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)

Radiological sacroiliac (SI) changes were found in 3 patients, 2 with primary hyperparathyroidism (1 also with associated chondrocalcinosis) and 1 with osteomalacia. Osteomalacia was due to celiac disease. None of the 3 patients, all females, had a history of psoriasis, urethritis, iritis or chronic colitis. There was no renal function impairment. Peripheral joints were affected in the patient with associated condrocalcinosis. HLA B 27 was negative in all cases. Low back pain and vertebral stiffness were present in the patient with osteomalacia. A dramatic improvement in pain and stiffness ensued after vitamin D injections. These SI lesions, which may simulate ankylosing spondylitis, were attributable to subchondral bone changes related to the metabolic bone diseases. In the case of osteomalacia the SI lesions were predominantly on the right side, where there was a Looser's zone on the ischial ramus suggesting that pseudofractures could be a cause of SI changes. Metabolic osseous diseases such as osteomalacia or primary hyperparathyroidism should be investigated in cases of HLA B 27 negative radiological "sacroiliitis".
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PMID:[Sacroiliac changes, HLA-B27 negative, in primary hyperparathyroidism and osteomalacia]. 46 71

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

Does a sojourn at high altitude during the winter and spring improve vitamin D status (and possibly suppress parathyroid hormone [PTH]) in patients with ankylosing spondylitis (AS)? In 73 patients with AS, serum concentrations of 25-hydroxy-vitamin D [25(OH)D] and PTH were determined before and after a three-week rehabilitation treatment at Bad Gastein (1000 m above sea level). At the first examination, serum 25(OH)D was median (25th, 75th percentile) 15.5 ng mL-1 (10.0 ng mL-1, 20.6 ng mL-1). Thirteen patients (18%) had a 25(OH)D concentration below 8 ng mL-1. In 53 patients (73%) the level was below 20 ng mL-1. After the sojourn, 25(OH)D significantly (p = 0.02) increased to 19.7 (11.3, 24.6) ng mL-1. PTH did not change significantly, being 32 (22.4, 43.9) pg mL-1 before and 30.3 (24.1, 39.9) pg mL-1 after the sojourn. Analysing different periods of sojourn, a significant (p < 0.001) increase in 25(OH)D was found in April but not in the other months. Patients with ankylosing spondylitis may have extremely low levels of 25(OH)D. The results of the present study suggest that a sojourn at high altitude in early spring is liable to reduce vitamin D deficiency.
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PMID:Serum 25-hydroxyvitamin D and parathyroid hormone in patients with ankylosing spondylitis before and after a three-week rehabilitation treatment at high altitude during winter and spring. 1138 78

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

In this study, the relation between osteoporosis and vitamin D and the disease activity in patients with ankylosing spondylitis (AS) was investigated. A hundred patients with AS and 58 healthy individuals were included in the study. In addition to the routine blood and urine tests, serum 25-(OH)D3, parathormone (PTH), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), total calcium, ionized calcium, and phosphorous levels of all participants were also measured. Bone mineral density (BMD) measurements were performed at the anterior-posterior and lateral lumbar and femur regions. Anterior-posterior and lateral thoracic and lumbosacral radiography was performed on all participants. The disease activity was evaluated by Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), functional status by Bath Ankylosing Spondylitis Functional Index (BASFI), and mobility by Bath Ankylosing Spondylitis Metrology Index (BASMI). In the patient group, BMD values obtained from the lateral lumbar and femur regions and serum vitamin D levels were lower than the control group. A negative relation was determined between the lateral lumbar BMD values and ESR, CRP, and BASDAI scores of patients with AS. The ESR, CRP levels, and BASMI scores of the AS patients with osteoporosis were significantly higher, when compared to patients without osteoporosis. The negative correlation between serum 25-(OH)D3 level and ESR, CRP levels did not reach a statistically significant level in patients with AS; the positive correlation between PTH levels and ESR, and the negative correlation between CRP and BASDAI also did not reach a statistically significant level. Vitamin D deficiency in AS may indirectly lead to osteoporosis by causing an increase in the inflammatory activity. The present authors believe that it would be beneficial to monitorize vitamin D levels together with BMD measurements in order to determine the patients under osteoporosis risk.
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PMID:The relation between osteoporosis and vitamin D levels and disease activity in ankylosing spondylitis. 1968 57

Vitamin D research is discussed in light of the hypothesis that the lower average levels of vitamin D frequently observed in autoimmune disease are not a sign of deficiency. Instead, it is proposed that the lower levels result from chronic infection with intracellular bacteria that dysregulate vitamin D metabolism by causing vitamin D receptor (VDR) dysfunction within phagocytes. The VDR dysfunction causes a decline in innate immune function that causes susceptibility to additional infections that contribute to disease progression. Evidence has been accumulating that indicates that a number of autoimmune diseases can be reversed by gradually restoring VDR function with the VDR agonist olmesartan and subinhibitory dosages of certain bacteriostatic antibiotics. Diseases showing favorable responses to treatment so far include systemic lupus erythematosis, rheumatoid arthritis, scleroderma, sarcoidosis, Sjogren's syndrome, autoimmune thyroid disease, psoriasis, ankylosing spondylitis, Reiter's syndrome, type I and II diabetes mellitus, and uveitis. Disease reversal using this approach requires limitation of vitamin D in order to avoid contributing to dysfunction of nuclear receptors and subsequent negative consequences for immune and endocrine function. Immunopathological reactions accompanying bacterial cell death require a gradual elimination of pathogens over several years. Practical and theoretical implications are discussed, along with the compatibility of this model with current research.
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PMID:Reversing bacteria-induced vitamin D receptor dysfunction is key to autoimmune disease. 1975 26


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