Marketing Scoops: Scientists Trace Lupus To One of The World’s Most Common Viruses

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One of the world’s most common viral infections could underlie virtually every case of lupus, according to a recent study providing the strongest evidence yet for a link. The research, led by scientists at Stanford University, has found that the Epstein-Barr virus (EBV) could be the trigger behind the ‘cruel mystery‘……..Continue reading….

By: Carly Cassella

Source: ScienceAlert

Critics:

Lupus, formally called systemic lupus erythematosus (SLE), is an autoimmune disease in which the body’s immune system mistakenly attacks healthy tissue in many parts of the body. Symptoms vary among people and may be mild to severe. Common symptoms include painful and swollen joints, fever, chest pain, hair loss, mouth ulcers, swollen lymph nodes, feeling tired, and a red rash which is most commonly on the face.

Often there are periods of illness, called flares, and periods of remission during which there are few symptoms. Children up to 18 years old develop a more severe form of SLE termed childhood-onset systemic lupus erythematosus. Lupus is Latin for ‘wolf’: the disease was so-named in the 13th century as the rash was thought to appear like a wolf’s bite. The cause of SLE is not clear. It is thought to involve a combination of genetics and environmental factors.

Among identical twins, if one is affected there is a 24% chance the other one will also develop the disease. Female sex hormones, sunlight, smoking, vitamin D deficiency, and certain infections are also believed to increase a person’s risk. The mechanism involves an immune response by autoantibodies against a person’s own tissues. These are most commonly anti-nuclear antibodies and they result in inflammation. Diagnosis can be difficult and is based on a combination of symptoms and laboratory tests.

There are a number of other kinds of lupus erythematosus including discoid lupus erythematosus, neonatal lupus, and subacute cutaneous lupus erythematosus. There is no cure for SLE, but there are experimental and symptomatic treatments. Treatments may include NSAIDs, corticosteroids, immunosuppressants, hydroxychloroquine, and methotrexate. Although corticosteroids are rapidly effective, long-term use results in side effects.

Alternative medicine has not been shown to affect the disease. Men have higher mortality.^[9] SLE significantly increases the risk of cardiovascular disease, with this being the most common cause of death. While women with lupus have higher-risk pregnancies, most are successful. Rate of SLE varies between countries from 20 to 70 per 100,000. Women of childbearing age are affected about nine times more often than men.

While it most commonly begins between the ages of 15 and 45, a wide range of ages can be affected. Those of African, Caribbean, and Chinese descent are at higher risk than those of European descent. Rates of disease in the developing world are unclear. SLE is one of several diseases known as “the great imitator” because it often mimics or is mistaken for other illnesses. SLE is a classical item in differential diagnosis, because SLE symptoms vary widely and come and go unpredictably.

Diagnosis can thus be elusive, with some people having unexplained symptoms of SLE for years before a definitive diagnosis is reached. Common initial and chronic complaints include fever, malaise, joint pains, muscle pains, and fatigue. Because these symptoms are so often seen in association with other diseases, these signs and symptoms are not part of the diagnostic criteria for SLE. When occurring in conjunction with other signs and symptoms, however, they are considered suggestive.

While SLE can occur in both males and females, it is found far more often in women, and the symptoms associated with each sex are different.^[9] Females tend to have a greater number of relapses, a low white blood cell count, more arthritis, Raynaud syndrome, and psychiatric symptoms. Males tend to have more seizures, kidney disease, serositis (inflammation of tissues lining the lungs and heart), skin problems, and peripheral neuropathy.

As many as 70% of people with lupus have some skin symptoms. The three main categories of lesions are chronic cutaneous (discoid) lupus, subacute cutaneous lupus, and acute cutaneous lupus. People with discoid lupus may exhibit thick, red scaly patches on the skin. Similarly, subacute cutaneous lupus manifests as red, scaly patches of skin but with distinct edges. Acute cutaneous lupus manifests as a rash. Some have the classic malar rash (commonly known as the butterfly rash) associated with the disease.

This rash occurs in 30–60% of people with SLE. Hair loss, mouth and nasal ulcers, and lesions on the skin are other possible manifestations. The most commonly sought medical attention is for joint pain, with the small joints of the hand and wrist usually affected, although all joints are at risk. More than 90 percent of those affected will experience joint or muscle pain at some time during the course of their illness.

Unlike rheumatoid arthritis, lupus arthritis is less disabling and usually does not cause severe destruction of the joints. Fewer than ten percent of people with lupus arthritis will develop deformities of the hands and feet. People with SLE are at particular risk of developing osteoarticular tuberculosis. A possible association between rheumatoid arthritis and SLE has been suggested, and SLE may be associated with an increased risk of bone fractures in relatively young women.

Anemia is common in children with SLE and develops in about 50% of cases. Low platelet count (thrombocytopenia) and low white blood cell count (leukopenia) 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.

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.

Steroids are sometimes prescribed as an anti-inflammatory treatment for lupus; however, they can increase one’s risk for heart disease, high cholesterol, and atherosclerosis. SLE can cause pleuritic pain as well as inflammation of the pleurae known as pleurisy, which can rarely give rise to shrinking lung syndrome involving a reduced lung volume. Other associated lung conditions include pneumonitis, chronic diffuse interstitial lung disease, pulmonary hypertension, pulmonary emboli, and pulmonary hemorrhage.

Some studies have found that vitamin D deficiency (i.e., a low serum level of vitamin D) often occurs in patients with SLE and that its level is particularly low in patients with more active SLE. Furthermore, 5 studies reported that SLE patients treated with vitamin D had significant reductions in the activity of their disease.

However, other studies have found that the levels of vitamin D in SLE are not low, that vitamin D does not reduce their SLE’s activity, and/or that the vitamin D levels and responses to vitamin D treatment varied in different patient populations (i.e., varied based on whether the study was conducted on individuals living in Africa or Europe).

Because of these conflicting findings, the following middle ground has been proposed for using vitamin D to treat SLE: Patients with SLE that have 25-hydroxyvitamin D₂ plus 25-hydroxyvitamin D₃ serum levels less than 30 ng/ml should be treated with vitamin D to keep these levels at or above 30 ng/ml or, in patients having major SLE-related organ involvement, at 36 to 40 ng/ml and

Patients with 25-hydroxyvitamin D₂ plus 25-hydroxyvitamin D₃ levels at or above 30 ng/ml should not be treated with vitamin D unless they have major SLE-related organ involvement in which case they should be treated with 25-hydroxyvitamin D₂ plus 25-hydroxyvitamin D₃ to maintain their serum vitamin D levels between 36 and 40 ng/ml.

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