CLINICAL TRIALS PROFILE FOR COLLAGENASE
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All Clinical Trials for collagenase
| Trial ID | Title | Status | Sponsor | Phase | Start Date | Summary |
|---|---|---|---|---|---|---|
| NCT00004409 ↗ | Phase II Randomized Study of Collagenase in Patients With Residual Type Dupuytren's Disease | Completed | State University of New York | Phase 2 | 1995-08-01 | OBJECTIVES: Evaluate the safety and efficacy of collagenase in improving flexion deformity, range of motion, and grip strength in patients with residual Dupuytren's disease. |
| NCT00014742 ↗ | Phase III Randomized Study of Collagenase in Patients With Residual Stage Dupuytren's Disease | Completed | State University of New York | Phase 3 | 1969-12-31 | OBJECTIVES: I. Compare the safety and efficacy of clostridial collagenase vs placebo in terms of improving the degree of flexion deformity, range of finger motion, and grip strength in patients with residual stage Dupuytren's disease. II. Compare the overall clinical success rate, time to return to normal finger contracture to within 0-5 degrees of normal (zero degrees), and frequency of cord rupture in the joint of patients treated with these regimens. III. Compare the baseline change in degree of finger flexion deformity, range of motion of the treated finger, and strength of hand grip (in pounds) in patients treated with these regimens. IV. Compare the frequency distribution of the number of patients with reduction in finger contracture to within 0-5 degrees of normal (zero degrees) and the number who require re-treatment with open-label collagenase after treatment with these regimens. |
| NCT00261144 ↗ | Collagenase in the Treatment of Cellulite | Unknown status | Stony Brook University | Phase 2 | 2013-02-01 | The purpose of this study is to determine if collagenase injection will reduce or eliminate the appearance of cellulite of the thigh. |
| NCT00261196 ↗ | Collagenase in the Treatment of Adhesive Capsulitis (Frozen Shoulder) | Withdrawn | Biospecifics Technologies Corp. | Phase 2 | 2006-01-01 | The purpose of this study is to test collagenase injection therapy to dissolve adhesions causing frozen shoulder. |
| NCT00261196 ↗ | Collagenase in the Treatment of Adhesive Capsulitis (Frozen Shoulder) | Withdrawn | Stony Brook University | Phase 2 | 2006-01-01 | The purpose of this study is to test collagenase injection therapy to dissolve adhesions causing frozen shoulder. |
| NCT00261209 ↗ | Collagenase in the Treatment of Zone II Flexor Tendon Adhesions in the Hand | Completed | Stony Brook University | Phase 1/Phase 2 | 2005-01-01 | The purpose of this study is to dissolve flexor tendon adhesions associated with failed tendon repair surgery. |
| NCT00294775 ↗ | Effect of Angiotensin II Receptor Blockers (ARB) on Left Ventricular Reverse Remodelling After Aortic Valve Replacement in Severe Valvular Aortic Stenosis | Unknown status | Odense University Hospital | Phase 3 | 2006-02-01 | The consequence of aortic valve stenosis (AVS) is increased pressure load on the left ventricle which causes left ventricular (LV) hypertrophy, and myocardial stretch will cause activation of cardiac peptides and activation of the renin angiotensin aldosterone system (RAAS). The consequence of LV hypertrophy is increased chamber-stiffness and delayed active LV relaxation which initially will cause diastolic and later systolic dysfunction. In heart failure (HF) and ischemic heart disease the degree of diastolic dysfunction has been demonstrated to correlate with functional class, neurohormonal activation and prognosis which also recently have been suggested for AVS. With longstanding elevated filling pressures the left atrium (LA) will dilate. Only limited data are available on the degree and importance of LA dilatation in AVS. When apparent, symptoms of HF in AVS are associated with high mortality rates. If LV systolic dysfunction also is present prognosis will deteriorate further. In these cases aorta valve replacement (AVR) is recommended. AVR will normalize pressure overload and thereby decreases LV hypertrophy. Previously it was believed that in time LV hypertrophy regressed towards normal and even normalized. Recent studies however have demonstrated that LV hypertrophy regression mainly happens during the first year after AVR, and little subsequent changes are seen during the remaining 10 years. Furthermore, patients that experience most regression of hypertrophy have more favourable outcome and better functional class than patients with less regression of hypertrophy. Thus absence of reverse remodelling is associated with poor outcome after AVR. Importantly the regression of LV hypertrophy is closely paralleled by decreasing RAAS hyperactivity. RAAS hyperactivity may be attenuated pharmacologically with angiotensin II receptor blockers (ARB) which in systemic hypertension with LV hypertrophy has been associated with reverse remodelling. The hypothesis is that in patients undergoing AVR for symptomatic AVS, 12 months post operative blockade of the angiotensin II receptor will accelerate LV and LA reverse remodelling, reduce filling pressures and suppress neurohormonal activation compared with conventional therapy. This will lead to improved exercise tolerance and due to improved left atrial function reducing the risk of atrial arrythmias. |
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