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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

In the last years it has been recognized that patients with systemic lupus erythematosus (SLE) are at high risk of osteoporosis (OP) and fractures, both occurring through disease-specific (chronic arthritis, reduced physical activity, induction of cytokines promoting bone resorption, renal impairment, endocrine factors) and nondisease-specific mechanisms (sunshine avoidance with consequent vitamin D deficiency, glucocorticoids, immunosuppressants and chronic anticoagulants). Regarding anticoagulants, subcutaneous heparin is crucial against the risk of recurrent thromboembolism or pregnancy loss, specifically in patients with SLE and anti-phospholipid syndrome (APS). Thus heparin-induced OP represents one of the hazards of this treatment, first because heparin must be used long-term and secondly because pregnancy and lactation themselves may predispose to OP and fractures. Current data suggest the use of prophylaxis with calcium and vitamin D in all patients treated with heparin during pregnancy. Nevertheless glucocorticoid-induced OP (GIOP) is considered the most serious risk factor for OP and fractures in SLE patients. All guidelines recommend general measures and supplementation with calcium and vitamin D in all patients. However when considering premenopausal patients, there is no generally recommended treatment. Bisphosphonates, which are considered the first choice therapy for the prevention and treatment of GIOP, should be used 'cautiously' in these patients. Therefore the potential risks and lack of efficacy data on fracture risk reduction in premenopausal patients must be weighed against their proven efficacy in postmenopausal patients.
Lupus 2004
PMID:Risk factors for osteoporosis in female patients with systemic lupus erythematosus. 1548 12

A connection between vitamin D deficiency and severe health problems including various types of cancer has been demonstrated. We have shown that patients that have to protect themselves against solar UV radiation for medical reasons, including patients with xeroderma pigmentosum (XP), basal cell nevus syndrome (BCNS), lupus erythematodes (LE) or transplant recipients, are at risk to develop vitamin D deficiency. We conclude that 25-hydroxyvitamin D serum levels as a measure of vitamin D status have to be analyzed in patients that have to protect themselves against solar UV radiation for medical reasons. Suboptimal vitamin D status has to be substituted (e.g. via oral treatment) to protect against serious vitamin D deficiency-related health problems without increasing the risk to develop solar UV-induced skin cancer. Our finding that protection against solar UV radiation causes vitamin D deficiency underlines the need for re-defining dermatological recommendations for solar UV protection in skin cancer prevention programs.
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PMID:Sunlight, skin cancer and vitamin D: What are the conclusions of recent findings that protection against solar ultraviolet (UV) radiation causes 25-hydroxyvitamin D deficiency in solid organ-transplant recipients, xeroderma pigmentosum, and other risk groups? 1720 18

The identification of vitamin D receptor in cells involved in the immune response and the discovery that activated dendritic cells produce vitamin D hormone suggested that vitamin D could exert immunoregulatory effects. Patients with autoimmune diseases such as multiple sclerosis, rheumatoid arthritis and systemic lupus erythematosus (SLE) show low 25-OH vitamin D serum levels. In particular, SLE patients have multiple risk factors for vitamin D deficiency and disease severity seems correlated with lower 25-OH vitamin D serum levels. Treatment of vitamin D deficiency could be particularly important in SLE patients due to concomitant insults on their tissues such as bone, and in view of the possible immunomodulatory effects exerted by vitamin D.
Lupus 2008 Jan
PMID:Review: vitamin D, immunity and lupus. 1808 76

Despite the improvement of systemic lupus erythematosus (SLE) survival observed in the last decades, the long-term prognosis of these patients remains poor mainly due to complications of the disease and/or of its treatment. Therefore, in order to improve SLE prognosis, we should try to avoid long-term complications by adopting, early in the disease course, some strategies directed to prevent infections, atherosclerosis and cancer. Moreover, since it has been shown that autoantibodies appear before clinical manifestations in SLE, the question of whether or not asymptomatic individuals with a reliable positive serology should be treated arises. Other than advising these individuals to avoid sun exposure, drugs implicated in drug-induced lupus and cigarette smoking, the use of vitamin D and hydroxychloroquine could be considered. Finally, early SLE diagnosis has led to a modification of disease clinical spectrum at disease onset with an increased frequency of mild disease manifestations over severe ones. Thus great effort should be made in order to identify early in the disease course risk factors for the development of severe SLE manifestations. Finally patients with mild disease carrying factors predictive of severe manifestations should be treated more aggressively than we have done up to now.
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PMID:Preventive strategies in systemic lupus erythematosus. 1819 Aug 77

Vitamin D deficiency is highly prevalent and is increasingly thought to be an important risk factor in many diseases that have high morbidity and mortality, including lupus. Vitamin D is an immunomodulatory hormone with effects on T cells, B cells, and dendritic cells. Animal models of autoimmune disease and epidemiologic studies suggest a role for vitamin D as a modifiable environmental factor in autoimmune disease. Recommendations are available regarding screening for and repletion of vitamin D deficiency. More research is needed to understand the role of vitamin D as an immunomodulator and to determine the optimal range of serum 25-hydroxyvitamin D for musculoskeletal, cardiovascular, and immune health.
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PMID:The link between vitamin D deficiency and systemic lupus erythematosus. 1866 6

The research projects of the European Forum on Antiphospholipid Antibodies are representative of how dynamic is this area of investigation. The present review is focused on the most recent projects of the Forum on the aetiopathogenic aspects of the antiphospholipid syndrome (APS). Studies on the genetic background of the APS are ongoing in order to better define the proximity between APS and full-blown systemic lupus erythematosus. However, the analysis of the polymorphisms of genes coding for inflammatory mediators may offer new information on the role of inflammatory processes in triggering thrombotic events as well as the whole susceptibility for developing the vascular manifestations. A systematic and wide detection of serological markers of infectious processes will give new insight on the role of infectious agents in favouring autoimmunity in APS. Owing to the well-known role of vitamin D(3) defect in autoimmune disease, the detection of vitamin plasma levels in APS patients will offer the rationale for a possible therapeutic supplementation. Additional projects are aimed to better characterize the diagnostic/prognostic value of antiphospholipid antibodies (aPL) by defining their epitope specificity and binding avidity. Pregnancy complications represent the obstetric side of APS. Research projects are focussed on the role of complement activation in placenta damage and on the potential ability of aPL to affect the fertility. Finally, a study has been planned in order to draw definitive conclusions on the associations between aPL and atherosclerosis.
Lupus 2009 Sep
PMID:European Forum on Antiphospholipid Antibodies: research in progress. 1967 94

Recent research has implicated vitamin D deficiency (serum levels of 25-hydroxyvitamin D <50 nmol/L) with a number of chronic conditions, including autoimmune conditions such as multiple sclerosis, lupus, and psoriasis, and chronic conditions such as osteoporosis, osteoarthritis, metabolic syndrome, fibromyalgia and chronic fatigue syndrome. It has been assumed that low levels of 25-hydroxyvitamin D (25-D) accurately indicate vitamin D storage and vitamin D receptor (VDR)-mediated control of calcium metabolism and innate immunity. To evaluate this assumption, 25-D and 1,25-dihydroxyvitamin D3 (1,25-D) levels were measured in 100 Canadian patients with these conditions. Additionally, other inflammatory markers (CK, CRP) were measured. Results showed a strong positive association between these autoimmune conditions and levels of 1,25-D >110 pmol/L. However, there was little association with vitamin D deficiency or the other inflammatory markers, meaning that the results challenge the assumption that serum levels of 25-D are a sensitive measure of the autoimmune disease state. Rather, these findings support the use of 1,25-D as a clinical marker in autoimmune conditions. High levels of 1,25-D may result when dysregulation of the VDR by bacterial ligands prevents the receptor from expressing enzymes necessary to keep 1,25-D in a normal range.
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PMID:Vitamin D metabolites as clinical markers in autoimmune and chronic disease. 1975 77

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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