Another new B-cell-suppressing treatment is belimumab (Benlysta). Belimumab blocks the stimulation of the B cells (a B-lymphocyte stimulator or BLyS-specific inhibitor) and is approved for the treatment of adults with active autoantibody-positive systemic lupus erythematosus who are receiving standard therapy. It is important to note that the efficacy of belimumab has not been evaluated in patients with severe active lupus nephritis or severe active central nervous system lupus. Belimumab has not been studied in combination with other biologic therapies or intravenous cyclophosphamide.
Anemia is common in children with SLE and develops in about 50% of cases. Low platelet and white blood cell counts may be due to the disease or a side effect of pharmacological treatment. People with SLE may have an association with antiphospholipid antibody syndrome (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.
The underlying trigger to develop these antibodies in lupus is unknown, although experts believe that a combination of genetic, environmental, and possibly hormonal factors are involved. The fact that lupus can run in families suggests that there is a genetic basis for its development, but so far no single “lupus gene” has been identified. Experts suspect that several different genes may be involved in determining an individual’s chance of developing the disease, as well as which tissues and organs are affected, and how severe the disease will be if it does occur. Other factors being investigated as contributing to the onset of lupus are overexposure to sunlight, stress, certain drugs, and viruses and other infectious agents.
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. 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).
An inflammatory response (inflammation) occurs when tissues are injured by bacteria, trauma, toxins, heat, or any other cause. The damaged cells release chemicals including histamine, bradykinin, and prostaglandins. These chemicals cause blood vessels to leak fluid into the tissues, causing swelling. This helps isolate the foreign substance from further contact with body tissues.
Chemokines are low-molecular-weight proteins that stimulate recruitment of leukocytes. They are secondary pro-inflammatory mediators that are induced by primary pro-inflammatory mediators such as interleukin-1 (IL-1) or tumor necrosis factor (TNF). The physiologic importance of this family of mediators is derived from their specificity. Unlike the classic leukocyte chemo-attractants, which have little specificity, members of the chemokine family induce recruitment of well-defined leukocyte subsets. Thus, chemokine expression can account for the presence of different types of leukocytes observed in various normal or pathologic states.
Acute Cutaneous Lupus results in flat red patches on the cheeks and nose called a malar or butterfly rash that looks quite like sunburn. These patches may also appear on the arms, legs, trunk and any other area that is commonly exposed to the sun. Patients with Acute Cutaneous Lupus can also manifest oral ulcers, hives and temporary hair loss. Acute Cutaneous Lupus is more common in people living with SLE.
The principal receptors on animal cells for binding most extracellular matrix proteins—including collagens, fibronectin, and laminins—are the integrins. Integrins, like other cell adhesion molecules, differ from cell-surface receptors for hormones and for other extracellular soluble signal molecules in that they usually bind their ligand with lower affinity and are usually present at about tenfold to a hundredfold higher concentration on the cell surface. If the binding were too tight, cells would presumably become irreversibly glued to the matrix and would be unable to move—a problem that does not arise if attachment depends on large numbers of weak adhesions. This is an example of the “Velcro principle” mentioned earlier. Like other transmembrane cell adhesion proteins, however, integrins do more than just attach a cell to its surroundings. They also activate intracellular signaling pathways that communicate to the cell the character of the extracellular matrix that is bound.
SLE is undoubtedly a potentially serious illness with involvement of numerous organ systems. However, it is important to recognize that most people with SLE lead full, active, and healthy lives. Periodic increases in disease activity (flares) can usually be managed by varying medications. Since ultraviolet light can precipitate and worsen flares, people with systemic lupus should avoid sun exposure. Sunscreens and clothing covering the extremities can be helpful. Abruptly stopping medications, especially corticosteroids, can also cause flares and should be avoided. People with SLE are at increased risk of infections as SLE-related complications, especially if they are taking corticosteroids or immunosuppressive medications. Therefore, any unexpected fever should be reported to medical professionals and evaluated.
Next, Ms. Everett reviewed some of the key foods that are important for your diet. She emphasized that balance is essential – that is, to not eat too much of one thing and not enough of another. Different foods have different nutritional components. Included in the important foods that Ms. Everett highlighted were a variety of fruits and vegetables; foods low in calories and saturated fats; and foods high in antioxidants, fiber, calcium, vitamin D, and Omega 3 fatty acids.
When lupus starts affecting other organs of the body, doctors often prescribe drugs that suppress the immune system, says Kramer. (Lupus causes the body’s immune system to mistakenly attack itself. Immunosuppressive medications help stop that from happening.) One such example, is Cytoxan (cyclophosphamide), originally an anticancer drug. It suppresses the immune system and may be used to reduce inflammation of the kidney, or nephritis, says Dr. Kaplan.
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