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PubMedDate not supplied

The enigma of autonomic failure in diabetes.

The extent of autonomic failure in diabetes and the damage that results both in terms of structure and function is seldom realised. This article focuses on the consequences of autonomic denervation of several different forms of smooth muscle, notably those of arterial wall, vas deferens, stomach, iris and bronchial wall. The clinical implications of these changes are described, in particular the problems arising from vascular (and vas deferens) calcification and abnormalities of vascular reactivity; insulin-induced postural hypotension and the splanchnic circulation; the anaemia of autonomic neuropathy from failure of erythropoietin production; gastromyopathy as a cause of gastroparesis; iritis as a symptom related to diabetic autonomic neuropathy (DAN); the concept of an autoimmune basis for DAN; and failure of bronchial reactivity and respiratory arrests in DAN. The importance of clinical observation leading to clinical experiment and research, together with the stimulation of ideas by collaboration with clinical colleagues in other disciplines is emphasised throughout.

Autonomic Nervous System Diseases↗
PubMed1998

[Anomalies of phosphate and calcium metabolism in chronic renal insufficiency].

The disturbances of calcium and phosphate metabolism in chronic renal failure involve mainly two hormones, namely calcitriol and parathyroid hormone. They are thought to start with a reduction in calcitriol synthesis, probably due to several mechanisms, and with a reduced action of calcitriol at its target tissues, including the parathyroid cell. They may lead to several complications of clinical importance including both secondary hyperparathyroidism, in the presence or absence of vitamin D deficiency, and hypoparathyroidism. The corresponding expression at the bone level may be osteitis fibrosa, osteomalacia or adynamic bone disease. These complications are frequently associated with soft tissue calcifications, mainly vascular and periarticular, with serious clinical consequences in some patients.

Bone Diseases↗
PubMed1998

Mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS) syndrome: an autopsy report.

Autopsy reports of patients with mitochondrial encephalopathy with lactic acidosis and strokelike episode (MELAS) are rare. This report documents the clinical and autopsy findings of a 47-year-old woman with MELAS syndrome. The diagnosis was corroborated by documenting a mitochondrial DNA mutation tRNA-Leu (UUR) at position 3243. The patient's clinical history was marked by schizophrenia, peptic ulcer disease, constipation requiring hemicolectomy, migraine headaches, deafness, and a left temporal lobe infarct. At autopsy, a muscle biopsy demonstrated numerous ragged red fibers and a partial cytochrome C oxidase deficiency. By electron microscopy, increased numbers of slightly hypertrophic mitochondria were observed focally within myocytes and vessel walls; paracrystalline mitochondrial inclusions were not seen. The brain at autopsy showed mild cerebral atrophy and diffuse cortical gliosis. Prominent bilateral basal ganglia calcifications and vascular sclerosis were present, and a small remote left temporal lobe infarct was seen.

DNA Mutational Analysis↗
PubMed2003

Improvement in lower-extremity peripheral arterial disease by nocturnal hemodialysis.

A 42-year-old man with end-stage renal disease (ESRD) was referred for conversion to nocturnal hemodialysis (NHD) therapy from conventional hemodialysis (CHD) therapy because of refractory intermittent claudication secondary to peripheral arterial disease (PAD). The patient was initiated on CHD therapy in 1976 and subsequently had undergone two unsuccessful renal transplantations. While on CHD therapy, his clinical course was complicated by worsening vascular and soft-tissue calcification. Extensive dystrophic soft-tissue calcification was noted bilaterally in his hands, lower extremities, and sacral region, requiring surgical excision. Lower-extremity arterial Doppler scans documented vascular calcification and a pronounced decrease in peripheral arterial flow bilaterally. After conversion to NHD therapy (7.5 h/session five times weekly), the patient became symptom free and had significant clinical improvements in (1) hemodynamics, measured by clinic blood pressure and two-dimensional echocardiography, (2) biochemical profile, and (3) a sustained improvement in arterial Doppler flow measured by duplex Doppler ultrasound. We conclude that NHD was able to improve lower-extremity PAD in our patient. Further observational and interventional studies are required to investigate the therapeutic potential of NHD for the treatment of PAD in patients with ESRD.

Adult↗
PubMed2004

Phenotypic modulation of vascular smooth muscle cells during medial arterial calcification: a role for endothelin?

We have previously shown that an endothelin receptor antagonist can regress medial arterial calcification in a rat model. The aim of this study was to characterize the phenotypic changes of vascular smooth muscle cells during calcification and mineral loss, in order to understand better the underlying mechanisms. Control Wistar rats were compared with rats treated only with warfarin/ vitamin K1 (15 mg/kg per day) for 8 weeks, or in combination with darusentan (30 mg/kg per day) for the final 4 weeks. Vascular smooth muscle cell, bone cell and macrophage phenotypes were evaluated by the local expression of alpha-actin, tartrate-resistant acid phosphatase and ED-1, respectively. Proteins involved in the modulation of bone resorption like osteopontin and osteoprotegerin were also evaluated by immunohistochemistry. The warfarin/vitamin K1 treatment increased medial arterial calcification ninefold (P < 0.05). At sites of calcification, there was a decrease in alpha-actin localization, and an appearance of osteopontin immunostaining. Histochemical and immunostaining for osteoclast and macrophage markers, as well as for osteoprotegerin, were negative. Although the extent of calcification foci was reduced by darusentan, protein localization in the calcified areas was not modified. Thus, the development of medial arterial calcification produces a phenotypic change in vascular smooth muscle cells that does not appear to be normalized in regions remaining calcified during mineral loss.

Animals↗
PubMed2003

The effects of sevelamer and calcium acetate on proxies of atherosclerotic and arteriosclerotic vascular disease in hemodialysis patients.

BACKGROUND: We recently determined that in hemodialysis patients, the use of calcium salts to correct hyperphosphatemia led to progressive coronary artery and aortic calcification as determined by sequential electron beam tomography (EBT) while the use of the non-calcium-containing binder sevelamer did not. Whether the specific calcium preparation (acetate vs. carbonate) might influence the likelihood of progressive calcification was debated. METHODS: To determine whether treatment with calcium acetate was specifically associated with hypercalcemia and progressive vascular calcification, we conducted an analysis restricted to 108 hemodialysis patients randomized to calcium acetate or sevelamer and followed for one year. RESULTS: The reduction in serum phosphorus was roughly equivalent with both agents (calcium acetate -2.5 +/- 1.8 mg/dl vs. sevelamer -2.8 +/- 2.0 mg/dl, p = 0.53). Subjects given calcium acetate were more likely to develop hypercalcemia (defined as an albumin-corrected serum calcium > or =10.5 mg/dl) (36 vs. 13%, p = 0.015). Treatment with calcium acetate (mean 4.6 +/- 2.1 g/day - equivalent to 1.2 +/- 0.5 g of elemental calcium) led to a significant increase in EBT-determined calcification of the coronary arteries (mean change 182 +/- 350, median change +20, p = 0.002) and aorta (mean change 181 +/- 855, median change +73, p < 0.0001). These changes were similar in magnitude to those seen with calcium carbonate. There were no significant changes in calcification among sevelamer-treated subjects. CONCLUSION: Despite purported differences in safety and efficacy relative to calcium carbonate, calcium acetate led to hypercalcemia and progressive vascular calcification in hemodialysis patients.

Acetates↗
PubMed2005

Bisphosphonates and atherosclerosis: why?

The increasing knowledge on bone calcification processes has revealed some similarities with vascular tissue, where calcifications of arteries and cardiac valves contribute to several cardiovascular problems, such as heart failure, systolic hypertension, and myocardial and peripheral ischemic disease. Bisphosphonates have been used extensively for over two decades for the treatment of diseases associated with excessive bone resorption, i.e., osteoporosis, osteolytic bone metastasis, hypercalcemia and Paget's disease, by blocking osteoclastic function. Etidronate, pamidronate and clodronate has been shown to inhibit the development of experimental atherosclerosis, and proposed mechanisms for this action include inhibition of arterial calcification and lipid accumulation, degradation of atherogenic LDL-cholesterol and reduced foam cell formation. Bisphosphonates inhibit various enzymes involved in cholesterol biosynthesis and suppress macrophages in atheromatous lesions. The possibility of pharmacological agents that effectively treat both osteoporosis and atherosclerosis is attractive, however, current evidence is not conclusive and further research is necessary to confirm these actions in the clinical setting.

Apoptosis↗
PubMedDate not supplied

[Venous calcification].

Explore the source record for details and available documents.

Calcification, Physiologic↗
PubMedDate not supplied

Evaluation of small caliber vascular prostheses implanted in small children: activated angiogenesis and accelerated calcification.

Healing characteristics of small-caliber vascular prostheses used in small children have rarely been observed because removing specimens are troublesome. Modified Blalock Taussig shunt procedures were performed using small caliber expanded polytetrafluoroethylene (ePTFE) vascular grafts and fabric grafts in 13 patients with congenital heart disease. At the time of total corrective procedures, a piece of 10 ePTFE grafts in 10 patients and six fabric grafts in four patients were removed from the distal pulmonary anastomosis, and evaluated. The implantation duration was from 11 months to 5 years and 7 months (mean, 2 years and 6 months). At removal, average patient age was 4 years and all grafts were patent. Microscopically, the wall of three ePTFE grafts were calcified, and macrophages were immunohistologically observed in the graft wall. Thrombus formation, intimal hyperplasia, and pannus detachment was common. In the fabric grafts, many capillaries infiltrated the interstices and often reached the lumen from the perigraft side. These results suggested that in cyanotic small children, angiogenesis in and around fabric grafts was active and calcification was accelerated in ePTFE grafts. Complete endothelialization throughout the length, caused by angiogenesis, might be possible in small children when highly porous fabric vascular prostheses are used.

Blood Vessel Prosthesis↗
PubMed2005

Local delivery of osteopontin attenuates vascular remodeling by altering matrix metalloproteinase-2 in a rabbit model of aortic injury.

OBJECTIVE: Vascular remodeling, often accelerated after cardiovascular procedures, may result in stenosis or aneurysm formation. The bone-associated protein osteopontin has been suggested to be involved in vascular remodeling, yet the effect of locally applied osteopontin in an acute vascular injury model of aortic calcification has not been examined. METHODS: Vascular healing of rabbit thoracic aortas treated locally with recombinant osteopontin (dose: 1 microg; n = 16) or albumin (control, n = 16) after acute injury created by end-to-end anastomosis was evaluated. Matrix metalloproteinase-2 level was quantified by gelatin zymography. Proliferation of smooth muscle cells was detected by immunostaining for proliferative cell nuclear antigen. RESULTS: Osteopontin-treated aortas showed significantly diminished vascular remodeling with less calcification (P = .001) and reduced anastomotic luminal stenosis (4% vs 28%, P = .002) compared with controls 2 months postsurgery. Moreover, osteopontin-treated aortas revealed a thickened adventitia with increased fibrosis (P = .006). Matrix metalloproteinase-2 level was up-regulated 2-fold with osteopontin treatment compared with control at 1 week, returning to baseline by 1 month. Staining for proliferation cell nuclear antigen disclosed an increase in proliferation cell nuclear antigen-positive smooth muscle cells in the media of osteopontin-treated aortas at 1 week, normalizing by 1 month. CONCLUSIONS: These data suggest a beneficial effect of locally applied osteopontin after acute injury possibly by altering matrix metalloproteinase-2 activity and smooth muscle cell proliferation. Brief application of osteopontin may effectively enhance vascular healing by reducing calcification and thus maintaining luminal integrity. The role of the osteopontin-related increase in adventitial fibrosis on vascular healing has to be explored.

Animals↗
PubMed2006

Mitral and aortic annular calcification are highly associated with systemic calcified atherosclerosis.

BACKGROUND: Atherosclerosis has been implicated as a cause of valvular calcification. The aim of this study was to determine whether atherosclerotic calcification in multiple vascular areas is significantly associated with aortic or mitral annular calcification independent of traditional risk factors. METHODS AND RESULTS: A total of 1242 consecutive asymptomatic patients free of clinical coronary heart disease were studied by electron-beam computed tomography for the extent of calcium due to atherosclerosis in 5 distinct vascular beds and calcium in the aortic and mitral annuli. Nearly 24% had calcium in the aortic annulus, whereas 8% were found to have mitral annular calcification. Age and a history of hypertension were the only traditional cardiovascular risk factors that were independently associated with prevalent calcification in the aortic and mitral annuli. After adjustment for age, gender, and cardiovascular disease risk factors, subjects with calcium in the thoracic aorta had the highest odds for the presence of aortic annular calcium (OR=3.9, P<0.01), whereas those with calcium in the abdominal aorta had the highest odds for mitral annular calcification (OR=5.1, P=0.01). Standardized increases in calcium in the abdominal aorta (OR=2.0, P<0.01) and iliacs (OR=1.8, P=0.01) were significantly associated with calcium in the aortic annulus after adjustment for the extent of calcium in the other vascular beds, whereas the thoracic aorta was significantly associated (OR=1.4, P=0.02) with calcium in the mitral annulus. CONCLUSIONS: This study supports the hypothesis that calcification of the mitral and aortic annuli is related to atherosclerosis in other vascular beds.

Adult↗
PubMed2004

[Calcification of heart valves in hemodialized patients and their cardiosurgical correction].

Development of vascular and systemic calcification is one of the more serious and often occurring complications in hemodialyzed patients. The cardiac valves calcifications are of the essential importance. They are result of the very complicated calcification process connected with hyperphosphataemia, hyperparathyroidism, calcium carbonate administering and active vitamin D3 metabolites as well as using dialysis fluids with high concentration of calcium. Elevated P and Ca x P product are both significant predictors of cardiovascular mortality in hemodialized patients. We describe two patients with cardiac failure because of cardiac valves calcification. Both patients underwent artificial valves implantation. The patients showed a marked improvement of the quality of life and haemodynamic status.

Adult↗
PubMed1995

Islet cell tumors of the pancreas: pathologic-imaging correlation among size, necrosis and cysts, calcification, malignant behavior, and functional status.

OBJECTIVE: The purpose of our study was to correlate the imaging and pathologic features of islet cell tumors with regard to tumor size, necrosis and cysts, calcification, malignant behavior, and functional status. MATERIALS AND METHODS: We retrospectively reviewed the clinical, pathologic, and imaging features of all 133 cases of pathologically proved islet cell tumors of the pancreas seen at the Armed Forces Institute of Pathology. Clinical data, including the patients' symptoms and serologic characteristics, were used to distinguish hyperfunctioning tumors (those causing symptoms related to elevated serum polypeptide levels) from nonhyperfunctioning tumors; hyperfunctioning tumors were divided further into insulin-producing and non-insulin-producing types. All patients had at least one cross-sectional imaging study, including CT (n = 118), sonography (n = 42), or MR imaging (n = 22). Clinical, pathologic, and imaging features were evaluated and correlated with tumor size, necrosis and cysts, calcification, local invasion, vascular invasion, metastases, and functional status. RESULTS: Islet cell tumors with areas of necrosis or cystic change found pathologically and on imaging studies (56/133) were larger (8.4 cm in mean transverse diameter) than homogeneous solid lesions (2.9 cm in mean transverse diameter) and were predominantly non-insulin producing (48/56) and nonhyperfunctioning (36/56). Of the 43 insulinomas, 35 were small (2.2 cm in mean transverse diameter), solid, and homogeneous. Larger size also was associated with calcification and malignant behavior, including local invasion, vascular invasion, and distant metastases. CONCLUSION: Our findings show that cystic and necrotic islet cell tumors are usually non-insulin-producing and nonhyperfunctioning neoplasms and larger than the typically solid and small insulinomas. Calcification, local invasion, vascular invasion, and metastatic disease are more commonly seen with larger neoplasms.

Adenoma, Islet Cell↗
PubMed2003

Endochondral bone formation in the heart: a possible mechanism of coronary calcification.

During the atherosclerotic process, calcification occurs and is associated with a high likelihood of adverse events. Coronary calcification has been perceived as a passive precipitation of mineral. Recently, calcification associated with atherosclerosis has been found to be the result of an organized, regulated process that is similar to the process of calcification in bone. Mineralization in skeletal tissue can form by endochondral ossification in which mesenchymal cells differentiate into chondroblasts and produce a cartilage matrix which then degenerates and is remodeled to form bone. In this study, hearts from oophorectomized, aged female Sprague Dawley rats were found to contain areas of cartilage. Micro-computerized tomography radiogrammetry provided quantitative images of the architecture and confirmed the calcified tissue. Histological analysis revealed staining for several markers consistent with cartilage and bone tissue: acid phosphatase and bone matrix proteins, osteocalcin, osteopontin, osteonectin, and bone sialoprotein. In addition, cartilage types II, X, and procollagen type I were present. The presence of chondrocytes in the aged rat heart provides insights into the process of calcification in coronary arteries. Many proteins associated with calcification in bone are present in the cartilage that is present in vascular tissue, suggesting that endochondral calcification is another possible mechanism by which calcification of vascular tissue may occur.

Aging↗
PubMed2026

Imaging techniques for assessing the hand in systemic sclerosis: a systematic review.

BACKGROUND: Systemic sclerosis (SSc) is a rare autoimmune connective tissue disease frequently associated with hand involvement, leading to significant functional impairment. Imaging techniques provide unique opportunities to visualize and quantify structural and functional abnormalities of the hand, supporting diagnosis, monitoring, and treatment evaluation. This systematic review summarizes the imaging techniques used in SSc. METHODS: A systematic search of PubMed and Embase was conducted. Eligible studies included original research articles in English that applied or evaluated imaging techniques of the hands in SSc, published after 2000. Ultrasound and nailfold capillaroscopy were excluded, given their established use. Screening was performed independently by two authors. Findings were synthesized by clinical manifestations, study quality was assessed using the QUADAS-2 tool. RESULTS: Sixty-one studies met the inclusion criteria. In total, 25 distinct imaging techniques were identified, enabling assessment of various hand structures, including vascular involvement, inflammation, fibrosis, calcifications, erosions, and bone marrow edema. Vascular imaging was most extensively studied, particularly in the context of Raynaud's phenomenon and digital ischemia, with multiple techniques demonstrating impaired perfusion and altered thermoregulatory responses. MRI consistently detected subclinical inflammatory and erosive changes of joints and soft tissues,. CT-based techniques provided detailed assessment of calcinosis cutis, while optical and photoacoustic methods showed promise for quantifying skin fibrosis. CONCLUSION: Imaging techniques provide valuable, complementary insights into hand involvement in SSc, often revealing subclinical disease. Despite promising results, limited standardization and longitudinal validation currently restrict clinical implementation. Future studies should focus on harmonizing protocols and validating against clinically meaningful outcomes.

Humans↗
PubMed2003

Cardiac and pulmonary calcification in a hemodialysis patient: partial regression 4 years after parathyroidectomy.

AIMS: The reversibility of extraskeletal calcifications in dialysis patients is an important and unresolved issue. Although periarticular calcifications have been shown to be reversible, little data are available on vascular or parenchymal calcifications. CASE HISTORY: A patient on maintenance hemodialysis with severe hyperparathyroidism, hypercalcemia and hyperphosphatemia was admitted to undergo parathyroidectomy. A preoperative total body bone scintigraphy was performed to better evaluate a lytic lesion in the pelvis, the histology of which proved to be a "brown tumor". The scan showed the typical findings of renal osteodystrophy, but also a diffuse extra-skeletal uptake of bone tracer in the lungs, kidneys, femoral arteries and myocardium. After surgery, good control of serum calcium, phosphate (Ca x P product < 50 mg2/dl2) and PTH levels was maintained during 4 years of follow-up. Bone scans were repeated after 2 and 4 years, showing marked improvement of periarticular uptake at the ends of long bones. Extraosseous calcium deposition was still markedly evident, but progressively decreased (at 4 years: heart -36%, lungs -18%). CONCLUSION: In this dialysis patient, extraskeletal calcification of visceral organs (particularly in the heart and the lungs) due to prolonged hypercalcemia and hyperphosphatemia was partially reversible by parathyroidectomy followed by good long-term control of serum phosphate and calcium.

Adult↗