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Systemic Lupus Erythematosus

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tanya crocker

on 3 March 2011

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Transcript of Systemic Lupus Erythematosus

Case Study A 25-year-old African American woman, previously
well, came to the University Hospital of Brooklyn
complaining of a 2-week history of lower abdominal
pain and occasional dysuria. She also related a
1-week history of fever, loss of appetite, generalized
weakness, a nonspecific cough, and a single
episode of vomiting on the day of her visit. She had
been to 2 different physicians within the previous
week, who had prescribed various antibiotics for a
presumed diagnosis of upper respiratory tract infection
and pelvic inflammatory disease, respectively.
Her medical history was notable for childhood
illnesses of atopic dermatitis, migraines, and occasional
nonspecific chest pains. She also received
treatment for gonorrhea and chlamydial infection
when she was 20 years old. When examined, she was a young, alert, wellappearing
woman. She was afebrile, her pulse rate
was 100 beats per minute, and her blood pressure
was 104/64 mmHg. She had no skin lesions or
lymphadenopathy. Her eyes were normal on examination.
Her chest sounds were clear with no friction
rubs, and she had no murmurs or rubs. Her
abdomen was soft with mild suprapubic tenderness,
minimal guarding, and no rebound tenderness.
Bowel sounds were present. She had no vaginal
discharge, cervical motion tenderness, or adnexal
masses. Her uterine size was normal. Her extremities
showed no joint swelling or tenderness. Neurologically,
she was unremarkable. Laboratory studies disclosed the following values:
sodium 139 mEq/L
potassium 3.8 mEq/L
chloride 105 mEq/L
bicarbonate 21 mEq/L
bloodurea nitrogen 10 mg/dL
creatinine 0.6 mg/dL
glucose 84 mg/dL
aspartate aminotransferase 119 U/L (normal 14–50 U/L)
alanine aminotransferase 76 U/L (normal 10–65 U/L)
protein 8.2 g/dL
albumin 3.7 g/dL
calcium 8.5 mg/dL
totalbilirubin 1.3 mg/dL (normal 0.2–1.3 mg/L). A CBC:
1.62 X 10^3/uL
Neutrophils 73%
band cells 15%
lymphocytes 15%
monocytes 5%
and atypical lymphocytes 2%
Hemoglobin 11.8 g/dL
hematocrit 35.8%, and
platelets 183,000/uL
a white cell count of 12–20 per high-power field Lab results The patient was admitted to the hospital with a
differential diagnoses of urinary tract infection,
neutropenia secondary to human immunodeficiency
virus (HIV) infection or acquired immunodeficiency
syndrome (AIDS), and possible perihepatitis
complicating pelvic inflammatory disease. Connective tissue workup showed a antinuclear
antibody (ANA) titer 1:1280, anti– double-stranded
DNA antibody positive, anti-DNA titer 1:640, anti-
Smith antibody positive, anti-ribonucleoprotein
positive, anti-SSA and anti-SSB negative, complements
C4 10 mg/dL (normal 16–47 mg/dL), C3
16 mg/dL (normal 83–201 mg/dL), anticardiolipin
antibodies were elevated, immunoglobulin G (IgG)
was 23 g/L (normal 0–14 g/L) and IgM 24 mg/L
(normal 0–9 mg/L). Lupus anticoagulant was negative.
Tests for gonorrhea, chlamydial infection,
and HIV were all negative. A diagnosis of SLE pancreatitis was made on the fourth day of admission, and steroids were started. Lupus Lupus is a chronic, autoimmune disease that can damage any part of the body (skin, joints, and/or organs inside the body). Lupus is also a disease of flares and remissions. It is believed that 5 million people throughout the world have a form of lupus.
Lupus strikes mostly women of childbearing age (15-44).
However, men, children, and teenagers develop lupus, too.
Women of color are 2-3 times more likely to develop lupus.
People of all races and ethnic groups can develop lupus.
More than 16,000 new cases of lupus are reported annually across the country Genes No gene or group of genes has been proven to cause lupus. Lupus does, however, appear in certain families, and when one of two identical twins has lupus, there is an increased chance that the other twin will also develop the disease. These findings, as well as others, strongly suggest that genes are involved in the development of lupus. Although lupus can develop in people with no family history of lupus, there are likely to be other autoimmune diseases in some family members. Certain ethnic groups (people of African, Asian, Hispanic/Latino, Native American, Native Hawaiian, or Pacific Island descent) have a greater risk of developing lupus, which may be related to genes they have in common. Environment While a person’s genes may increase the chance that he or she will develop lupus, it takes some kind of environmental trigger to set off the illness or to bring on a flare. Examples include:

ultraviolet rays from the sun
ultraviolet rays from fluorescent light bulbs
sulfa drugs, which make a person more sensitive to the sun, such as: Bactrim® and Septra® (trimethoprim-sulfamethoxazole); sulfisoxazole (Gantrisin®); tolbutamide (Orinase®); sulfasalazine (Azulfidine®); diuretics
sun-sensitizing tetracycline drugs such as minocycline (Minocin®)
penicillin or other antibiotic drugs such as: amoxicillin (Amoxil®); ampicillin (Ampicillin Sodium ADD-Vantage®); cloxacillin (Cloxapen®)
an infection
a cold or a viral illness
exhaustion
an injury
emotional stress, such as a divorce, illness, death in the family, or other life complications
anything that causes stress to the body, such as surgery, physical harm, pregnancy, or giving birth Pathophysiology Pathogenic autoantibodies in patients with lupus have particular properties that enable them to cause disease. Clinical investigations and studies in laboratory mice have shown that IgG antibodies with high-affinity binding to double-stranded DNA tend to be more strongly associated with tissue damage than IgM or lower-affinity IgG antibodies. Production of these high-affinity IgG antibodies are “driven” by antigens.
The term “antigen-driven” refers to a process in which antigen binds immunoglobulin on the surface of B lymphocytes, thereby stimulating the cells to proliferate.
The higher the affinity of the surface immunoglobulin for the antigen, the more strongly the cells are stimulated and the more they proliferate.
In the presence of the stimulating antigen, there is a continuous selective pressure favoring B cells that display on their surface and secrete immunoglobulins with high affinity for that antigen.
In general, this antigen-driven process can occur only in B lymphocytes that are being stimulated by T lymphocytes as well as by antigen. This process is known as T-lymphocyte help.
What are the Symptoms of Lupus Because lupus can affect so many different organs, a wide range of symptoms can occur. These symptoms may come and go, and different symptoms may appear at different times during the course of the disease.
The most common symptoms of lupus, which are the same for females and males, are:
extreme fatigue (tiredness)
headaches
painful or swollen joints
fever
anemia
edema in feet, legs, hands, and/or around eyes
pain in chest on deep breathing (pleurisy)
butterfly-shaped rash across cheeks and nose
photosensitivity
hair loss
abnormal blood clotting
mouth or nose ulcers A 25-year-old African American woman, previously in good health, came to the Hospital complaining of lower abdominal pain and occasional dysuria for the previous 2 weeks. She also reported fever, loss of appetite, generalized weakness, a nonspecific cough for the previous week, and vomiting on the day of her visit.
She has been taking various antibiotics for the last week, prescribed to her by 2 different doctors. These doctors had presumed diagnoses of upper respiratory tract infection and pelvic inflammatory disease, respectively. The patient was admitted to the hospital with a differential diagnosis of urinary tract infection, neutropenia secondary to human immunodeficiency virus (HIV) infection or acquired immunodeficiency syndrome (AIDS), and possible perihepatitis complicating pelvic inflammatory disease. She was allowed nothing by mouth, given intravenous fluids, and started empirically on antibiotics. By day 3 of admission her serum lipase had doubled to 1445 U/L and her white cell count had dropped to 0.92 10^3/uL. Her gastrointestinal discomfort had resolved, and she reported feeling better. A diagnosis of SLE pancreatitis was made on the fourth day of admission, and steroids were started No gene or group of genes has been proven to cause lupus. Lupus does, however, appear in certain families, and when one of two identical twins has lupus, there is an increased chance that the other twin will also develop the disease. These findings, as well as others, strongly suggest that genes are involved in the development of lupus. Although lupus can develop in people with no family history of lupus, there are likely to be other autoimmune diseases in some family members. Certain ethnic groups (people of African, Asian, Hispanic/Latino, Native American, Native Hawaiian, or Pacific Island descent) have a greater risk of developing lupus, which may be related to genes they have in common. Systemic lupus erythematosus (SLE), also called lupus, is an autoimmune disorder in which the body’s immune system incorrectly attack the body’s own tissues and organs, leading to inflammation and damage.
The cause of lupus is unknown, but it has been associated with genetic, environmental, and infectious causes.
While a person’s genes may increase the chance that he or she will develop lupus, it takes some kind of environmental trigger to set off the illness or to bring on a flare. Examples include:

•ultraviolet rays from the sun
•ultraviolet rays from fluorescent light bulbs
•sulfa drugs, which make a person more sensitive to the sun, such as: Bactrim® and Septra® (trimethoprim-sulfamethoxazole); sulfisoxazole (Gantrisin®); tolbutamide (Orinase®); sulfasalazine (Azulfidine®); diuretics
•sun-sensitizing tetracycline drugs such as minocycline (Minocin®)
•penicillin or other antibiotic drugs such as: amoxicillin (Amoxil®); ampicillin (Ampicillin Sodium ADD-Vantage®); cloxacillin (Cloxapen®)
•an infection
•a cold or a viral illness
•exhaustion
•an injury
•emotional stress, such as a divorce, illness, death in the family, or other life complications
•anything that causes stress to the body, such as surgery, physical harm, pregnancy, or giving birth
Lupus most commonly affects women of childbearing age but also occurs in children, adolescents, and men.
The disorder may affect almost all organs in the body, with the kidney being most commonly involved. The disorder may be mild in some cases (for example, only involving the skin) and very severe in other cases (affecting multiple organs, including the brain).
The disease course is characterized by flares (intervals of active disease) and remissions (intervals of inactive disease).
People of all races and ethnic groups can develop lupus.
It is believed that 5 million people throughout the world have a form of lupus.
Sex
More than 90 percent of people with lupus are women.
Age
Symptoms and diagnosis occur most often when women are in their childbearing years, between the ages of 15 and 44.
Race
In the United States, lupus is more common in people of color -- African Americans, Hispanics/Latinos, Asian Americans, Native Americans, Native Hawaiians and Pacific Islanders -- than in the Caucasian population. It also appears that lupus develops at an earlier age and is more severe among members of these ethnic groups.
Family History
Relatives of people with lupus have an approximately 5-13 percent chance of developing lupus. However, only about 5 percent of children will develop lupus if their mother has lupus. Prevalence
•ranges from approximately 40 cases per 100,000 persons among Northern Europeans to more than 200 per 100,000 persons among blacks
•In the United States, the number of patients with lupus exceeds 250,000.
•The life expectancy of such patients has improved from an approximate 4-year survival rate of 50% in the 1950s to a 15-year survival rate of 80% today.
•Even so, a patient in whom lupus is diagnosed at 20 years of age still has a 1 in 6 chance of dying by 35 years of age, most often from lupus or infection.
•Later, myocardial infarction and stroke become important causes of death.
Because lupus can affect so many different organs, a wide range of symptoms can occur. These symptoms may come and go, and different symptoms may appear at different times during the course of the disease.
The most common symptoms of lupus, which are the same for females and males, are:
•extreme fatigue (tiredness)
•headaches
•painful or swollen joints
•fever
•anemia
•edema in feet, legs, hands, and/or around eyes
•pain in chest on deep breathing (pleurisy)
•butterfly-shaped rash across cheeks and nose
•photosensitivity
•hair loss
•abnormal blood clotting
•mouth or nose ulcers Forms of Lupus
Systemic Lupus Erythematosus
Cutaneous Lupus Erythematosus
Drug-induced Lupus Erythematosus
Neonatal Lupus Systemic Lupus Erythematosus
is the most common form of lupus, and is what most people mean when they refer to "lupus." Systemic lupus can be mild or severe. Some of the more serious complications involving major organ systems are:
•inflammation of the kidneys (lupus nephritis), which can affect the body’s ability to filter waste from the blood and can be so damaging that dialysis or kidney transplant may be needed
•an increase in blood pressure in the lungs (pulmonary hypertension)
•inflammation of the nervous system and brain, which can cause memory problems, confusion, headaches, and strokes
•inflammation in the brain’s blood vessels, which can cause high fevers, seizures, behavioral changes,
•hardening of the arteries (coronary artery disease), which is a buildup of deposits on coronary artery walls that can lead to a heart attack
•Cutaneous refers to the skin, and this form of lupus is limited to the skin. Although there are many types of rashes and lesions (sores) caused by cutaneous lupus, the most common rash is raised, scaly and red, but not itchy.
•Another common example of cutaneous lupus is a rash over the cheeks and across the bridge of the nose, known as the butterfly rash
•Other rashes or sores may appear on the face, neck, or scalp (areas of the skin that are exposed to sunlight or fluorescent light), or in the mouth, nose, or vagina
•Hair loss and changes in the pigment, or color of the skin are also symptoms of cutaneous lupus
Cutaneous Lupus Erythematosus:

•Cutaneous refers to the skin, and this form of lupus is limited to the skin. Although there are many types of rashes and lesions (sores) caused by cutaneous lupus, the most common rash is raised, scaly and red, but not itchy.
•Another common example of cutaneous lupus is a rash over the cheeks and across the bridge of the nose, known as the butterfly rash
•Other rashes or sores may appear on the face, neck, or scalp (areas of the skin that are exposed to sunlight or fluorescent light), or in the mouth, nose, or vagina
•Hair loss and changes in the pigment, or color of the skin are also symptoms of cutaneous lupus
Drug Induced Lupus

• Drug-induced lupus is a lupus-like disease caused by certain prescription drugs. The symptoms of drug-induced lupus are similar to those of systemic lupus, but only rarely will any major organs be affected.
• The drugs most commonly connected with drug-induced lupus are hydralazine (used to treat high blood pressure or hypertension), procainamide (used to treat irregular heart rhythms), and isoniazid (used to treat tuberculosis). Drug-induced lupus is more common in men because they are given these drugs more often; however, not everyone who takes these drugs will develop drug-induced lupus. The lupus-like symptoms usually disappear within six months after these medications are stopped. Neonatal Lupus:

• Neonatal lupus is a rare condition that affects infants of women who have lupus and is caused by antibodies from the mother acting upon the infant in the womb.
• ~ 25% of women with SLE have spontaneous abortions
• At birth, the infant may have a skin rash, liver problems, or low blood cell counts, but these symptoms disappear completely after several months with no lasting effects.
• Some infants with neonatal lupus are born with a serious heart defect.
• With proper testing, physicians can now identify at-risk mothers and the infant can be treated at or before birth.
• Most infants of mothers with lupus are entirely healthy. Pathogenesis Pathogenic autoantibodies in patients with lupus have particular properties that enable them to cause disease. Clinical investigations and studies in laboratory mice have shown that IgG antibodies with high-affinity binding to double-stranded DNA tend to be more strongly associated with tissue damage than IgM or lower-affinity IgG antibodies. Production of these high-affinity IgG antibodies are “driven” by antigens.
The term “antigen-driven” refers to a process in which antigen binds immunoglobulin on the surface of B lymphocytes, thereby stimulating the cells to proliferate.
The higher the affinity of the surface immunoglobulin for the antigen, the more strongly the cells are stimulated and the more they proliferate.
In the presence of the stimulating antigen, there is a continuous selective pressure favoring B cells that display on their surface and secrete immunoglobulins with high affinity for that antigen.
Thus, B cells expressing antibodies with a higher affinity for the antigen will outcompete those with weaker affinities for function and survival.
In general, this antigen-driven process can occur only in B lymphocytes that are being stimulated by T lymphocytes as well as by antigen. This process is known as T-lymphocyte help. Figure 2 shows a B cell and a T cell interacting and stimulating each other. T-cell cytokines affect B cells by stimulating cell division, switching antibody production from IgM to IgG and promoting a change in the molecular sequence of the secreted antibody so that it binds more strongly to the driving antigen.
Thus, T-cell help makes possible the production of high-affinity IgG autoantibodies. These kinds of antibodies are closely linked to tissue damage in lupus.
The autoantigen-specific B cells and T cells that interact to produce injurious autoantibodies are absent in healthy people. Several mechanisms could account for the absence of such cells. These mechanisms include removal (deletion) of the autoreactive B cells, inactivation of the cells so that they remain in the body but are anergic, or a change in the light chain of the antibody expressed by an autoreactive B lymphocyte (so-called receptor editing) such that the antibody loses the ability to bind autoantigen.
Serum levels of interleukin-10 are consistently high in patients with lupus, and they correlate with the activity of the disease. Interleukin-10 has a number of biologic effects, including stimulation of polyclonal populations of B lymphocytes.
Blocking this cytokine could reduce the production of pathogenic autoantibodies.
This diagram summarizes the pathogenesis of lupus and the targets of some new drugs that are currently being evaluated in clinical trials.
If autoantibodies are the proximate agents of tissue damage in patients with lupus, then treatments aimed at reducing autoantibody levels could be effective.
Serum levels of interleukin-10 are consistently high in patients with lupus, and they correlate with the activity of the disease. Interleukin-10 has a number of biologic effects, including stimulation of polyclonal populations of B lymphocytes.
Blocking this cytokine could reduce the production of pathogenic autoantibodies.
This diagram summarizes the pathogenesis of lupus and the targets of some new drugs that are currently being evaluated in clinical trials.
If autoantibodies are the proximate agents of tissue damage in patients with lupus, then treatments aimed at reducing autoantibody levels could be effective.
• Routine Blood Tests
– Usually your doctor will first request a complete blood count (CBC). Your blood is made up of red blood cells, white blood cells, platelets, and serum. The complete blood count measures the levels of each. In cases of lupus, these blood tests may reveal low numbers
• Urine Tests
– Because your body’s waste is processed by the kidneys, testing a sample of urine (called a 'spot urine' test) can reveal any problems with the way your kidneys are functioning.
• Antibodies
– The antibodies your body makes against its own normal cells and tissues play a large role in lupus. Many of these antibodies are found in a panel, or group, of tests that are ordered at the same time. The test you will hear most about is called the ANA test. Antinuclear antibodies
•Other Blood Tests
–Some blood tests measure levels of proteins that are not antibodies. The levels of these proteins can alert your doctor that there is inflammation somewhere in your body.
–Complement is the name of a group of proteins that protect the body against infections. They work by strengthening the body’s immune reactions. Complement proteins are used up by the inflammation caused by lupus, which is why people with inflammation due to active lupus often have low complement levels
•Blood Clotting Time Tests
–The rate at which your blood begins to clot is important: if it clots too easily, a blood clot, called a thrombus, can break free and travel through the body. Blood clots can cause damage such as a stroke or miscarriage. If your blood does not clot quickly enough, you could be at risk for excessive bleeding if you are injured.
•Tissue Biopsies
–The skin and kidney are the most common sites biopsied in someone who may have lupus.
–The results of the biopsy can show the amount of inflammation and any damage being done to the tissue.
–Further tests can be performed on the tissue sample to look for autoimmune antibodies and to determine whether the problem is due to lupus or is caused by some other factor, such as infection or medication.
Treatments:
• Because the symptoms of lupus vary from one person to another, the treatment of the disease is tailored to the specific problems that arise in each person
• Today, doctors are using a wide variety of medicines to treat lupus -- ranging in strength from mild to extremely strong
– Anti-Inflammatories
– Corticosteroids
– Antimalarials
– Immunosuppressives (Immune Modulators)
– Anticoagulants
• The goal of any treatment plan is to:
– reduce inflammation caused by lupus
– suppress your overactive immune system
– prevent flares, and treat them when they occur
– control symptoms like joint pain and fatigue
– minimize damage to organs
Drug-induced lupus was first identified almost 50 years ago and has been the subject of many research studies. However, the causes of this disorder are only beginning to be understood.

One view is that the offending drugs interfere with enzymes that would otherwise suppress certain genes. The result is a non-specific hyperimmune condition.
Considerable circumstantial evidence suggests that it is not the drug itself but the metabolic change the drug undergoes in the body that makes it able to react with the immune system.
One possibility is that when these drug metabolites bind to certain proteins, drug-protein complexes are produced. These then activate drug-specific lymphocytes, which damage surrounding tissue or stimulate neighboring lymphocytes.
In one mouse study, a drug metabolite was placed in the thymus (one of the main lymphoid organs that forms T lymphocytes). The result was production of the type of autoantibodies that are seen in drug-induced lupus. These findings point to the human thymus as the place where the DILE process begins.
It is possible that more than one process causes drug-induced lupus. Although most cases of SLE probably arise spontaneously, the similarities in the signs and symptoms between SLE and DILE suggest that similar immune problems are involved in both diseases. The ANAs in drug-induced lupus are primarily autoantibodies that are able to react with a histone-DNA complex, which is the major component of the nucleus of all cells.

A special laboratory test to detect certain antibodies to this histone-DNA complex is a sensitive marker for lupus-like disease brought on by many drugs Treatments Lab Results Lupus Environment Signs and Symptoms of Lupus Diagnosis Case Study The naming of the disease dates back to the 13th century. The physician Rogerius thought the facial lesions characteristic of the cutaneous form of the disease reminiscent of a wolf's bite and so named the disease Lupus which is Latin for wolf. These lesions were described in 1833 by Cazeneva as "erythema centrifugum" while the distinctive malar or "butterfly rash" was first described by Ferdinand von Hebra in 1846. The first illustrations of the Lupus Erythematosus was in von Hebra's 1856 book "The Atlas of Skin Diseases"

The first recognition of systemic Lupus came in 1872 by Moriz Kaposi the son-in-law of von Hebra. Kaposi described two distinct forms of the disease; the previously described discoid or cutaneous form of the disease, and a more serious, possibly life-threatening disseminated form (SLE). Furthermore, Kaposi described symptoms of the disseminated form including subcutaneous nodules, arthritis with synovial hypertrophy, lymphadenopathy, fever, weight loss, anemia and CNS involvement.

More recently Lupus has been recognized as an autoimmune disorder with the discovery of the LE cell in 1948 by MM Hargraves et al in 1948. This cell was discovered in the bone marrow of patients with the disseminated form of the disease. The cell is described as being "the result of... phagocytosis of free nuclear material with a resulting round vacuole containing partially digested and lysed nuclear material..." The American College of Rheumatology (ACR) has developed clinical and laboratory criteria to help physicians diagnose and classify lupus. Having 4 of the 11 criteria at one time or individually over time, suggests a diagnosis of lupus.

1. Malar rash- Face rash that is butterfly shaped and covers the bridge of the nose and spreads across the cheeks
2. Scaly rash, called a discoid rash, which appears as raised, scaly patches
3. Sun-related rash, which appears after exposure to sunlight
4. Mouth sores, which are usually painless
5. Joint pain and swelling that occurs in two or more joints
6. Swelling of the linings around the lungs or the heart
7. Kidney disease
8. A neurological disorder, such as seizures or psychosis
9. Low blood counts (RBC,WBC, PLT)
10. Positive antinuclear antibody tests, which indicate that you may have an autoimmune disease
11. Other positive blood tests that may indicate an autoimmune disease, such as a positive double-stranded anti-DNA test, positive anti-Sm test, positive anti-phospholipid antibody test or false-positive syphilis test Laboratory tests Blood tests:

Complete blood count:
Results may indicate anemia, which commonly occurs in lupus. A low white blood cell or platelet count may occur in lupus as well.

Erythrocyte sedimentation rate:
This blood test determines the rate at which red blood cells settle to the bottom of a tube in an hour. A faster than normal rate may indicate a systemic disease, such as lupus.

Blood Clotting Time Tests
Prothrombin time (PT)
Partial thromboplastin time (PTT)
Urinalysis

An examination of a sample urine may show increased protein levels or red blood cells, which may occur if lupus has affected the kidneys. Lupus can attack the kidneys without any warning signs, so these tests are very important.

A spot urine test can reveal any problems with the way the kidneys are functioning
The most common urine tests look for cell casts, and proteinuria
A collection of urine over a 24-hour period can also give important information. Antibodies

Antibodies the body makes against its own normal cells and tissues play a large role in lupus. Many of these antibodies are found in a panel, or group, of tests that are ordered at the same time.

Antinuclear antibodies (ANA)
Antibodies that connect, or bind, to the nucleus of the cell. This process damages, and can destroy, the cells.
The ANA blood test is a sensitive test for lupus, since these antibodies are found in 97% of people with the disease.
When three or more typical features of lupus are present (such as involvement of the skin, joints, kidneys, lungs, heart, blood, or nervous system) a positive ANA test will confirm a diagnosis of lupus.

Antibodies to double-stranded DNA (anti-dsDNA)
Target the DNA inside the cell nucleus.
Anti-dsDNA antibodies are found in half of the people with lupus.
Other tests
Chest X-ray. An image of your chest may reveal abnormal shadows that suggest fluid or inflammation in your lungs. It may also show an enlarged heart as a result of a buildup of fluid within the pericardium.
Electrocardiogram (ECG). This test measures the pattern of electrical impulses generated in your heart. It can help identify irregular rhythms or damage.
Tissue Biopsies
The skin and kidney are the most common sites biopsied in someone who may have lupus.
oThe results of the biopsy can show the amount of inflammation and any damage being done to the tissue.
Other tests

Chest X-ray
Image of the chest may reveal abnormal shadows that suggest fluid or inflammation in the lungs. It may also show an enlarged heart as a result of a buildup of fluid within the pericardium.

Electrocardiogram (ECG)
Measures the pattern of electrical impulses generated in the heart. It can help identify irregular rhythms or damage.

Tissue Biopsies
The skin and kidney are the most common sites biopsied in someone who may have lupus.
The results of the biopsy can show the amount of inflammation and any damage being done to the tissue. Once diagnosed with lupus, the doctor will develop a treatment plan based on patient’s age, symptoms, general health, and lifestyle.

The goals of any treatment plan are to:
reduce inflammation caused by lupus
suppress an overactive immune system
prevent flares, and treat them when they occur
control symptoms like joint pain and fatigue
minimize damage to organs Standard Treatments Anti-Inflammatories

Anti-inflammatory medications help to relieve many of the symptoms of lupus by reducing inflammation and pain. For many people with lupus, an anti-inflammatory drug may be the only medication they need to control their lupus.

Aspirin: pain-reducing, anti-inflammatory, and anticoagulant properties that can control some of the symptoms of lupus.
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs): suppress inflammation and are especially useful for joint pain and stiffness.
Ex. ibuprofen (Motrin®) & celecoxib (Celebrex®) Corticosteroids

Drugs designed to work like the body’s naturally occurring hormones produced by the adrenal glands, in particular cortisol. Cortisol helps regulate blood pressure and the immune system, and it is the body’s most potent anti-inflammatory hormone.

Steroid medications work quickly to decrease the swelling, warmth, tenderness, and pain that are associated with inflammation. They do this by lessening the immune system’s response.

Prednisone is the most commonly prescribed steroid for lupus Antimalarials

Most often prescribed for skin rashes, mouth ulcers, and joint pain, but also can be effective in mild forms of lupus where inflammation and blood clotting are a concern.

Antimalarials improve lupus by decreasing autoantibody production, protecting against the damaging effects of ultraviolet light from the sun and other sources, and improving skin lesions.

hydroxychloroquine (Plaquenil®) and chloroquine (Aralen®) Anticoagulants

Blood clots can be a life-threatening symptom of lupus, these drugs are used to thin your blood to prevent it from clotting too easily.

Low-dose aspirin
Heparin (Calciparine®, Liquaemin®)
Warfarin (Coumadin®) Immunosuppressives

Used to control inflammation and the overactive immune system, especially when steroids have been unable to bring lupus symptoms under control, or when a person cannot tolerate high doses of steroids.

Cyclophosphamide (Cytoxan®): developed to fight cancer. It has been shown to improve kidney and lung disease.
Methotrexate (Rheumatrex™): Also developed to fight cancer, and is known as the "gold standard" for the treatment of rheumatoid arthritis. It has also been shown to be very effective in treating skin lesions, arthritis, and pleuritis in people with lupus.
Azathioprine (Imuran®): It blocks inflammation pathways in lupus and helps to lower the steroid dosage and improve liver and kidney disease. Investigational Treatments Biologics

Genetically engineered compounds that interfere with the action of cells involved in the immune response.

LJP 394 (Riquent™): may be able to block the production of the anti-double-stranded DNA (dsDNA) antibodies believed to promote lupus kidney disease, without suppressing the entire immune system or causing adverse side effects.
Atacicept (TACI-Ig): was designed to interrupt several stages of B cell development and may inhibit cells responsible for making antibodies. LymphoStat-B™
developed to disrupt activation of B lymphocytes by interfering with BLyS, a protein required for B cell activity. Several other related therapies (atacicept and belimumab) that also block B cell activation via the BLyS pathway are being tested for lupus.

Rituximab (Rituxan®, anti-CD20)
targets a specific protein known as CD20 that appears on the surface of B cells. Rituxan binds to CD20 and is believed to work with the body’s own immune system to attack and kill the marked B cells.

Epratuzumab
an anti-CD22 antibody designed to bind to the CD22 antigen on B cells and may control lupus disease by depleting B cells and by controlling or modulating B cell function. References
JAMA. 2005;293(24):3130 (doi:10.1001/jama.293.24.3130) Sarah Ringold; Cassio Lynm; Richard M. Glass http://jama.ama-assn.org/cgi/content/full/293/24/3130
Anisur Rahman, Ph.D., and David A. Isenberg, M.D. NEJM 358;9 www.nejm.org february 28, 2008
Lupus Foundation http://www.lupus.org/newsite/index.html
http://en.wikipedia.org/wiki/Lupus
Works Cited
Duncan, H. V., and G. Achara. "A Rare Initial Manifestation of Systemic Lupus Erythematosus--Acute Pancreatitis: Case Report and Review of the Literature." The Journal of the American Board of Family Medicine 16.4 (2003): 334-38. Google Scholar. Web. 10 Feb. 2011. <http://www.jabfm.org/cgi/reprint/16/4/334>.
Hochberg, MD, MPH, Marc C. "LUPUS FOUNDATION OF AMERICA - The History of Lupus Erythematosus." Lupus Foundation of America. Web. 15 Feb. 2011. <http://www.lupus.org/webmodules/webarticlesnet/templates/new_aboutintroduction.aspx?articleid=1520&zoneid=9>.
Lupus Foundation of America. Web. 13 Mar. 2011. <http://www.lupus.org/newsite/index.html>.
Ringold, MD, Sarah, and Cassio Lynm, MA. "Systemic Lupus Erythematosus, June 22/29, 2005, Ringold Et Al. 293 (24): 3130 — JAMA." JAMA, the Journal of the American Medical Association, a Weekly Peer-reviewed Medical Journal Published by AMA — JAMA. Ed. Richard M. Glass, MD. Web. 13 Feb. 2011. <http://jama.ama-assn.org/content/293/24/3130.full>.
Staff, Mayo Clinic. "Lupus - MayoClinic.com." Mayo Clinic. 20 Oct. 2009. Web. 23 Feb. 2011. <http://www.mayoclinic.com/health/lupus/DS00115>.
"Systemic Lupus Erythematosus." Wikipedia, the Free Encyclopedia. 7 Nov. 2001. Web. 02 Mar. 2011. <http://en.wikipedia.org/wiki/Lupus>. Tanya Crocker
John Lydick
Stefanie Atanasoski Complement:
Group of proteins that protect the body against infections. They work by strengthening the body’s immune reactions. Low complement levels can be found in lupus since these proteins are used up by the inflammation process caused by the disease.

C-reactive protein (CRP):
A protein produced by the liver, and high levels of CRP in the blood may indicate inflammation due to lupus.

Kidney and liver assessment:
Blood tests can assess how well the kidneys and liver are functioning. Lupus can affect these organs. Antibodies to phospholipids (aPLs)
Can cause narrowing of blood vessels, leading to blood clots in the legs or lungs, stroke, heart attack, or miscarriage.
The most commonly measured aPLs are lupus anticoagulant, anticardiolipin antibody, and anti-beta2 glycoprotein I.
Nearly 30% of people with lupus will test positive for antiphospholipid antibodies.

*Phospholipids found in lupus are also found in syphilis, and the blood test cannot always tell the difference between the two diseases.

Syphilis test: Approximately 20% of those with lupus will have a false-positive syphilis test result. Antibodies to histone
Target the protein that surrounds the DNA molecule
Sometimes found in people with systemic lupus but are more often seen in people with drug-induced lupus.

Antibodies to Sm
Target Sm proteins in the cell nucleus
Found in 30-40% of people with lupus, the presence of this antibody almost always means one has lupus. Anti-IL6
elevated levels of Interleukin 6 in blood, urine, and kidneys have been seen in people with active lupus. Treatment with anti-IL-6 may be able to suppress inflammation induced by autoreactive B cells and autoreactive T cells.

Eculizumab (anti C5a)
developed to inhibit the complement component C5. Complement is a collection of proteins that can become overactive or misdirected by autoantibodies in a disease like lupus.

Anti-IL10:
an antibody that blocks the activity of IL10, which is important in the activation of B cells in lupus. Monoclonal Antibodies

The monoclonal antibody approach has been used to target both B and T lymphocytes, the white blood cells responsible for autoantibody production in lupus.
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