Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied bone mineral metabolism prospectively in 113 children with chronic rheumatic diseases (juvenile arthritis, systemic lupus erythematosus, and juvenile dermatomyositis) to determine the relationship of serum levels of osteocalcin to rheumatic disease activity and corticosteroid usage, and to determine, in part, the cause of osteopenia in this population. Disease activity was quantitated by historical, clinical, and serologic means and an activity score derived. The 113 children were divided according to the expression of their disease, which was active (group 1: mean score 3.42, mean erythrocyte sedimentation rate 28 mm/hr) or inactive (group 2: score 1.7, erythrocyte sedimentation rate 15 mm/hr) (p less than 0.02 group 1 vs group 2 for each value), or which remitted during the study (group 3). We found that serum levels of osteocalcin, but not those of ionized calcium, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and parathyroid hormone, were reduced in group 1 children even before corticosteroid therapy was employed. Children in both group 2 and group 3 had normal osteocalcin levels despite the use of corticosteroids. The reduced levels of osteocalcin were predictive of a reduction in bone mass measured by photon absorptiometry in 16 of 19 children so studied. We conclude that skeletal abnormalities that result in a reduced bone mass occur in the clinical course of the majority of children with active chronic rheumatic diseases, are associated with reduced osteocalcin levels, and are not related to the use of corticosteroids. Serum osteocalcin levels may be a sensitive marker for reduced osteoblast activity and bone formation in children with chronic rheumatic diseases.
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PMID:Abnormalities in serum osteocalcin values in children with chronic rheumatic diseases. 231 4

We prospectively determined the frequency of atlantoaxial subluxation in a group of patients with systemic lupus erythematosus (SLE) and analyzed its relationship with tendinous laxity, Jaccoud's syndrome and other features of the disease. Five of 59 patients (8.5%) had atlantoaxial subluxation. No patient presented atlantoaxial subluxation in neutral lateral cervical radiographs but all 5 had anterior atlantoaxial subluxation in full flexion films; one patient also had lateral subluxation. The 5 patients with atlantoaxial subluxation were compared with the remaining 54. Mean SLE disease duration was longer in patients with atlantoaxial subluxation (12 years) than in those without (6.6 years) (p less than 0.01). Jaccoud's syndrome, patellar tendon elongation and articular hypermobility were significantly more frequent in patients with atlantoaxial subluxation. The presence or history of arthritis failed to distinguish patients with and without atlantoaxial subluxation, while chronic renal failure and increased serum parathyroid hormone levels were significantly associated to the presence of atlantoaxial subluxation. We suggest that atlantoaxial subluxation is further evidence of tendinous alterations seen in patients with SLE.
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PMID:Atlantoaxial subluxation in systemic lupus erythematosus: further evidence of tendinous alterations. 231 18

Serum procollagen type I carboxyterminal propeptide (PICP) has been shown to be a useful marker of bone formation in patients undergoing haemodialysis. However, PICP levels has not been evaluated in depth in patients maintained on continuous ambulatory peritoneal dialysis (CAPD). Therefore serum and dialysate levels of PICP, its peritoneal clearance (Clp), mass transfer (MTp), and its possible relationship with osteocalcin, parathyroid hormone (PTH), and bone histomorphometry were studied in a group of CAPD patients. Serum PICP was just above the normal range with significant amounts detected in the dialysate but no correlations were found between levels of serum PICP, dialysate PICP, and Clp-PICP. One patient with systemic lupus and osteitis fibrosa had extraordinarily high serum and dialysate levels of PICP. The patient later developed sclerosing peritonitis. No associations were seen between serum PICP and Clp-PICP and any of the 18 bone histomorphometric parameters evaluated. Dialysate level of PICP correlated negatively with mineral appositional rate (r = -0.62, P < 0.01) and mineralization lag time (r = 0.64, P < 0.01). MTp-PICP correlated positively with mineral appositional rate (r = 0.65, P < 0.01). Serum osteocalcin and serum PTH levels did not correlate to serum, dialysate, Clp or MTp measurements of PICP. These results suggest that measurements of PICP in CAPD patients do not give substantial information as an non-invasive marker of bone histology.
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PMID:Type I procollagen propeptide in patients on CAPD: its relationships with bone histology, osteocalcin, and parathyroid hormone. 859 3

Although osteoporosis has traditionally been considered a disease of women, men also incur substantial bone loss with aging, and elderly men have age-specific hip fracture incidence rates and vertebral fracture prevalence rates that are at least half those in women. Early postmenopausal bone loss (which results in the syndrome of type I osteoporosis) is due to the direct skeletal consequences of estrogen deficiency, manifested by an increase in bone resorption without an adequate increase in bone formation. Recent evidence indicates that even late postmenopausal bone loss (type II or 'smile' osteoporosis) in women may be due to estrogen deficiency. In particular, the late consequences of estrogen deficiency in elderly women result in abnormalities in calcium homeostasis and increases in parathyroid hormone secretion, leading to increased bone resorption and bone loss. The etiology of bone loss in aging men has remained relatively unclear. Recent evidence from a male deficient in estrogen receptor-alpha and in two males with aromatase deficiency indicate that estrogen may play a significant role in bone metabolism in men. Moreover, several large epidemiologic studies have found that bone mineral density correlates better with serum estrogen than testosterone in aging men. Thus estrogen deficiency may lead to bone loss in men.
Lupus 1999
PMID:Osteoporosis: gender differences and similarities. 1045 20

We studied the effect of alphacalcidol (1-alpha-hydroxycholecalciferol) on bone metabolism in patients who were placed on glucocorticoid therapy. We selected 41 women (age: 32-52 yrs) who were recently diagnosed with systemic lupus erythematodes, multiple sclerosis, rheumatoid arthritis or asthma bronchiale. Patients did not have other disease or take drugs known to influence bone metabolism. Patients were randomly enrolled into two groups and were given 5-25 mg prednisone daily. After 4 weeks, group A (n = 21) received 0.5-1.0 microgram (mean = 0.54 +/- 0.03 microgram) alphacalcidol and group B (control; n = 20) was given 500 mg calcium daily for three years. There were no significant differences in age and steroid doses between groups. Serum calcium (Ca), osteocalcin (OC), collagen I C-terminal propeptide (PICP), parathyroid hormone (PTH), and urinary calcium and deoxypyridinoline crosslink excretion (DPD) were measured before corticosteroid administration, and before alphacalcidol or calcium treatment as well as 6 weeks, 6 months, and 1, 2, and 3 years later. Bone mineral density (BMD) was examined before treatment and 6 months, 1, 2, and 3 years later by DEXA and SPA. OC and PICP decreased significantly after 4 weeks on steroid in both groups and increased in group A but not in group B after 6 weeks of treatment with alphacalcidol and remained unchanged for 3 years. Serum PTH increased in both groups after 4 weeks of glucocorticoid treatment and was reduced in group A, but not in group B, after 6 weeks on alphacalcidol. Serum Ca, urinary Ca, and DPD did not change significantly in either group during the study period. Lumbar spine and femoral neck BMD were significantly reduced in group B after 6 months and 1 year, respectively, and continued to decrease during the study, while no significant change in group A was observed. BMD of the radius did not change in either group for 2 years but there was a significant reduction by the third year in group B. Based on these results, alphacalcidol treatment appears to be effective in preventing glucocorticoid-induced bone loss in these patients by reducing secondary hyperparathyroidism and stimulating bone formation.
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PMID:Prevention of corticosteroid-induced osteoporosis by alfacalcidol. 1076 37

Induced apoptosis of autoreactive T-lymphocyte precursors in the thymus is crucial for the prevention of autoimmune disorders. IGF-I and prolactin, which are lymphocyte growth factors, may have the potential to suppress apoptosis in thymocytes and thus encourage autoimmunity; conversely, dietary fish oil rich in omega-3 fats appears to upregulate apoptosis in lymphocytes. Since whole-food vegan diets may downregulate systemic IGF-I activity, it is proposed that such a diet, in conjunction with fish oil supplementation and treatment with dopamine agonists capable of suppressing prolactin secretion, may have utility for treating and preventing autoimmune disorders. This prediction is consistent with the extreme rarity of autoimmune disorders among sub-Saharan black Africans as long as they followed their traditional quasi-vegan lifestyles, and with recent ecologic studies correlating risks for IDDM and for multiple sclerosis mortality with animal product and/or saturated fat consumption. Moreover, there is evidence that vegan or quasi-vegan diets are useful in the management of rheumatoid arthritis, multiple sclerosis, and possibly SLE. The dopamine agonist bromocryptine exerts anti-inflammatory effects in rodent models of autoimmunity, and there is preliminary evidence that this drug may be clinically useful in several human autoimmune diseases; better tolerated D2-specific agonists such as cabergoline may prove to be more practical for use in therapy. The moderate clinical utility of supplemental fish oil in rheumatoid arthritis and certain other autoimmune disorders is documented. It is not unlikely that extra-thymic anti-inflammatory effects contribute importantly to the clinical utility of vegan diets, bromocryptine, and fish oil in autoimmunity. The favorable impact of low latitude or high altitude on autoimmune risk may be mediated by superior vitamin D status, which is associated with decreased secretion of parathyroid hormone; there are theoretical grounds for suspecting that parathyroid hormone may inhibit apoptosis in thymocytes. Androgens appear to up-regulate thymocyte apoptosis, may be largely responsible for the relative protection from autoimmunity enjoyed by men, and merit further evaluation for the management of autoimmunity in women. It will probably prove more practical to prevent autoimmune disorders than to reverse them once established; a whole-food vegan diet, coupled with fish oil and vitamin D supplementation, may represent a practical strategy for achieving this prevention, while concurrently lowering risk for many other life-threatening 'Western' diseases.
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PMID:Upregulation of lymphocyte apoptosis as a strategy for preventing and treating autoimmune disorders: a role for whole-food vegan diets, fish oil and dopamine agonists. 1146 Nov 85

The aim of this study was to evaluate bone mineral density (BMD), biochemical markers of bone turnover, and hormone levels in men with systemic lupus erythematosus (SLE). BMD at L2-L4 lumbar vertebrae (LS), left proximal femur neck, and radius at the ultradistal and mid-33% region was measured by dual-energy X-ray absorptiometry in 23 men with SLE (mean age, disease duration, and cumulative corticosteroid dose were 45.6 years, 11.9 years, and 33.410 g, respectively) and 40 healthy, age- and sex-matched controls. Biochemical markers of bone turnover, parathyroid hormone and 25-hydroxyvitamin D (25-OH-D), testosterone, and dehydroepiandrosterone sulfate (DHEAS) levels were measured. There was no difference in BMD between the SLE and control group. The prevalence of osteoporosis was 17.4% (4 out of 23), found at LS. Biochemical markers of bone turnover were within the reference range. There was a high prevalence of hypovitaminosis D (65.2%), hypotestosteronism (62.5%), and hypodehydroepiandrosterone sulfate (100%). There was no correlation between BMD and duration of disease, corticosteroid doses, SLE Disease Activity Index (SLEDAI), SLE Collaboration Clinics/American College of Rheumatology (SLICC/ARC) damage index, or markers of bone turnover. Bone-specific alkaline phosphatase (BSAP) (r, -0.500; P=0.018) and DHEAS (r, -0.511; P=0.013) correlated with the daily corticosteroid dose. Despite corticosteroid therapy, bone mass in men with SLE was not decreased.
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PMID:Bone mineral density, biochemical markers of bone turnover, and hormonal status in men with systemic lupus erythematosus. 1176 29

Primary hyperparathyroidism (PHP) is a metabolic illness that results from autonomous secretion of parathyroid hormone and is one of the most common causes of hypercalcemia. We present the case of a 47-year-old female with a previous diagnosis of systemic lupus erythematosus (SLE) in whom clinical (diffuse bone pain, emotional lability, jaw tumor) and laboratory features (calcium= 13.5 mg/dL, phosphate= 1.8 mg/dL, alkaline phosphatase= 3028 U/L, PTH intact= 1472 pg/dL) prompted the diagnosis of PHP secondary to parathyroid adenoma as demonstrated by the anatomopathology. After treatment with calcitonin spray 400 UI per day, IV pamidronate 90 mg/week, and subtotal parathyroidectomy, the patient status improved with normal laboratory tests. This is the second report to describe the coexistence of these two disorders in a single patient. Although the pathophysiology of the association of PHP and SLE is not known, the recognition of this association has a practical implication since the therapeutical strategy is completely different.
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PMID:[Primary hyperparathyroidism in a patient with systemic lupus erythematosus]. 1576 20

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

Vitamin D as a part of the endocrine system is an important component in the interaction between the kidney, bone, parathyroid hormone, and the intestine, which maintains extracellular calcium level within normal limits, in order to keep the vital physiologic process and skeletal integrity. Vitamin D is also associated with hypertension, muscular function, immunity, and ability to encounter infection, autoimmune disease, and cancer. The role of vitamin D in immunity is a feedback reaction of paracrine to eliminate inflammation or to influence CD4 T-cell differentiation and or to increase the function of T suppressor cell or combination between both. The active form of vitamin D produces and maintains self immunologic tolerance, some studies show that 1,25(OH)2D inhibits induction of disease in autoimmune encephalomyelitis, thyroiditis, type-1 diabetes mellitus, inflammatory bowel disease (IBD), systemic lupus erythematosus, and collagen-induced arthritis and Lyme arthritis.
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PMID:Vitamin D and autoimmune disease. 1769 36


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