Preventive measures are necessary to minimize the risks of steroid-induced osteoporosis and accelerated atherosclerotic disease. [146] The American College of Rheumatology (ACR) Guidelines for the prevention of glucocorticoid-induced osteoporosis suggest the use of traditional measures (eg, calcium, vitamin D) and the consideration of prophylactic bisphosphonate therapy.
Rheumatologists have long been concerned that the female hormone estrogen or treatment with estrogen may cause or worsen lupus. Recent research showed that estrogen therapy can trigger some mild or moderate flares of lupus, but does not cause symptoms to get much worse. Yet, estrogen can raise the risk of blood clots. Thus, you should not take estrogen if your blood tests show antiphospholipid antibodies (meaning you already have a high risk of blood clots).

A randomized, double-blind, placebo-controlled trial in 40 patients with juvenile-onset SLE suggests that cholecalciferol supplementation for 24 weeks is effective in decreasing disease activity and improving fatigue in these patients. Compared with the placebo group, patients receiving oral cholecalciferol 50,000 IU/week demonstrated significant improvement in Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) scores (P = 0.010) and European Consensus Lupus Activity Measurement (ECLAM) scores (P = 0.006), along with a reduction of fatigue related to social life, as measured by the Kids Fatigue Severity Scale (K-FSS) score (P = 0.008). [110]
It also recommends intravenous Ig with/without GCs or RTX plus GCs for patients who are refractory to high-dose GCs, those with life-threatening bleeding, those requiring urgent surgery and those with infections (strong recommendation based on moderate certainty of the evidence). Cost and availability, however, may prompt the use of IS instead of RTX although there are no data to support this assertion (table 4).
There are assertions that race affects the rate of SLE. However, a 2010 review of studies which correlate race and SLE identified several sources of systematic and methodological error, indicating that the connection between race and SLE may be spurious.[100] For example, studies show that social support is a modulating factor which buffers against SLE-related damage and maintains physiological functionality.[100] Studies have not been conducted to determine whether people of different racial backgrounds receive differing levels of social support.[100] If there is a difference, this could act as a confounding variable in studies correlating race and SLE. Another caveat to note when examining studies about SLE is that symptoms are often self-reported. This process introduces additional sources of methodological error. Studies have shown that self-reported data is affected by more than just the patients experience with the disease- social support, the level of helplessness, and abnormal illness-related behaviors also factor into a self-assessment. Additionally, other factors like the degree of social support that a person receives, socioeconomic status, health insurance, and access to care can contribute to an individual’s disease progression.[100][101] Racial differences in lupus progression have not been found in studies that control for the socioeconomic status [SES] of participants.[100][102] Studies that control for the SES of its participants have found that non-white people have more abrupt disease onset compared to white people and that their disease progresses more quickly. Non-white patients often report more hematological, serosal, neurological, and renal symptoms. However, the severity of symptoms and mortality are both similar in white and non-white patients. Studies that report different rates of disease progression in late-stage SLE are most likely reflecting differences in socioeconomic status and the corresponding access to care.[100] The people who receive medical care have often accrued less disease-related damage and are less likely to be below the poverty line.[102] Additional studies have found that education, marital status, occupation, and income create a social context which contributes to disease progression.[100]
Many types of wild seafood provide omega-3 fats that help reduce inflammation levels. The best choices are wild salmon, sardines, mackerel, halibut, trout and anchovies. Aim to consume these omega-3 foods about two to three times weekly, or consider supplementing. Just be sure to buy “wild-caught” to reduce intake of things like heavy metals found in farm-raised fish, plus limit intake of fish high in mercury.
Intravenous immunoglobulins may be used to control SLE with organ involvement, or vasculitis. It is believed that they reduce antibody production or promote the clearance of immune complexes from the body, even though their mechanism of action is not well understood.[87] Unlike immunosuppressives and corticosteroids, IVIGs do not suppress the immune system, so there is less risk of serious infections with these drugs.[88]

As with all autoimmune conditions, lupus is a disease of the immune system. Your immune system has a very sophisticated mechanism for keeping you safe that it uses to identify the foreign substances that you come into contact with every day, such as allergens, toxins, infections, and even food. If your immune system deems anything dangerous, it will produce antibodies to ward off the harmful intruders.
Since a large percentage of people with SLE have varying amounts of chronic pain, stronger prescription analgesics (painkillers) may be used if over-the-counter drugs (mainly nonsteroidal anti-inflammatory drugs) do not provide effective relief. Potent NSAIDs such as indomethacin and diclofenac are relatively contraindicated for people with SLE because they increase the risk of kidney failure and heart failure.[83]
However, the mainstays of treatment are corticosteroids such as prednisone (Deltasone), hydrocortisone, methylprednisolone (Medrol), and dexamethasone (Decadron, Hexadrol). These drugs heavily suppress inflammation but can cause short-term side effects including swelling, increased appetite, and weight gain and long-term side effects including stretch marks on the skin, weakened or damaged bones, high blood pressure, damage to the arteries, diabetes, infections, and cataracts.
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.
Prognosis is typically worse for men and children than for women; however, if symptoms are present after age 60, the disease tends to run a more benign course. Early mortality, within 5 years, is due to organ failure or overwhelming infections, both of which can be altered by early diagnosis and treatment. The mortality risk is fivefold when compared to the normal population in the late stages, which can be attributed to cardiovascular disease from accelerated atherosclerosis, the leading cause of death for people with SLE.[83] To reduce the potential for cardiovascular issues, high blood pressure and high cholesterol should be prevented or treated aggressively. Steroids should be used at the lowest dose for the shortest possible period, and other drugs that can reduce symptoms should be used whenever possible.[83]

Lupus is an inflammatory autoimmune disease that can affect multiple parts of the body including the various organ systems. Doctors prescribe traditional pharmaceutical medications to manage symptoms and prevent flare ups of the disease that can cause more serious problems and complications. Many patients choose to supplement their pharmaceutical care with alternative treatments and lifestyle adjustments like using diet and exercise to minimize lupus symptoms. We discuss this further in our  blog, Lupus/Chronic Illness: The Mind/Body Connection. There exists two major diets widely discussed in the autoimmune world. One is the anti-inflammatory diet and one is called the Paleo Diet.
Gene regulation is the process of turning genes on and off. During early development, cells begin to take on specific functions. Gene regulation ensures that the appropriate genes are expressed at the proper times. Gene regulation can also help an organism respond to its environment. Gene regulation is accomplished by a variety of mechanisms including chemically modifying genes and using regulatory proteins to turn genes on or off.

Lupus is an incredibly complex autoimmune disease and diagnosing lupus can take a lot of time and many doctor visits. Patients will often get diagnosed with other “overlap” diseases such as rheumadoid arthritis (RA), Sjogren’s Syndrome, scleroderma, fibromyalgia or Raynaud’s Phenomenon even before a diagnosis of lupus is made. This can be incredibly frustrating for you as well as your doctors. Understanding the process of getting a lupus diagnosis is one of the most common questions we get here as well as a main topic in the discussions on our Facebook page and our other social media platforms. The goal of this blog is to give a clear understanding of the diagnosis process and provide the tools needed to go back to your doctor (or a new doctor) armed with the information you need.
Since SLE patients can have a wide variety of symptoms and different combinations of organ involvement, no single test establishes the diagnosis of systemic lupus. To help doctors improve the accuracy of the diagnosis of SLE, 11 criteria were established by the American Rheumatism Association. These 11 criteria are closely related to the symptoms discussed above. Some people suspected of having SLE may never develop enough criteria for a definite diagnosis. Other people accumulate enough criteria only after months or years of observation. When a person has four or more of these criteria, the diagnosis of SLE is strongly suggested. Nevertheless, the diagnosis of SLE may be made in some settings in people with only a few of these classical criteria, and treatment may sometimes be instituted at this stage. Of these people with minimal criteria, some may later develop other criteria, but many never do.
Discoid Lupus is the most common form of Cutaneous Lupus. People living with Discoid Lupus complain of a red, raised and scaly lesion on the face, scalp or parts of the body. Manifestations on the face form across the cheeks, nose and ears. Over time, these lesions can produce scarring and skin discoloration (darkly colored and/or lightly colored areas). Typically, these lesions occur on areas of the body that are exposed to sunlight or fluorescent lights. If lesions appear in the scalp or involve the hair follicles, areas of hair loss may develop which could be permanent if the hair follicle is completely destroyed. They are often not itchy or painful. 
Lupus is an incredibly complex autoimmune disease and diagnosing lupus can take a lot of time and many doctor visits. Patients will often get diagnosed with other “overlap” diseases such as rheumadoid arthritis (RA), Sjogren’s Syndrome, scleroderma, fibromyalgia or Raynaud’s Phenomenon even before a diagnosis of lupus is made. This can be incredibly frustrating for you as well as your doctors. Understanding the process of getting a lupus diagnosis is one of the most common questions we get here as well as a main topic in the discussions on our Facebook page and our other social media platforms. The goal of this blog is to give a clear understanding of the diagnosis process and provide the tools needed to go back to your doctor (or a new doctor) armed with the information you need.
Your gut is somewhat permeable to allow very small molecules (micronutrients) pass through the intestinal wall. It’s how you absorb your food. Many factors can damage your gut, including gluten, infections, medications and stress. This damage allows much larger particles such as toxins, microbes, and undigested food particles to “leak through” your gut and enter your bloodstream, triggering an immune response. We know from the research of Dr. Alessio Fasano that leaky gut is a necessary precursor to autoimmunity, meaning if you’re dealing with lupus, you also have a leaky gut. Not to mention, your gut is where nearly 80% of your immune system lives. So in order to overcome lupus, you must first repair your gut.
I recommend that everyone remove gluten from their diets because it’s simply an inflammatory food, and this is particularly critical for anyone with an autoimmune condition. I also highly recommend that anyone with an autoimmune condition remove all grains and legumes from your diet as well. These foods contain proteins known as lectins, which act as a natural pesticide for crops and can wreak havoc on the lining of your gut. My cookbook, The Autoimmune Solution Cookbook, contains over 150 specially designed recipes to help make following an autoimmune-friendly protocol easy and delicious!
Often, people with lupus experience weight loss or gain due to loss of appetite, unhealthy dietary habits, or decreased energy and mobility. If you experience weight loss or loss of appetite, talk to your doctor. S/he can help you determine the cause of the problem and take strides to correct it. Weight gain can be caused by many factors, including reduced activity levels and overeating due to steroid use or increased stress. However, remember that women with lupus between the ages of 35 and 44 experience a risk of heat attack that is 50x that of the normal population. Therefore, it is very important that you try to stick to a diet that is low in cholesterol and saturated fats. A low-sodium diet is also essential for people suffering from high blood pressure (above 120/80 mmHg for people with lupus) and kidney disease.
Deal with one problem at a time, Keep finding ways to enjoy the outdoors but stay away from the sun. Florescent lights also seem to cause flareups in skin from my wife’s experience. A good book I read called “The Sun Is My Enemy” covers an experience that follows what you describe, and it helps to understand the symptoms and life long effects than need addressing but don’t determine quality or length of life.
The male hormone DHEA (dehydroepiandrosterone), produced in the adrenals, seems to help and may reduce the need for prednisone. Although DHEA is available over-the-counter, don’t take it without medical supervision. It presents an increased risk of heart attack and breast and prostate cancer so it is vital that a physician monitor anyone taking it for lupus. Furthermore, over-the-counter brands of DHEA may not be as reliable as prescription forms.
One food for people with lupus to avoid is alfalfa. Alfalfa tablets have been associated with reports of a lupus-like syndrome or lupus flares. The lupus-like effects may include muscle pain, fatigue, abnormal blood test results, changes in how the immune system functions, and kidney problems. These reactions may be due to the amino acid L-canavanine (found in alfalfa seeds and sprouts, but not in leaves), which can activate the immune system and increase inflammation.
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.
Based on the identified evidence the panel concluded that compared with GCs alone, the addition of other IS (CYC, MMF or TAC) is associated with significant benefits, higher remission rates and lower progression rates to end-stage renal disease (ESRD). Head-to-head comparisons between MMF, TAC and high-dose CYC showed that MMF and TAC are associated with less adverse effects than high-dose CYC. Between low and high-dose CYC the balance favours the former because of better safety profile and comparable efficacy, although this conclusion is based on one trial that included predominantly Caucasians. RTX did not provide additional benefits when combined with MMF.

Intravenous immunoglobulins may be used to control SLE with organ involvement, or vasculitis. It is believed that they reduce antibody production or promote the clearance of immune complexes from the body, even though their mechanism of action is not well understood.[87] Unlike immunosuppressives and corticosteroids, IVIGs do not suppress the immune system, so there is less risk of serious infections with these drugs.[88]


Synovitis is an inflammation of the joint lining, called synovium. The symptoms are often of short duration and may change location although when caused by overuse tend to remain in one joint. The pain is usually more severe than expected based on the appearance of the joint on examination. In fact, sometimes there is pain without swelling or even tenderness in the joint, in which case the symptom is called “arthralgias” (literally meaning “joint pain” in Greek). Although synovitis has many different causes, the most common cause in an active healthy person is overuse.
It can be very scary to receive a lupus diagnosis, have your life disrupted and cause you to become uncertain about the future. The good news is that strides are continually being made in the discovery of better diagnostic tools and more effective medications. With the combination of correct treatment, medication, and living a healthy lifestyle, many people with lupus can look forward to a leading a long and productive life. 
When Griffiths et al compared the corticosteroid-sparing effect of cyclosporine with azathioprine in patients with severe SLE, they concluded that azathioprine may be considered first-line therapy, whereas cyclosporine requires close monitoring of blood pressure and serum creatinine. However, the investigators noted that in patients who are unable to tolerate azathioprine, cyclosporine may be considered. [136]
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.
Disease-modifying antirheumatic drugs (DMARDs) are used preventively to reduce the incidence of flares, the progress of the disease, and the need for steroid use; when flares occur, they are treated with corticosteroids. DMARDs commonly in use are antimalarials such as hydroxychloroquine and immunosuppressants (e.g. methotrexate and azathioprine). Hydroxychloroquine is an FDA-approved antimalarial used for constitutional, cutaneous, and articular manifestations. Hydroxychloroquine has relatively few side effects, and there is evidence that it improves survival among people who have SLE.[83] Cyclophosphamide is used for severe glomerulonephritis or other organ-damaging complications. Mycophenolic acid is also used for treatment of lupus nephritis, but it is not FDA-approved for this indication, and FDA is investigating reports that it may be associated with birth defects when used by pregnant women.[86]

Intravenous immunoglobulins may be used to control SLE with organ involvement, or vasculitis. It is believed that they reduce antibody production or promote the clearance of immune complexes from the body, even though their mechanism of action is not well understood.[87] Unlike immunosuppressives and corticosteroids, IVIGs do not suppress the immune system, so there is less risk of serious infections with these drugs.[88]
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. Because of early recognition and management of SLE, end-stage renal failure occurs in less than 5%[27][28] of cases; except in the black population, where the risk is many times higher.
The panel suggests SOC alone over adding other immunosuppressant (IS) in adult patients with SLE with MSK manifestations (weak recommendation based on low certainty of the evidence). It suggests also adding either MTX, LFN, belimumab or ABT to those failing to respond to SOC (weak recommendation based on low to moderate certainty of the evidence). Cost and availability may favour MTX (table 1).
It is important to understand that osteoporosis has no symptoms. There is no pain in the bones where individuals with osteoporosis would hypothetically feel sore, so it is important to speak with your doctor to have a regular bone mass density test performed. Again, there is a high risk of osteoporosis for people with lupus because of often decreased physical activity, vitamin D deficiency, medication side effects, and the additional risk of kidney disease. Listed below are nutritional tips to follow:
Autoantibodies directed against various nuclear antigens including DAutoantibodies directed against various nuclear antigens including DNA, RNA, histones, acidic nuclear proteins, or complexes of these molecular elements. Antinuclear antibodies are found in systemic autoimmune diseases including systemic lupus erythematosus, Sjogren’s syndrome, scleroderma, polymyositis, and mixed connective tissue disease. Autoantibodies directed against various nuclear antigens including DNA, RNA, histones, acidic nuclear proteins, or complexes of these molecular elements. Antinuclear antibodies are found in systemic autoimmune diseases including systemic lupus erythematosus, Sjogren’s syndrome, scleroderma, polymyositis, and mixed connective tissue disease.
Antinuclear antibody (ANA) testing and anti-extractable nuclear antigen (anti-ENA) form the mainstay of serologic testing for SLE. Several techniques are used to detect ANAs. Clinically the most widely used method is indirect immunofluorescence (IF). The pattern of fluorescence suggests the type of antibody present in the people's serum. Direct immunofluorescence can detect deposits of immunoglobulins and complement proteins in the people's skin. When skin not exposed to the sun is tested, a positive direct IF (the so-called lupus band test) is an evidence of systemic lupus erythematosus.[70]

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There are assertions that race affects the rate of SLE. However, a 2010 review of studies which correlate race and SLE identified several sources of systematic and methodological error, indicating that the connection between race and SLE may be spurious.[100] For example, studies show that social support is a modulating factor which buffers against SLE-related damage and maintains physiological functionality.[100] Studies have not been conducted to determine whether people of different racial backgrounds receive differing levels of social support.[100] If there is a difference, this could act as a confounding variable in studies correlating race and SLE. Another caveat to note when examining studies about SLE is that symptoms are often self-reported. This process introduces additional sources of methodological error. Studies have shown that self-reported data is affected by more than just the patients experience with the disease- social support, the level of helplessness, and abnormal illness-related behaviors also factor into a self-assessment. Additionally, other factors like the degree of social support that a person receives, socioeconomic status, health insurance, and access to care can contribute to an individual’s disease progression.[100][101] Racial differences in lupus progression have not been found in studies that control for the socioeconomic status [SES] of participants.[100][102] Studies that control for the SES of its participants have found that non-white people have more abrupt disease onset compared to white people and that their disease progresses more quickly. Non-white patients often report more hematological, serosal, neurological, and renal symptoms. However, the severity of symptoms and mortality are both similar in white and non-white patients. Studies that report different rates of disease progression in late-stage SLE are most likely reflecting differences in socioeconomic status and the corresponding access to care.[100] The people who receive medical care have often accrued less disease-related damage and are less likely to be below the poverty line.[102] Additional studies have found that education, marital status, occupation, and income create a social context which contributes to disease progression.[100]

What are the causes and types of arthritis? Arthritis is a term that describes around 200 conditions that cause pain in the joints and the tissues surrounding the joints. The most common form of arthritis is osteoarthritis. Other related conditions include gout and fibromyalgia. The article looks at the types, causes, and treatments, including natural remedies. Read now


Some patients with mild lupus, with a little joint pain or rash can be managed with anti-inflammatory drugs such as nonsteroidal anti-inflammatory drugs, or NSAIDs, such as ibuprofen or naproxen, says Stuart D. Kaplan, MD, the chief of rheumatology at South Nassau Communities Hospital in Oceanside, New York. These drugs can also help manage fever and inflammation of the heart and lining around the lungs. (2)

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