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(1/3283) Broncholithiasis: rare but still present.

Broncholithiasis is a rare but distinct and potentially dangerous pulmonary problem that still needs to be considered in the differential diagnosis of some patients with bronchial obstruction. Broncholiths originate from calcified material in peribronchial lymph nodes eroding into the tracheobronchial tree. The clinical and chest X-ray signs are usually non-specific, but the diagnosis can nowadays be made based on clinical suspicion, CT-scan and fibre-optic bronchoscopy findings, so that a malignant cause of airway obstruction can be ruled out. The removal of broncholiths during fibre-optic bronchoscopy is seldom possible and rather dangerous. They can be removed safely by rigid bronchoscopy with the aid of Nd-YAG laser photocoagulation. Thoracotomy is indicated in complicated cases with fistula formation or severe bleeding.  (+info)

(2/3283) Role of glutaraldehyde in calcification of porcine aortic valve fibroblasts.

Glutaraldehyde-treated porcine aortic valve xenografts frequently fail due to calcification. Calcification in the prostheses begins intracellularly. In a previous study, various types of cell injury to canine valvular fibroblasts, including glutaraldehyde treatment, led to calcification. An influx of extracellular Ca2+ into the phosphate-rich cytosol was theorized to be the mechanism of calcification. To test the Ca2+ influx theory, cytosolic Ca2+ and Pi concentrations were assessed in glutaraldehyde-treated porcine aortic valve fibroblasts, and their relationship to a subsequent calcification was studied. Glutaraldehyde caused an immediate and sustained massive cytosolic Ca2+ increase that was dose dependent and a several-fold increase in Pi. Calcification of cells followed within a week. The earliest calcification was observed in blebs formed on glutaraldehyde-treated cells. Live control cells or cells fixed with glutaraldehyde in Ca2+-free solution did not calcify under the same conditions. Concomitant increases in Ca2+ and Pi in glutaraldehyde-treated cells appear to underlie the mechanism of calcification, and the presence of extracellular Ca2+ during glutaraldehyde fixation promotes calcification.  (+info)

(3/3283) Histology and tissue chemistry of tidemark separation in hamsters.

Adult articular cartilage is divided by the tidemark into a deep calcified layer and a more superficial uncalcified layer. Histologic examination of articular cartilage from the knee joint of golden Syrian hamsters 123 days of age or older revealed defects at the tidemark in the tibia. Defects ranged from small separations of the calcified and uncalcified layers along the tidemark to progressively larger defects apparently formed by dissolution. These larger defects appeared as cavities in the noncalcified cartilage, had smooth rather than rough edges, frequently contained coalesced debris, and often resulted in a bulge in the articular surface. Occasionally, these large defects broke through the articular surface. Defects were not observed in tibial cartilage of younger (<90 days old) hamsters or in femoral cartilage from hamsters of any age. Exercise neither protected against nor increased the severity of the defects. Collagen cross-linking by pyridinoline was examined as a function of age and increased from 1,090 to 3,062 micromoles of pyridinoline/mole of hydroxyproline over the period of 1-9 months of age but was not correlated with defect formation. With increasing age, these focal tidemark defects could lead to osteoarthrosis-like cartilage lesions.  (+info)

(4/3283) Incidence and clinical relevance of coronary calcification detected by electron beam computed tomography in heart transplant recipients.

BACKGROUND: Patients treated by cardiac transplantation who survive beyond one year are at significant risk from fatal coronary artery disease. The development of coronary artery calcification in these patients is discussed and methods available to detect it are reviewed. OBJECTIVES: To assess the clinical importance of coronary artery calcium in heart transplant recipients. METHODS: In a cohort of 102 cardiac transplant recipients, electron beam computed tomography was used to measure calcium in the coronary arterial wall 63 days to 9.1 years (median 4.6 years) after transplantation. The results were compared with angiographic findings and with conventional coronary disease risk factors. The patients were followed for a mean of 2.12 years (1.2-4.02 years) to assess the relationship between these findings and future cardiac events. RESULTS: Forty-one (40.2%) had a stenosis of > 24% in one or more major coronary artery at angiography. Forty-six (45%) had a coronary calcium score > 0. The absence of calcium had a negative predictive value with respect to angiographic disease in any vessels of 87.5%. Logistic regression revealed that dyslipidaemia, systemic hypertension and organ ischaemic time were significant predictors of calcification. At follow-up, both an abnormal coronary angiogram and coronary calcium were found to be the only significant predictors of late events. Multivariate analysis suggested that the detection of coronary calcium did not offer any additional predictive information over that provided by the angiogram itself. CONCLUSION: Electron beam computed tomography is well suited to the assessment of calcium in the coronary arteries of heart transplant recipients, although the mechanisms of this calcification remain poorly understood. Calcium is detected more frequently than would be suggested by studies using intravascular ultrasound. It is associated with the presence of angiographic disease, and with some conventional risk factors for coronary disease. At follow-up the presence of coronary calcium was associated with an adverse clinical outcome, as it is in conventional ischaemic heart disease.  (+info)

(5/3283) Renal biopsy in the milk-alkali syndrome.

In milk-alkali syndrome the degree of renal impairment varies greatly. Few reports have been published describing structural changes on renal biopsy. In three illustrative cases, impairment of renal function was related to morphological changes shown on percutaneous biopsy. Milk-alkali syndrome should be considered as a cause of renal dysfunction in patients with a long history of dyspensia.  (+info)

(6/3283) Degenerative changes in aortic root allografts placed in the right ventricular outflow tract of growing puppies.

Differently prepared aortic root allografts were implanted in the right ventricular outflow tract of growing puppies to determine the site of origin and progress of degenerative changes in these conduits. The three preparations assessed were as follows: group A, fresh and sterile grafts; group B, antibiotic sterilized grafts in nutrient medium; and group C, beta-propiolactone sterilized grafts. Although calcification of the aortic wall occurred in all groups, the aortic leaflets were minimally affected. A correlation between viability and lack of calcification and between viability and long-term function is emphasized.  (+info)

(7/3283) Calcific myonecrosis.

Calcific myonecrosis is a rare and late sequela of compartment syndrome, which becomes symptomatic years after the initial trauma. We diagnosed this condition in a 64-year old man, 42 years after he sustained a shot-gun wound to the right lower leg. Total excision of a peripherally calcified, cystic mass, continuous with the anterior tibial muscle belly resulted in complete resolution of symptoms. Consideration of the diagnosis is warranted in patients with a history of major injury who develop a soft tissue mass in the traumatized compartment. The treatment of choice is marginal excision.  (+info)

(8/3283) Angiographic correlation of CT calcification in the carotid siphon.

BACKGROUND AND PURPOSE: Calcification in the coronary arteries has been correlated with significant vessel stenosis. The predictive value of calcification within the carotid siphon has not been characterized; however, stenosis in the carotid siphon is potentially important in determining management of patients with ipsilateral carotid bifurcation stenosis. The purpose of this study was to determine optimal parameters for assessing carotid siphon calcification on head CT scans and to compare the CT findings with angiographic results. METHODS: We performed a retrospective review of patients referred for diagnostic carotid arteriography. Those patients who also had undergone a head CT study at our institution were selected. The CT scans and angiograms of 64 patients (128 vessels) were reviewed. Carotid siphon calcification on CT scans was characterized on brain and bone windows as mild, moderate, or severe. Comparison was then made with angiographic findings. RESULTS: The sensitivity and specificity of CT for depicting greater than 50% angiographic stenosis in the carotid siphon were 86% and 98%, respectively, for bone windows and 100% and 0%, respectively, for brain windows. The positive predictive value (PPV) for a stenosis of greater than 50% as evidenced by severe calcification was 86% on bone windows and 11% on brain windows. The PPV for mild and moderate calcification on bone windows was 2.5% and 0%, respectively. CONCLUSION: Severe CT calcification in the carotid siphon as characterized on bone windows correlates with a carotid siphon stenosis of greater than 50% as determined angiographically. Therefore, the identification of severe calcification offers a potential noninvasive method for identifying stenosis of the carotid siphon. This information may be essential in determining management and prognosis for patients with carotid bifurcation stenosis.  (+info)