View clinical trials related to Arthropathy, Neurogenic.
Filter by:Diabetic foot represents a major medical , social and economic problem worldwide. Charcot's neuroarthropathy, being a common cause of diabetic foot, has been an intriguing topic of research for endocrinologists, podiatrists and surgeons. After its first description by JEAN-MARTIN CHARCOT in 1868, many theories have been put forward regarding its pathophysiology , but not much research has been done for its prevention and treatment , specially the inactive stage. The course of Charcot 's neuroarthropathy is triphasic , with the diagnosis being usually missed in the active stage, henceforth the patients often come to us with a deformed foot. As a consequence , the osteoclastic activity in active stage renders the foot bones demineralized and weak, thus being susceptible to fracture and fragmentation. Teriparatide is recombinant human (1-34) parathyroid molecule that has been approved for post-menopausal osteoporosis and in men with primary or secondary osteoporosis. It acts by preferentially stimulating osteoblast over osteoclast activity resulting in new bone formation and an increase in the rate of bone remodeling which manifest as an increase in skeletal mass and bone mineral density . Keeping the pathophysiology of Charcot's foot in mind, teriparatide may be used as potential treatment for inactive Charcot's neuroarthropathy but there are no studies or randomized trials in this setting, till date. We hypothesize that teriparatide may increase the remodeling of foot bones in Charcot's neuroarthropathy, improve bone mineral density, subsequently leading to a reduction in the risk of fractures and progression of deformities. This study plans to compare the effects of teriparatide in diabetes patients with inactive Charcot's foot in a placebo controlled design.
Polyneuropathy is a complication of diabetes mellitus which leads to decreased sensation in arms and legs. This in turn can lead to the development of (infected) foot ulcers. Charcot's disease can also be a consequence of polyneuropathy. Patients with Charcot's disease suddenly develop a red, warm and swollen foot, like an infection. Charcot's disease leads to foot fractures. After these fractures have healed, the shape of the foot can be dramatically altered. This altered shape of the foot increases the risk of developing foot ulcers. Nerves are important in regulating the inflammatory response. This study aims to investigate whether the inflammatory response is different in patients with polyneuropathy with and without a history of Charcot's disease.
The condition Charcot foot has been known in more than 130 years, and yet there still remains a large effort to find the cause, diagnostic and medical treatment of the condition. Charcot neuroarthropathy is a progressive disease of bone and joints characterized by often-painless bone and joint destruction in limbs that have lost sensory innervation. The incidence of acute Charcot among diabetic patients is 0,2 % the prevalence is 7,5 %. In the group of patients with neuropathy the prevalence is even higher –29%. The diagnosis is often made on a clinical basis, particularly in the early stages of the condition. The aim of this study is to find a method that makes the diagnosis primarily on the basis of paraclinical information. Clinical presentation: The typical patients have had diabetes in 10 years and have distal symmetrical neuropathy. The common lesion is unilateral with an acute phase, which may occur either spontaneously or be triggered by a minor trauma. The foot becomes swollen, warm, red and oedematous. Some patients have pain, and the condition could be misdiagnosed as cellulites, acute gout, deep vein thrombosis and osteomyelitis. If the patient has a foot ulcer it is important to rule out osteomyelitis and cellulites. In the initial phase it is difficult to make the right diagnose because Charcot is a rare condition. This leads to a delay in the treatment of the Charcot foot, which, for the moment, is reduction of weight bearing. The patient is equipped with an air cast, and the non weight-bearing regime is in some cases maintained in 12 months. The chronic Charcot is characterized by established deformity. The deformity can be in different sites in the foot, the most common is in the mid foot. Because of the deformity there is abnormal weight pressure on the weight bearing sites on the foot. This is associated with callus formation and there is a higher risk for ulceration.
This study will evaluate the safety and effectiveness of anakinra (Kineret ) for treating patients with neonatal onset multisystem inflammatory disease (NOMID), also known as chronic infantile neurological, cutaneous and arthropathy (CINCA) syndrome. This disease can cause rash, joint deformities, brain inflammation, eye problems, and learning difficulties. Immune suppressing medicines commonly used to treat NOMID do not completely get rid of the disease symptoms and, if used for a long time in high doses, can cause harmful side effects. Anakinra, approved by The Food and Drug Administration for treating rheumatoid arthritis in adults, blocks a substance called IL-1 that may be an important factor in causing the inflammation in NOMID. Patients 2 years of age and older with NOMID whose disease symptoms appeared by at least 6 months of age may be eligible for this study. During a 3-week observation before beginning medication, patients will have a physical examination and evaluation of their condition. They will keep a daily diary of symptoms ratings, and will have blood drawn once a week to measure inflammation and monitor disease. At the end of this period, patients will be admitted to the NIH Clinical Center for 5 days to start daily anakinra injections, given under the skin of the thigh, upper arm, or belly. They will also be taught how to self-inject the medication. After 3 months on medication, patients will be randomly assigned to: 1) continue taking anakinra, or 2) receive a placebo injection (an inactive substance identical in appearance to the study drug). Follow-up visits at NIH for 5 days each will be scheduled at 1, 3, and 12 months, plus one visit between months 5 and 7. During this time, patients will undergo the following procedures: - Magnetic resonance imaging (MRI) scans of the brain and of affected joints. This test uses a magnetic field and radio waves to image the parts of the body under study. Patients who cannot lie still during the brain scan will be sedated. Only patients who do not require sedation will have their joints scanned. - Lumbar puncture (spinal tap). A local anesthetic is given and a needle is inserted in the space between the bones in the lower back where the cerebrospinal fluid circulates below the spinal cord. A small amount of fluid is collected through the needle for analysis. - Examinations by specialists, including an ophthalmologist (eye exam); otolaryngologist (ear, nose and throat exam and hearing test); neurologist (evaluate neurological symptoms such as headache, weakness, walking difficulties, blurred vision); dermatologist (skin exam with photography for record of rashes and joint changes); psychologist or psychiatrist (test memory and learning ability); rehabilitation medicine specialist (evaluate ability walk, move, and use the hands); speech therapist (evaluate ability to talk). - X-rays of joints and bones to look for changes during treatment with anakinra. - DEXA scan to examine bone density. - Blood samples to assess overall clinical condition, measure blood levels of anakinra, and - with the patient's agreement - to perform DNA studies to look for gene differences associated with NOMID. - Skin biopsy (optional) to examine how gene differences in NOMID are related to the rash. - Quality of life questionnaires and review of symptom ratings diaries. Between NIH visits, patients will be evaluated by their local doctor once a month for a checkup, blood tests, symptoms review, evaluation of drug side effects, and completion of quality of life questionnaires.