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)

Nutritional status for six captive canid species (n=34) and four captive ursid species (n=18) were analyzed. The species analyzed included: African wild dog (Lycaon pictus), arctic fox (Alopex lagopus), gray wolf (Canis lupus), maned wolf (Chrysocyon brachyurus), Mexican wolf (Canis lupus baleiyi), red wolf (Canis rufus), brown bear (Ursus arctos), polar bear (Ursus maritimus), spectacled bear (Tremarctos ornatus), and sun bear (Ursus malayanus). Diet information was collected for these animals from each participating zoo (Brookfield Zoo, Fort Worth Zoo, Lincoln Park Zoological Gardens, and North Carolina Zoological Park). The nutritional composition of the diet for each species at each institution met probable dietary requirements. Blood samples were collected from each animal and analyzed for vitamin D metabolites 25(OH)D and 1,25(OH)(2)D, vitamin A (retinol, retinyl stearate, retinyl palmitate), vitamin E (alpha-tocopherol and gamma-tocopherol) and selected carotenoids. Family differences were found for 25(OH)D, retinol, retinyl stearate, retinyl palmitate and gamma-tocopherol. Species differences were found for all detectable measurements. Carotenoids were not detected in any species. The large number of animals contributing to these data, provides a substantial base for comparing the nutritional status of healthy animals and the differences among them.
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PMID:Serum concentrations of vitamin D metabolites, vitamins A and E, and carotenoids in six canid and four ursid species at four zoos. 1113 48

The production of high-affinity pathogenic autoantibodies in systemic lupus erythematosus (SLE) may result from aberrant immune regulation. Since 1,25 dihydroxy vitamin D(3) (1,25 D(3)) has immunoregulatory activity, we examined effects of 1,25 D(3) and its analogs HM, V, MC1288, and KH1060 on autoantibody production and proliferation of SLE PBMC. We found, in SLE, a higher percentage of T, B, and NK expressing vitamin D(3) receptors (VDRs) (P = 0.034, 0.006, 0.012, respectively). Incubating SLE PBMC with 1,25 D(3) compounds significantly reduced proliferation, polyclonal and anti-dsDNA IgG production, and the percentages of CD3(+)/DR(+) T and B (CD19(+)) cells, while elevating NK (CD16(+)) cells (P < 0.001). 1,25 D(3) analogs were more potent than the natural compound: KH1060 up-regulated CD14 expression by SLE monocytes (P < 0.001), inhibited polyclonal and anti-dsDNA IgG production by SLE-derived B lymphoblasts, and induced apoptosis of activated B lymphoblasts. These data suggest that 1,25 D(3) compounds can offer novel approaches to the clinical management of SLE.
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PMID:Vitamin D(3) and its synthetic analogs inhibit the spontaneous in vitro immunoglobulin production by SLE-derived PBMC. 1128 44

The patient with systemic lupus erythematosus (SLE) is at risk of osteoporosis through several factors: the inflammatory disease itself, disease-related co-morbidity, and its treatment. Bone loss is apparent early in the disease and this may be confounded primarily by treatment with corticosteroids. Patients should be assessed for additional risk factors for osteoporosis and general lifestyle measures adopted. Bone mineral density measurement should be considered in SLE patients at high risk of osteoporosis, particularly those starting corticosteroids and in postmenopausal women. Calcium and vitamin D supplementation provide general prophylaxis and are a suitable first-line option. Hormone replacement should be used in hypogondal subjects unless contra-indicated. In subjects at high fracture risk, particularly in postmenopausal women, bisphosphonate therapy should be considered as these agents have been shown to significantly reduce vertebral fracture risk. These measures should reduce the burden of osteoporosis and fracture in patients with lupus.
Lupus 2001
PMID:Osteoporosis in systemic lupus erythematosus: prevention and treatment. 1131 58

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

Regulation of calcium homeostasis during pregnancy is complex. Clinically significant bone mass loss is infrequent; however a subset of women may develop symptomatic osteoporosis related to pregnancy. Lactation is a period of special risk for bone loss. Whatever the effect of heparin on bone loss, vertebral fractures are rare in women treated with heparin during pregnancy. Low molecular weight heparins may have a less deleterious effect on bone than unfractionated heparin. Women with autoimmune diseases, particularly those with lupus and/or the antiphospholipid syndrome may receive heparin throughout pregnancy. Corticosteroids must be reduced as much as possible in these women, and calcium plus vitamin D are recommended. Finally, indications for heparin use must be clearly justified and advice regarding breastfeeding must be offered.
Lupus 2001
PMID:Lupus pregnancy: is heparin a risk factor for osteoporosis? 1167 46

This report highlights the finding of ulcerative plantar keratoderma in two patients with systemic lupus erythematosus (SLE). Both patients suffered from painful plantar ulcerations and fissures; in one patient there was diffuse desquamation over the entire plantar surface, while the other patient's lesions were focal and accentuated over weight-bearing surfaces. Other etiologies for keratoderma including papulosquamoua disease, contact dermatitis, tinea and primary keratodermas were excluded. Both patients were resistant to multiple topical therapies including super-potent topical corticosteroids, vitamin D analogues and retinoids, but did report moderate relief with hydrocolloid dressings applied over super-potent topical corticosteroids and pressure off-loading measures. Lupus-associated keratoderma can be recurrent and recalcitrant to treatment, often necessitating aggressive therapy and particular attention to advanced wound care methodologies. While not a specific cutaneous sign of lupus, it should be recognized as a cause for considerable morbidity.
Lupus 2001
PMID:Ulcerating plantar keratoderma in association with systemic lupus erythematosus. 1167 55

In recent years there has been an effort to understand possible noncalcemic roles of vitamin D, including its role in the immune system and, in particular, on T cell-medicated immunity. Vitamin D receptor is found in significant concentrations in the T lymphocyte and macrophage populations. However, its highest concentration is in the immature immune cells of the thymus and the mature CD-8 T lymphocytes. The significant role of vitamin D compounds as selective immunosuppressants is illustrated by their ability to either prevent or markedly suppress animal models of autoimmune disease. Results show that 1,25-dihydroxyvitamin D3 can either prevent or markedly suppress experimental autoimmune encephalomyelitis, rheumatoid arthritis, systemic lupus erythematosus, type I diabetes, and inflammatory bowel disease. In almost every case, the action of the vitamin D hormone requires that the animals be maintained on a normal or high calcium diet. Possible mechanisms of suppression of these autoimmune disorders by the vitamin D hormone have been presented. The vitamin D hormone stimulates transforming growth factor TGFbeta-1 and interleukin 4 (IL-4) production, which in turn may suppress inflammatory T cell activity. In support of this, the vitamin D hormone is unable to suppress a murine model of the human disease multiple sclerosis in IL-4-deficient mice. The results suggest an important role for vitamin D in autoimmune disorders and provide a fertile and interesting area of research that may yield important new therapies.
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PMID:Vitamin D: its role and uses in immunology. 1172 33

Numerous inflammatory rheumatic diseases occurring in premenopausal women require the use of high doses of glucocorticoids (GC). It was believed for many years that premenopausal women were, at least to some extent, protected from bone loss associated with GC therapy. However, epidemiological studies performed in premenopausal women with systemic lupus erythematosus, demonstrate that these patients have lower bone mineral density as compared to age-matched controls. This is explained in part by the underlying disease and in part by treatment with GC. The American College of Rheumatology recommends life style adaptation, supplementation with calcium and vitamin D in patients receiving, or initiating therapy with >/=5 mg equivalent prednisone/day. Bisphosphonates are recommended, but they should be used with caution in young women as they cross the placenta and can affect skeletal remodeling in the foetus. Bisphosphonates have a prolonged terminal half-life and data on their safety extends to 10 years. It is therefore critical to inform premenopausal women about the risks of bisphosphonates and to recommend bisphosphonates with shorter terminal half-life.
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PMID:Management of glucocorticoid induced osteoporosis in premenopausal women with autoimmune disease. 1284 50

The aim of this study was to analyse the heterogeneity of bone mineral density (BMD) reduction across measurement sites in female systemic lupus erythematosus (SLE) patients on glucocorticoid (CS) treatment. The study population consisted of two subgroups: 32 women at a mean (SD) age of 43.2 (12.0) years, SLE duration of 13.4 (6.2) years, treated with a mean cumulative prednisone dose of 34.4 g; and 16 women at a mean age of 36.1 (9.0) years, SLE duration of 3.2 (2.0) years, never treated with glucocorticoids (control group). The participants underwent a standardised interview, medical record review, blood sampling and BMD examination of the lumbar spine, femoral neck and distal forearm by dual-energy X-ray absorptiometry. CS-treated participants were supplemented with daily calcium (1200 mg) and vitamin D (500 UI). During the study mean daily glucocorticoid dose was 10 mg prednisone equivalent. The controls did not receive either corticosteroids or calcium and vitamin D. BMD and laboratory parameters were re-examined at the end of the second year. At baseline 22 (68.7%) of the CS-treated participants had osteoporosis at least at one major site, compared to 18.8% of the controls. The BMD reduction was proportional to the trabecular bone content at the specific measurement site. At baseline mean T scores in the CS-treated group were the highest at the forearm (-1.03 +/- 1.13), followed by the hip (-1.32 +/- 1.26), AP spine (-1.87 +/- 1.46) and lateral spine (-2.90 +/- 1.50). At follow-up lateral spine bone loss was 5.54% per year, the total hip and the forearm lost 3.59% and 0.33%, respectively, compared to annual losses of 1.02% (AP spine), 1.30% (lateral spine), 0.83% (total hip) and 0.11% (forearm) in the control group. The heterogeneity of BMD reduction in our SLE population emphasises the need for the targeted use of bone densitometry in steroid-treated patients. Attention should be paid to trabecular-rich sites, and fracture risk should be specifically determined.
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PMID:Bone mineral density changes in women with systemic lupus erythematosus. 1457 64

We studied the effect of 1-year transdermal estrogen replacement therapy (ERT) on bone mineral density (BMD) and biochemical markers of bone turnover in osteopenic postmenopausal systemic lupus erythematosus (SLE) patients in a randomized, double-blind, placebo-controlled trial. SLE patients were randomly allocated to treatment (estradiol; 50 microg transdermal 17beta-estradiol; n=15) or placebo ( n=17) group. Both groups received 5 mg continuous oral medroxyprogesterone acetate, 500 mg calcium and 400 IU vitamin D(3). L(1)-L(4) spine (LS), left femur and total hip BMD were measured at baseline and at 6 and 12 months. Serum osteocalcin (OC) and degradation products of C-terminal telopeptides of type-I collagen (CTx) levels were measured at baseline and 3, 6, 9, and 12 months. There was a significant difference in the percentage change of LS BMD at 6 months between the two groups (103.24+/-3.74% (estradiol group) vs 98.99+/-3.11% (placebo group); P<0.005). There was a significant decrease within the estradiol group in the CTx levels between baseline and all subsequent visits ( P<0.05). There was no significant difference in SLE disease activity index, Systemic Lupus International Collaborating Clinics/American College of Rheumatology (ACR) damage index and corticosteroid dose during the study period. Transdermal estradiol may prevent bone loss in postmenopausal SLE women at the lumbar spine and femur, with no increase in disease activity among postmenopausal SLE women receiving transdermal ERT. The high dropout rate (8/15) leads us to the conclusion that efficacy of HRT in a high-risk group such as SLE women can be attained only in a small number of patients, provided all inclusion/exclusion criteria are strictly adhered to.
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PMID:The effect of 1-year transdermal estrogen replacement therapy on bone mineral density and biochemical markers of bone turnover in osteopenic postmenopausal systemic lupus erythematosus patients: a randomized, double-blind, placebo-controlled trial. 1586 11


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