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

1) Antiphospholipid antibody syndrome may be associated with unusual sites of thrombosis. 2) Laboratory evaluation involves testing for antiphospholipid antibodies: lupus anticoagulant and anticardiolipin antibodies. 3) Acute management of thrombosis involves immediate anticoagulation. Low-molecular-weight heparins are as safe and effective as unfractionated heparin in this setting. Arterial events may require emergent thrombolytic therapy. Monitoring of the APTT with unfractionated heparin in the presence of a lupus anticoagulant is ineffective; these patients require monitoring of antifactor Xa levels or the use of LMWH, which does not require monitoring. 4) The pharmacokinetics of LMWH change in pregnancy, resulting in a shorter plasma half-life and larger volume of distribution. Monitoring of antifactor Xa levels is necessary. 5) Chronic anticoagulation is best achieved with warfarin, with significantly decreased rates of recurrent events when the INR is > or = 3.0. Long-term, if not life-long, anticoagulation is often necessary. Warfarin is teratogenic, and individuals desiring pregnancy will need to convert to therapeutic, not prophylactic, doses of either unfractionated heparin or LMWH. 6) As part of optimal management of thrombosis in APS, additional risk factors for thrombosis should be eliminated or reduced. These include comorbid illnesses such as hypertension and hyperlipidemia, as well as smoking. 7) Tamoxifen, raloxifene, oral contraceptives, and hormone replacement therapy are all associated with an increased risk of DVT in the general population. In APS patients receiving therapeutic anticoagulation, the addition of these drugs should not increase thrombosis risk. In APS patients not receiving anticoagulant therapy, these hormonal therapies may increase the thrombosis risk.
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PMID:Management of thrombosis in women with antiphospholipid syndrome. 1121 45

Dendritic cells (DCs) in the patient and animal models of systemic lupus erythematosus (SLE) are abnormal, but the detailed mechanism is unclear. Estrogen can modulate DCs in biological condition and estrogen concentration is related to the onset and development of SLE. So the control of estrogen on DCs might lead to the disorder of DCs. To prove the hypothesis, we detected the effects of 17beta-estradiol (E2) on bone marrow (BM)-derived DCs in SLE murine model-(NZB x NZW) F1 (NZB/w F1) female mice before and after the disease onset. We found that E2 mainly enhanced the expression of surface molecule CD40, MHCII and the stimulation activity of immature DCs, but weakened the activity of mature DCs. E2 decreased the production of cytokines IL-6, IL-10, IL-12 and TNFalpha of DCs in young mice, but increased them in old mice. Tamoxifen could antagonize the E2 effect. E2 changed the expression of estrogen receptor-alpha (ER alpha) in DCs. The level of ER alpha in DCs of various old mice and the differentiation states varied. The results suggest that E2 can modulate the functions of BM-derived DCs in SLE pathology. The modulation is achieved by binding ER. The effects of E2 on DCs are different depending on the progression of SLE and cell differentiation status. This might be due to the difference of ER expression.
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PMID:Estrogen modulates bone marrow-derived DCs in SLE murine model-(NZB x NZW) F1 female mice. 1838 42

Tamoxifen is a selective oestrogen receptor modulator (SERM) with an established role in the treatment and chemoprevention of hormone-related breast cancer. It is also cardioprotective and increases bone mineral density. However, due to pleiotrophic ligand-receptor properties, its role in a variety of seemingly unrelated disorders, including multiple sclerosis, Parkinson's disease, Alzheimer's disease, systemic lupus erythematosus and urological cancers, has been investigated in many studies. The non-patented drug tamoxifen confers a significant advantage over newer drugs in being inexpensive and well-tolerated with a known side-effect profile. This review highlights the interaction of tamoxifen on oestrogen receptors (ERs) and assesses whether this agent continues to have future applications in a variety of clinical settings, both as a therapy in early and established disease and usage as a prophylactic in those at risk of debilitating conditions. Indeed, it may have as-yet-unknown benefit(s) in a variety of conditions, both as a prophylactic in those at high-risk and also as in novel therapeutic strategies in established disease. Future clinical studies may seek to establish the exact future role and efficacy for SERMs both in men and women. Perhaps a multi-functional SERM such as tamoxifen may be the aspirin of the 21(st) century.
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PMID:The multiple applications of tamoxifen: an example pointing to SERM modulation being the aspirin of the 21st century. 1875 31

Encapsulating peritoneal sclerosis (EPS) is a serious and often fatal complication of long-term PD with severe malnutrition and poor prognosis. It causes progressive obstruction and encapsulation of the bowel. This retrospective study reviews our experience and that reviewed in the literature concerning EPS. It refers to a total of 1966 patients treated with chronic PD between 1974 and 2008. Twenty one of them (1.1%) developed EPS, with the incidence increasing with the duration of PD. Mean age of our patients with EPS was 43, ranging from 18 to 71 years, 8 were men and 13 women with a mean body mass index (BMI) of 21.6 kg/m(2). Only one patient had Type II diabetes, 15 patients had glomerular disease, and six of these 15 had an autoimmune disease such as Wegener's granulomatosis and SLE. Thirteen patients developed EPS while on PD, 7 within 2 years after transfer to HD, and only one after renal transplantation. However, 7 patients had a previous renal transplant before returning to PD and subsequently developing EPS. Interestingly, we did not observe more episodes of EPS after transplantation. In the patients who developed EPS, the peritonitis rate over the period of observation was 1/15.6 pt-months and was due to Staphylococcus aureus, coagulase-negative staphylococcus, Pseudomonas and fungi. A history of peritonitis was not a prerequisite for developing EPS, since one patient had no episodes of peritonitis and 4 had just one previous episode. Fifteen patients presented with peritonitis within 4 months before the diagnosis of EPS with particularly virulent micro-organisms such as S. aureus, Candida, Pseudomonas, Corynebacterium, and Peptostreptococcus. Eleven patients were treated with hypertonic dextrose solutions (4.25 g/dl of dextrose) and seven with icodextrin, indirectly suggesting problems with ultrafiltration. Nine of 21 patients were on beta-blockers. The diagnosis of EPS was made either surgically or radiologically with signs of small bowel obstruction in combination with severe malnutrition. Eleven of our patients (52%) had evidence of small bowel obstruction and 14 patients required total parenteral nutrition (TPN). Tamoxifen (10-20 mg daily) was started in 6 patients, 4 of whom are alive and 2 deceased 3 and 5 years after EPS was diagnosed. Of the 12 patients who were not given tamoxifen, 2 are alive and 10 died. No side effects of tamoxifen were reported. Only 7 of our patients (33%) died during the first year after the diagnosis of EPS. Currently, 4 patients are on HD and 3 have had a renal transplant. Six patients of the fourteen who underwent surgery (42.8%) died within the first 6 months after operation and five died after an average of 6.6 years, mostly due to cardiovascular causes, three are still alive. As EPS becomes more prevalent with longer duration of PD, large multicenter prospective studies are needed to establish its incidence and identify risk factors, therapeutic approach, and prognosis.
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PMID:Encapsulating peritoneal sclerosis: a single-center experience and review of the literature. 2092 72