Why the butterfly? People living with Lupus often have a rash on their face called a malar rash. Commonly called a 'butterfly' rash, it appears across the nose and cheeks, in the shape of a butterfly's wings. You will find a different butterfly on each page, representing how different Lupus is for each person. What's New in Lupus News - Archived Articles



Monday December 31 5:19 PM ET / Drug Helps Arthritis, but Has Side Effects: Study
NEW YORK (Reuters Health) - Patients in the early stages of rheumatoid arthritis may have less joint damage if they take the steroid drug prednisone, according to the results of a study conducted in the Netherlands. However, long-term use of the drug--even at relatively low doses--appears to increase the risk of bone fractures, experts warn.
Rheumatoid arthritis is a disease in which the immune system attacks the lining of joints, causing pain, stiffness and inflammation. The disease can ultimately cause joint destruction and disability. The condition is more common in women than in men and can be diagnosed in people in their 30s and 40s.
Corticosteroids, such as prednisone, are used to treat many conditions such as arthritis, asthma and lupus, and taking them is known to cause bone thinning.
Writing in the January issue of the journal Annals of Internal Medicine, Dr. Amalia A. van Everdingen and colleagues report the results of their study on the use of prednisone to slow the progression of rheumatoid arthritis. Other drugs are known to slow joint damage seen in rheumatoid arthritis patients, and the researchers wanted to find out if prednisone could be safely used in the same way.
In the study, the researchers prescribed 10 milligrams (mg) of prednisone to 41 patients who were known to have rheumatoid arthritis for less than one year. Forty other patients, who also had the condition for less than one year received an inactive placebo.
After 6 months of treatment, those taking prednisone had less joint stiffness, swelling and tenderness, and they were less likely to take other medications such as nonsteroidal anti-inflammatory drugs compared with those taking the placebo, the authors report. They also note that x-rays showed less joint damage in those taking prednisone.
However, after 2 years, those taking prednisone were more likely to have cracks in their spinal bones than those taking a placebo. Five patients in the prednisone groups compared with two people in the placebo group developed fractures in the small bones of their backs.
Low doses of the drug may be useful when combined with other drugs known to slow the progression of the disease, van Everdingen and colleagues conclude.
In an accompanying editorial, Dr. Theodore Pincus of Vanderbilt University Medical Center in Nashville, Tennessee, and colleagues take issue with the notion that 10 mg of prednisone should be considered ``low-dose.''
``A dosage of 10 mg per day may be regarded as 'intermediate' or even 'high' by some clinicians, including ourselves,'' the editorialists write.
``Prednisone, in doses of 5 mg or less, appears to provide considerable clinical benefit to many, if not most, patients with rheumatoid arthritis and seems well tolerated in many patients,'' Pincus and colleagues conclude.



Smoking Ups Lupus Risk: Report / Thursday December 20 1:13 PM ET
NEW YORK (Reuters Health) - Smokers are at increased risk of developing the autoimmune disease systemic lupus erythematosus, according to the results of a recent study.
Lupus can occur in several forms, but systemic lupus erythematosus (SLE)--usually referred to simply as lupus--is the most serious type. It is an incurable disease marked by inflammation and damage to tissue and organs throughout the body, including the joints, skin, heart, kidney and central nervous system. Lupus is an autoimmune disorder, meaning it occurs when the immune system mistakenly attacks the body's own tissue.
``The results of this study provide further evidence for smoking as an important risk factor for the development (of lupus),'' Dr. Najeeb O. Ghaussy and colleagues from the University of New Mexico Health Sciences Center in Albuquerque write in their report published in the Journal of Rheumatology.
``This is the first study showing an association between SLE and smoking in a predominantly Hispanic group,'' they add.
The researchers interviewed 125 patients with SLE and 125 healthy adults who were matched by age and sex to the lupus patients.
The investigators found that people who were current smokers were seven times more likely than nonsmokers to have lupus. Those who were former smokers were nearly four times as likely to develop lupus as never-smokers.
``It is not surprising that cigarettes might have some effect on autoimmunity, as there are at least 55 chemical factors that affect cell growth or viability in cigarette smoke including carbon monoxide, cyanide, hydrazine, hydroquinone and others,'' Ghaussy and colleagues point out.
``It is also possible that cigarette smoking may act in concert with other environmental triggers, such as infection, to initiate the autoimmune process,'' the authors add.



Study Suggests Potential New Way to Treat Lupus by Amy Norton / Thursday, November 15 5:21PM ET
NEW YORK (Reuters Health) - New research into lupus suggests how the immune system goes awry in the disease--a discovery scientists say could lead to better, more targeted treatments for lupus in the next few years.
Lupus can occur in several forms, but systemic lupus erythematosus (SLE)--usually referred to simply as lupus--is the most serious type. It is an incurable disease marked by inflammation and damage to tissue and organs throughout the body, including the joints, skin, heart, kidney and central nervous system. Lupus is an autoimmune disorder, meaning the immune system mistakenly attacks the body's own tissue.
The new study, reported in the November 16th issue of Science, suggests how this misguided immune system attack unfolds.
In experiments with blood from SLE patients, researchers at the Baylor Institute for Immunology Research in Dallas, Texas, were able to zero in on an immune system protein called interferon-alpha as the possible instigator of the autoimmune response in lupus.
The finding suggests that a drug that would act against interferon-alpha could fight the disease, lead investigator Dr. Jacques Banchereau told Reuters Health.
``We are very, very eager to get an antagonist'' to interferon-alpha, he said, noting that such a drug could be available for initial trials in the next 2 years.
Drugs that suppress the immune system are already part of lupus treatment, but these treatments are ``nonspecific'' in their targeting of immune function, the Texas researchers note. And while they help many patients, the drugs carry side effects such as nausea, hair loss and an increased risk of infection and cancer. Suppressing only interferon-alpha could potentially provide a more targeted treatment.
Banchereau said there is a particular need for new treatments for children with SLE, 20% of whom die of organ damage from the disease.
Interferon-alpha has previously been found at high levels in the blood of SLE patients. In their experiments, Banchereau and his colleagues found that in SLE patients' blood, immune system cells called monocytes develop into large pools of dendritic cells, which are responsible for triggering other immune system cells to attack. Banchereau likened this transformation to a ``bunch of reservists becoming marines.''
This overly large population of active dendritic cells, he explained, may then begin triggering attacks on normal body tissue. And the culprit that appears to induce monocytes to become dendritic cells is interferon-alpha.
``Thus,'' the researchers conclude, ``unabated induction of dendritic cells by interferon-alpha may drive the autoimmune response in SLE.''



New Survey Reveals Chronic Fatigue Syndrome is as Disabling or Debilitating As Lupus, Multiple Sclerosis and Rheumatoid Arthritis / Lack of Test to Detect the Illness Remains Greatest Barrier to Diagnosis
CHARLOTTE, N.C., Nov. 15 /PRNewswire/ -- Thirteen years after a group of scientists coined the term chronic fatigue syndrome (CFS) to describe a mysterious medical condition, many medical professionals are acknowledging it as a seriously disabling condition in need of treatment, concluded a survey released today by The Chronic Fatigue and Immune Dysfunction Syndrome (CFIDS) Association of America.
Three-quarters of medical professionals responding to the survey believe that CFS, also known as CFIDS, is as or more disabling than other chronic diseases such as lupus, multiple sclerosis, or rheumatoid arthritis. But despite the severe nature of the illness, diagnosis remains problematic. Half of the survey respondents cited the lack of a proven diagnostic test to be the greatest barrier to accurately identifying CFS. Thirty-five percent feel lack of a known cause of the illness is a barrier to diagnosis, and 31% feel there is not enough basic knowledge about CFS among the medical community.
Currently, health care practitioners are using a number of different methods to diagnose CFS. Almost three-quarters (72%) rely on exclusion of other common causes for symptoms; 68% use a patient history; and 25% use laboratory tests. Practitioners also rely on documenting the presence of symptoms other than fatigue. When respondents were asked what one symptom other than fatigue made them more likely to suspect CFS, or without which they would not make a diagnosis, the most common answer was post-exertional malaise (incapacitating fatigue lasting more than 24 hours after physical or mental exertion).
Lack of basic knowledge among practitioners and the absence of a diagnostic test means that more research and awareness of CFS is needed. Seventy-seven percent of the medical professionals surveyed felt that the amount of available professional education about CFS is not adequate. In addition, a large majority of respondents (87%) indicated that there should be more funding for research on the illness.
"These survey findings confirm that CFS is increasingly recognized as a serious, debilitating illness, and medical professionals still lack the core knowledge and tests they need to diagnosis CFS quickly and accurately," stated Kim Kenney, President and Chief Executive Officer of The CFIDS Association of America. "Much has been learned about CFS, but it is now very apparent that there is still a great need for research and education in the medical community."
The four-page survey was mailed to 8,100 medical professionals around the country, with a total of 865 completed surveys returned. The medical professionals polled came from a variety of disciplines including internal medicine, family/general practice, psychiatry/psychology, neurology, nursing and medical research.
About CFS (or CFIDS):
CFS is a serious and complex illness that affects many different body systems. There is no known cause. It is characterized by incapacitating fatigue (experienced as profound exhaustion and extremely poor stamina), neurological problems and numerous other symptoms. CFS can be severely debilitating and can last for many years. CFS is often misdiagnosed because it can resemble other disorders including mononucleosis, multiple sclerosis, fibromyalgia, Lyme disease, post-polio syndrome, and autoimmune diseases such as lupus. CFS is also known as myalgic encephalomyelitis (ME).



Human Genome Sciences wins OK to test lupus drug
NEW YORK, Nov 1 (Reuters) - U.S. regulators have given approval for Human Genome Sciences Inc. to begin Phase I human trials of LymphoStat-B for treatment of systemic lupus in adults who are already receiving standard treatments for the autoimmune disease, the company said on Thursday.
Human Genome Sciences , a biotechnology firm based in Rockville, Maryland, said it hopes in the future to test the experimental monoclonal antibody -- formerly known as Anti-BLyS -- against other autoimmune ailments such as rheumatoid arthritis.
Autoimmune diseases are conditions in which the body's own overactive immune system attacks healthy joints and tissues. Systemic lupus erythematosus causes episodes of inflammation in joints, tendons and other connective tissues and organs. About 90 percent of people with lupus are young women in their late teens to 30s.
Symptoms vary considerably in seriousness and frequency, ranging from rashes or hair loss to life-threatening kidney damage and blood disorders. Flare-ups appear to be triggered by sunlight in many patients, but rarely occur after menopause.
LymphoStat-B, which binds and inactivates the BLyS protein that is believed to stimulate the immune system, was discovered in a collaboration between Human Genome Sciences and British biotechnology firm Cambridge Antibody Technology Inc. as part of their first collaboration.
"Autoimmune diseases represent the third-greatest clinical burden after cardiovascular disease and cancer and currently have no cure," said Robert Kimberly, director of clinical immunology at the University of Alabama at Birmingham.
Although not curable, doctors currently treat lupus with standard pain and anti-inflammatory drugs like aspirin. People with severe symptoms are given steroids to tame inflammation and drugs like azathioprine to suppress the immune system.



Wednesday October 31 5:23 PM ET / Scientists Learn How Lupus Destroys Nervous System by Merritt McKinney
NEW YORK (Reuters Health) - Scientists announced on Wednesday that they may have identified how the autoimmune disease lupus destroys the central nervous system. Antibodies produced by the disease seem to kill nerves by latching on to a receptor on neurons, according to a report in the November issue of the journal Nature Medicine.
The discovery eventually may lead to new therapies for the disease, one of the investigators told Reuters Health. In people with lupus, or systemic lupus erythematosus (SLE) as it is officially known, the immune system loses the ability to differentiate between its own cells and outside invaders, and antibodies attack healthy cells. The condition can vary widely in severity, manifesting as skin rash and arthritis or leading to damage to the kidneys, heart, lungs and brain to varying degrees. There is no cure. The disease disproportionately affects women, particularly those of child-bearing age and of African or Asian descent.
If the central nervous system is affected, the resulting damage can cause a variety of problems including headache, paranoia, mania, schizophrenia and stroke. Exactly how lupus antibodies kill nerve cells has been a mystery, however.
Now Dr. Betty Diamond, of Albert Einstein College of Medicine in New York, and colleagues have discovered in experiments with human tissue and mice that lupus antibodies latch on to a common receptor found on nerves. Once the antibodies attach to these receptors--known as the NR2 subunits of the NMDA receptor--they trigger the death of neurons. The research eventually may lead to new therapies for lupus, one of the study's co-authors told Reuters Health. ``New insights into disease mechanism often lead to new therapeutics,'' said Dr. Bruce T. Volpe, of the Burke Medical Research Institute of Weill Medical College of Cornell University in White Plains, New York.
``Our work suggests a new hypothesis for the clinical symptom of cognitive decline in patients with lupus,'' he said. ''Now we need to test it.''
He explained that the antibodies ``cross react'' with ordinary molecules in the body, meaning that they recognize the molecules by mistake. This ``accidental recognition'' may destroy the cell, Volpe said. Now that researchers have formulated a new hypothesis about how lupus damages the nervous system, there are many questions to answer, according to Volpe. The next steps, he said, include seeing how frequently the nerve-killing antibodies are present in people with lupus and whether the presence of the antibodies is linked to neurological symptoms.
It will also be important to find out whether the process of cross-reactivity, or accidental recognition, is involved in other immune diseases that affect the nervous system, Volpe said.
The authors of an accompanying editorial agree that the research may open the door to new treatments if it is confirmed. And future research may show that similar types of ''cross-reactivities'' also play a role in other types of lupus-related tissue damage, according to Drs. Brian L. Kotzin and Elizabeth Kozora, of the University of Colorado Health Sciences Center in Denver.
But the editorialists caution that the results of the experiments, which included samples from only a few lupus patients, are preliminary.



Tuesday October 30 5:22 PM ET / Autoimmune-Disease Proteins Higher After Pregnancy
NEW YORK (Reuters Health) - Women who suffer from autoimmune disorders such as rheumatoid arthritis and multiple sclerosis may find relief during pregnancy but their symptoms may become even worse after they give birth.
Now, a preliminary study suggests that increased levels of certain stress hormones during the final trimester of pregnancy may suppress immune system proteins involved in inflammation, a hallmark of autoimmune disorders. But in the weeks after pregnancy, levels of these hormones fall sharply, resulting in higher levels of inflammatory proteins that may contribute to arthritis and multiple sclerosis.
``This finding has important implications for understanding why immune disorders may subside during pregnancy but flare up again after birth,'' Dr. Duane Alexander, director of the National Institute of Child Health and Human Development (NICHD) in Bethesda, Maryland, said in a prepared statement.
Multiple sclerosis occurs when the body's immune system attacks the central nervous system and destroys myelin, the protective coating that insulates nerve fibers in the brain and spine. The destruction of myelin can lead to numbness, muscle weakness and stiffness. In rheumatoid arthritis, the immune system attacks the lining of the joints, causing pain, stiffness and inflammation. There is no cure for either disease.
In the new study, researchers led by Dr. Ilia J. Elenkov of Georgetown University Medical Center in Washington, DC, measured levels of various immune system proteins in the blood of 18 healthy pregnant women during their third trimester and in the weeks after birth.
According to results published in the October issue of the Journal of Clinical Endocrinology and Metabolism, levels of interleukin-12 (IL-12) were about three times lower in the final trimester of pregnancy compared with levels measured after birth. Similarly, levels of tumor necrosis factor (TNF)-alpha were about 40% lower during the third trimester. IL-12 and TNF-alpha are proteins that trigger the body's immune system to fight disease but are also involved in the swelling and tissue destruction that marks autoimmune disorders.
Meantime, levels of cortisol, norepinephrine and 1,25-dihydroxyvitamin were higher in the third trimester compared with levels measured after birth. Previous studies have shown that these hormones can suppress levels of IL-12 and TNF-alpha, the researchers explain.
While further studies are needed, the findings may ultimately help scientists to understand the processes involved in autoimmune disorders and develop new treatments for conditions such as multiple sclerosis and rheumatoid arthritis, the NICHD's Alexander said.



Friday October 12 02:40 AM EDT / Prepping for the Patch (HealthScoutNews)
If you're about to get a patch test to see if you're allergic to something, there are two things you should always do first: avoid the sun for at least a week, and tell your dermatologist about any medications -- prescription or not -- you are taking. That's because sun exposure and many drugs can alter patch-test results by suppressing the immune system. This, in turn, could keep an allergic reaction from showing up on a patch test.
The most common drugs likely to interfere? Topical and oral corticosteroids; high blood-pressure drugs, especially calcium-channel blockers (such as diltiazem); nonsteroidal anti-inflammatory medications, prescription or not (such as aspirin, ibuprofen, and Feldene); and cyclosporine, an immune suppressant used for severe psoriasis, lupus and organ transplants.
In addition, retinoid drugs (including Retin-A) and products containing capsaicin (such as Zostrix) may make you more sensitive to some allergens, causing more severe reactions to patch tests than normal.



MCP Hahnemann University Researcher Reports Successful Treatment of Aplastic Anemia Opens Door for Treatment of All 80 Autoimmune Diseases
PHILADELPHIA, Oct. 5 /PRNewswire/ -- A newly proven cure for Severe Aplastic Anemia, a fatal bone marrow failure disorder, has broad implications for a similar cure for the entire array of 80 autoimmune diseases (i.e., Lupus Erythematosus, Crohn's Disease and Rheumatoid Arthritis), which afflict many people, according to Professor of Medicine at MCP Hahnemann University, Isadore Brodsky, M.D., who was a member of the research study led by his son, Robert Brodsky, published in the October 2, 2001 issue of the Annals of Internal Medicine.
The remedy, which chiefly consists of a ten-times higher dosage of what has been considered the standard administration of the nearly 50-year-old chemotherapy drug, Cyclophosphamide (Cytoxan), has been proven in clinical studies of 19 patients from MCP Hahnemann University, Johns Hopkins University, and the University of Maryland.
The high dosage of Cytoxan -- which was once thought too toxic to withstand -- can be used as the primary treatment for severe Aplastic Anemia who are not ideal candidates for bone marrow transplantation. Until now, months to years of immune therapy or bone marrow transplantation has been required to treat the devastating disease of Severe Aplastic Anemia. The use of Cytoxan is only a four-day therapy and produces "durable treatment-free remission." The remedy, according to the study, had 73 percent of the patients off all medication at 2 years. At 50 months, 65 percent of the patients were in treatment-free remission.
In severe Aplastic Anemia, the immune system attacks the stem cells, the progenitors of all blood cells produced in the bone marrow, and renders them incapable of making new oxygen-carrying red blood cells, infection-fighting white cells and clot-inducing platelets.
Like the other autoimmune diseases, Severe Aplastic Anemia occurs when the body's immune system inexplicably goes haywire, turns paranoid, and begins to attack itself. Even normal healthy body proteins suddenly are seen as the enemy and attacked.
As Dr. I. Brodsky explained, the impact of Cytoxan is that the marrow stem cell reconstitutes the bone marrow and "reboots" the patient's immune system, allowing it function normally without any further therapy.
Preliminary trials in treating other autoimmune diseases -- such as Lupus Erythematosus, Crohn's Disease, Rheumatoid Arthritis and neurologic disorders -- with similar high doses of Cytoxan were previously published in "Annals of Internal Medicine."
The conclusion at that time, prior to the final outcomes of these current trials, was that the high dose treatment of Cyclophosphamide "can induce complete remission in patients with refractory, severe autoimmune disease. Reemergence of marrow function is similar to that seen after autologous transplantation and does not carry the risk for re-infusion of autoaggressive lymphocytes with the autograft."
The results have been published the October 2, 2001, "Annals of Internal Medicine" under the headline: Durable Treatment-Free Remission after High-Dose Cyclophosphamide Therapy for Previously Untreated Severe Aplastic Anemia. The lead researcher of the report is MCP Hahnemann University graduate (1989), Dr. Robert Brodsky, now with Johns Hopkins Oncology Center, in collaboration with his father, Dr. Isadore Brodsky.



The PolyTiter(TM) System Received FDA Clearance as an Aid in the Diagnosis and Management of Autoimmune Diseases
CORTLANDT MANOR, N.Y., Sept. 25 /PRNewswire/ -- The PolyTiter Immunofluorescent Titration System (PolyTiter System) is based on the principle that the intensity of the fluorescence produced by a specimen in the Immuno-fluorescent assay (IFA) is related to the endpoint titer of the specimen. The PolyTiter System permits the linear regulation of the illumination, paralleling the dilution effect. By controlling the illumination of an IFA slide in a manner parallel to specimen dilution, the system supports establishing the titer of the specimen from a single dilution. Unlike automated systems that measure all available light, it is the technician who decides which features on the slide are to be measured by looking at the selected object (speckles, nucleoli, etc).
The optical device allows for semi-quantitative determination of the patient titer from the initial well by regulating, using a digital control pad, the amount of light illuminating on the sample wells. The titer value is determined from the standard curve via software calculations using a computer which is interfaced to the PolyTiter System.
Polymedco's president, Andrew Cervasio, states, "The PolyTiter System represents the first major innovation in IFA testing in several decades. The system will allow for more effective patient management and results."
The system enables standardization among technologists and laboratories while reducing test turnaround time. Flexibility is provided by allowing usage of most commercially available substrate slides and microscopes.
The complete PolyTiter System includes the microscope adapter, keypad, computer, and substrate slides.
Autoantibodies are immunoglobulins produced by the immune system in response to several pathological conditions referred to as autoimmune diseases. Antinuclear antibodies (ANA) are directed against many nuclear antigens and these antibodies play a key role in the diagnosis, classification, prognosis, and treatment of these diseases. Positive ANA results usually occur in autoimmune diseases such as systemic lupus erythrematosus (SLE), mixed connective tissue disease (MCTD), Rheumatoid Arthritis (RA), Sjogren's Syndrome (SS), and Progressive Systemic Sclerosis (PSS).
Autoimmune diseases cause significant and chronic morbidity and disability. Nearly 9 million Americans are currently affected with an autoimmune disease.


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