Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arthritic temporomandibular joints were investigated for intra-articular temperature and joint fluid content of calcitonin gene-related peptide. Eleven patients (16 joints) with rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, or chronic unspecific polyarthritis or monarthritis participated in the study. The intra-articular temperature varied between 35.5 and 37.5 degrees C, with a mean of 36.5 degrees C. The concentration of calcitonin gene-related peptide varied between 7.5 and 749.0 pmol/l, with a mean of 108.6 pmol/l. There was a positive correlation between the intra-articular temperature and the joint fluid concentration of calcitonin gene-related peptide. The plasma level of the peptide was on an average 5% of the joint fluid level.
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PMID:Relation between intra-articular temperature of the arthritic temporomandibular joint and presence of calcitonin gene-related peptide in the joint fluid. A clinical study. 827 69

Three months postpartum, a 33-year-old woman with ankylosing spondylitis (AS) suffered multiple vertebral fractures. Bone mineral density was 61-67% of age-matched normal values at the lumbar spine and proximal femur, and an initial iliac crest bone biopsy revealed osteoporosis and osteomalacia. Secondary causes of bone disease were excluded, and the patient was treated with calcium, vitamin D, and nasal spray calcitonin (400 u/day). Over 4 years, she has shown partial recovery of bone mass and almost complete resolution of osteomalacia. Osteoporosis and fracture occur in patients with AS, yet this case represents a rare association between AS and both osteomalacia and postpregnancy spinal osteoporosis.
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PMID:Osteomalacia and osteoporosis in a woman with ankylosing spondylitis. 915 86

Salmon calcitonin (especially intranasal) provides an interesting analgesic effect in a series of painful conditions including reflex sympathetic dystrophy syndrome, adhesive capsulitis, ankylosing spondylitis, rheumatoid arthritis, vertebral crush fractures and metastasis, phantom limb pain, etc. In addition, in preliminary series, calcitonin shows an unexpected benefit to vasomotor changes and peptic ulcer. Yet the experience in these conditions is limited and needs confirmation. By comparison with the injectable, the intranasal route seems particularly interesting because of less undesirable effects, and a more rapid and probably more powerful analgesia.
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PMID:Calcitonin in reflex sympathetic dystrophy syndrome and other painful conditions. 1200 65

Trigeminal neuralgia (TN) has been recognized as one of the most common neurovascular syndromes caused by the vascular contact of the trigeminal nerve in its root entry zone (REZ) with a branch of the superior or anterior inferior cerebellar arteries, leading to a demyelinization of trigeminal sensory fibers within either the nerve root or, less commonly, the brainstem. There is a lack of certainty regarding the aetiology and pathophysiology of TN, therefore the treatment of trigeminal neuropathic pain disorders continues to be a major therapeutic challenge. The identification of novel therapeutic agents for the treatment of these disorders is important. Calcitonin (especially intranasal) provides an interesting analgesic effect in a series of painful conditions including reflex sympathetic dystrophy syndrome, adhesive capsulitis, ankylosing spondylitis, rheumatoid arthritis, vertebral crush fractures and metastasis, phantom limb pain, etc. Exogenous calcitonin is thought to cross the blood-brain barrier and to accumulate slowly in the brain, inducing analgesia once sufficient receptors are occupied. We hypothesize that calcitonin may has anti - trigeminal neuralgia properties. From the clinical point of use, the analgesic effect of calcitonin will be beneficial throughout the whole period of medical treatment of trigeminal neuralgia patients.
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PMID:Could calcitonin be a useful therapeutic agent for trigeminal neuralgia? 1834 43

Biological therapy is a thriving area of research and development, and is well established for chronic forms of rheumatoid arthritis (RA) and ankylosing spondylitis (AS). However, there is no clinically validated biological therapy for osteoarthritis (OA). Chronic forms of OA are increasingly viewed as an inflammatory disease. OA was largely regarded as a "wear and tear disease". However, the disease is now believed to involve "low grade" inflammation and the growth of blood vessels and nerves from the subchondral bone into articular cartilage. This realization has focused research effort on the development and evaluation of biological therapy that targets proinflammatory mediators, angiogenic factors and cytokines in articular cartilage, subchondral bone and synovium in chronic forms of OA. This review article provides an overview of emerging biological therapy for OA, and discusses recent molecular targets implicated in angiogenesis and neurogenesis and progress with antibody-based therapy, calcitonin, and kartogenin, the small molecule stimulator of chondrogenesis.
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PMID:The future of osteoarthritis therapeutics: emerging biological therapy. 2417 Feb 55