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)

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

22,049 adults were surveyed in a ten-year epidemiological study. The frequency of common rheumatic symptoms in Shantou population was much lower than that in northern China. The prevalence of ankylosing spondylitis, rheumatoid arthritis, osteoarthritis, osteoporosis and gout was 0.20%-0.32%, 0.20%-0.26%, 8.3%-10.8%, 12.4% and 0.15%-0.17% respectively. The frequency of HLA-B27 was 4.1% among general population and 90.6% in ankylosing spondylitis. The most commonly involved sites of osteoarthritis were lumbar spine, neck, and knee; but hands and hip were rarely involved. 85% subjects under investigation were found to be short of calcium intake. The differences between the north and the south of China in the prevalence of rheumatic symptoms may be related to the diversities in consciousness of seeking medical advice, reduction of bone content, climate and ergonomics.
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PMID:[10-year epidemiological study on rheumatic diseases in Shantou area]. 1037 16

The term chondrocalcinosis is often used to describe the radiological or pathological features of calcified joint cartilage, and it usually indicates the deposition in cartilage of calcium pyrophosphate dihydrate. The prevalence of chondrocalcinosis increases with age, with dramatic increases occurring in the decades past age 60. In younger patients with chondrocalcinosis, either clinical evidence of associated metabolic diseases leading to the chondrocalcinosis or familial disease occurrence usually can be detected. We report a 42-year-old Chinese woman with ankylosing spondylitis and arthritis involving multiple peripheral joints. Severe chondrocalcinosis was detected incidentally in this patient, however, subsequent studies revealed no associated metabolic disease or familial susceptibility and the clinical features of this patient were different from those of ankylosing chondrocalcinosis (pseudoankylosing spondylitis). The cause of chondrocalcinosis in this patient remains unknown, but joint damage and repair could have been initiating or aggravating factors of the chondrocalcinosis.
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PMID:Ankylosing spondylitis with severe chondrocalcinosis: case report. 1058 32

The association between rheumatological and thyroid disorders has long been known, the most common being the association of rheumatoid arthritis and autoimmune thyroiditis. Little is known as to possible thyroid involvement in ankylosing spondylitis (AS). In 22 female patients with AS and 22 healthy age-matched control subjects parameters of thyroid gland function, rheumatic activity, as well as a subtle drug anamnesis of the rheumatic medication, and an ultrasonographic examination of the thyroid gland were determined. Thyroid function was tested by intravenous injection of 400 microg thyrotropin-releasing hormone (TRH). In parallel basal levels of reverse-T3 (rT3), calcium and anti-thyroid antibodies were estimated. In the AS-group an enlarged thyroid volume was seen in 10 cases, basal FT4, FT3 and TT3 were significantly lower, TSH and TT4 were found to be in the normal range and rT3 was significantly increased. The prevalence of anti-thyroid antibodies was significantly higher in the AS-group. The AS-patients responded as well as the controls with thyroid hormone secretion to TRH, within an observation period of 2 hours. No differences were observed in TSH response. Free serum calcium showed in both groups no significant difference. To summarize our results, female patients with AS showed a
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PMID:Thyroid disorders in female patients with ankylosing spondylitis. 1058 2

Diclofenac (DCLF) is a nonsteroidal anti-inflammatory drug that is widely used for the treatment of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, and acute muscle pain conditions. Toxic doses of DCLF can cause nephrotoxicity in humans and experimental animals. However, whether this DCLF-induced nephrotoxicity involves apoptotic cell death in addition to necrosis is unknown. The goals of this investigation were to determine whether DCLF-induced nephrotoxicity involves oxidative stress and apoptotic type genomic DNA fragmentation, and if so, whether DCLF-induced oxidative stress and DNA fragmentation cause apoptotic cell death in mouse kidneys. Male ICR mice (CD-1; 25-45 g), fed ad libitum, were administered nephrotoxic doses of DCLF (100, 200, 300 mg/Kg, po) and sacrificed 24 h later. Blood was collected to evaluate renal injury (BUN), lipid peroxidation (MDA: malondialdehyde levels), and superoxide dismutase (SOD) activity (a marker of oxidative stress). Kidney tissues were analyzed both quantitatively and qualitatively to determine the degree and type of DNA damage, and evaluated histopathologically for the presence of apoptotic characteristics in the nucleus of diverse types of kidney cells. Results show that diclofenac is a powerful nephrotoxicant (at 100, 200, and 300 mg/kg: 4.7-, 4.9-, and 5.0-fold increases in BUN compared to the control, respectively) and a strong inducer of oxidative stress (significant increase in MDA levels). Oxidative stress induced by DCLF was also coupled with massive kidney DNA fragmentation (100, 200, and 300 mg/kg: 3-, 8-, and 10-fold increases compared to control, respectively). A dose-dependent increase in MDA levels and SOD activity was also observed, which indicated a link between oxidative stress and nephrotoxicity. Qualitative analysis of DNA fragmentation by gel electrophoresis showed a DNA ladder indicative of Ca2+-Mg2+-endonuclease activation. Histopathological examination of kidney sections revealed numerous apoptotic nuclei across proximal and distal tubular cell linings. Collectively, these data for the first time suggest that DCLF-induced nephrotoxicity may involve production of reactive oxygen species leading to oxidative stress and massive genomic DNA fragmentation, and these two free radical mediated events may ultimately translate into apoptotic cell death of kidney cells in vivo, and reveal a DNA-active role for DCLF.
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PMID:Diclofenac induced in vivo nephrotoxicity may involve oxidative stress-mediated massive genomic DNA fragmentation and apoptotic cell death. 1144 Aug 26

A 39-year-old woman presented with symptoms of pain in the lumbar region and lower extremities. Physical findings included restricted movement of the lumbar spine, sacroiliac joint tenderness, positive Schober's test (10-12.5 cm), and bilaterally positive Mennel and Fabere tests. Although these symptoms and findings were suggestive of ankylosing spondylitis, osteomalacia was diagnosed with the appearance of multiple pseudofractures in her pelvic X-ray and laboratory abnormalities. All her symptoms and signs resolved in 6 months with vitamin D and calcium treatment.
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PMID:A case of osteomalacia mimicking ankylosing spondylitis. 1156 83

Vertebral fractures due to osteoporosis are a common but frequently unrecognized complication of ankylosing spondylitis (AS) and various factors may contribute to the development of osteoporosis in AS. It is known that inflammatory activity in rheumatic disease (i.e., proinflammatory cytokines) itself plays a possible role in the pathophysiology of bone loss. 1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) seems to be another possible candidate for mediatory function in regulating both the inflammatory process and bone turnover. The aim of this study was to evaluate the relation between disease activity, bone turnover and calciotropic hormones. In 70 patients with established AS and an age- and sex-matched control group, the relation between disease activity (erythrocyte sedimentation rate, C-reactive protein, Bath Ankylosing Spondylitis Disease Activity Index), and serum levels of vitamin D metabolites, parathyroid hormone (PTH), bone alkaline phosphatase (bAP) and urinary pyridinium cross-links were determined. Serum levels of 1,25(OH)2D3 (p<0.01) and PTH (p<0.01) were negatively correlated with disease activity, the excretion of urinary pyridinium crosslinks showed a positive correlation with disease activity (p<0.01), and 1,25(OH)2D3 and PTH were positively correlated with bAP (p<0.01). These results indicate that high disease activity in AS is associated with an alteration in vitamin D metabolism and increased bone resorption. Furthermore, the decreased levels of 1,25(OH)2D3 may contribute to a negative calcium balance and inhibition of bone formation. Our results suggest further research is necessary to determine whether low levels of 1,25(OH)2D3 as an endogenous immune modulator suppressing activated T cells and cell proliferation may accelerate the inflammation process in AS.
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PMID:Relationship between disease activity and serum levels of vitamin D metabolites and parathyroid hormone in ankylosing spondylitis. 1184 29

Vertebral fractures due to osteoporosis are a common but frequently unrecognized complication in established ankylosing spondylitis (AS). It is known that inflammatory activity in rheumatic diseases (i.e., proinflammatory cytokines) itself plays a possible role in the pathophysiology of bone loss. The aim of this study was to analyze whether inflammatory activity and an alteration of the vitamin D metabolism play a substantial role in the loss of bone mass in AS. In this cross-sectional study, 58 patients with established AS and an age- and sex-matched control group were examined. The vitamin D status was investigated, as was, in parallel, the relationship to disease activity (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP], Bath Ankylosing Spondylitis Disease Activity Index [BASDAI]), markers of bone metabolism (parathyroid hormone [PTH], 1.25 vitamin D3, 25 vitamin D3), calcium, bone alkaline phosphatase (bone-AP), urine cross-links, and plasma tumor necrosis factor alpha (TNFalpha). Bone mineral density was measured by quantitative computed tomography (QCT) of the lumbar spine. Osteoporosis was diagnosed in early as well as in progressive stages of AS (23/58=39.6%). Furthermore, serum levels of 1.25 vitamin D3 and PTH were negatively correlated with disease activity and TNFalpha. The excretion of cross-links showed a positive correlation with disease activity and TNFalpha, and 1.25 vitamin D3 and PTH were positively correlated with bone-AP. TNFalpha also positively correlated with disease activity. AS patients with osteoporosis showed significantly increased CRP, ESR, cross-links and PTH and a significantly decreased 1.25 D3. Osteoporosis is frequent in AS and high disease activity is associated with an alteration in vitamin D metabolites and increased levels of bone resorption in active AS. Our findings propose a close association of BMD, bone metabolism and inflammatory activity, possibly related to vitamin D inflammation interactions.
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PMID:Association of 1.25 vitamin D3 deficiency, disease activity and low bone mass in ankylosing spondylitis. 1617

Secondary osteoporosis is common among patients being evaluated for osteoporosis. All men and premenopausal women with unexplained bone loss or a history of a fragility fracture should undergo a work-up for secondary osteoporosis. Also, postmenopausal women with risk factors for secondary osteoporosis should be carefully evaluated. The evaluation should include a thorough history, physical examination, bone mineral density testing, and laboratory testing. While there is no consensus for a cost-effective laboratory evaluation, some recommendations include: 25-hydroxyvitamin D, parathyroid hormone (PTH), serum and urine calcium, phosphate, creatinine, liver function tests, a complete blood count, testosterone in men, and thyroid-stimulating hormone. After a thorough review of the evaluation for secondary osteoporosis, this chapter reviews the pathophysiology and treatment of secondary osteoporotic disorders, including vitamin D insufficiency, osteomalacia, the osteoporosis of erosive inflammatory arthritis, ankylosing spondylitis, systemic lupus erythematosus, and osteoporosis related to anti-androgenic therapy for prostate cancer and aromatase inhibitor therapy for breast cancer. Physicians have a significant responsibility to evaluate and treat the underlying medical problem that is the cause of secondary osteoporosis and to optimize bone health in the individual patient.
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PMID:The management of secondary osteoporosis. 1630 Nov 95

A 50-year-old man without family history of metabolic bone disease was referred to our hospital with a 5-year history of progressively worsening spinal and bilateral diffuse leg pain and proximal muscle weakness. Two years before admission, he was diagnosed as ankylosing spondylitis by a rheumatologist and was maintained on low-dose prednisone therapy without benefit. He developed progressive spinal and thoracic deformities, resulting in a 10 cm loss in height in the preceding 2 years. On physical examination, marked thoracic kyphosis and pectus carinatum was noted. Plain radiograph revealed pseudofracture in the right femoral neck. Laboratory findings showed a normal level of serum calcium, elevated level of serum alkaline phosphatase and inappropriately increased urinary phosphate excretion despite extreme hypophosphatemia. He was diagnosed as adult-onset hypophosphatemic osteomalacia caused by renal phosphate wasting. Serum fibroblast growth factor 23 was the upper limit of normal despite extreme hypophosphatemia and no neoplastic lesion potentially inducing hypophosphatemic osteomalacia could be identified in a thorough search including imaging studies of his entire body. Oral administration of phosphate and activated vitamin D together with dipyridamole relieved the persistent pain and weakness, and he became fully ambulatory.
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PMID:Sporadic adult-onset hypophosphatemic osteomalacia caused by excessive action of fibroblast growth factor 23. 1831 Sep 82


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