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Discover the confidence, skills and tools that others like you have gained from Us in Lupus. Us in Lupus is designed to give you more than just the facts about lupus. It's a resource designed by GSK that offers people living with lupus the skills, tools, and confidence they need to help them face lupus. It's a set of tools to help you identify, track, and make sense of all of your symptoms.

Lupus Symptom: Joint Pain

You may also receive Speaking of Lupus , our award-winning series of self-help booklets that can help you boost your skills and confidence. Using these tools can help you to better manage your lupus and make the most of interactions with your healthcare team. Living With Lupus. Contact a lupus support specialist toll-free:. Some have the classic malar rash or butterfly rash associated with the disease. Hair loss , mouth and nasal ulcers, and lesions on the skin are other possible manifestations.

The most commonly sought medical attention is for joint pain , with the small joints of the hand and wrist usually affected, although all joints are at risk. More than 90 percent of those affected will experience joint or muscle pain at some time during the course of their illness. Fewer than ten percent of people with lupus arthritis will develop deformities of the hands and feet. A possible association between rheumatoid arthritis and SLE has been suggested, [19] and SLE may be associated with an increased risk of bone fractures in relatively young women.

People with SLE may have an association with antiphospholipid antibody syndrome [23] a thrombotic disorder , wherein autoantibodies to phospholipids are present in their serum. Abnormalities associated with antiphospholipid antibody syndrome include a paradoxical prolonged partial thromboplastin time which usually occurs in hemorrhagic disorders and a positive test for antiphospholipid antibodies; the combination of such findings have earned the term " lupus anticoagulant -positive".

Another autoantibody finding in SLE is the anti-cardiolipin antibody , which can cause a false positive test for syphilis. SLE may cause pericarditis —inflammation of the outer lining surrounding the heart, myocarditis —inflammation of the heart muscle, or endocarditis —inflammation of the inner lining of the heart. It involves either the mitral valve or the tricuspid valve. Atherosclerosis also occurs more often and advances more rapidly than in the general population. SLE can cause pleuritic pain as well as inflammation of the pleurae known as pleurisy , which can rarely give rise to shrinking lung syndrome involving a reduced lung volume.

Painless passage of blood or protein in the urine may often be the only presenting sign of kidney involvement. Acute or chronic renal impairment may develop with lupus nephritis , leading to acute or end-stage kidney failure. The histological hallmark of SLE is membranous glomerulonephritis with "wire loop" abnormalities.

Neuropsychiatric syndromes can result when SLE affects the central or peripheral nervous system. The American College of Rheumatology defines 19 neuropsychiatric syndromes in systemic lupus erythematosus. A common neurological disorder people with SLE have is headache , [34] although the existence of a specific lupus headache and the optimal approach to headache in SLE cases remains controversial. Neurological disorders contribute to a significant percentage of morbidity and mortality in people with lupus.

Eye involvement is seen in up to one-third of people. In addition, the medications used to treat SLE can cause eye disease: long-term glucocorticoid use can cause cataracts and secondary open-angle glaucoma, and long-term hydroxychloroquine treatment can cause vortex keratopathy and maculopathy. While the most pregnancies are positive there is a greater risk of adverse events. Neonatal lupus is the occurrence of SLE symptoms in an infant born from a mother with SLE, most commonly presenting with a rash resembling discoid lupus erythematosus , and sometimes with systemic abnormalities such as heart block or enlargement of the liver and spleen.

Fatigue in SLE is probably multifactorial and has been related to not only disease activity or complications such as anemia or hypothyroidism , but also to pain , depression , poor sleep quality, poor physical fitness and lack of social support. SLE is presumably caused by a genetic susceptibility coupled with an environmental trigger which results in defects in the immune system. One of the factors associated with SLE is vitamin D deficiency.

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SLE does run in families, but no single causal gene has been identified. Instead, multiple genes appear to influence a person's chance of developing lupus when triggered by environmental factors. Since SLE is associated with many genetic regions, it is likely an oligogenic trait, meaning that there are several genes that control susceptibility to the disease. SLE is regarded as a prototype disease due to the significant overlap in its symptoms with other autoimmune diseases.

Drug-induced lupus erythematosus is a generally reversible condition that usually occurs in people being treated for a long-term illness. Drug-induced lupus mimics SLE. However, symptoms of drug-induced lupus generally disappear once the medication that triggered the episode is stopped. More than 38 medications can cause this condition, the most common of which are procainamide , isoniazid , hydralazine , quinidine , and phenytoin.

Discoid cutaneous lupus is limited to skin symptoms and is diagnosed by biopsy of rash on the face, neck, scalp or arms. SLE is triggered by environmental factors that are unknown.

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In SLE, the body's immune system produces antibodies against itself, particularly against proteins in the cell nucleus. These antibody attacks are the immediate cause of SLE. People with SLE have intense polyclonal B-cell activation, with a population shift towards immature B cells. T cells, which regulate B-cell responses and infiltrate target tissues, have defects in signaling, adhesion, co-stimulation, gene transcription, and alternative splicing.

In the complement system low C3 levels are associated with systemic lupus erythematosus [63]. These cells normally engulf B cells that have undergone apoptosis after somatic hypermutation. Also, uningested apoptotic nuclei can be found outside of TBMs.

Lupus Handbook: These Are the Faces of Lupus - A G Moore - Book |

This material may present a threat to the tolerization of B cells and T cells. Dendritic cells in the germinal center may endocytose such antigenic material and present it to T cells, activating them.

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  • Also, apoptotic chromatin and nuclei may attach to the surfaces of follicular dendritic cells and make this material available for activating other B cells that may have randomly acquired self-specificity through somatic hypermutation. Impaired clearance of dying cells is a potential pathway for the development of this systemic autoimmune disease.

    Systemic lupus erythematosus

    This includes deficient phagocytic activity and scant serum components in addition to increased apoptosis. SLE is associated with defects in apoptotic clearance, and the damaging effects caused by apoptotic debris. When apoptotic material is not removed correctly by phagocytes, they are captured instead by antigen-presenting cells, which leads to development of antinuclear antibodies. Monocytes isolated from whole blood of people with SLE show reduced expression of CD44 surface molecules involved in the uptake of apoptotic cells. Most of the monocytes and tingible body macrophages TBMs , which are found in the germinal centres of lymph nodes , even show a definitely different morphology; they are smaller or scarce and die earlier.

    Serum components like complement factors, CRP , and some glycoproteins are, furthermore, decisively important for an efficiently operating phagocytosis.

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    With SLE, these components are often missing, diminished, or inefficient. Recent research has found an association between certain people with lupus especially those with lupus nephritis and an impairment in degrading neutrophil extracellular traps NETs. The clearance of early apoptotic cells is an important function in multicellular organisms. It leads to a progression of the apoptosis process and finally to secondary necrosis of the cells if this ability is disturbed. Necrotic cells release nuclear fragments as potential autoantigens , as well as internal danger signals, inducing maturation of dendritic cells DCs , since they have lost their membranes' integrity.

    Increased appearance of apoptotic cells also stimulates inefficient clearance.

    What is systemic lupus erythematosus (SLE)?

    That leads to maturation of DCs and also to the presentation of intracellular antigens of late apoptotic or secondary necrotic cells, via MHC molecules. Autoimmunity possibly results by the extended exposure to nuclear and intracellular autoantigens derived from late apoptotic and secondary necrotic cells.

    B and T cell tolerance for apoptotic cells is abrogated, and the lymphocytes get activated by these autoantigens; inflammation and the production of autoantibodies by plasma cells is initiated. A clearance deficiency in the skin for apoptotic cells has also been observed in people with cutaneous lupus erythematosus CLE. In healthy conditions, apoptotic lymphocytes are removed in germinal centers GC by specialized phagocytes, the tingible body macrophages TBM , which is why no free apoptotic and potential autoantigenic material can be seen.

    In some people with SLE, buildup of apoptotic debris can be observed in GC because of an ineffective clearance of apoptotic cells. Autoreactive B cells can accidentally emerge during somatic hypermutation and migrate into the germinal center light zone.