Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0003873 (rheumatoid arthritis)
 53,068 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

IL-3, a cytokine with hematopoietic differentiating capability, induced murine bone marrow cells to differentiate into cells resembling osteoclasts. The cells resulting from treatment with IL-3 were multi-nucleated and demonstrated tartrate-resistant acid-phosphatase activity, as do resident osteoclasts found in bone. IL-3-induced osteoclast-like cell development in the absence of serum-derived vitamin D metabolites, and a mAb that inhibited IL-3-induced proliferation of an addicted cell line also inhibited the development of osteoclasts in the presence of IL-3. The same Ab had no effect on 1 alpha, 25-dihydroxyvitamin D3-induced differentiation of osteoclasts. This newly described function of IL-3 may indicate a role for activated T cells in the bone resorption seen with rheumatoid arthritis.
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PMID:IL-3 induces differentiation of bone marrow precursor cells to osteoclast-like cells. 280 96

Although low-dose oral corticosteroid therapy cannot be considered remittive, it has earned a place in the therapeutic armamentarium for rheumatoid arthritis. Major clinical trials of a group using corticosteroid compared with a control group have not been done since the 1950s. One of these three large trials showed some slowing of the destructive joint changes of rheumatoid arthritis with use of low doses of corticosteroid. However, these agents have well-known side effects, especially when used long-term. Elderly patients or those who have features of the disease that indicate progression (eg, multiple joint involvement, elevated ESR, early evidence of erosion on x-ray films) are likely to benefit from carefully controlled doses of a corticosteroid. Because these drugs diminish bone formation and arthritis itself accelerates osteoporosis, supplemental calcium and vitamin D are useful adjuncts. A remittive agent and aspirin-like drug should be prescribed along with the corticosteroid. Abrupt withdrawal of even a very low dose of corticosteroids in rheumatoid arthritis patients causes a flare.
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PMID:Oral steroids in rheumatoid arthritis. Helpful but not remittive. 331 40

Osteocalcin is the most abundant noncollagenous protein of bone and is regarded as the best biochemical marker for bone formation. The synthesis of this protein in osteoblasts is stimulated by 1.25-Dihydroxyvitamin D3 (1.25(OH)2D3). The aim of this study was to examine the rate of bone formation measured by osteocalcin in patients (pts) with rheumatoid arthritis (RA) (n = 58) and osteoarthrosis (OA) (n = 14) and its dependence on various parameters of calcium and phosphate metabolism, especially vitamin D metabolites. Furthermore we compared the significance of alkaline phosphatase and osteocalcin as a parameter for bone turnover in these patients. According to treatment pts with RA were divided into four groups: one receiving gold salts (n = 14), one glucocorticoids (n = 13), one chloroquine (n = 14), and one nonsteroidal antiinflammatory drugs (NSAID) (n = 17). Pts with OA and RA treated with NSAID showed significantly lower values of osteocalcin than pts with RA treated with glucocorticoids or gold. In contrast to osteocalcin, alkaline phosphatase was significantly higher in all pts with RA than in pts with OA. 1.25(OH)2D, which was significantly (p less than 0.05) elevated in pts with RA treated with glucocorticoids, correlated significantly with parathyroid hormone (PTH). These data indicate that bone metabolism, at least in pts with OA and RA treated with NSAID is characterized by a decreased bone formation which is probably compensated in part in pts treated with glucocorticoids, as 1.25(OH)2D and PTH are significantly (p less than 0.05) elevated. Furthermore, the osteocalcin values were closely correlated with 1.25(OH)2D in pts with OA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Osteocalcin and bone metabolism in rheumatoid arthritis and osteoarthritis]. 349 36

The response of circulating 1,25-dihydroxyvitamin D [1,25-(OH)2D] to challenge with vitamin D treatment both before and after 7-10 days of prednisone therapy (25 mg/day) was investigated in five anephric subjects, six patients with chronic renal failure (CRF), two patients with vitamin D intoxication and four patients with hypoparathyroidism. In anephric subjects serum 25-hydroxyvitamin D [25-(OH)D] rose from 58 +/- 48 (SD) to 377 +/- 221 (SD) nmol/l after administration of 150 micrograms of 25-(OH)D3 for 1 month. Serum 1,25-(OH)2D, which was barely detectable in only two out of five patients under basal conditions, rose to 30 +/- 21 pmol/l after 2 weeks of therapy with 25-(OH)D3, but fell to 10 +/- 5 pmol/l during prednisone treatment. In CRF patients circulating 1,25-(OH)2D rose from 37 +/- 24 to 58 +/- 24 pmol/l during 25-(OH)D3 therapy, but fell to 41 +/- 31 pmol/l during prednisone treatment. In two patients with rheumatoid arthritis, hypercalcaemia due to vitamin D intoxication was associated with raised levels of 1,25-(OH)2D (288 and 317 pmol/l). Administration of prednisone resulted in suppression of 1,25-(OH)2D levels (132 and 96 pmol/l respectively) and reduction of serum calcium to within the normal range. In the hypoparathyroid patients prednisone therapy did not affect circulating 25-(OH)D levels but serum 1,25-(OH)2D fell from 192 +/- 42 to 117 +/- 23 pmol/l and serum calcium from 2.41 +/- 0.21 to 2.20 +/- 0.05 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Extrarenal synthesis of 1,25-dihydroxyvitamin D: sensitivity to glucocorticoid treatment. 349 10

A 35-year-old white male with rheumatoid arthritis who had developed hypercalcemia, hypercalciuria, and nephrolithiasis was found to be abnormally sensitive to vitamin D as a result of lack of regulation of circulating 1,25-dihydroxyvitamin D (1,25-(OH)2D). An increase in daily intake of vitamin D from 10 micrograms (400 units) per day to 50 micrograms (2000 units) per day produced an abnormal elevation in serum 1,25-(OH)2D, hypercalcemia, and hypercalciuria which were corrected by prednisone. Serum 25-hydroxyvitamin D initially was abnormally low, and increased with vitamin D to values which were in the low normal range. There were significant positive correlations between serum 1,25-(OH)2D (p less than .05) and serum calcium and between serum 1,25-(OH)2D and urinary calcium (p less than .05). Serum immunoreactive parathyroid hormone, initially in the lower range of normal, decreased further during hypercalcemia. A radiograph of the chest, gallium scan, and serum angiotensin-converting enzyme activity were normal. No granulomas or evidence of lymphoma were found in biopsies of the liver and of several lymph nodes. It is concluded that the abnormal calcium metabolism in this patient resulted from increased circulating 1,25-(OH)2D and that the defect in vitamin D metabolism was not related to sarcoidosis, other granulomatous disease, Hodgkin's disease, or lymphoma. The relationship, if any, of the abnormal metabolism of vitamin D and calcium to rheumatoid arthritis remains to be established.
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PMID:Abnormal calcium metabolism caused by increased circulating 1,25-dihydroxyvitamin D in a patient with rheumatoid arthritis. 350 40

One-hundred and two patients with rheumatoid arthritis (RA) were studied. They were divided into three groups according to treatment with gold salts, penicillamine or glucocorticoids. Blood samples were drawn between November and January and four different metabolites of vitamin D (25(OH)D3, 24,25 (OH)2D3, 25,26 (OH)2D and 1,25 (OH)2D) were measured and compared to values from normal subjects. The mean serum concentrations of 25(OH)D3 in all three patient groups were significantly lower than those of the controls (p less than 0.01-0.001). The mean serum concentrations of 24,25 (OH)2D3 and 25,26 (OH)2D were not significantly different from the control values, whereas 1,25 (OH)2D concentrations were significantly lower in the penicillamine and steroid groups (p less than 0.05-0.01). When patients were stratified according to functional classes, we found a significant inverse relation between serum concentrations of 25(OH) D3, 24,25(OH)2D3, 25,26(OH)2D and the functional class, but not between 1,25(OH)2D and the functional class. We conclude that the decreased serum 25(OH)D3 concentration found in patients with RA is likely to be caused by decreased exposure to sunlight due to decreased activity, and thus is a result of the disease rather than a pathogenetic factor. Whether the small decrease in serum 1,25(OH)2D is of clinical significance and related to the development of osteoporosis in patients with RA is probably doubtful.
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PMID:Serum concentration of vitamin D metabolites in rheumatoid arthritis. 362 43

Serum and urinary variables of bone mineral metabolism were studied in 49 postmenopausal women with rheumatoid arthritis (RA). Results were compared to those in a sex, age and menopausal age matched control group. No patient took corticosteroids, or had any disease other than RA which might affect bone. Total serum calcium was low in patients with RA compared to controls (9.0 +/- 0.5 mg% vs 9.3 +/- 0.3 mg%, p less than 0.005), but was normal when corrected for albumin (9.5 +/- 0.6 mg% vs 9.3 +/- 0.4 mg%, NS). Serum phosphorus was significantly higher in patients with RA than in controls (3.6 +/- 0.3 mg% vs 3.3 +/- 0.4 mg%, p less than 0.001) as well as serum alkaline phosphatase activity (107.6 +/- 27.2 IU/l vs. 9.6 +/- 28.91 IU/l). Serum creatinine, vitamin D and parathyroid hormone levels were comparable in both groups. Urinary hydroxyproline and mucopolysaccharide excretions were higher in patients with RA than controls, both for fasting (respectively 0.089 +/- 0.028 vs 0.039 +/- 0.023, p less than 0.001 and 0.072 +/- 0.027 vs 0.047 +/- 0.019, p less than 0.001) and for 24 h values (50.3 +/- 17.9 mg vs 36.2 +/- 15.4 mg, p less than 0.001 and 54.6 +/- 26.0 mg vs 41.7 +/- 16.5 mg, p less than 0.05). Urinary calcium excretion was comparable in the 2 groups. Our findings of raised serum phosphorus and alkaline phosphatase activity, raised urinary hydroxyproline and mucopolysaccharides excretion suggest that in patients with RA there is a higher metabolic activity of bone. In none of the patients could any indication of osteomalacia or of parathyroid overactivity be found.
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PMID:Mineral metabolism in postmenopausal women with active rheumatoid arthritis. 370 43

Calcium and bone metabolism in 29 rheumatoid arthritis (RA) patients were compared with those in 27 postmenopausal osteoporotic patients. Signs of vitamin D deficiency were found in 20 RA patients, including 12 who took recommended amounts of vitamin D in their diets and were exposed to sufficient sunlight, and in none of the osteoporotic patients. There were no signs of malabsorption. In six out of 15 patients we found increased liver enzyme activity, which may have a role in vitamin D metabolism. We propose the influence of non-steroidal anti-inflammatory drugs (NSAIDs) on vitamin D metabolism in the liver as a possible explanation.
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PMID:Bone metabolism in rheumatoid arthritis compared with postmenopausal osteoporosis. 394 43

Long-term glucocorticoid treatment might interfere with the vitamin D metabolism. The serum concentrations of 25-OHD were significantly reduced whereas the circulating levels of 1,25-(OH)2D were normal in 50 patients with rheumatoid arthritis on long-term treatment with small doses of prednisone. The bone mineral content of the forearm was significantly reduced, but the degree of bone loss did not correlate with duration of treatment or dose of prednisone given. Quantitative bone histomorphometry was performed in 18 patients. Apart from a significant correlation between serum 25-OHD and the fractional trabecular bone volume, no relationships were observed between bone histomorphometry and vitamin D metabolites or serum iPTH. The results indicate that the bone loss was due to a decreased osteoblastic activity rather than to an impaired vitamin D metabolism.
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PMID:Bone mineral loss, bone histomorphometry and vitamin D metabolism in patients with rheumatoid arthritis on long-term glucocorticoid treatment. 400 84

An evaluation of mineral metabolism was performed in 41 patients with RA and the pertinent data were compared to bone mineral content in patients either untreated or treated with different doses of corticosteroids. Our study confirms that osteoporosis is a common finding even in rheumatoid patients never treated with corticosteroids. Moreover, in patients treated with such drug the loss of bone mineral content was related to the dosage rather than to the length of treatment. In all cases no overt biochemical derangement was observed. According to our study, parathyroid hormone does not seem to influence the development of osteoporosis in rheumatoid arthritis, while a relative deficiency of calcitonin along with an inadequate vitamin D metabolism could play some role.
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PMID:Mineral metabolism and bone mineral content in rheumatoid arthritis. Effect of corticosteroids. 401 12


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