Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CALCIFICATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,243 records · Page 69Linked to original sources

Sonographic appearance and significance of arcuate artery calcification.

During routine pelvic ultrasonography, we observed calcification of the arcuate branches of the uterine artery in eight patients. Calcification was manifest as symmetric, hyperechoic foci with acoustic shadowing in the periphery of the uterine myometrium. Uterine arterial calcification is important to recognize, as patients often have severe underlying systemic disease. Arcuate artery calcification can be differentiated from other pathologic causes of calcification in the uterus.

Adult↗

Antenatal detection of idiopathic arterial calcification with hydrops fetalis.

Idiopathic arterial calcification of infancy, or occlusive infantile arterial calcification, is a rare cause of arterial calcification. This condition is inherited as an autosomal recessive pattern, which is almost always fatal. In most of the 100 cases described in the literature, the diagnosis was made at autopsy; a few cases have been reported in which an antemortem diagnosis was made on the basis of radiographic or sonographic demonstration of arterial calcification. The clinical characteristics are extremely variable, and respiratory distress with cardiac failure is the most common finding. Hypertension that is refractory to treatment is present in most cases. Most infants die before the age of 6 months, and very few have survived for more than 1 year. Mortality in this condition is caused by myocardial ischemia due to coronary artery involvement or refractory cardiac failure. The purpose of this report is to describe the prenatal diagnosis of idiopathic arterial calcification. Fewer than 10 cases of antenatal detection of this condition have been reported in the literature. This case is 1 of 2 cases with the earliest diagnosis of this condition so far (Table 1).

Adult↗

Simultaneous occurrence of calcification and amyloid deposit in pilomatricoma.

Amyloid deposition was encountered in 10 of 16 samples of pilomatricoma, indicating that the deposition of amyloid is nearly as common as calcification in pilomatricoma. In addition, a simultaneous occurrence of calcification and amyloid deposit in pilomatricoma was recognized in 9 of 16 samples. The calcification and the deposition of amyloid developed topographically in the same area within the shadow cell masses. Such an area was revealed as moderately basophilic, amorphous, or hyalinized by H&E staining. Electron microscopy revealed spotty calcium deposits in amyloid. No light chains of human immunoglobulin were detected in the amyloid-deposited area. Amyloid in this tumour may facilitate calcification or serve as a matrix for subsequent calcification.

Adolescent↗

Periarticular calcification in systemic lupus erythematosus.

OBJECTIVE: To describe the radiologic manifestations of periarticular calcification in patients with systemic lupus erythematosus (SLE) and to investigate clinical variables associated with its occurrence. METHODS: Hand radiographs and clinical records of 52 patients who had 4 or more features of the 1982 revised criteria for classifying SLE and who had no other collagen vascular diseases were analyzed retrospectively. RESULTS: Periarticular calcifications were found in 7 patients (13.5%) near the distal and proximal interphalangeal (DIP and PIP) joints and metacarpophalangeal (MCP) joints. No significant association with calcification was noted for the following variables: age at disease onset, duration of the disease, sex, the maximum value of the serum calcium, organic phosphate, and uric acid, Raynaud's phenomenon, lupus nephritis, femoral avascular necrosis, central nervous system lupus, proteinuria, or the use of drugs such as corticosteroids, synthetic vitamin D, and nonsteroidal antiinflammatory drugs. However, a significant association was noted with the use of furosemide (p < 0.01 by chi-square). In 5 patients periarticular calcification was observed during or just after hyperuricemia had developed while taking diuretics. CONCLUSION: Periarticular calcification in patients with SLE was seen in the DIP, PIP, and MCP joints, and appeared to be associated with the use of diuretics. If patients with SLE are prescribed a diuretic regimen, crystal associated arthritis should be considered as a possibility when diagnosing oligoarthritis.

Adult↗

Reversible peritoneal calcification in a patient treated by CAPD.

The patient, a female, aged 65 years, developed diffuse peritoneal calcification nine years after commencing CAPD therapy. No abdominal symptoms or evidence of peritonitis were discovered during this period. Before peritoneal calcification was detected, a dialysate with a high glucose concentration (3.86%) had been used once daily for 16 months. In the case of this patient, it was not possible to discover any of the previous indicated etiologies of peritoneal calcification such as significantly elevated values for the product Ca x P, overt secondary hyperparathyroidism, or relapsing peritonitis. It was realized that the use of a high-glucose dialysate in a patient on long-term CAPD treatment had been one causative factor. After peritoneal calcification had been confirmed, the calcium concentration of the dialysate changed from 3.5 mEq/l to 2.5 mEq/l and the patient was put on a regime of 2.0 g alumigel (aluminum-containing phosphate binders) a day. Eight months later, a CT scan was taken. The peritoneal calcification has clearly been mitigated. At present, CAPD therapy is being continued in the absence of any abdominal symptoms.

Aged↗

Recurrent pregnancy loss associated with endometrial hyperechoic areas (endometrial calcifications): a case report and review of the literature.

Endometrial calcifications occur sporadically and are associated with infertility. Previous uterine trauma during instrumentation and/or uterine infection are likely involved in their pathogenesis. The association between endometrial calcifications and recurrent pregnancy loss has been very infrequently reported. A 28-year-old woman with a history of two consecutive first trimester pregnancy losses presented with ultrasonographic hyperechoic endometrial areas associated with histologic endometrial calcification foci. A third pregnancy conceived before starting micronized oral progesterone supplementation also spontaneously aborted at eight weeks. During the fourth pregnancy, progesterone supplementation was taken for the initial 12 weeks. The endometrial lesions were no longer detectable and the pregnancy progressed to term without complications. Endometrial calcifications, related to intrauterine bone tissue, have been previously treated with curettage or with endoscopic surgery, and to the best of our knowledge, have not been reported to disappear spontaneously. In this case, regression of the endometrial calcifications and a favorable pregnancy outcome occurred in concert with oral micronized progesterone supplementation. A combination of transvaginal ultrasonography and endometrial biopsy appears to be an effective method for diagnosing and monitoring of this rare condition.

Abortion, Habitual↗

Calcification and degeneration following mitral valve reconstruction in patients requiring chronic dialysis.

BACKGROUND AND AIM OF THE STUDY: Abnormal calcium homeostasis in patients with end-stage renal failure results in dystrophic calcification; this limits the use of heterograft tissue valve prostheses in patients on chronic dialysis. Mitral valve reconstruction offers advantages over mitral replacement in many patients without renal failure, and offers theoretical advantages in patients requiring dialysis. This study was performed to determine the outcome of mitral valve reconstruction in patients with renal failure requiring chronic dialysis. METHODS: Ten patients with end-stage renal failure and on chronic dialysis who underwent mitral valve repair were identified retrospectively and followed for clinical and echocardiographic outcome. All patients had good results immediately following surgical valve mitral repair, with no more than mild mitral regurgitation and low transmitral gradients on intraoperative transesophageal echocardiography. RESULTS: Clinical and echocardiographic follow up was available for eight patients at an average of 2.3 +/- 1.4 years after surgery. Despite there being no significant valve calcification at the time of surgery, visible mitral leaflet calcification was evident in seven of these patients, and the transmitral gradient for the group was significantly increased (from 4.8 +/- 1.7 mmHg to 8.3 +/- 3.9 mmHg, p = 0.04). Two patients required reoperation for failed mitral repair; one at six months due to chordal rupture, and one at 15 months due to mitral calcification with stenosis. CONCLUSION: Despite good early surgical results, there was accelerated calcification of the repaired mitral valve, a rapid increase in postoperative mitral gradients, and a high incidence of failure of the reconstruction. Additional prospective studies are required to evaluate the optimal intervention for patients with end-stage renal failure who require mitral valve surgery.

Calcinosis↗

Preimplant ultrastructure and calcification tendency of various biological aortic valves.

BACKGROUND AND AIM OF THE STUDY: In recent years a number of fixation and anti-calcification methods have been developed, but little is yet known about the calcification process of biological valves. The aims of this study were to: (i) perform a systematic ultrastructural investigation on various biological valves; and (ii) determine the extent of calcification of these valves in a subcutaneous rat model. METHODS: The following porcine aortic prostheses were investigated: Toronto-SPV, Intact, Freestyle, Mosaic and Hancock-II. Samples taken from the valve leaflets, and in the case of the Freestyle and Toronto-SPV valves also from the aortic wall, were examined ultrastructurally using scanning and transmission electron microscopy. Other samples were implanted subcutaneously in Wistar rats for 12 weeks. The calcium content of the samples was measured using atomic absorption spectrophotometry. RESULTS: All valves examined showed a considerable loss of the endothelial cover. Significant changes in valve ultrastructure were also detected. With regard to calcium content, two valve groups could be distinguished (p <0.05): (i) those with high calcium content, e.g. Toronto-SPV and Intact (>40 mg/g dry tissue); and (ii) those with low calcium content, e.g. Mosaic, Freestyle and Hancock-II (<5 mg/g). CONCLUSION: Fixation methods have pronounced effects on the ultrastructural integrity of bioprostheses. The degenerative calcification of bioprostheses can be effectively inhibited by glutaraldehyde-free fixation and anti-calcification treatments.

Animals↗

Metastatic calcification of the cardiac conduction system with heart block: an under-reported entity in chronic renal failure patients.

Systemic metastatic calcification is a common complication of chronic renal failure. Cardiac involvement is particularly ominous, especially when the cardiac conduction system is affected. Conduction defects, arrhythmias, and sudden death have all been reported with conduction system calcification; however, these are relatively under-reported or unrecognized causes of cardiac morbidity and mortality. We describe a 40-year-old man with Von Hippel-Lindau disease who had been maintained on hemodialysis for two years following bilateral nephrectomies for renal cell carcinoma. The patient presented with symptomatic complete heart block that had progressed from Mobitz type I atrioventricular block. Two months later, while being internally paced, the patient died unexpectedly after a complicated hospital admission. Postmortem revealed extensive vascular, myocardial, and conduction system calcification. Conduction system calcification may cause sudden death in chronic renal failure patients during hospital admission, or unexpectedly while the patient is in the community. Knowledge of this condition is necessary to detect it, as the conduction system is not routinely examined. A routine abbreviated conduction system examination is warranted for patients with systemic metastatic calcification, especially if they have sudden death or a known history of heart block.

Adult↗

[Asymptomatic familial basal ganglia calcification with autosomal dominant inheritance: a family report].

We report here a pedigree of basal ganglia calcification with autosomal dominant inheritance. Following a traffic accident, the proband, a seven-year-old boy, was incidentally noted by cranial computed tomography to have calcification of the bilateral basal ganglia. Six affected members spanning three generations, aged from 5 to 57 years, also had calcification in various degree. None of them had clinical symptoms. There were neither abnormal data nor any characteristic physical symptoms associated with parathyroid disorders. There was no consanguinity. Both sexes were affected and the sex ratio was 0.5. Male-to-male transmission was documented. These findings suggested an autosomal dominant trait. The clinico-radiological findings in our pedigree were different from those of the previously reported cases of familial basal ganglia calcification, that infants were affected and that clinical symptoms were absent in elderly patients. These facts suggest our pedigree is a new type of familial basal ganglia calcification with autosomal dominant inheritance.

Basal Ganglia Diseases↗

Postpartum follow-up of hepatic calcification detected by prenatal ultrasound.

The causes of parenchymal hepatic calcification are mostly transplacental infection of TORCH complex, ischaemic necrosis, or tumours of foetal liver including haemangioma, hamartoma, teratoma, hepatoma, and hemangioendothelioma. Vascular pathologies like hepatic artery aneurysm, haematoma, calcified thromboemboli of portal vein and hepatic veins can also cause hepatic calcification. We present a case of hepatic calcification which was first diagnosed by prenatal ultrasound. In the postpartum follow-up, we observed that the calcifications had decreased in number and size. The causes and results of hepatic calcification or underlying disease are discussed with analysis of the literature.

Adult↗

Analysis of calcium deposits in calcific periarthritis.

OBJECTIVE: To determine if hydroxyapatite (HAP), octacalcuim phosphate (OCP), or tricalcium phosphate (TCP) can be found in the calcium deposits in calcific periarthritis. METHODS: Thirty-six specimens from 34 patients who had acute inflammation and roentgenographically recognized calcification in soft tissue were analyzed. Twenty-three patients with calcific tendinitis in the shoulder and 11 with calcific periarthritis at other sites were included. We prepared 2 kinds of samples from each specimen; a dried sample (washed and dried calcific deposit), and a sample heated to 1,000 degrees C. All were analyzed by X-ray diffraction, Raman spectroscopy, infrared absorption spectroscopy, and X-ray fluorescence spectrometry for calcium and phosphorus molar ratio. Synthetic HAP was used as the control in each analysis. RESULTS: The X-ray diffraction patterns of all dried samples were similar to those of HAP and carbonate apatite. We found no diffraction patterns of OCP or TCP. However, an OH- group at 3570cm(-1) was observed with Raman spectroscopy for samples heated to 1,000 degrees C and synthetic HAP, but not for the dried samples. Infrared absorption spectroscopy also confirmed an OH- group for samples heated to 1,000 degrees C and synthetic HAP, and confirmed that dried samples contained carbonate. CONCLUSION: Calcium deposits are composed of carbonate apatite. HAP, OCP, and TCP were not identified in any deposits.

Adult↗

Differential coronary artery calcification detected by electron beam computed tomography as an indicator of coronary stenosis among patients with stable angina pectoris.

BACKGROUND: The detection of coronary artery calcification by electron beam computed tomography (EBCT) has been suggested as an indicator of atherosclerosis and coronary artery disease (CAD). There is no consensus on the correlation between coronary calcification and angiographically significant stenosis on an artery-by-artery basis. OBJECTIVE: To examine the relationship between coronary calcification score (CCS) and the presence of significant CAD on an artery-by-artery basis in patients with stable angina pectoris. METHODS AND RESULTS: EBCT and coronary angiogram (CAG) were evaluated in 71 patients with stable angina and in nine control subjects. The CCSs of each of the four major coronary arteries were highest in patients with significant CAD (n=43), followed by patients with insignificant CAD (n=5), patients with syndrome X (n=23) and control subjects, respectively. Calcification scores of the four major coronary arteries appeared to have different predictive power for significant stenosis on the same vessel. For left main (LM) and left anterior descending (LAD) coronary arteries, CCSs of vessels with significant stenoses were not different from those without significant stenoses (values expressed as medians: LM 0 versus 1; LAD 98.5 versus 70; not significant). Calcification scores of left circumflex (LCX) and right coronary arteries (RCA) were significantly higher in vessels with significant stenosis (LCX 49.5 versus 0; RCA 53 versus 1; P<0.05). CCSs appeared to be moderately useful to predict significant stenoses in these two vessels (areas under receiver operating characteristic curves: LCX 0.68+/-0.08, 95% CI 0.52 to 0.81; RCA 0.71+/-0.08, 95% CI 0.55 to 0.84). CONCLUSIONS: The CCSs of RCA and LCX arteries, but not those of LM and LAD arteries, may predict significant angiographic stenosis on an artery-by-artery basis among patients with stable angina pectoris.

Aged↗

Tissue damage and calcification may be independent mechanisms of bioprosthetic heart valve failure.

BACKGROUND AND AIM OF THE STUDY: Porcine bioprosthetic valves have excellent hemodynamics and do not require anticoagulation, but have limited durability. Cusp tearing is a major cause of bioprosthetic valve failure. It has been suggested that the mechanism of bioprosthetic valve failure is stiffening by calcification, which leads to elevated stresses and secondary collagen fiber damage and leaflet tearing. This thesis was tested in explanted porcine bioprostheses. METHODS: A total of 60 explanted porcine bioprosthetic valves was tested mechanically, and 15 explanted valves were examined grossly and histologically. Circumferentially and radially oriented samples of cusp tissue were tested uniaxially in a materials testing machine and compared with five controls. RESULTS: Mean (+/-SD) duration of implantation was 10.9+/-5.6 years. Circumferential specimens from explants were less extensible than controls (11.0+/-5.5% versus 24.5+/-2.8% strain, p <0.001), and failed at lower tensions (973+/-733 versus 3075+/-911 N/m, p = 0.001) and at lower strains (21.2+/-8.1% versus 47.3+/-7.1% strain, p <0.001). Radial specimens from explants were less extensible (28.7+/-6.8% versus 39.2+/-5.9% strain, p = 0.002) and failed at lower strains (60.3+/-17.3% versus 112.2+/-24.9% strain, p <0.001) than the controls. The stiffness of the explants was unchanged from controls in both circumferential and radial samples. There were no differences between explants and controls in radial and circumferential stiffness, and in radial failure strength. Calcification was mild and diffuse in most of the tested samples. Tears were found in areas without calcific deposits, along with breaks in collagen fiber bundles. CONCLUSION: These results do not support the thesis that calcification stiffens glutaraldehyde-fixed porcine bioprostheses, except when the entire cusp is transformed into a solid mass of mineral. Rather, leaflet tears may develop as a result of accumulated mechanical damage that is independent of calcification.

Animals↗

Generalized calcification of the liver in advanced schistosomiasis japonica--a case report.

A generalized calcification of the liver was seen in a plain abdominal radiograph of an old male with schistosomiasis japonica and a myeloma. Autopsy disclosed advanced fibrosis of the liver, and histologically, numerous calcified ova with calcification of the surrounding tissue were seen in the thick fibrous bands. Calcification of schistosoma ova so intense as to exhibit a generalized hepatic calcification has never been described in the literature. It is not clear whether the number of ova and the period of their presence are the only factors that determine the degree of liver calcification.

Aged↗

[A case of idiopathic brain calcification associated with dyschromatosis symmetrica hereditaria, aplasia of dental root, and aortic valve sclerosis].

The patient was a 23-year-old woman. She was the product of a full-term pregnancy and normal delivery. At age 3, she was observed to have eruptions on the face and extremities. Gait disturbance and abnormal posture appeared when she was 17-year-old. Mental deterioration followed several years later, and these symptoms progressed gradually. On examination at age 23, mixture of hyperpigmented and hypopigmented macules were observed on the face and the dorsal aspects of the extremities. We diagnosed her skin lesion as dyschromatosis symmetrica hereditaria (DSH) based on dermatological findings, normal minimal erythema dose and normal unscheduled DNA synthesis of her skin fibroblasts. Neurologically, she showed moderate mental deterioration, dystonic posture, dystonic and spastic gait, and generalized hyperreflexia. Laboratory examinations, including parathyroid function, were normal. Brain CT scan revealed severe symmetrical calcifications in the basal ganglia, cerebral white matter, and dentate nucleus. She also showed aplasia of dental root and aortic valve sclerosis. Her father also revealed the same clinical features including skin lesion, movement disorder, mental deterioration, and severe aortic valve calcification. So we diagnosed this patient as familial idiopathic brain calcification associated with DSH, aplasia of dental root, and aortic valve sclerosis. Constellation of these clinical features does not match any previously established type of familial idiopathic brain calcification or hereditary dystonia. However, Patrizi et al reported a patient with DSH associated with torsion dystonia who was very similar to our patient. We propose that our patient and the patient reported by Patrizi et al construct a distinct clinical entity in familial idiopathic brain calcification or hereditary dystonia.

Adult↗

Acute calcific discitis in adults.

Acute calcific discitis in the pediatric population is a well-described entity and may rarely involve the adult population. Acute calcific discitis does occur in adults, presenting clinically with the abrupt onset of severe back pain with a classic radiographic calcification of the disc similar to that of a discogram; it resolves with nonsurgical symptomatic treatment. To our knowledge, no cases of "idiopathic" adult calcific discitis have been reported in the orthopedic literature. We report 2 adult patients with symptomatic thoracic disc calcifications that closely resemble those observed in children and briefly discuss the relevant clinical and radiographic features, along with a review of the literature.

Adult↗

[Diagnosis and treatment of cervical disc calcification in children].

OBJECTIVES: To investigate the diagnosis and treatment cervical disc calcification in children. METHODS: 13 children with cervical disc calcification were analysed retrospectively. Cervical pain was observed after influenza in 5 children, suddenly cervical pain in 3, sudden wryneck in 3 cases. Two children with this disease were accidentally found after injury. RESULTS: 14 calcifications of cervical disks were found in 13 children. Clinical symptoms disappeared after symptomatic management. Calcification disappeared in 5 months. CONCLUSIONS: Cervical disc calcification in children is a kind of benign self-limited disease. Correst understanding of pathophysiologic course of this disease helps to avoid unnecessary surgery.

Adolescent↗