In more severe cases, medications that modulate the immune system (primarily corticosteroids and immunosuppressants) are used to control the disease and prevent recurrence of symptoms (known as flares). Depending on the dosage, people who require steroids may develop Cushing's syndrome, symptoms of which may include obesity, puffy round face, diabetes mellitus, increased appetite, difficulty sleeping and osteoporosis. These may subside if and when the large initial dosage is reduced, but long-term use of even low doses can cause elevated blood pressure and cataracts.
The role of the immune system in causing diseases is becoming better understood through research. This knowledge will be applied to design safer and more effective treatment methods. For example, completely revising the immune system of people with extremely aggressive treatments that virtually temporarily wipe out the immune system is being evaluated. Current studies involve immune eradication with or without replacement of cells that can reestablish the immune system (stem-cell transplantation).
The term undifferentiated connective tissue diseases is used to define conditions characterized by the presence of signs and symptoms suggestive of a systemic autoimmune disease that do not satisfy the classificative criteria for defined connective tissue diseases (CTD) such as systemic lupus erythematosus (SLE), Sjögren’s syndrome (SS), rheumatoid arthritis (RA) and others. A small percentage of patients presenting with an undifferentiated profile will develop during the first year follow up of a full blown CTD, however an average of 75% will maintain an undifferentiated clinical course. These patients may be defined as having a stable undifferentiated connective tissue diseases (UCTD). The most characteristic symptoms of UCTD are represented by arthritis and arthralgias, Raynaud’s phenomenon, leukopenia, while neurological and kidney involvement are virtually absent. Eighty percent of these patients have a single autoantibody specificity, more frequently anti-Ro and anti-RNP antibodies. Stable UCTD are considered as distinct clinical entities and therefore it has been proposed to define those conditions as UCTD. Classificative criteria have also been proposed and a work to better define them is still under way.

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]


Vasculitis affecting medium and small arteries, particularly at the point of bifurcation and branching. Segmental inflammation and fibrinoid necrosis of blood vessels lead to ischemia of the areas normally supplied by these arteries. Signs and symptoms depend on the location of the affected vessels and organs, but patients usually present with symptoms of multisystem disease, including fever, malaise, weight loss, hypertension, renal failure, myalgia, peripheral neuritis, and gastrointestinal bleeding; these may occur episodically. Unlike most types of vasculitis, PAN does not affect glomerular capillaries although other renal vessels are involved. The disease is associated with hepatitis B and C.
The EULAR recommendations indicate that in pregnant women with SLE, prednisolone, azathioprine, hydroxychloroquine (unnecessary discontinuation of hydroxychloroquine during pregnancy may result in lupus flares), and low-dose aspirin may be used. [61] Prednisone, prednisolone, and methylprednisolone are the corticosteroids of choice during pregnancy because of their minimal placental transfer. However, mycophenolate mofetil, cyclophosphamide, and methotrexate are strictly contraindicated. [61]
Everett adds that eating fish for protein is particularly good. Fish — especially salmon, tuna, and mackerel — contain omega-3 fatty acids, which are important because they help fight inflammation, she says. Omega-3s, which are also available as supplements, may decrease your risk for heart disease. This may be especially important for women with lupus because they have at least double the risk of heart disease compared with women who don't have lupus, according to a review of studies published in August 2013 in Seminars in Arthritis and Rheumatism. “Lupus is an independent risk factor for heart disease, so you should maintain a heart-healthy diet that helps fight inflammation and keeps you at a healthy weight," Everett says.
Fernández-Nebro A, Rúa-Figueroa Í, López-Longo FJ, Galindo-Izquierdo M, Calvo-Alén J, Olivé-Marqués A, Ordóñez-Cañizares C, Martín-Martínez MA, Blanco R, Melero-González R, Ibáñez-Rúan J, Bernal-Vidal JA, Tomero-Muriel E, Uriarte-Isacelaya E, Horcada-Rubio L, Freire-González M, Narváez J, Boteanu AL, Santos-Soler G, Andreu JL, Pego-Reigosa JM 2015, ‘Cardiovascular Events in Systemic Lupus Erythematosus: A Nationwide Study in Spain From the RELESSER Registry’, EAS-SER (Systemic Diseases Study Group of Spanish Society of Rheumatology). Medicine (Baltimore), vol. 94, no. 29, viewed 22 September 2017, https://www.ncbi.nlm.nih.gov/pubmed/26200625
People with lupus should know that most rashes, and sometimes other symptoms, are aggravated by sun exposure, so you’ll want to avoid it or use sun protection. It’s critical to talk to your doctor about skin rashes and lesions that you observe, as many are treated differently, and some can be signs that the disease is progressing or changing. You may need other treatments, too.
For resistant skin disease, other antimalarial drugs, such as chloroquine (Aralen) or quinacrine, are considered and can be used in combination with hydroxychloroquine. Alternative medications for skin disease include dapsone and retinoic acid (Retin-A). Retin-A is often effective for an uncommon wart-like form of lupus skin disease. For more severe skin disease, immunosuppressive medications are considered as described below.

Most autoimmune diseases affect one specific system. For example, Rheumatoid Arthritis involves the joints, and Multiple Sclerosis affects the brain and spinal cord. Lupus, on the other hand, affects more than one system simultaneously. No matter what organ or system is being attacked, all autoimmune diseases are similar in that they are an immune response caused by systemic inflammation that leads your body to attack itself.


If you have lupus, you may experience dry mouth. Your eyes may feel gritty and dry, too. That’s because some people with lupus develop Sjogren’s disease, another autoimmune disorder. Sjogren’s causes the glands responsible for tears and saliva to malfunction, and lymphocytes can accumulate in the glands. In some cases, women with lupus and Sjogren’s may also experience dryness of the vagina and skin.
Acute cutaneous LE typically presents in the third decade of life and is frequently associated with active SLE. There are localized and generalized forms of ACLE. The localized form is the frequently described malar, or “butterfly” rash, which refers to erythema that occurs over both cheeks, extends over the nasal bridge, and spares the nasolabial folds. These lesions are classically transient, sun-induced, and non-scarring, although dyspigmentation can occur. Patients may initially mistake this rash for a sunburn, and only seek medical attention when it persists for several days. A fine surface scale and/or edema may be associated with the erythema. Malar rashes have been reported to be present in up to 52% of SLE patients at the time of diagnosis, with clinical activity of the rash paralleling that of the systemic disease. This rash can be confused with acne rosacea and seborrheic dermatitis, however the former is associated with the formation of papules and pustules, and the latter occurs within the nasolabial folds.

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.
(1) SOC; (2) SOC plus methotrexate (MTX); (3) SOC plus leflunomide (LFN); (4) SOC plus belimumab; (5) SOC plus abatacept (ABT); (6) other options: azathioprine (AZA), mycophenolate mofetil (MMF), cyclosporine A (CsA) or rituximab (RTX) (online supplementary tables S2.1.1, S2.1.4, S2.1.6, S2.1.7, S2.2.11, S2.1.11, S2.1.12, S2.1.14, S2.1.15, S2.1.17, S2.2.1, S2.2.2, S2.2.4, S3.1.1, S3.1.3–S3.1.6, S3.2.1, S3.2.2, S12.2–S12.5, S12.8–S12.10).
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]
Next, a doctor will usually prescribe a corticosteroid such as prednisone, which has a variety of unpleasant and dangerous side effects. Long term prednisone therapy can cause muscle wasting and osteoporosis, and those side effects require additional monitoring and medication. If the steroids stop controlling the symptoms, then a host of other serious medications are prescribed that either modulate or suppress the immune system as a whole. Plaquenil and belimumab (Benlysta) are some of the drugs used, and they have very harsh side effects including hair loss, muscle atrophy, blood disorders and increased susceptibility to infections.
(1) SOC; (2) SOC plus methotrexate (MTX); (3) SOC plus leflunomide (LFN); (4) SOC plus belimumab; (5) SOC plus abatacept (ABT); (6) other options: azathioprine (AZA), mycophenolate mofetil (MMF), cyclosporine A (CsA) or rituximab (RTX) (online supplementary tables S2.1.1, S2.1.4, S2.1.6, S2.1.7, S2.2.11, S2.1.11, S2.1.12, S2.1.14, S2.1.15, S2.1.17, S2.2.1, S2.2.2, S2.2.4, S3.1.1, S3.1.3–S3.1.6, S3.2.1, S3.2.2, S12.2–S12.5, S12.8–S12.10).
There is no single diagnostic test for systemic lupus. The test you will hear most about is called the antinuclear antibody (ANA) test. This is not a specific test for lupus, however. In fact, a variety of laboratory tests are used to detect physical changes or conditions in your body that can occur with lupus. Each test result adds more information to the picture your doctor is forming of your illness.

Disease that results when the immune system mistakenly attacks the body’s own tissues. Examples include multiple sclerosis, type 1 diabetes, rheumatoid arthritis, and systemic lupus erythematosus. Autoimmune diseases can affect almost any part of the body, including the heart, brain, nerves, muscles, skin, eyes, joints, lungs, kidneys, glands, the digestive tract, and blood vessels. The classic sign of an autoimmune disease is inflammation, which can cause redness, heat, pain, and swelling.

Today, physicians treat lupus using a wide variety of medicines, ranging in strength from mild to extremely strong. Prescribed medications will usually change during a person’s lifetime with lupus. However, it can take months—sometimes years—before your health care team finds just the right combination of medicines to keep your lupus symptoms under control.

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