pt is hvng fvr wth jnts pain since a month anable to lift her both uppr lmb

Friends today I am discussing about High uric acid problem. Patient have pain in joints in sole of feet just take pain killer never try to rule out whether uric acid is high or any other cause. I am telling in detail. Hyperuricemia (High Uric Acid) What Is Hyperuricemia? Hyperuricemia is an excess of uric acid in the blood. Uric acid passes through the liver, and enters your bloodstream. Most of it is excreted (removed from your body) in your urine, or passes through your intestines to regulate "normal" levels. Normal Uric acid levels are 2.4-6.0 mg/dL (female) and 3.4-7.0 mg/dL (male). Normal values will vary from laboratory to laboratory. Also important to blood uric acid levels are purines. Purines are nitrogen-containing compounds, which are made inside the cells of your body (endogenous), or come from outside of your body, from foods containing purine (exogenous). Purine breaks down into uric acid. Increased levels of uric acid from excess purines may accumulate in your tissues, and form crystals. This may cause high uric acid levels in the blood. Uric acid formation may occur when the blood uric acid level rises above 7 mg/dL. Problems, such as kidney stones, and gout (collection of uric acid crystals in the joints, especially in your toes and fingers), may occur. What Causes Hyperuricemia? Causes of high uric acid levels (hyperuricemia) can be primary (increased uric acid levels due to purine), and secondary (high uric acid levels due to another disease or condition). Sometimes, the body produces more uric acid than it is able to excrete. Causes of High Uric Acide Levels: Primary hyperuricemia Increased production of uric acid from purine Your kidneys cannot get rid of the uric acid in your blood, resulting in high levels Secondary hyperuricemia Certain cancers, or chemotherapy agents may cause an increased turnover rate of cell death. This is usually due to chemotherapy, but high uric acid levels can occur before chemotherapy is administered. After chemotherapy, there is often a rapid amount of cellular destruction, and tumor lysis syndrome may occur. You may be at risk for tumor lysis syndrome if you receive chemotherapy for certain types of leukemia, lymphoma, or multiple myeloma, if there is a large amount of disease present. Kidney disease - this may cause you to not be able to clear the uric acid out of your system, thus causing hyperuricemia. Medications - can cause increased levels of uric acid in the blood Endocrine or metabolic conditions -certain forms of diabetes, or acidosis can cause hyperuricemia Elevated uric acid levels may produce kidney problems, or none at all. People may live many years with elevated uric acid levels, and they do not develop gout or gouty arthritis (arthritis means "joint inflammation"). Only about 20% of people with elevated uric acid levels ever develop gout, and some people with gout do not have significantly elevated uric acid levels in their blood. Symptoms of Hyperuricemia: You may not have any symptoms. If your blood uric acid levels are significantly elevated, and you are undergoing chemotherapy for leukemia or lymphoma, you may have symptoms kidney problems, or gouty arthritis from high uric acid levels in your blood. You may have fever, chills, fatigue if you have certain forms of cancer, and your uric acid levels are elevated (caused by tumor lysis syndrome) You may notice an inflammation of a joint (called "gout"), if the uric acid crystals deposit in one of your joints. (*Note- gout may occur with normal uric acid levels, too). You may have kidney problems (caused by formation of kidney stones), or problems with urination Things You Can Do About Hyperuricemia: Make sure you tell your doctor, as well as all healthcare providers, about any other medications you are taking (including over-the-counter, vitamins, or herbal remedies). Remind your doctor or healthcare provider if you have a history of diabetes, liver, kidney, or heart disease. Follow your healthcare provider's instructions regarding lowering your blood uric acid level and treating your hyperuricemia. If your blood levels are severely elevated, he or she may prescribe medications to lower the uric acid levels to a safe range. If you have an elevated blood uric acid level, and your healthcare provider thinks that you may be at risk for gout, kidney stones, try to eat a low purine diet. Foods that are high in purine include: All organ meats (such as liver), meat extracts and gravy Yeasts, and yeast extracts (such as beer, and alcoholic beverages) Asparagus, spinach, beans, peas, lentils, oatmeal, cauliflower and mushrooms Foods that are low in purine include: Refined cereals - breads, pasta, flour, tapioca, cakes Milk and milk products, eggs Lettuce, tomatoes, green vegetables Cream soups without meat stock Water, fruit juice, carbonated drinks Peanut butter, fruits and nuts Keep well hydrated, drinking 2 to 3 liters of water per day, unless you were told otherwise. Take all of your medications for hyperuricemia as directed Avoid caffeine and alcohol, as these can contribute to problems with uric acid and hyperuricemia. Avoid medications, such as thiazide diuretics (hydrochlortiazide), and loop diuretics (such as furosemide or Lasix®). Also, drugs such as niacin, and low doses of aspirin (less than 3 grams per day) can aggravate uric acid levels. Do not take these medications, or aspirin unless a healthcare provider who knows your condition told you. If you experience symptoms or side effects, especially if severe, be sure to discuss them with your health care team. They can prescribe medications and/or offer other suggestions that are effective in managing such problems. Drugs or Treatments That May Be Prescribed by Your Doctor: Your doctor or healthcare provider may prescribe medications if you have a high blood uric acid levels. These may include: Non-steroidal anti-inflammatory (NSAID) agents and Tylenol®- such as naproxen sodium and ibuprofen may provide relief of gout-related pain. Gout may be a result of a high uric acid level. If you are to avoid NSAID drugs, because of your type of cancer or chemotherapy you are receiving, acetaminophen (Tylenol() up to 4000 mg per day (two extra-strength tablets every 6 hours) may help. It is important not to exceed the recommended daily dose of Tylenol, as it may cause liver damage. Discuss this with your healthcare provider. Uricosuric Drugs: These drugs work by blocking the reabsorption of urate, which can prevent uric acid crystals from being deposited into your tissues. Examples of uricosuric drugs include probenecid, and sulfinpyrazone. Xanthine oxidase inhibitors - Such as allopurinol, will prevent gout. However, it may cause your symptoms of gout to be worse if it is taken during an episode of painful joint inflammation. Allopurinol may also be given to you, if you have a certain form of leukemia or lymphoma, to prevent complications from chemotherapy and tumor lysis syndrome - and not necessarily to prevent gout. With high levels of uric acid in your blood, as a result of your disease, the uric acid will collect and form crystals in your kidneys. This may occur during chemotherapy, and may cause your kidneys to fail. When to Contact Your Doctor or Health Care Provider: Localized joint pain (especially in a toe or finger joint), that is red and inflamed. Shortness of breath, chest pain or discomfort; should be evaluated immediately. Feeling your heart beat rapidly (palpitations). Bleeding that does not stop after a few minutes. The top five homeopathic medicines for elevated uric acid levels include Colchicum, Benzoic Acid, Ledum Pal, Guaiacum, and Lithium Carb. Colchicum – Homeopathic Medicine for Uric Acid Colchicum Autumnale (commonly known Meadow Saffron) is a homeopathic remedy derived from the freshly dug up bulb of herb colchicum autumnale. This herb belongs to the family Liliaceae and is a native of Great Britain and Ireland. Colchicum is especially indicated in cases where high uric acid levels give rise to the onset of gout. There may be a sharp pain in the great toe. The affected parts may be swollen and very hot to touch. There could be great sensitivity to touch along with extreme pain. The pains could be more intense in the evening and at night. Colchicum may be indicated almost as a specific medicine in most cases of high uric acid levels. Slightest effort to move the legs gives rise to a sharp, shooting and unbearable pain in the toe. Walking may also be difficult. The person needing this remedy has intense swelling and pain in the big toe that is worse from motion. The toe pain also worsens from slightest touch, with the tendency of evening aggravation of the toe pain. Benzoic Acid – Homeopathic Medicine for Uric Acid When Signs Show up In Urine Benzoic Acid is homeopathic medicine for uric acid that is indicated when the signs of high uric acid show urinary symptoms. Uric acid crystals may be deposited in the kidneys or the urinary tract, giving rise to stones. On examination, the urine may exhibit very high levels of uric acid. The color of urine may also keep changing from dark brown to pale yellow. Benzoic acid may also be indicated when there are joint complaints, like a crackling sensation in the joints. The great toe may be swollen, causing difficulty in walking or even moving the limb. Cracking in the knee joint on movement may also be felt. In some cases, nodes from the deposition of urate crystals may be present on the knees. Homeopathic medicine Benzoicum Acidum also works well in cases of knee pain gets worse from drinking wine. It is also indicated as a general medicine in all cases of raised uric acid levels. Ledum Pal – Homeopathic Medicine for Uric Acid with Ankle Pain Ledum Palustre is a homeopathic medicine derived from a small flowering shrub, commonly known as Marsh tea. Marsh tea is a low growing evergreen shrub that only grows up to a height of one meter. The shrub belongs to the heath family and is a native of northern Europe. It is also widely distributed in British America and around Canadian lakes. Ledum pal is indicated when the high levels of uric acid in the blood result in the deposition of the crystals in the joint spaces. The first attack of pain could be triggered by an increased intake of meat or alcohol. Ledum Pal is a very beneficial homeopathic medicine for gout leading to ankle pain. The person needing Ledum Pal has pain and swelling in the ankle. The pain from the ankle may radiate up the leg, and movement tends to intensify the ankle pain. Guaiacum – Homeopathic Medicine for Uric Acid Homeopathic medicine Guaiacum is prepared from the resin obtained from the woods of Guaiacum officinale. Commonly known as Lignum Vite Resin, it belongs to the family Zygophyllaceae and is a native of tropical America. It is a well-indicated remedy to treat high uric acid levels and works well in chronic cases where the deformities and contractures set in. Intolerance to heat in any form, the affecting joints being extremely hot to touch, bad smell from the body are other symptoms. It is given in acute cases where the affected limb is painful, stiff and immobile. Lithium Carb – Homeopathic Medicine for Uric Acid with Stiffness Lithium Carb is a homeopathic medicine used to treat raised uric acid levels. The high levels of uric acid give rise to an unusual stiffness all over the body. Another peculiar feature is itching all over the skin of the joints. The pains are relieved by pouring hot water. Uric acid may get deposited in the joint spaces to give rise to nodosities which can be felt externally. The nodes may also be felt in the finger joints. In severe cases, they may be felt in the ear pinna

35 years old female suffering from recurrent painless nonitchy swelling for last 5 years. No h/o respiratory distress. No family history of such lesions. She is a known Hypertensive and for that she is on Telmisertan 40 mg/day. Patient has been treated with Levocetirizine 10mg twice a day for six months and Monteleukast 10 mg at night for six months, but no relief. Only responding to short courses of systematic Steroid 2 mg /kg with tapering dose. 1). Diagnosis 2). D/D 3). Investigations 4). Management. Please give your answers in chronological order.

A close relative (53yrs, female, hypertensive, no history of diabetes and tobacco) was admitted in ICU for 15 days due to severe viral pneumonia/ARDS. The pneumonia is now almost cured, but the patient has developed these gangrene like dead cells on her fingers. Most likely cause is a thrombus developed in wrist due to pic line used during pneumonia treatment. The vascular surgeons took a call to not take surgical intervention at that time due to severity of lung damage and started heparin. She is out of ICU for last 1 week, but still getting fever multiple times everyday. All the blood tests for bacterial infections are coming negative. The doctors at the hospital are saying that they will wait for sometime and then probably amputate the affected area. Is there any way to heal this without surgery? Also, could gangrene be cause of fever? Edit: I have attached the image of Doppler report. Also heparin is going on for last 20 days.

Lupus is a chronic autoimmune disease in which the body’s immune system becomes hyperactive and attacks normal, healthy tissue. This results in symptoms such as inflammation, swelling, and damage to joints, skin, kidneys, blood, the heart, and lungs. Under normal function, the immune system makes proteins called antibodies in order to protect and fight against antigens such as viruses and bacteria. Lupus makes the immune system unable to differentiate between antigens (a substance capable of inducing a specific immune response) and healthy tissue. This leads the immune system to direct antibodies against the healthy tissue – not just antigens – causing swelling, pain, and tissue damage. History The history of lupus can be divided into three periods: classical, neoclassical, and modern. This article concentrates on developments in the present century which have greatly expanded our knowledge about the pathophysiology, clinical-laboratory features, and treatment of this disorder. Lupus in the classical period (1230-1856) The history of lupus during the classical period was reviewed by Smith and Cyr in 1988. Of note are the derivation of the term lupus and the clinical descriptions of the cutaneous lesions of lupus vulgaris, lupus profundus, discoid lupus, and the photosensitive nature of the malar or butterfly rash. The word ‘lupus’ (Latin for ‘wolf’) is attributed to the thirteenth century physician Rogerius who used it to describe erosive facial lesions that were reminiscent of a wolf’s bite. Classical descriptions of the various dermatologic features of lupus were made by Thomas Bateman, a student of the British dermatologist Robert William, in the early nineteenth century; Cazenave, a student of the French dermatologist Laurent Biett, in the mid-nineteenth century; and Moriz Kaposi (born Moriz Kohn), student and son-in-law of the Austrian dermatologist Ferdinand von Hebra, in the late nineteenth century. The lesions now referred to as discoid lupus were described in 1833 by Cazenave under the term “erythema centrifugum,” while the butterfly distribution of the facial rash was noted by von Hebra in 1846. The first published illustrations of lupus erythematosus were included in von Hebra’s text, Atlas of Skin Diseases, published in 1856. Lupus in the neoclassical period (1872- 1948) The Neoclassical era of the history of lupus began in 1872 when Kaposi first described the systemic nature of the disorder: “…experience has shown that lupus erythematosus … may be attended by altogether more severe pathological changes, and even dangerous constitutional symptoms may be intimately associated with the process in question, and that death may result from conditions which must be considered to arise from the local malady.” Kaposi proposed that there were two types of lupus erythematosus; the discoid form and a disseminated (systemic) form. Furthermore, he enumerated various signs and symptoms which characterized the systemic form, including: subcutaneous nodules arthritis with synovial hypertrophy of both small and large joints lymphadenopathy fever weight loss anemia central nervous system involvement The existence of a systemic form of lupus was firmly established in 1904 by the work of Osler in Baltimore and Jadassohn in Vienna. Over the next thirty years, pathologic studies documented the existence of nonbacterial verrucous endocarditis (Libman-Sacks disease) and wire-loop lesions in individuals with glomerulonephritis; such observations at the autopsy table led to the construct of collagen disease proposed by Kemperer and colleagues in 1941. This terminology, ‘collagen vascular disease,’ persists in usage more than seventy years after its introduction. Lupus in the modern era (1948-present) The sentinel event which heralded the modern era was the discovery of the LE cell by Hargraves and colleagues in 1948. The investigators observed these cells in the bone marrow of individuals with acute disseminated lupus erythematosus and postulated that the cell “…is the result of…phagocytosis of free nuclear material with a resulting round vacuole containing this partially digested and lysed nuclear material…”. This discovery ushered in the present era of the application of immunology to the study of lupus erythematosus; it also allowed the diagnosis of individuals with much milder forms of the disease. This possibility, coupled with the discovery of cortisone as a treatment, changed the natural history of lupus as it was known prior to that time. Two other immunologic markers were recognized in the 1950s as being associated with lupus: the biologic false-positive test for syphilis and the immunofluorescent test for antinuclear antibodies. Moore, working in Baltimore, demonstrated that systemic lupus developed in 7 percent of 148 individuals with chronic false-positive tests for syphilis and that a further 30 percent had symptoms consistent with collagen disease. Friou applied the technique of indirect immunofluorescence to demonstrate the presence of antinuclear antibodies in the blood of individuals with systemic lupus. Subsequently, there was the recognition of antibodies to deoxyribonucleic acid (DNA) and the description of antibodies to extractable nuclear antigens (nuclear ribonucleoprotein [nRNP], Sm, Ro, La), and anticardiolipin antibodies; these autoantibodies are useful in describing clinical subsets and understanding the etiopathogenesis of lupus. The Lupus Erythematosus cell is discovered. This discovery ushered in the present era of the application of immunology to the study of lupus erythematosus; it also allowed the diagnosis of individuals with much milder forms of the disease. This possibility, coupled with the discovery of cortisone as a treatment, changed the natural history of lupus as it was known prior to that time. Two other immunologic markers were recognized in the 1950s as being associated with lupus: the biologic false-positive test for syphilis and the immunofluorescent test for antinuclear antibodies. Moore, working in Baltimore, demonstrated that systemic lupus developed in 7 percent of 148 individuals with chronic false-positive tests for syphilis and that a further 30 percent had symptoms consistent with collagen disease. Friou applied the technique of indirect immunofluorescence to demonstrate the presence of antinuclear antibodies in the blood of individuals with systemic lupus. Subsequently, there was the recognition of antibodies to deoxyribonucleic acid (DNA) and the description of antibodies to extractable nuclear antigens (nuclear ribonucleoprotein [nRNP], Sm, Ro, La), and anticardiolipin antibodies; these autoantibodies are useful in describing clinical subsets and understanding the etiopathogenesis of lupus. Genetic component recognized The familial occurrence of systemic lupus was first noted by Leonhardt in 1954 and later studies by Arnett and Shulman at Johns Hopkins. Subsequently, familial aggregation of lupus, the concordance of lupus in monozygotic twin pairs, and the association of genetic markers with lupus have been described over the past twenty years. Molecular biology techniques have been applied to the study of human lymphocyte antigen (HLA) Class II genes to determine specific amino acid sequences in these cell surface molecules that are involved in antigen presentation to T-helper cells in individuals with lupus. These studies have resulted in the identification of genetic-serologic subsets of systemic lupus that complement the clinico-serologic subsets noted earlier. It is hoped by investigators working in this field that these studies will lead to the identification of etiologic factors (e.g., viral antigens/proteins) in lupus. Over the last decade or so, we have witnessed significant advances in the understanding of the genetic basis of lupus, and of the immunological derangements which lead to the clinical manifestations of the disease. Advances have been made in the assessment of the impact of the disease in general, and in minority population groups, in particular and efforts are being made towards defining lupus biomarkers which may help both to predict disease outcome and to guide treatments. Prevalence and incidence Lupus appears to be a relatively uncommon disease. The prevalence has been estimated in several different countries mostly, however, in the developed world, using different techniques of case ascertainment. The authors of one metaanalysis (including those studies in Europe and North America) suggested an overall weighted mean prevalence of 24/100,000 population.Three English studies have produced prevalence estimates of: 12/100,000, 25/100,000 and 28/100,000 and the only study in N Ireland estimated a rate of 254/100,000. Studies in countries which include predominantly white populations have resulted in lower prevalence estimates (e.g. England) when compared with studies among populations with a significant proportion of Afro-Caribbeans, Asians and Hispanics. It is more difficult to estimate incidence for a rare disease but studies in both North America and Europe have produced estimates that are similar (approximately 1 – 8 cases per 100,000 persons per year).The lowest rates of incidence were seen among Caucasian Americans, Canadians and Spaniards and the highest rates among Asian (10.0 cases /100,000) and Afro-Caribbean (21.9 cases /100,000) residents of the UK. In an average UK practice list of 3000 patients, therefore, a GP would not expect to see a new case of lupus more often than every 7-10 years. Types There are three main types of lupus: Systemic lupus erythematosus (eh-RITH-eh-muh-TOE-sus) is the most common form. It’s sometimes called SLE, or just lupus. The word “systemic” means that the disease can involve many parts of the body such as the heart, lungs, kidneys, and brain. SLE symptoms can be mild or serious. Systemic lupus Discoid lupus erythematosus mainly affects the skin. A red rash may appear, or the skin on the face, scalp, or elsewhere may change color. Discoid lupus Drug-induced lupus is triggered by a few medicines. It’s like SLE, but symptoms are usually milder. Most of the time, the disease goes away when the medicine is stopped. More men develop drug-induced lupus because the drugs that cause it, hydralazine and procainamide, are used to treat heart conditions that are more common in men. Risk factors Risk factors for developing lupus include: Gender – more than 90% of people with lupus are women. Before puberty, boys and girls are equally likely to develop the condition Age – symptoms and diagnosis of lupus often occur between the ages of 15-45. Around 15% of people who are later diagnosed with lupus, experienced symptoms before the age of 18 Race – in the US, lupus is more common, more severe and develops earlier in African-Americans, Hispanics/Latinos, Asian-Americans, Native Americans, Native Hawaiians and Pacific Islanders than in the white population Family history – first-degree or second-degree relatives of a person with lupus have a 4-8% risk of developing lupus. One study suggests that sisters of lupus patients have as high as a 10% chance of developing lupus. In another 10-year prospective study, researchers observed a 7% incidence of lupus in first-degree relatives of lupus patients. Causes Many (but not all) scientists believe that lupus develops in response to a combination of factors both inside and outside the body, including hormones, genetics, and environment. Hormones Hormones are the body’s messengers. They regulate many of the body’s functions. Because nine of every 10 occurrences of lupus are in females, researchers have looked at the relationship between estrogen and lupus. While men and women both produce estrogen, its production is much greater in females. Many women have more lupus symptoms before menstrual periods and/or during pregnancy when estrogen production is high. This may indicate that estrogen somehow regulates the severity of lupus. However, no causal effect has been proven between estrogen, or any other hormone, and lupus. And, studies of women with lupus taking estrogen in either birth control pills or as postmenopausal therapy have shown no increase in significant disease activity. Researchers are now focusing on differences between men and women, beyond hormone levels, which may account for why women are more prone to lupus and other autoimmune diseases. Genetics Researchers have now identified more than 50 genes which they associate with lupus. These genes are more commonly seen in people with lupus than in those without the disease, and while most of these genes have not been shown to directly cause lupus, they are believed to contribute to it. In most cases, genes are not enough. This is especially evident with twins who are raised in the same environment and have the same inherited features yet only one develops lupus. Although, when one of two identical twins has lupus, there is an increased chance that the other twin will also develop the disease (30% percent chance for identical twins; 5-10% percent chance for fraternal twins). Lupus can develop in people with no family history of it, but 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 Most researchers today think that an environmental agent, such as a virus or possibly a chemical, randomly encountered by a genetically susceptible individual, acts to trigger the disease. Researchers have not identified a specific environmental agent as yet but the hypothesis remains likely. While the environmental elements that can trigger lupus and cause flares aren’t fully known, the most commonly cited are ultraviolet light (UVA and UVB); infections (including the effects of the Epstein-Barr virus), and exposure to silica dust in agricultural or industrial settings. Symptoms Lupus can have many symptoms, and they differ from person to person. Some of the more common ones are Pain or swelling in joints Muscle pain Fever with no known cause Red rashes, most often on the face (also called the “butterfly rash”) Chest pain when taking a deep breath Hair loss Pale or purple fingers or toes Sensitivity to the sun Swelling in legs or around eyes Mouth ulcers Swollen glands Feeling very tired Symptoms may come and go. When you are having symptoms, it is called a flare. Flares can range from mild to severe. New symptoms may appear at any time. Diagnosis and test Diagnosing lupus is difficult because signs and symptoms vary considerably from person to person. Signs and symptoms of lupus may vary over time and overlap with those of many other disorders. No one test can diagnose lupus. The combination of blood and urine tests, signs and symptoms, and physical examination findings leads to the diagnosis. Laboratory tests Blood and urine tests may include: Complete blood count: This test measures the number of red blood cells, white blood cells and platelets as well as the amount of hemoglobin, a protein in red blood cells. Results may indicate you have 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. The sedimentation rate isn’t specific for any one disease. It may be elevated if you have lupus, another inflammatory condition, cancer or an infection. Kidney and liver assessment: Blood tests can assess how well your kidneys and liver are functioning. Lupus can affect these organs. Urinalysis. An examination of a sample of your urine may show an increased protein level or red blood cells in the urine, which may occur if lupus has affected your kidneys. Antinuclear antibody (ANA) test. A positive test for the presence of these antibodies — produced by your immune system — indicates a stimulated immune system. While most people with lupus have a positive ANA test, most people with a positive ANA do not have lupus. If you test positive for ANA, your doctor may advise more-specific antibody testing. Imaging tests If your doctor suspects that lupus is affecting your lungs or heart, he or she may suggest: Chest X-ray. An image of your chest may reveal abnormal shadows that suggest fluid or inflammation in your lungs. Echocardiogram. This test uses sound waves to produce real-time images of your beating heart. It can check for problems with your valves and other portions of your heart. Biopsy Lupus can harm your kidneys in many different ways, and treatments can vary, depending on the type of damage that occurs. In some cases, it’s necessary to test a small sample of kidney tissue to determine what the best treatment might be. The sample can be obtained with a needle or through a small incision. Treatment and medications Treatment for lupus depends on your signs and symptoms. Determining whether your signs and symptoms should be treated and what medications to use requires a careful discussion of the benefits and risks with your doctor. As your signs and symptoms flare and subside, you and your doctor may find that you’ll need to change medications or dosages. The medications most commonly used to control lupus include: Nonsteroidal anti-inflammatory drugs (NSAIDs): Over-the-counter NSAIDs, such as naproxen sodium (Aleve) and ibuprofen (Advil, Motrin IB, others), may be used to treat pain, swelling and fever associated with lupus. Stronger NSAIDs are available by prescription. Side effects of NSAIDs include stomach bleeding, kidney problems and an increased risk of heart problems. Antimalarial drugs: Medications commonly used to treat malaria, such as hydroxychloroquine (Plaquenil), also can help control lupus. Side effects can include stomach upset and, very rarely, damage to the retina of the eye. Corticosteroids: Prednisone and other types of corticosteroids can counter the inflammation of lupus but often produce long-term side effects including weight gain, easy bruising, thinning bones (osteoporosis), high blood pressure, diabetes and increased risk of infection. The risk of side effects increases with higher doses and longer term therapy. Immunosuppressants: Drugs that suppress the immune system may be helpful in serious cases of lupus. Examples include azathioprine (Imuran, Azasan), mycophenolate (CellCept), leflunomide (Arava) and methotrexate (Trexall). Potential side effects may include an increased risk of infection, liver damage, decreased fertility and an increased risk of cancer. A newer medication, belimumab (Benlysta), also reduces lupus symptoms in some people. Side effects include nausea, diarrhea and fever. Prevention There is no known way to prevent Lupus since there is no known cause as yet. You can help manage flare-ups though: Avoid known triggers such as sunlight, stress, and lack of sleep Manage your diet Get adequate exercise