Active clinical trials for "Calcinosis"

In this mono-center,open,three-armes, controlled, randomized phase I study the progress of aortic valve calcification with and without vitamin K supplementation will be investgated. This will be done by means of measurements of concentrations from osteocalcine and MPG in blood serum, echocardiography, cardiac computed tomography and cardiac MRI

Calcinosis cutis refers to a group of disorders characterized by calcium deposition in the skin (1). The disorders are classified according to etiology into the following types: dystrophic, metastatic, iatrogenic, and idiopathic (1,2). Dystrophic calcification occurs in the setting of varicosities, infection, tumors, and connective tissue disorders (1). The connective tissue disorders most commonly associated with calcinosis cutis are systemic sclerosis and dermatomyositis, although it has also been reported in patients with systemic lupus erythematosus, undifferentiated connective tissue disorder, and mixed connective tissue disorder (2). The pathophysiology of calcinosis cutis is not well understood, and there is a broad range of severity seen, from benign localized, small nodules to large, severely debilitating lesions (2). Although many therapies have been investigated for treatment of calcinosis cutis, including calcium channel blockers, colchicine, minocycline, intravenous immunoglobulin, and bisphosphonates, results have been mixed at best (2). Surgical removal is sometimes feasible in the case of a localized lesion, however, recurrence after surgery is common (2). Recently, several authors have reported cases of dramatic resolution of dystrophic calcinosis cutis lesions with topical sodium thiosulfate preparations (1,3,4). Systemic sodium thiosulfate therapy is commonly used to treat calciphylaxis in patients with renal disorders with very few adverse events (1). A search of the literature to date yields no formal studies that aim to determine whether topical sodium thiosulfate is truly an effective therapy for calcinosis cutis. As a result, patients are often treated with therapies that are unproven or ineffective and their calcinosis cutis eventually leads to significant pain and disability. Research Question: Does treatment of dystrophic calcinosis cutis with topical sodium thiosulfate result in diminution of the lesion and associated pain? Objective: The objective of this pilot study is to investigate whether topical sodium thiosulfate is an effective therapy for calcinosis cutis. This study will also determine the feasibility of our protocol and provide information to help direct a future full-scale trial.

Patients with chronic kidney disease (CKD) have a higher mortality rate than the general population, with cardiovascular disease (CVD) accounting for approximately 50% of deaths. Vascular calcification is a common finding in patients with CKD. Furthermore, patients with CKD develop secondary hyperparathyroidism, partly because of a decrease of calcitriol synthesis on the kidney. Treatment of secondary hyperparathyroidism includes use of activated vitamin D including calcitriol and paricalcitol. Recent evidence in dialysis patients suggest an improved survival in patients using paricalcitol compared to calcitriol. Studies in uremic rats suggests that there are differential effects of calcitriol and paricalcitol in expression of markers of soft-tissue calcification independent of calcium-phosphorus product. Calcitriol increased calcification of vascular smooth muscle cells cultured in calcification media. There was also significant increase in pulse pressure in animals treated with calcitriol. The investigators hypothesize that these different forms of vitamin D may have differential effects in vascular calcification progression in CKD patients.

The purpose of this study is to evaluate the clinical effect of chewing gum containing maltitol, on re-mineralization of early caries following daily chewing for 6 months by school children, compared to a xylitol gum, gum base and a no gum group.

Aortic stenosis is the most common valvular heart disease and an important public-health problem. Surgical or interventional aortic valve replacement are based on symptoms and measures of valvular and ventricular function using echocardiography.There is no uniform pattern of progression. Instead, marked differences not only between individuals, but also during the time course of the disease can be observed. Several prospective studies have been performed to enhance the predictability of disease behavior. Individually it is still prone to large errors and hard to predict aortic stenosis progression. Therefore, in patients with aortic sclerosis without severe stenosis, it is desirable to find a strong predictor of rapid disease progression. This would allow anticipating cardiovascular deterioration by identifying individuals at particular risk. Study Hypothesis In patients with aortic sclerosis, increased serum calcification propensity, as measured by the T50-Test, is related to the amount of stenosis progression in one year.

Vascular calcification is a frequent complication in dialysis patients and is strongly associated with mortality. Its pathogenesis is complex and involves a series of markers that act on the vascular microenvironment. There is evidence that aldosterone is one of the biomarkers and may have a role in osteoinductive pathways.The aim of this study was to evaluate the effect of spironolactone, an inhibitor of mineralocorticoid receptor, in the progression of coronary calcification in patients undergoing peritoneal dialysis.

The purpose of this trial is to examine the effect of increasing dialyse magnesium on serum calcification propensity in subjects with end-stage renal disease treated with haemodialysis.

Vascular calcification is the leading cause of death in patients with end stage renal disease (ESRD) in hemodialysis. The protein matrix Gla vitamin K dependent (MGP) is a potent inhibitor of the vascular calcification. Objective: To evaluate the effect of vitamin K2 on vascular calcification in patients on hemodialysis. Materials and Methods: A prospective, randomized, double-blind study will be performed. The study subjects will be divided into a control (1000 µl of saline) or treated group (1000 µl containing 2000 µg of Vitamin K2). Vitamin K2 will be administered three times a week intravenously at the end of each dialysis session. Blood samples for biochemical determinations and vascular calcification will be assessed before and after 6 months of treatment through carotid Doppler ultrasound.

The purpose of this study is to test whether active vitamin D (calcitriol) protects bones from weakening and protects blood vessels from calcium deposits over the first year of kidney transplantation.

Cardiovascular disease (CVD) is the commonest cause of mortality in patients with chronic kidney disease (CKD) and end-stage kidney disease (ESKD). Reasons for the greater incidence of CVD in this group include traditional CVD risk factors of hypertension, dyslipidemia and diabetes but more importantly also include non-traditional risk factors such as calcium and phosphate imbalance. The latter is thought most likely to contribute to vascular calcification, especially for those on dialysis, and this in turn leads to arterial stiffness and left ventricular hypertrophy, the two commonest cardiovascular complications. Arterial stiffness and calcification have been found to be independent predictors of all-cause and cardiovascular mortality in CKD. Few studies, though, have looked at both structural and functional changes associated with calcification and there have been very few interventional studies addressing this issue. Control of calcium and phosphate levels in CKD can occur with the use of medications that reduce elevated serum phosphate (phosphate binders, mostly calcium-based) and those to treat hyperparathyroidism (vitamin D and more recently calcium sensing receptor agonists called calcimimetics). These pharmacological managements addressing calcium and phosphate imbalance reduce vascular calcification and CVD. Bisphosphonate therapy may also have a role in reduction of calcification. Low bone mineral density (BMD) is common in CKD patients and predicts increased fracture risk similar to the general population. Bisphosphonate therapy improves BMD and lowers the fracture risk. Bisphosphonates may also have a role in secondary hyperparathyroidism to reduce hypercalcemia and allow for more aggressive calcitriol treatment. Recent studies have addressed the possibility of bisphosphonates reducing the progression of vascular calcification in CKD and revealed that the extent of calcification may be suppressed in association with a reduction in chronic inflammatory responses. The investigators aim to perform a prospective, randomised study assessing the impact of alendronate on cardiovascular and bone mineral parameters. This will be a single-centre study involving subjects with CKD Stage 3 (those patients with GFR between 30 and 59ml/min). Arterial stiffness (by pulse wave analysis and pulse wave velocity) and vascular calcification (using CT scans through superficial femoral artery) will be followed as well as serum markers of calcium, phosphate and PTH. Differences in these end-points will be compared between participants taking alendronate and those not. The study will be conducted over a 12 month period and the investigators aim to recruit about 50 patients (25 on alendronate and 25 control).