Lupus Information - Journal Articles
Rev Rhum Engl Ed. 1999 Feb;66(2):102-5. Optical neuromyelitis or Devic's syndrome is a very uncommon neurological manifestation of systemic lupus erythematosus. It is also associated with antiphospholipid antibodies, limited responsiveness to glucocorticoid treatment and a poor prognosis. We report the case of a female systemic lupus erythematosus patient who developed recurrent flares of optical neuritis and transverse myelitis. These flares consistently responded to glucocorticoid therapy. Despite the absence of overt anticardiolipin antibodies in the course of the disease, long-term anticoagulant therapy has been introduced with positive results. Treatments are usually of limited efficacy in Devic's syndrome. In our patient, however, aggressive glucocorticoid treatment resulted in prolonged survival.
Annals of the Rheumatic Diseases 2006;65:57-63; doi:10.1136/ard.2005.035733 Conclusions: Reduced uptake of apoptotic cells by MDM from patients with SLE is not an intrinsic defect but is serum dependent and associated with decreased levels of C1q, C4, and C3.
OBJECTIVE: Magnetisation transfer imaging (MTI) provides information about brain damage with increased pathological specificity over conventional MRI and detects subtle abnormalities in the normal appearing brain tissue, which go undetected with conventional scanning. Brain MRI and MTI findings were compared in patients with multiple sclerosis (MS) and systemic immune mediated diseases (SIDs) affecting the CNS to investigate their roles in understanding the nature of brain damage in these diseases. METHODSBrain dual echo, T1 weighted and MTI scans were obtained in patients affected by systemic lupus erithematosus (SLE) with (NSLE, n=9) and without clinical CNS involvement (n=15), Behçet's disease (BD) (n=5), Wegener's granulomatosis (WG) (n=9), and antiphospholipid antibody syndrome (APLAS) (n=6). Ten patients with clinically definite MS and 15 healthy controls also underwent the same scanning protocol. Brain MRI and MT ratio (MTR) images of the same subject were coregistered and postprocessed to obtain MTR histograms of the whole brain and of the NABT. RESULTSBrain hyperintense lesions were found in all patients with MS and with NSLE and in 5/15 patients with SLE, 5/9 with WG, 1/5 with BD, and 3/6 with APLAS. The lesion burden in the brain was significantly higher in patients with MS compared with all the other disease groups. All MTR histogram parameters were significantly different among patient subgroups. Patients with MS had significantly lower average MTR than all except patients with NSLE and significantly lower peak height and location than patients with SLE. patients with NSLE had significantly lower average MTR than patients with SLE. CONCLUSIONSMicroscopic brain tissue damage is relevant in patients with MS, but, apart from patients with NSLE, it seems to be absent in systemic immune mediated diseases, even in the presence of macroscopic MRI lesions or clinical evidence of CNS involvement. (J Neurol Neurosurg Psychiatry 2000;68:170-
BMJ 1997;314:1349 (3 May)
Vandana Mehta Rai MD, and C Balachandran MD Dermatology Online Journal: 11 (2): 27 Department of Skin and Sexually Transmitted Diseases, Kasturba Medical College,Manipal Karnataka. firstname.lastname@example.org
Lupus. 2000;9(4):236-40. Many patients with systemic lupus erythematosus (SLE) develop cardiac manifestations during the course of their disease. Pericarditis is most commonly seen, with a reported prevalence of 60%. Myocardial involvement is present in only a minority of patients. In recent years, due to better noninvasive diagnostic techniques, valvular abnormalities can be demonstrated in an increasing number of patients. Depending on the technique used, valvulopathy can be demonstrated in up to 77% of SLE patients. Although most of the valvular lesions will be present without any symptoms, valve incompetence can result in congestive heart failure. Valvular lesions are associated with IgG anticardiolipin antibodies (aCL) and disease duration. We present a patient with SLE and secondary antiphospholipid syndrome (APS) who developed acute congestive heart failure due to pancarditis. Endocarditis, together with left ventricular dysfunction and pericardial effusion, were present. The endocarditis caused hemodynamically significant mitral valve insufficiency due to thickening of the mitral cusps. Just two weeks prior to the occurrence of congestive heart failure echocardiography had been normal. Treatment with high dose corticosteroids resulted in a gradual, almost complete recovery. Literature concerning cardiac manifestations in lupus is reviewed.
Samy Fenniche MD, Sana Triki MD, Rym Benmously MD, Hayet Marrak, MD Feiza Ben Ammar MD, Insaf Mokhtar MD Dermatology Online Journal 11 (2): 11 Dermatology Department, Habib Thameur Hospital, Tunis.
Ryumachi. 1999 Oct;39(5):778-83. A 50-year-old female was admitted to a local hospital because of dyspnea, and diagnosed as having left heart failure secondary to mitral regurgitation. After the improvement of congestive heart failure, polyarthralgia, fever, and positive anti-nuclear antibody were pointed out. She was referred to our hospital for the further evaluation. Serological test showed anti-double stranded DNA antibodies, anti-SS-A antibodies, anti-beta 2-GPI antibodies and biological false positive for syphilis. The diagnosis of SLE has been made from the clinical signs and the serology. Therefore mitral valvular lesion of this patient was considered to be one of the symptoms of SLE. We reported a rare case in which left heart failure was a initial clinical manifestation of SLE.
J Rheumatol 2006;33:50-6 Conclusion. Nondiabetic patients with SLE have evidence of significant decrease in sensitivity to insulin, and overall this population has a high prevalence of the metabolic syndrome (18%). Insulin resistance in the context of SLE was not strongly related to current or recent steroid therapy; it was, however, associated with higher levels of ox-LDL. Insulin resistance may therefore represent an additional CHD risk factor in patients with SLE.
First Release Sept 15 2006; J Rheumatol 2006;33:2192-8. Conclusion. Although premenopausal women with SLE have more disease activity than postmenopausal women with SLE, we have shown that there is a constant rate of improvement over time, be it in the premenopause, across the menopause, or postmenopause. This improvement is not due to change in menopausal status. Thus clinicians should not be anticipating the postmenopausal era in a patient's course as a period of natural disease improvement.
Lupus Research Institute (LRI) Funds Initial Findings
Arthritis Rheum. 1999 Feb;42(2):338-46. CONCLUSION: Young women with SLE are at substantially increased risk of AMI, CHF, and CVA. The relative odds of these conditions decrease with age among women with SLE.
J Rheumatol 2006;33:188-90
J Neurol Neurosurg Psychiatry. Published Online First: 24 February 2006. doi:10.1136/jnnp.2005.084285 © 2006 by BMJ Publishing Group Ltd
Pediatr Nephrol. 2000 May;14(5):416-21. A 14-year-old African-American girl was diagnosed with antiphospholipid-positive systemic lupus erythematosus (SLE) in July 1994. The course was complicated by nephrotic syndrome, sepsis, hemolytic anemia, acute renal failure, saphenous vein thrombosis, cutaneous vasculitis, mesenteric vasculitis, appendicitis, hemorrhagic cystitis, and avascular necrosis of the hips. In August 1997, she developed ovarian and fallopian tube complications secondary to SLE. Genitourinary complications of SLE, however, are uncommon, and ovarian vasculitis has not previously been reported as a complication of SLE. This report describes the course of an adolescent patient with SLE and focuses specifically on her genitourinary complications.
Arthritis Research & Therapy 2006, 8:R81 doi:10.1186/ar1951. Conclusion: Impairment of the TGF-β1 system in SLE not only may impact on the autoimmune pathophysiology of the disease but also may modulate the development of atherosclerosis and the increased risk for cardiovascular disease. Low activation of TGF-β1 is associated with increased apoptosis of PBMCs, increased carotid IMT, high levels of LDL-cholesterol and more severe SLE disease score. The factors in blood that modulate activation of TGF-β1 remain obscure, but the link with LDL-cholesterol opens up a novel atherogenic pathway that requires further study.
Seminars in Arthritis and Rheumatism Volume 36, Issue 4 , February 2007, Pages 238-245 PSORIASIS-SPONDYLITIS-SLE-SS-SAUDI. Conclusions: CVID should be suspected in any SLE patient with recurrent sinopulmonary infections in the absence of SLE activity and/or immunosuppressive treatment.
US Pharm. 2006;5:39-48. Due to the broad clinical and immunologic manifestations and varying symptoms of SLE, the disease should be suspected in patients who present with clinical symptoms affecting two or more of the organ systems listed in table 1.1 Diagnosis of SLE can be challenging because patients are prone to unpredictable exacerbations, remissions, and conditions that can mimic disease flares. Therefore, it is important to note that no single test can determine whether a person has SLE. Diagnosis is based on characteristic clinical features and laboratory criteria.6 The revised 1982 American College of Rheumatology (ACR) criteria for classification of SLE requires the presence of at least four of 11 conditions at any time during a patient's medical history (table 2).13,14 The ACR classification criteria are the most widely used to confirm and categorize patients with a diagnosis of SLE. Since these criteria also classify patients for clinical research studies and often lack sensitivity to milder forms of SLE, the ACR criteria may be less accurate in patients with mild disease.6,15 Consequently, the ACR criteria should not be used solely to exclude or confirm a diagnosis of SLE.
J Rheumatol 2006;33:2184-91. Conclusion. Brain perfusion SPECT is a sensitive tool for identifying brain impairment in SLE-related migraine, although the mechanisms of brain damage remain to be elucidated. Besides confirming focal hypoperfusion in some patients, in 4 patients statistical analysis revealed interictal hypofunction of the anterior cingulate cortex, a key structure for cortical elaboration of pain in the midline network.
J Intern Med. 2005 Jun;257(6):485-95
This article suggests an INR of 3 to 4 for patients with APS. Dr. Petri is one of the leading APS specialists and this webpage would be good to show your doctor if you are having a problem getting him/her to take you seriously that our INRs need to be higher. American Family Physician® > Vol. 57/No. 11 (June, 1998)
Arthritis Research & Therapy 2007, 9:R44 doi:10.1186/ar2184.
Chicky Dadlani MD, Melissa Pulitzer MD, and Stephen D Prystowsky MD. Dermatology Online Journal 14 (5): 5. Department of Dermatology, New York University.
Orthopaedic Nursing; March/April 2006; Volume 25 Number 2; Pages 140 - 145
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