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PubMed2001

Familial calcium crystal diseases: what have we learned?

The spectrum of heterotopic calcification or ossification is expanding because of the reports of several kindreds with calcium pyrophosphate deposition disease, apatite deposition disease, and others with less common syndromes associated with extracellular matrix calcification, such as fibrodysplasia ossificans progressiva and related syndromes. Genomic DNA studies in both humans and mice provide a shortcut to understanding the genetic basis of promotion and prevention of ECM calcification. Mutation in the COL2A1 gene has been identified in one family with spondyloepiphyseal dysplasia and calcium pyrophosphate and apatite crystalline deposits. In another kindred with precocious osteoarthritis without spondyloepiphyseal dysplasia, the phenotype was linked to markers of chromosome 8. In four other kindreds, the phenotypes were linked to an area of chromosome 5p. Two genes located in this region, which are expressed in articular cartilage, are being investigated as possible calcium pyrophosphate deposition disease genes. The results of linkage studies in three kindreds with articular/periarticular ADD with the COL2A1 gene were noninformative. Two different mouse mutations, the ank/ank and the ttw/ttw mice, are associated with intra-articular and ligament apatite deposits caused by a decrease in extracellular pyrophosphate concentrations, mimicking human arthritis caused by apatite deposition disease. Mutations in the matrix GLA protein, both in mice and in humans, are also associated with vascular and articular calcification. These mouse mutations provide cutting-edge information in the investigation of the mechanisms of apatite deposition in humans.

Calcinosis↗
PubMed1986

Magnesium, lipids and vascular diseases. Experimental evidence in animal models.

The possible role of Mg in the pathogenesis of vascular disease has recently received increasing attention. Accumulating evidence indicates that Mg strongly influences vascular tone and responsiveness to pressor agents and that Mg deficiency may be associated with an increased risk of hypertension. Moreover, experimental Mg deficiency produces vascular lesions with calcifications while increasing the dietary intake of Mg has been shown to prevent atheroma and thrombotic complications. The modifications of lipid metabolism during experimental Mg deficiency have been recently characterized. Severe Mg deficiency in weanling rats produces a marked hypertriglyceridemia and a decrease in the percentage of cholesterol transported by high-density lipoprotein. The decreased clearance of circulating triglycerides appears to be the major mechanism contributing to hyperlipemia. The same animals were found to have a reduced insulin response after intravenous glucose challenge and a slight reduction in heparin release lipoprotein lipase. A marked reduction in plasma activity of LCAT and a significant decrease in esterified/total plasma cholesterol ratio have also been reported. Severe Mg deficiency in weanling rats produces marked changes in the fatty acid pattern of total plasma lipids, as shown by decreased levels of stearic acid, increased of oleic acid and linoleic acid, and decreased levels of arachidonic acid. Platelets from Mg-deficient rats become more sensitive to thrombin. Such an increased sensitivity of platelets may in turn play an important role in initiating the vascular lesion as well as in thrombotic complications. In view of these experimental data in animal models, more work seems necessary in man to assess the effect of Mg on lipid metabolism and vascular disease.

Absorption↗
PubMed1995

Vascular effects of diet-induced hypercalcemia after balloon artery injury in giant Flemish rabbits.

To determine whether metastatic calcification during neointima formation can result in neointimal calcification that simulates advanced human atherosclerosis, 32 giant Flemish rabbits (weight 5.5 +/- 0.6 kg) underwent overstretch balloon injury of bilateral iliac arteries and received diet therapy for 8 weeks: high cholesterol (2%) and low calcium-vitamin D2 regimen (250 mg of calcium carbonate orally 5 times weekly and 50,000 U of calciferol intramuscularly 3 times weekly; group 1; n = 5); low cholesterol (0.5%) and high calcium-vitamin D2 regimen (500 mg of calcium carbonate orally 5 times weekly and 100,000 U of calciferol intramuscularly three times weekly; group 2; n = 19); or 0% cholesterol and high calcium-vitamin D2 regimen (group 3; n = 8). The incidence of vascular calcification was highest (71.4%) in group 2. Eighty-one percent of calcification was medial. Residual strain measurements of 7 thoracic aortas from group 2 compared to normal thoracic aortas from 8 control rabbits showed that residual strain was significantly increased in the calcified atherosclerotic aortas (12.3% vs 5.2%; p = 0.001). We conclude that diet-induced hypercalcemia predominantly affects the media despite the presence of concomitant neointima formation from balloon artery injury with or without hypercholesterolemia and increases the residual strain more than twofold compared to normal thoracic aortas.

Animals↗
PubMed2003

Cardiac valves in patients with Q fever endocarditis: microbiological, molecular, and histologic studies.

The pathologic features of Q fever endocarditis, which is caused by Coxiella burnetii, were histologically evaluated in cardiac valves from 28 patients. We used quantitative image analysis to compare valvular fibrosis, calcifications, vegetations, inflammation, and vascularization due to Q fever endocarditis with that due to non-Q fever endocarditis and valvular degeneration. We also studied the presence of C. burnetii in valves by immunohistochemical analysis, culture, and polymerase chain reaction (PCR). Histologically, Q fever endocarditis was characterized by significant fibrosis and calcifications, slight inflammation and vascularization, and small or absent vegetations. Despite antibiotic treatment, non-statistically significant variations at the histologic level were observed. These pathologic features could be confused with noninfectious valvular degenerative damage. We found that the detection of C. burnetii in cardiac valves by immunohistochemical analysis, culture, and PCR decreased significantly only after 1 year of antibiotic treatment, which emphasizes the long persistence of this organism in valve tissues. Pathologic and immunohistochemical analyses may contribute to the diagnosis of Q fever endocarditis.

Adult↗
PubMed1983

Histopathology of the eye in Cockayne's syndrome.

The eyes of a 44-month-old boy with Cockayne's syndrome had retinal pigmentary abnormalities that included variable pigmentation and excessive lipofuscin deposition in the retinal pigment epithelium and unusual pigmented cells in the retina and subretinal space. There was optic nerve atrophy with loss of nerve fibers and myelin sheaths and also atrophy of the retinal nerve fiber and ganglion cell layers consistent with the histologic features of a demyelinating disease. Widespread pigment dispersion was found in the anterior segment. There was no evidence of vascular disorder, ocular calcification, neuronal storage disorder, or dystrophic corneal changes.

Child, Preschool↗
PubMed2005

Proliferation and progesterone receptor status in benign meningiomas are not age dependent.

BACKGROUND: Some authors have suggested that the biology of meningiomas differs according to a patient's age. Proliferation, vascularity, and hormonal status in meningiomas can be used to describe changes during aging. In the current study, proliferation activity with the Ki-67/MIB-1 antibody was evaluated by immunohistochemistry in meningioma tissue specimens from young and elderly patients. METHODS: Over the past 25 years, tissue samples from 1766 patients with meningiomas were evaluated. Of these, 588 tumor specimens from 554 patients who underwent surgery between 1990 and 2000 were evaluated immunohistochemically. The proliferation index (LI) and progesterone receptor (PR) in meningiomas were quantitatively estimated in elderly (age > or = 70 years) and young patients (age < 70 years). Patients' charts including surgical records, discharge letters, pathology reports, and imaging studies were reviewed. Correlations with histologic subtype, disease recurrence-free survival, resection grade, location, size, vascularity, and tumor calcification were calculated as well. Only patients with a well documented follow-up were included in the statistical evaluation (n = 385). RESULTS: Compared with the young group of 344 patients with meningioma (age < 70 years; mean age, 51.9 years; range, 18-69 years), the elderly population (age > or = 70 years; n = 41; mean age, 74.9 years; range, 70-88 years) showed a male-to-female ratio of 3.2: 1. Both groups had an identical median Ki-67 LI of 3.0% and a PR status of 56.1% versus 58.4 %. No statistically significant differences in disease recurrence-free survival could be found in the two groups. CONCLUSIONS: Proliferation rates and PR status in benign intracranial meningiomas did not appear to be age dependent.

Adolescent↗
PubMed1989

Study of the bone pathology in early mucolipidosis II (I-cell disease).

Histological examination of the bones obtained on autopsy of a 5-month-old child with mucolipidosis II (I-cell disease) revealed inhibition of the growth plate calcification with defective vascular invasion and signs of hyperparathyroidism. These findings are the chondro-osseous basis of the early radiological ricket-like appearance of bones in the neonatal period or soon thereafter. Whether the early skeletal abnormalities of mucolipidosis II result from a primary enzymatic defect of cartilage and bone cells or from factors controlling bone metabolism deserves further study.

Dysostoses↗
PubMed1996

Primary diaphragmatic schwannoma with a typical target appearance: correlation of CT and MR imagings and histologic findings.

A rare case of benign diaphragmatic schwannoma in a 38-year-old female is reported. Precontrast computed tomography (CT) showed an encapsulated well-defined round homogeneous tumor with central calcification, measuring approximately 5 cm in diameter, arising from the left diaphragm. Contrast-enhanced CT and gadolinium-enhanced T1-weighted magnetic resonance (MR) imaging showed focal enhancement in the central portion of the tumor. The tumor showed a typical target appearance of increased peripheral signal intensity and decreased central signal intensity on unenhanced T2-weighted images. Pathological examination of resected specimens of the tumor showed two zonal histological components: a hypercellular portion of spindle cells with nuclear palisading (Antoni A tissue) and a hypocellular portion of cells with cystic degeneration, together with focal calcification and hemangeomatous vascular changes (Antoni B tissue). We consider the radiological characteristics of diaphragmatic schwannoma on CT and MR imagings to represent the geographic difference between the histologic zones of the tumor.

Adult↗
PubMed2001

Role of receptor activator of nuclear factor-kappaB ligand and osteoprotegerin in bone cell biology.

Receptor activator of nuclear factor (NF-kappaB) ligand (RANKL), its cellular receptor, receptor activator of NF-kappaB (RANK), and the decoy receptor osteoprotegerin (OPG) constitute a novel cytokine system. RANKL produced by osteoblastic lineage cells and activated T lymphocytes is the essential factor for osteoclast formation, fusion, activation, and survival, thus resulting in bone resorption and bone loss. RANKL activates its specific receptor, RANK located on osteoclasts and dendritic cells, and its signaling cascade involves stimulation of the c-jun, NF-kappaB, and serine/threonine kinase PKB/Akt pathways. The effects of RANKL are counteracted by OPG which acts as a soluble neutralizing receptor. RANKL and OPG are regulated by various hormones (glucocorticoids, vitamin D, estrogen), cytokines (tumor necrosis factor alpha, interleukins 1, 4, 6, 11, and 17), and various mesenchymal transcription factors (such as cbfa-1, peroxisome proliferator-activated receptor gamma, and Indian hedgehog). Transgenic and knock-out mice with excessive or defective production of RANKL, RANK, and OPG display the extremes of skeletal phenotypes, osteoporosis and osteopetrosis. Abnormalities of the RANKL/OPG system have been implicated in the pathogenesis of postmenopausal osteoporosis, rheumatoid arthritis, Paget's disease, periodontal disease, benign and malignant bone tumors, bone metastases, and hypercalcemia of malignancy, while administration of OPG has been demonstrated to prevent or mitigate these disorders in animal models. RANKL and OPG are also important regulators of vascular biology and calcification and of the development of a lactating mammary gland during pregnancy, indicating a crucial role for this system in extraskeletal calcium handling. The discovery and characterization of RANKL, RANK, and OPG and subsequent studies have changed the concepts of bone and calcium metabolism, have led to a detailed understanding of the pathogenesis of metabolic bone diseases, and may form the basis of innovative therapeutic strategies.

Animals↗
PubMed1998

[Diagnostic imaging for therapy control of primary bone tumors].

Adjuvant chemotherapy has significantly improved the prognosis of patients with bone sarcomas. Preoperative diagnostic imaging of tumor response to such therapy has become a mainstay for the assessment of prognosis, planning of surgery and further treatment. During therapy, responding tumors show characteristic changes on conventional radiography, angiography, sonography, radionuclide studies, CT and MR. The usefulness and the limitations of each imaging modality in assessing response to therapy are reviewed. The diagnostic importance of specific changes such as tumor volume reduction, calcification and tumor vascularization is discussed.

Adolescent↗
PubMed2004

Jejunal intussusception in a 10-year-old boy with blue rubber bleb nevus syndrome.

Jejunal intussusception in a Chinese 10-year-old boy affected by the blue rubber bleb nevus syndrome is presented and discussed. The syndrome is rare, sporadically found with possible dominant inheritance, and due to a gene mutation mapped on the short arm of chromosome 9. It presents with distinctive cutaneous and gastrointestinal malformations together with possible other organ involvement. Gastrointestinal malformations tend to bleed and lead to anaemia. Infrequent complications of the gastrointestinal malformations are volvulus, intestinal infarction and intussusception. The age of the patient and the jejunal intussusception precipitated by a vascular malformation containing calcifications (which were also found in different gut segments) make this case remarkable.

Child↗
PubMed2004

MRI of hemangiopericytoma in the sacrum.

Osseous hemangiopericytoma is rare. We present a case of a 30-year-old woman with low-back pain with radiation to the left buttock for 1 month. Magnetic resonance imaging (MRI) showed a tumor mass with areas of serpentine signal void pattern in the sacrum suggestive of a vascular tumor. Neither calcifications nor layered blood serum were noted. Histological diagnosis was compatible with osseous hemangiopericytoma.

Adult↗
PubMed1996

Renal function following cardiac arrest and resuscitation in the canine.

Organ malfunction often occurs following cardiac arrest and resuscitation. Renal function, inulin clearance (Cln), was examined in 27 dogs before and after (days 2, 4, and 6) cardiac arrest and resuscitation. Group A (n = 7) had no ventricular fibrillation (VF), but cardiopulmonary support was applied for 20 min, and three transthoracic countershocks were delivered. In groups B (n = 7), C (n = 7), and D (n = 6) VF was induced for 2.5, 5.0, and 7.5 min, respectively, followed by cardiopulmonary support for 20, 20, and 15 min, respectively. When necessary, epinephrine and sodium bicarbonate were given during resuscitation. Countershock was applied for defibrillation. Kidneys were examined histologically in groups C and D. Following cardiac arrest, Cln was significantly less in the arrested groups compared to the nonarrested group. Within group C, which received the most epinephrine, Cln correlated negatively with epinephrine administration, and with the energy applied for defibrillation. Histologically, group C showed the highest incidence of cortical tubular cytoplasmic vacuolization, regeneration, inflammation, and tubular casts. Groups C and D showed outer medullary tubular cytoplasmic vacuolization, renal vascular changes, and calcification. In conclusion, cardiac arrest and resuscitation may precipitate acute renal hypofunction as well as reversible and irreversible morphological changes in normal functioning canine kidneys. The confounding effect of pre-existing renal disease remains to be examined experimentally.

Animals↗
PubMed2005

Osteoprotegerin plasma concentrations correlate with severity of peripheral artery disease.

OBJECTIVE: Osteoprotegerin (OPG), a member of the tumor necrosis factor receptor family, is involved in the process of bone turnover and also in the pathogenesis of osteoporosis and premature calcification of the vascular system. In the present study on patients with peripheral artery disease (PAD), we correlated plasma OPG concentrations with severity of disease and the presence of cardiovascular risk factors. PATIENTS AND METHODS: Sixty-seven consecutive inpatients (26 females; mean age 70 years (S.D.: 12), undergoing percutaneous transluminal angioplasty (PTA) because of advanced symptomatic PAD of the lower extremities were studied. Severity grade of disease (clinical stage after "Fontaine", functional measurements in terms of the ankle brachial index (ABI) and "Bollinger score" of angiographies), biochemical parameters and a detailed cardiovascular risk profile were documented. Fasting plasma concentrations of OPG were measured by a commercial sandwich enzyme immunoassay. MAIN RESULTS: The mean plasma concentrations of OPG were 5.3 pmol/l (S.D.: 3.3). Plasma OPG concentrations in subjects with PAD, clinical stages III-IV (n=15) were 7.9 pmol/l (S.D.: 5.3) and were significantly higher than in patients without ischemic ulcerations (n=52; 4.6 pmol/l; S.D.: 2.0; p<0.01). The mean value of Bollinger score was 29.1 (S.D.: 19.8). OPG was positively correlated with Bollinger score of disease (r=0.31; p<0.02), age (r=0.58; p<0.01) and creatinine-values (r=0.32; p<0.01) and negatively correlated with ABI (r=-0.39; p<0.03). CONCLUSION: In patients with PAD, plasma OPG concentrations were significantly higher in subjects with ischemic ulcerations than in those without and were positively correlated with higher severity grade of disease, age and creatinine-values. Further studies are required to analyze the role of OPG as a diagnostic marker for severity of atherosclerotic disease and to assess a possible therapeutic potential as "vasculoprotegerin".

Aged↗
PubMed1999

Parathyroid hormone, vitamin D, and cardiovascular disease in chronic renal failure.

BACKGROUND: Parathyroid hormone and vitamin D have been shown to influence cardiac and vascular growth and function experimentally in human subjects with normal renal function. Because of the increased prevalence of hyperparathyroidism and altered vitamin D status in chronic renal failure, these alterations have been considered to contribute to the increased prevalence of cardiovascular disease and hypertension seen in this patient population. Methods and Results. In this article, we review experimental and clinical literature on the cardiovascular effects of parathyroid hormone and vitamin D and relate them to the development of cardiac and vascular dysfunction in uremia, such as: cardiomyopathy, myocardial hypertrophy, and fibrosis, as well as to myocardial ischemia; uremic glucose intolerance, dyslipidemia, and atherosclerosis; hypertension; and vascular and cardiac calcifications. CONCLUSIONS: The hyperparathyroid state and altered vitamin D status found in uremia contribute to the cardiovascular pathology seen clinically in uremia and also to the excess mortality from cardiovascular causes found in this patient group. The therapeutic implications of these observations are also discussed.

Cardiovascular Diseases↗
PubMed2004

Cardiac valves in patients with Whipple endocarditis: microbiological, molecular, quantitative histologic, and immunohistochemical studies of 5 patients.

The pathological features of Whipple endocarditis, which is caused by Tropheryma whipplei, were histologically evaluated in cardiac valves from 5 patients. We used quantitative image analysis to compare the valvular fibrosis, calcifications, vegetations, inflammation, and vascularization due to Whipple endocarditis with those due to non-Whipple endocarditis and degenerative valves. We also studied the presence of T. whipplei in valves by immunohistochemical analysis, culture, and polymerase chain reaction (PCR). In histologic analysis, Whipple endocarditis was characterized by significant fibrosis, a lack of calcifications, slight inflammation and vascularization, and vegetations of intermediate size. Inflammatory infiltrates consisted mainly of foamy macrophages and lymphocytes. We found that the detection of T. whipplei in cardiac valves, by immunohistochemical analysis, was correlated with the detection of the bacterium by culture and PCR. We report, for the first time, the immunodetection of T. whipplei in a surgically removed arterial embolus. Pathological and immunohistologic analyses may contribute to the diagnosis of Whipple endocarditis.

Adult↗