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)

In 576 patients quantitative scintigraphy of the sacroiliac joints and the spinal cord with 99mTc-Pyrophosphate was performed. 328 were patients with proven ankylosing spondylitis according to the New-York criteria. 120 were patients with a clinically and roentgenologically suspected ankylosing spondylitis and 128 persons formed a healthy control group. The count rate in small regions of interest (ROI) in the sacroiliac joints, the spinal cord and the os sacrum were compared on the basis of indexes. The scintigraphic data of patients with ankylosing spondylitis were compared with healthy control group and with the radiographic findings and radiologic staging of the disease: In a longitudinal follow-up study during 1 to 6 years these investigations were continued together with clinical and roentgenological checks. Quantitative bone scintigraphy provides characteristic indexes for ankylosing spondylitis, indicating the increased mineral metabolism of the sacroiliac joints and the spinal chord. Skeletal scintigraphy is recommended for early detection and monitoring of ankylosing spondylitis.
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PMID:[Diagnostic potentials of quantitative bone scintigraphy in spondylitis ankylopoietica: a comparison with x-ray findings]. 254 May 7

In this review we consider diseases associated with pathological mineralization/ossification, namely, ankylosing spondylitis (AS), osteoarthritis (OA), generalized artery calcification of infancy (GACI), vascular calcification as well as chondrocalcinosis (CC) and pseudo gout. Deciphering the key enzymes implicated in the calcification process is an objective of prime importance and the ultimate goal is to synthesize inhibitors of these enzymes in order to provide efficient alternate therapeutic strategies that will slow down the pathologic mineralization and complement the arsenal of anti-inflammatory drugs. One of the difficulties in the definition of diseases associated with pathologic mineralization/ossification lies in the controversial relationship between the type of calcification and the nature of the disease. Here, we propose to clarify this relationship by making a distinction between diseases associated with hydroxyapatite (HA) and calcium pyrophosphate dihydrate (CPPD) deposits. AS, OA, GACI and vascular calcification are usually characterized by mineralization/ossification associated with HA deposits, while CC and pseudo gout are mostly characterized by CPPD deposits. Although both HA and CPPD deposits may occur concomitantly, as in chronic pyrophosphate arthritis or in OA with CPPD, they are formed as a result of two antagonistic processes indicating that treatment of distinct diseases can be only achieved by disease-specific drug therapies. The hydrolysis of PPi, an inhibitor of HA formation, is mostly controlled by tissue non-specific alkaline phosphatase TNAP, while PPi production in the extracellular medium is controlled by ANK, a PPi transporter, and/or NPP1 which generates PPi from nucleotide triphosphates. Low PPi concentration may lead to a preferential deposition of HA while high PPi concentration will favor the formation of CPPD deposits. Thus, HA and CCPD deposition cannot occur concomitantly because they are determined by the Pi/PPi ratio which, in turn, depends on the relative activities of antagonistic enzymes, TNAP hydrolyzing PPi or ANK and NPP1 producing PPi. TNAP inhibitors could prevent HA formation in AS, in late OA, in GACI, as well as in vascular calcifications, while ANK or NPP1 inhibitors could slow down CCPD deposition in CC and pseudo gout.
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PMID:Ankylosing spondylitis, late osteoarthritis, vascular calcification, chondrocalcinosis and pseudo gout: toward a possible drug therapy. 2151 61