Lupus
The most common form of lupus, systemic lupus erythematosus (SLE) is a chronic, relapsing, inflammatory, and often febrile multisystemic disorder of the connective tissue. Systemic lupus erythematosus (SLE) is of unknown etiology, but it is thought to result from a disorder of the immune regulation system inducing an immune response against host antigens. This leads to inflammation and irreversible damage to target organs. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.
Systemic lupus erythematosus (SLE) is estimated to affect one in a thousand whites and one out of every 250 black women from 18 to 65 years of age. Joint and muscle pains are very common symptoms of systemic lupus erythematosus (SLE), with 90 percent of patients presenting with joint and/or muscle pain. Systemic lupus erythematosus (SLE) usually pursues a chronic course and may lead to death due to lesions affecting the kidneys, the central nervous system and other vital organs.
CAUSAL FACTORS: LUPUS
The precise etiology of systemic lupus erythematosus (SLE) remains elusive. Predisposing factors for the condition include genetics (certain types of human leukocyte antigens and null complement alleles), environmental factors including exposure to the sun, hormonal factors and use of some drugs such as sulfa antibiotics.
Systemic lupus erythematosus (SLE) is accompanied by the production of abnormal antibodies by the B-cells. Some of the autoantibodies, including antidouble-stranded DNA and anti-Smith, are specific for the condition. Others, including anti-RNP, anti-Rho and anti-La, are also present in other autoimmune diseases. One focus of current research is to determine whether or not the B cells themselves are intrinsically abnormal. An underlying factor in systemic lupus erythematosus (SLE) may be apoptosis (programmed cell death). In patients with systemic lupus erythematosus (SLE), cellular antigens exposed by apoptosis elicit an immune response.*
* Casciola-Rosen L, Rosen A, Petri M, Schlissel M. Surface blebs on apoptotic cells are sites of enhanced procoagulant activity: implications for coagulation events & antigenic spread in systemic lupus erythematosus. Proc Natl Acad Sci USA 1996;93:1624-9.
TREATMENT MODALITIES: LUPUS
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MEDICATIONS: LUPUS
Treatment for systemic lupus erythematosus (SLE) patients centres on prescribing medications that successfully manage the active phase of the disease without causing long-term damage. Traditional therapy for lupus is based on corticosteroids, which suppress the overreactive immune system. Corticosteroid therapy, however, is not specific and the inevitable side effects may themselves be fatal.
This recognition has led to a change in treatment protocols, with the intent of limiting exposure to corticosteroids. Doctors are now less reluctant to use immunosuppressive drugs such as azathioprine and cyclophosphamide to treat the condition. Treatment for active systemic lupus erythematosus (SLE) differs, depending on the organs involved and the severity of the disease.
Analgesics and Anti-inflammatories
NSAIDs
Nonsteroidal anti-inflammatory drugs (NSAIDs) are a group of drugs commonly used to treat active lupus because of their analgesic, anti-inflammatory, and antipyretic properties. NSAIDs inhibit the enzymes Cox-1 and Cox-2 (cyclooxygenase), which catalyze arachidonic acid to prostaglandins and leukotrienes. Arachidonic acid is released from membrane phospholipids as a response to inflammatory stimuli. The efficacy of NSAIDs differs from patient to patient. This is likely due to the pharmacokinetic differences among the various NSAIDs.
Through their inhibition of Cox-1 enzyme, NSAIDs can cause stomach irritation, bleeding, fluid retention, and decreased kidney function. Since NSAIDs bind to plasma proteins they may be displaced by or may displace other plasma-bound drugs such as coumadin, methotrexate, digoxin, cyclosporine, oral antidiabetic agents, and sulfa drugs. This interaction can enhance the therapeutic or toxic effects of either drug.
NSAIDs (particularly indomethacin) can interfere with the pharmacologic control of hypertension and cardiac failure in patients who take beta-adrenergic antagonists, angiotensin-converting enzyme inhibitors, or diuretics.
The long-term use of NSAIDs may have a damaging effect on chondrocyte function.
Adverse effects of NSAIDs (which can occur at any time), include renal failure, hepatic dysfunction, bleeding, and gastric ulceration.
Cox-2 Inhibitors
A relatively new sub-class of NSAID, known as Cox-2 inhibitors, work by blocking cyclooxygenase 2 enzyme which is involved in the inflammation pathway. By sparing cyclooxygenase 1 (Cox-1) enzyme, gastrointestinal toxicity is purportedly reduced. Due to their proclaimed reduction of gastro-intestinal side effects, Cox-2 inhibitors have claimed a large marketshare.
Unfortunately, recent studies have indicated that Cox-2 inhibitors can increase the risk of cardiovascular problems including angina, myocardial and cerebral infarction, thrombosis and sudden death, to four times that of traditional NSAIDs. A review of more than 48,000 patients taking rofecoxib revealed that 0.52% of patients taking an inactive placebo pill had a heart attack each year. The annual rate of heart attack was 0.74% for patients taking rofecoxib. One theory for this holds that Cox-1 enzyme plays a role in preventing the clot formation that leads to cardiovascular problems.
The assertion that Cox-2 inhibitors (rofecoxib, celecoxib) do not induce haemorrhage in the upper gastro-intestinal tract, is also under dispute. While studies confirm that Cox-2 inhibitors cause fewer gastro-intestinal events than traditional NSAIDs in the short-term, it is not yet known what the long-term effects of these drugs will have on the gastric mucosa.
*Important News Release September 2004
Vioxx®, the cox-2 inhibitor made by Merck, has been pulled from the market because of severe lethal side effects due to heart attack and stroke.
Acetaminophen
Acetaminophen is often prescribed to relieve mild to moderate pain. The drug possesses analgesic and antipyretic properties, but is not an anti-inflammatory. For this reason, it may usually be safely combined with an anti-inflammatory medication.
Overdosing can cause liver damage that may be severe enough to cause liver failure and death.
This damage occurs in a dose-related manner and is the leading cause of rapid onset liver failure in the US, Canada and the UK.
For the average healthy adult, the recommended maximum dose of acetaminophen over a 24-hour period is four grams (4000 mg) or eight extra-strength pills. (Each extra-strength pill contains 500 mg and each regular strength pill contains 325 mg.) A patient who drinks more than two alcoholic beverages per day, however, should not take more than two grams of acetaminophen over 24 hours. For children, the dose is based on weight and age.
A single dose of 7 to 10 grams of acetaminophen (14 to 20 extra-strength tablets) can cause liver injury in the average healthy adult. (This amount is about twice the recommended maximum dose for a 24-hour period.) In children, a single dose of 140 mg/kg body weight of acetaminophen can result in liver injury. However, amounts of acetaminophen as low as 3 to 4 grams in a single dose or 4 to 6 grams over 24 hours, have been reported to cause severe liver injury, sometimes resulting in death. Certain individuals, for example, those who regularly drink alcohol or those with hepatitis C, are more prone than others to developing acetaminophen-induced liver damage.
Cortisone
Cortisone is a steroid that reduces inflammation and swelling and that can influence regulation of the immune system.
Chronic use of corticosteroids may result in weight gain, hypertension, susceptibility to infection, capillary fragility, acne, excess hair growth, cataracts, glaucoma, diabetes, muscular atrophy, accelerated atherosclerosis, menstrual irregularities, irritability, insomnia and psychosis. Since steroids appear to cause premature death of osteoblasts and slow their replacement; osteoporosis and bone damage are of particular concern. Long-term use may also affect brain cells, causing memory loss. Certain side effects such as hypoglycemia, edema and hypertension can be minimized by treatment.
Oral prednisone is often prescribed when the symptoms of SLE are not being controlled by other treatments and there is concern about an imminent flare-up, or when the disease is severe or life threatening. Prednisone use needs to be carefully monitored because of its many side effects, and the drug must never be stopped abruptly.
Anti-Malarials
Anti-malarial medications (hydroxychloroquine, chloroquine) help to manage the fatigue, skin rashes and joint pain associated with lupus. They may take several months to take effect.
GI intolerance is the most common side effect of anti-malarial medications. Nausea and loss of appetite are particularly common in patients on the full dose. A twice daily dose may help to avoid gastrointestinal distress.
A more serious, although rare, side effect is loss of vision. This may occur if anti-malarials are taken in high doses over a long period of time. Patients should have an eye examination prior to anti-malarial therapy and follow-ups every six to12 months.
Cytotoxic Drugs
Cytotoxic (immunosuppressive) drugs are often prescribed to control severe cases of systemic lupus erythematosus (SLE) involving major organs, or severe muscle inflammation.
Side effects include decreased blood cell counts, sterility, increased risk of infection and a risk of developing certain types of cancer. Systemic lupus erythematosus (SLE) patients receiving cytotoxic drug therapy should have regular blood tests and be monitored closely.
Substances that may help modify the disease process
Nutricol®
Available as the OTC supplement Recovery® in many pharmacies, Nutricol® is proposed to reduce the inflammation that accompanies lupus. Nutricol® (Recovery®) is an anti-catabolic agent that works at cellular level to help stabilize the tissues. Biomedica Labs also believes that this proprietary blending of plant nutrients naturally increases the cells' receptivity to hormones such as insulin which are required to speed tissue repair.
Recovery® contains the active ingredient Nutricol®, a disease modifying anti-catabolic agent (DMAC), which Biomedica Labs is proud to introduce to health care professionals.
Over the past several years veterinarians have reported that Recovery® has been used successfully to alleviate lupus symptoms in ferrets.
Biostructural® Medicine goes beyond simply addressing symptoms and focuses on the degenerative process and optimal healing.
Nutricol® (Recovery®) may be safely combined with other medications or taken on its own to help counter inflammation and improve the quality and rate of healing.
Information for Doctors: Print an 6-page detailed information package that provides the following:
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Click here to view feedback from health professionals and users about the results noted from Recovery® with Nutricol®.