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  Systemic lupus erythematosus

Systemic lupus erythematosus also known as SLE or lupus (Latin word for “wolf”) is a chronic inflammatory autoimmune disorder involving many organ systems in the body. It is a Type III Hypersensitivity reaction which is a T-lymphocyte mediated disease, also called “Systemic Immune Complex Disease” (SICD). This immune-mediated disorder is potentially debilitating and sometimes fatal. The term autoimmune disease is described as a condition wherein the immune system of the body is attacking its own cells and tissues, resulting in widespread inflammation and tissue damage. SLE may affect any part of the body, but most of the time involves the heart, joints , skin, lungs, blood vessels and brain. There is a crude similarity between the butterfly-shaped malar or facial rash with that of a wolf’s face in some patients with SLE, hence; the term lupus was developed.

Systemic lupus erythematosus Skin diseases
Systemic lupus erythematosus


Although men can be diagnosed with lupus, it was found out that the disease primarily affects young women of childbearing age. Moreover, prevalence rate is noted to be higher among the following races: African-American, Asian, Hispanic and Native American women. This may be probably due to some socioeconomic factors. The exact etiology of the disease remains to be unknown and there is no consensus that has been developed on whether it is a single condition or a group of related diseases. SLE is thought to arise based on the three major mechanisms namely: genetic predisposition, environmental causes and drug-induced lupus (e.g. procainamide, hydralazine and quinidine).

Criteria have been established by the American College of Rheumatology (ACR) to identify SLE cases for the purpose of inclusion in clinical trials and were not intended to be used to diagnose individual patients.

However, a patient must present with 4 out of the 11 criteria, either at the same time or serially, during a given observation period to be classified as having SLE. These criteria include:

1. Malar rash
2. Discoid lupus (red, scaly patches on skin)
3. Photosensitivity
4. Mouth or nose ulcers
5. Arthritis
6. Proteinuria (More than 0.5g per day of protein in urine) or cellular casts present in the urine
7. Seizures or psychosis
8. Pleuritis (inflammation of the lung membrane) or pericarditis (inflammation of the heart membrane)
9. Hemolytic anemia (low red blood cell count), leukopenia (low white blood cell count), lymphopenia (low lymphocyte count) or thrombocytopenia (low platelet count)
10. Anti-DNA antibody sensitive but not specific; Anti-Sm antibody or false positive serological test for syphilis or antiphospholipid antibody positivity ; Anti-ss DNA; Antihistone Abs are present in 100% of drug-induced lupus; Prolonged PTT; Anticardiolipin and lupus anticoagulant; Complement levels are usually decreased
11. Positive fluorescence antinuclear antibody test (positive ANA).

Some doctors make a diagnosis on the basis of the abovementioned ACR classification criteria. However, since the criteria were established mainly for scientific research use then patients may have SLE despite never actually meeting the specified criteria. Some patients who have SLE may present with rarer manifestations such as lupus gastroenteritis, pancreatitis or cystitis, autoimmune inner ear disease, parasympathetic dysfunction, retinal and systemic vasculitis.

The mainstay of serologic testing for lupus is antinuclear antibody testing and anti-extractable nuclear antigen (anti-ENA). Antiphospholipid antibodies can likewise occur more often in SLE, and can predispose the patient for thrombosis but the Anti-Sm (Anti Smith) is the most sensitive and a more specific test. The Anti-dsDNA antibody test is the only marker to monitor prognosis in lupus. Other routine tests performed in SLE suspects are levels of complement system , complete blood count (CBC), serum electrolytes, renal and liver function tests.

There is no known cure for SLE. The standard treatment available for SLE is limited primarily to corticosteroids, anti-malarials (e.g. Plaquenil (hydroxycholoroquine), and chemotherapy drugs or immunosuppressants such as cyclophosphamide, methotrexate and azathioprine. The role of these medications is mainly controlling the disease and prevents flare ups. Typically, flares are treated with steroids and some DMARDs (disease-modifying antirheumatic drugs). DMARDs suppress the disease process, eventually reduce the need for steroid and finally, preventing flares. This is due to the fact the long term intake of steroids are as much as possible avoided because of its side-effects that manifest as obesity, diabetes, osteoporosis (Cushing syndrome).

Due to the advances in diagnosis and treatment of SLE, the over ten-years’ survival rate improved nowadays to over 90% of cases and many can live asymptomatically. Infection is the most common cause of death in SLE. This is related to the immunosuppression brought about by the medications used to manage the disease itself. Prognosis is poorer for men and children as compared to women however, if the onset of symptoms is over age 60, the disease tends to have a more benign course with better prognosis.

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