A handy guide to steroid therapy for arthritisThe inflammation underlying rheumatic diseases is driven by an over "anxious" immune system.
Glucocorticoids – sometimes called corticosteroids or “cortisone” are among the most potent, rapid, and reliable anti inflammatory agents available. Their beneficial effects are relatively short-lived and often overshadowed by the many potential side-effects.. Glucocorticoids are well absorbed orally. Many glucocorticoids require activation by the liver. In the blood corticosteroids are highly protein bound. Effects of glucocorticoids are far reaching. They decrease collagen synthesis and wound healing. They also promote the synthesis of glucose by the liver while at the same time increasing the accumulation of glycogen (another form of sugar) in body tissue. Simultaneously, they inhibit the action of insulin, decrease the production of fat while increasing the breakdown of fatty tissue. While the liver is stimulated to make more protein, protein is broken down at an accelerated rate in muscle. Corticosteroids also inhibit the absorption of calcium, inhibit collagen synthesis, and increase the excretion of calcium by the kidney. So how do steroids block inflammation? It appears they act at several key points in the inflammatory cascade. Steroids interfere with the ability of inflammatory cells to congregate and also block their ability to travel through blood vessel walls. Communication between inflammatory cells is also blocked. Prostaglandin synthesis is interfered with. Powerful enzymes that white blood cells ordinarily release during inflammation (superoxides) are prevented from leaving. Corticosteroids also reduce the synthesis of antibodies and suppress the immune response across the board. Remember that the adrenal glands normally produce corticosteroids in response to stress, infection, and inflammation. Corticosteroid therapy is aimed at mimicking this normal function. Unfortunately, we are not as effective as Mother Nature.
Also…while blocking inflammation is important in patients with arthritis, inflammation is an important normal process in defense and repair. The upshot of this that control of inflammation in arthritis with glucocorticoids carries a penalty- the production of unwanted side-effects. Corticosteroids are rapidly and widely distributed in tissues. They may increase the clearance of aspirin And occasionally increase the dose of warfarin needed for anticoagulation. Patients on diuretics are at increased risk of losing potassium. Patyients with chronic diseases often do not synthesize enough albumin. This is an important protein that steroids are bound to. When there is less albumin, more free corticostreroid drug is free in the system and there is the potential for more steroid toxicity. Corticosteroids may interfere with vaccination therapy. This is important because the response to killed vaccine response is less than normal, meaning a patient will not get the desired effect. And since the immune system is inhibited, live vaccines may lead to growth of the live organism in the patient. Skin testing responses are also blocked. When corticosteroids are given, the rule of thumb is this: higher and more frequent doses mean more potent and quicker effects on inflammation as well as more side-effects. Daily oral dosing in the morning is given to minimize the effect of adrenal suppression. Alternate day corticosteroids can be used for disease suppression during chronic therapy. Alternate therapy has fewer side-effects… but is also less potent. For severe rheumatic diseases, a high dose of short course therapy, can be given over 1 to 3 days. One method used is intravenous pulse therapy. High doses (1,000 mgs.) of methylprednisolone (Solumedrol) is given daily for three days. This appears to have an effect not only on acute inflammation but also on lymphocytes leading to a more potent effect on chronic inflammation as well. This allows the daily oral prednisone dose to be reduced. Adverse effects are relatively common. These compounds decrease calcium absorption from the GI tract. They also decrease collagen production by osteoblasts (cells that are responsible for making bone). Steroids shut down adrenal corticosteroid production by affecting the pituitary adrenal axis. Since adrenal steroid production is impaired, the adrenal glands will not be able to respond in the face to stressors such as illness, surgery, infection, or trauma. While alternate day therapy may decrease the risk of adrenal suppression, they do not remove it completely. Even short course or low dose corticosteroid therapy can lead to adrenal suppression. Unfortunately the positive effects of corticosteroids on inflammatory and immune responses also increase the risk of opportunistic infection. The effects of steroids on glucose and protein metabolism leads to increased blood sugar, fat deposits in undesirable areas such as the face and neck, disturbances in electrolytes in the blood, fluid retention, hypertension and elevation of blood lipids. Multiple undesirable effects occur on the skin. These include, acne, excess hair, easy bruising, decreased ability to heal, and purple stretch marks. In the eye, steroid therapy leads to cataracts and glaucoma. Muscle weakness and wasting may develop. Ulcers in the stomach develop more readily, particularly in patients treated concurrently with non steroidal anti inflammatory drugs. Pancreatitis is a complication as is accelerated hardening of the arteries. Other side effects of corticosteroids include spreading of infection, osteonecrosis (death of bone), psychiatric disturbances, bowel perforation, and masking of infection. Treatment with glucocorticoids needs to be individualized. One size does not fit all. Factors that need to be considered include: type of disease being treated, severity of condition, co-morbid conditions (other medical problems), and concomitant medications (other medicines). The dose of corticosteroids needed should be the lowest dose required for control of the disease. Adjustments in dose will vary depending on clinical response as well as laboratory results. Reductions in steroid dose need to be tailored to the situation. Abrupt decreases should be avoided since flares of disease may occur necessitating an increase in steroid dose and therefore prolongation of steroid therapy. Once steroid dosing has reached an acceptable level (and that is dependent on the rheumatologist), then conversion to an alternate day schedule may begin. Unfortunately, alternate dosing is not that effective for patient with rheumatoid arthritis and polymyalgia rheumatica. The key is to control disease.
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