of mortality. This article addresses some limitations of the concept of osteoporosis in CKD and compares bone and vascular disorders and mortality between non-selected general population and dialysis patients from the same geographic area. In the general population, all metabolic disorders increase with age, as well as vascular calcifications. The progression of vascular calcification was associated with a higher prevalence and incidence of bone fractures. In addition, both vascular calcifications and vertebral fractures were associated with higher mortality. A similar pattern was observed in dialysis patients with no increments in vertebral fractures, although with higher prevalence of vascular calcifications also both associated with higher mortality. Age was the strongest variable associated with all the analysed parameters, but some of the associations remained significant after age adjustment indicating the likely role of other common factors in the pathogenesis of bone and vascular disorders.

Bone Density↗
PubMed2005

[Risedronate: a possible treatment for extraosseous calcification].

A case report of 51 year-old female, diagnosed as CREST syndrome, presenting with an ectopic calcification in the left shoulder joint, which disappeared soon after the start of risedronate. She had been taking steroid and NSAIDs for the past four years, but the pain and the range of motion of her shoulder became worse and restricted progressively during the last three years only to form extraosseous calcification. Laboratory data showed normal renal function, no inflammatory changes, and no abnormalities in calcium and and phosphate metabolism including parathyroid hormone. Risedronate was administered for glucocorticoid-induced osteoporosis. Although the bone turnover markers, such as serum NTX (N-terminal telopeptides of type I collagen) and BSAP (bone specific alkaline phosphate), did not show remarkable changes, the pain disappeared a week later and the range of motion recovered a month later. The X-ray at 6 months risedronate treatment revealed a complete disappearance of the ectopic calcification. Risedronate, probably through a different process from etidronate, could prevent extraosseous calcification.

Anti-Inflammatory Agents, Non-Steroidal↗