Subacute Cutaneous Lupus can cause skin lesions on any part of the body. These lesions often form red, ring-shaped, scaly patches on the skin. These lesions do not itch and often appear on the chest as well as the upper back and neck; however, they may also be seen on the face and arms. Typically, these lesions occur on areas of the body that are exposed to sunlight or fluorescent lights. Furthermore, it is not uncommon for patients with SCLE to have associated joint disease.
Chronic fatigue syndrome (CFS) is a disorder that causes extreme fatigue. This fatigue is not the kind of tired feeling that goes away after you rest. Instead, it lasts a long time and limits your ability to do ordinary daily activities. The main symptom of CFS is severe fatigue that lasts for 6 months or more. You also have at least four of these other symptoms:
Whether you’re dealing with lupus, rheumatoid arthritis, Hashimoto’s or one of the hundreds of other autoimmune conditions out there, you have the power to beat your symptoms, regain your energy, and feel like yourself again. By following these steps to uncover the root cause of your illness, you CAN reverse your disease and live a life full of optimal health!
Before drinking alcohol, first double-check with your doctor to make sure that it is not forbidden with your medicines. Prednisone, non-steroidal anti-inflammatory drugs (NSAIDs), acetaminophen, antidepressants, opioids, warfarin and methotrexate can potentially have more side effects if taken with alcohol. If you do drink alcohol it is very important to drink only in moderation.
Although no one symptom qualifies someone as having lupus, certain clinical techniques can be used to narrow down the diagnosis. For example, a test for antinuclear antibodies (ANAs) in the blood is probably the first tool a physician will use. A positive ANA test does not necessarily mean that someone has lupus; in fact, one out of five normal women has a positive ANA. However, a negative ANA test greatly reduces the suspicion.
Recommendations are applicable to patients showing partial or total remission after induction therapy aiming at sustaining renal remission, preventing relapses and achieving the best long-term outcome. The following interventions were considered: (1) AZA; (2) MMF; (3) CYC; (4) TAC; and (5) CsA (online supplementary tables S1.1.1.7, S1.1.2.1, S1.1.2.2, S1.2.1, S1.2.3, S1.2.4, S1.2.5, S1.2.6, S1.2.7).
An increase in the size of an organ, structure, or the body due to growth rather than tumor formation. This term is generally restricted to an increase in size or bulk that results not from an increase in the number of cells but from an increase in a cellular component, e.g., proteins. It applies to any increase in size as a result of functional activity.
One of several different tests used to evaluate the condition of the respiratory system. Measures of expiratory flow and lung volumes and capacities are obtained. The forced vital capacity is one of the more important pulmonary function tests; it provides a measure of the amount of air that can be maximally exhaled after a maximum inspiration and the time required for that expiration. Pulmonary function tests can also determine the diffusion ability of the alveolar-capillary membrane.
Limitations of the test: Although almost all people with lupus have the antibody, a positive result doesn't necessarily indicate lupus. Positive results are often seen with some other diseases and in a smaller percentage of people without lupus or other autoimmune disorders. So a positive ANA by itself is not enough for a lupus diagnosis. Doctors must consider the result of this test along with other criteria.
B cells are essential for the development and pathogenesis of both systemic and organ-specific autoimmune diseases. Autoreactive B cells are typically thought of as sources of autoantibody, but their most important pathogenetic roles may be to present autoantigens to T cells and to secrete proinflammatory cytokines. A rate-limiting step in the genesis of autoimmunity then is the activation of autoreactive B cells. Here, mechanisms are discussed that normally prevent such activation and how they break down during disease. Integrating classic work with recent insights, emphasis is placed on efforts to pinpoint the precursor cells for autoantibody-secreting cells and the unique stimuli and pathways by which they are activated.
SLE is associated with defects in apoptotic clearance, and the damaging effects caused by apoptotic debris. Early apoptotic cells express “eat-me” signals, of cell-surface proteins such as phosphatidylserine, that prompt immune cells to engulf them. Apoptotic cells also express “find-me” signals, to attract macrophages and dendritic cells. When apoptotic material is not removed correctly by phagocytes, they are captured instead by antigen-presenting cells, which leads to development of antinuclear antibodies.[4]
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
The immune response is how your body recognizes and defends itself against bacteria, viruses, and substances that appear foreign and harmful.The immune system protects the body from possibly harmful substances by recognizing and responding to antigens. Antigens are substances (usually proteins) on the surface of cells, viruses, fungi, or bacteria. Nonliving substances such as toxins, chemicals, drugs, and foreign particles (such as a splinter) can also be antigens. The immune system recognizes and destroys substances that contain antigens. Your own body’s cells have proteins that are antigens. These include a group of antigens called HLA antigens. Your immune system learns to see these antigens as normal and usually does not react against them.
Micrograph of a section of human skin prepared for direct immunofluorescence using an anti-IgG antibody. The skin is from a person with systemic lupus erythematosus and shows IgG deposits at two different places. The first is a bandlike deposit along the epidermal basement membrane ("lupus band test" is positive); the second is within the nuclei of the epidermal cells (antinuclear antibodies are present).

Most people who have SLE have low levels of vitamin D and should take a vitamin D supplement regularly. Vitamin D is essential for proper function of the immune system and several studies have shown that people who have more severe lupus tend to have lower levels of vitamin D compared to those who have milder disease.  It is advised to talk with your consultant or GP about your vitamin D levels as you may already be prescribed calcium supplements which may contain vitamin D. Some dietary sources of vitamin D can be found HERE. It is important to bear in mind that most vitamin D is usually synthesised from sunlight on the skin, but with lupus you should be protecting yourself from exposure to UV.
Consuming foods in their natural, whole form limits your exposure to synthetic additives, toxins or pesticides. These chemicals are very commonly found in packaged products and non-organic foods (even many veggies and fruit!). Because those with lupus already have weakened immune systems, reducing exposure to synthetic hormones, chemicals, medications and heavy metals is usually crucial for recovery.
The clinical manifestations of systemic lupus erythematosus are fundamentally the same in children and adults.15 In two descriptive studies25,26 of children with the disease, the most frequent manifestations were fever, rash, arthritis, alopecia, and renal involvement. Compared with adults, children have a higher incidence of malar rash, anemia, leukocytopenia,27 and severe manifestations such as neurologic or renal involvement.28

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.
To minimize complications in pregnancy, SLE ideally should be well controlled for at least 4-6 months before conception. Obstetricians who handle high-risk pregnancies should optimally offer pregnancy planning consultation and monitor all pregnancies in patients with SLE. Suggestions for treatment of SLE during pregnancy are also included in the European League Against Rheumatism (EULAR) recommendations. High-dose aspirin and NSAIDs should be avoided in later pregnancy.

Because some treatments may cause harmful side effects, it is important to report any new symptoms to the doctor promptly. It is also important not to stop or change treatments without talking to the doctor first. In addition to medications for lupus itself, in many cases it may be necessary to take additional medications to treat problems related to lupus such as high cholesterol, high blood pressure, or infection.


The mechanism by which foreign antigens are taken into antigen-presenting cells (APCs) and broken up. Part of the antigen is then displayed (presented) on the surface of the APC next to a histocompatibility or self-antigen, activating T lymphocytes and cell-mediated immunity. T lymphocytes are unable to recognize or respond to most antigens without APC assistance.
The antinuclear antibody (ANA) test is used to detect autoantibodies that react against components of the nucleus of the body's cells. It's currently one of the most sensitive diagnostic tests available for diagnosing lupus (SLE). That's because 97 percent or more of people with lupus (SLE) have a positive ANA test result. A negative ANA test result means lupus (SLE) is unlikely. 

Another recent development is the shift regarding omega-3 fatty acids, which were believed to be beneficial in patients with lupus by decreasing inflammation. “We showed that omega-3 did not affect disease activity, improve endothelial function, or reduce inflammatory markers, though there was evidence that omega-3 may increase [low-density lipoprotein] LDL cholesterol,” said Dr Stojan. “We no longer recommend omega-3 supplementation in lupus patients.”


Maybe. Start by seeing your family doctor and a rheumatologist, a doctor who specializes in the diseases of joints and muscles such as lupus. Depending on your symptoms or whether your organs have been hurt by your lupus, you may need to see other types of doctors. These may include nephrologists, who treat kidney problems, and clinical immunologists, who treat immune system disorders.
“I have had severe lupus for over twenty years and find that diet doesn’t really change any symptoms. I eat meat, fish, dairy, gluten and sugar too…all in moderation. I eat lots of fruit and veg and avoid processed foods. The only thing I avoid is alcohol. I guess everyone is different but a well-balanced, healthy diet with exercise (when I’m up to it) is my formula.”
So what happens when you grow up and learn that you have lupus, or another equally devastating chronic illness?  Should all of your nutritional decisions now be based on what your body needs rather than what tastes best? Can they be one in the same?  If you are one of the lucky ones, they already are, and this transition is not quite as tough. But for others, the mandate that you should be choosing foods simply for their nutritional value may be yet, another “hard pill to swallow”, so to speak.  Thus, the lupus and diet dilemma.
The loss of self-tolerance is believed to be due to many hereditary and environmental factors and occurs when autoantigens are damaged, when they link with a foreign antigen, when the structure of a autoantigen is very similar to that of a foreign antigen (molecular mimicry), or when autoreactive T cells are not adequately controlled or are activated by nonspecific antigens. The changes in the appearance of the autoantigen or activation of autoreactive T-cells result in autoantigens being perceived as foreign. Inflammation and destruction of the tissues bearing the antigen occur because of the production of autoantibodies by B cells or the cytotoxicity of autoreactive T cells, which attack the autoantigens.
Dermatomyositis. Acute onset of confluent macular erythema in a periorbital and malar distribution (involving the cheeks and extending over the nasal bridge), with extension to the chin in a female with juvenile dermatomyositis. Note the perioral sparing. In some patients, there may be more extensive involvement of the face, including the perioral region, forehead, lateral face, and ears. In contrast to SLE , in dermatomyositis with malar erythema, the nasolabial folds are often not spared.
The panel suggests SOC alone over adding other IS in adult patients with SLE with cutaneous manifestations (weak recommendation based on low certainty of the evidence). It also suggests adding MTX, AZA, MMF, CsA, CYC or belimumab to patients failing to respond to SOC (weak recommendation based on low to moderate certainty of the evidence). Cost and availability may favour MTX and AZA (table 1).
Collagen is the major insoluble fibrous protein in the extracellular matrix and in connective tissue. In fact, it is the single most abundant protein in the animal kingdom. There are at least 16 types of collagen, but 80 – 90 percent of the collagen in the body consists of types I, II, and III. These collagen molecules pack together to form long thin fibrils of similar structure. Type IV, in contrast, forms a two-dimensional reticulum; several other types associate with fibril-type collagens, linking them to each other or to other matrix components. At one time it was thought that all collagens were secreted by fibroblasts in connective tissue, but we now know that numerous epithelial cells make certain types of collagens. The various collagens and the structures they form all serve the same purpose, to help tissues withstand stretching.
Over half of the people with SLE develop a characteristic red, flat facial rash over the bridge of their nose. Because of its shape, it is frequently referred to as the "butterfly rash" of SLE. The rash is painless and does not itch. The facial rash, along with inflammation in other organs, can be precipitated or worsened by exposure to sunlight, a condition called photosensitivity. This photosensitivity can be accompanied by worsening of inflammation throughout the body, called a "flare" of the disease.

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. The endocarditis of SLE is non-infectious, and is also called (Libman–Sacks endocarditis). It involves either the mitral valve or the tricuspid valve. Atherosclerosis also occurs more often and advances more rapidly than in the general population.[23][24]
Articular cartilage is the highly specialized connective tissue of diarthrodial joints. Its principal function is to provide a smooth, lubricated surface for articulation and to facilitate the transmission of loads with a low frictional coefficient. Articular cartilage is devoid of blood vessels, lymphatics, and nerves and is subject to a harsh biomechanical environment. Most important, articular cartilage has a limited capacity for intrinsic healing and repair. In this regard, the preservation and health of articular cartilage are paramount to joint health.
Photosensitive systemic lupus erythematosus (SLE) rashes typically occur on the face or extremities, which are sun-exposed regions. Although the interphalangeal spaces are affected, the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints are spared. Photo courtesy of Dr. Erik Stratman, Marshfield Clinic.
Photosensitive systemic lupus erythematosus (SLE) rashes typically occur on the face or extremities, which are sun-exposed regions. Although the interphalangeal spaces are affected, the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints are spared. Photo courtesy of Dr. Erik Stratman, Marshfield Clinic.
Genome-wide association studies (GWAS) revealed regions of linkage that were found on most chromosomes.[52] These studies are useful in identifying the genes that may be responsible for complex diseases such as SLE. Candidate gene loci implicated with SLE include multiple alleles from the HLA region, Fc-gamma receptor, and complement component system.[50] However, association does not prove that a specific form of a gene is responsible for the disease, as there may be other polymorphisms in the region that have a greater association effect.[50] However, because the biological role of most genes are not completely understood, it can be difficult to attribute phenotypic traits to certain genetic polymorphisms. Since SLE is associated with so many genetic regions, it is likely an oligogenic trait, meaning that there are several genes that control susceptibility to the disease.[50] Further complicating our understanding is the association of certain linkages with various ethnic groups.[50]
An antibody, produced by B cells in response to an altered autoantigen on one type of the body’s own cells, that attacks and destroys these cells. Autoantibodies are the basis for autoimmune diseases such as rheumatoid arthritis and diabetes mellitus. Several theories exist about why autoantibodies are formed. The most common theory proposes that AAbs develop as the result of a combination of hereditary and environmental risk factors that cause an autoantigen to be falsely recognized as alien by B cells; as a result, antibodies are produced for its destruction.

With variants known as discoid lupus, subacute cutaneous lupus, and systemic lupus erythematosus, lupus is one of several disorders of the immune system considered “autoimmune” in nature. These diseases occur when the immune system malfunctions and turns its infection-defense capabilities against the body, producing antibodies against healthy cells and tissues. These antibodies promote chronic inflammation and can damage organs and tissues. In lupus, these antibodies are known as antinuclear antibodies (ANA) because they target parts of the cell’s nucleus. Experts don’t yet fully understand all of the factors and triggers that cause inflammation and tissue damage in lupus, and research is ongoing.


SLE can also flare during or after pregnancy. Whether flares of SLE are more frequent during pregnancy is controversial. The flares do not seem to be exceedingly more serious than those in nonpregnant patients, although pregnancy outcomes are generally more likely to be complicated. Increased rates of hypertension during pregnancy, premature delivery, unplanned cesarean delivery, postpartum hemorrhage, and maternal venous thromboembolism are all more frequent in women with SLE.
Autoreactive B cells can accidentally emerge during somatic hypermutation and migrate into the germinal center light zone. Autoreactive B cells, maturated coincidentally, normally do not receive survival signals by antigen planted on follicular dendritic cells and perish by apoptosis. In the case of clearance deficiency, apoptotic nuclear debris accumulates in the light zone of GC and gets attached to FDC. This serves as a germinal centre survival signal for autoreactive B-cells. After migration into the mantle zone, autoreactive B cells require further survival signals from autoreactive helper T cells, which promote the maturation of autoantibody-producing plasma cells and B memory cells. In the presence of autoreactive T cells, a chronic autoimmune disease may be the consequence.

For some patients whose kidneys or central nervous systems are affected by lupus, a type of drug called an immunosuppressive may be used. Immunosuppressives, such as cyclophosphamide and mycophenolate mofetil, restrain the overactive immune system by blocking the production of immune cells. These drugs may be given by mouth or by IV infusion. The risk for side effects increases with the length of treatment.
Avoid calcium supplements, however, which Johns Hopkins researchers have found to potentially increase the risk of heart damage and arterial plaque buildup. “Due to the risk of accelerated atherosclerosis in lupus, we no longer recommend calcium supplementation and encourage a diet rich in calcium instead,” noted George Stojan, MD, a rheumatologist and assistant professor of medicine at Johns Hopkins.
One of several different tests used to evaluate the condition of the respiratory system. Measures of expiratory flow and lung volumes and capacities are obtained. The forced vital capacity is one of the more important pulmonary function tests; it provides a measure of the amount of air that can be maximally exhaled after a maximum inspiration and the time required for that expiration. Pulmonary function tests can also determine the diffusion ability of the alveolar-capillary membrane.
So what happens when you grow up and learn that you have lupus, or another equally devastating chronic illness?  Should all of your nutritional decisions now be based on what your body needs rather than what tastes best? Can they be one in the same?  If you are one of the lucky ones, they already are, and this transition is not quite as tough. But for others, the mandate that you should be choosing foods simply for their nutritional value may be yet, another “hard pill to swallow”, so to speak.  Thus, the lupus and diet dilemma.

The gene is the basic physical unit of inheritance. Genes are passed from parents to offspring and contain the information needed to specify traits. Genes are arranged, one after another, on structures called chromosomes. A chromosome contains a single, long DNA molecule, only a portion of which corresponds to a single gene. Humans have approximately 20,000 genes arranged on their chromosomes.


More serious organ involvement with inflammation occurs in the brain, liver, and kidneys. White blood cells can be decreased in SLE (referred to as leukopenia or leucopenia). Also, low blood-clotting factors called platelets (thrombocytopenia) can be caused by lupus. Leukopenia can increase the risk of infection, and thrombocytopenia can increase the risk of bleeding. Low red blood cell counts (hemolytic anemia) can occur.
Note: Ultimately, in patients with kidney disease from systemic lupus erythematosus (lupus nephritis), a kidney biopsy may be necessary to both define the cause of the kidney disease as being lupus-related as well as to determine the stage of the kidney disease in order to optimally guide treatments. Kidney biopsies are often performed by fine-needle aspiration of the kidney under radiology guidance, but in certain circumstances, a kidney biopsy can be done during an open abdominal operation.

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.
Lupus pregnancy deserves special review because it presents unique challenges. Pregnant women with SLE are considered high-risk pregnancies. These pregnancies require interactive monitoring generally by a skilled rheumatologist together with an obstetrician expert in high-risk pregnancies. Women with SLE who are pregnant require close observation during pregnancy, delivery, and the postpartum period. This includes fetal monitoring by the obstetrician during later pregnancy. These women can have an increased risk of miscarriages (spontaneous abortions) and can have flares of SLE during pregnancy. The presence of phospholipid antibodies, such as cardiolipin antibodies or lupus anticoagulant, in the blood can identify people at risk for miscarriages. Cardiolipin antibodies are associated with a tendency toward blood clotting. Women with SLE who have cardiolipin antibodies or lupus anticoagulant may need blood-thinning medications (aspirin with or without heparin) during pregnancy to prevent miscarriages. Other reported treatments include the use of intravenous gamma globulin for selected people with histories of premature miscarriage and those with low blood-clotting elements (platelets) during pregnancy. Pregnant women who have had a previous blood-clotting event may benefit by continuation of blood-thinning medications throughout and after pregnancy for up to six to 12 weeks, at which time the risk of clotting associated with pregnancy seems to diminish. Plaquenil has now been found to be safe for use to treat SLE during pregnancy. Corticosteroids, such as prednisone, are also safely used to treat certain manifestation of lupus during pregnancy.
Certain foods, including garlic and alfalfa sprouts, should be avoided by people with lupus. [For a more complete list of items to be avoided, please see the article “Things to Avoided” in the Lupus 101 section.] Recently controversy has also arisen over whether aspartame induces lupus. However, scientists have concluded that there is no evidence to suggest that aspartame causes lupus.
Other medicines. You may need other medicines to treat illnesses or diseases that are linked to your lupus — such as high blood pressure or osteoporosis. Many people with lupus are also at risk for blood clots, which can cause a stroke or heart attack. Your doctor may prescribe anticoagulants (“blood thinners”), such as warfarin or heparin, to prevent your blood from clotting too easily. You cannot take warfarin during pregnancy.

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Please Note: The material on this site is provided for informational purposes only and is not medical advice. Always consult your physician before beginning any diet or exercise program.

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