Lupus Treatment: Long-Term Corticosteroid Therapy


Lupus is a chronic multisystem autoimmune disease that is characterized by immune deregulation, resulting in the production of autoantibodies, likely to lead to a multiplicity of complications that can damage the vital body organs such as heart, lungs, kidney and brain. The lupus disease manifests itself as cutaneous vasculitis, (Scopelitis, 1992).

glomerulonephritis, cardiopulmonary, and cerebrovascular. Lupus is characterized by “Flares” of activity punctuated with periods of improvement and remission. Improvement periods can last weeks, months, or even years. Although treatment for lupus is varied in its course, it has no cure. However, corticosteroids and cytotoxics have been used in the past several decades to improve the prognosis of the disease. The most commonly used corticosteroids in the treatment of Systemic Lupus Erythematosus (SLE or Lupus) are Prednisone, prednisolone, methylprednisolone, and hydrocortisone. The long-term systemic use of corticosteroids is one of the most important issues in the management of SLE due to their potential risk and benefits. (Scopelitis, 1992).

The lupus ailment is classified into three types and these are namely;

The systematic lupus erythematosus- This is the most common type of lupus and very serious of all. People with type of lupus develop rashes on the face which resemble the bite or scratch of a wolf. It is approximated that more than 15% of the people start to develop this ailment when they are teenagers. This type of lupus affects skin, joints and tendons. It may also affect vital body organs like brain, lungs, heart and kidneys.

Discoid lupus- this kind of lupus is related to skin disease and therefore causes rashes on the face, neck, scalp and ears. It is regarded to be a rare form of lupus than systematic lupus erythematosus. Almost 10% of discoid patients develop into a mild form of systematic lupus erythematosus. This type of lupus does not affect the body organs but it might leave permanent scars after healing of the rashes, (Fessel, 1975).

Discoid lupus- this kind of lupus is related to skin disease and therefore causes rashes on the face, neck, scalp and ears. It is regarded to be a rare form of lupus than systemic lupus erythematosus. Almost 10% of discoid patients develop into a mild form of systematic lupus erythematosus. This type of lupus does not affect the body organs but it might leave permanent scars after healing of the rashes.

This study focuses on the risks and benefits of corticosteroid therapy and will try to answer the question on whether the benefits of long-term corticosteroid use outweigh the risks in systemic lupus autoimmune disease. The research question of this study will therefore be:

Do the benefits of long-term prednisone therapy in the treatment of systemic lupus out weigh the negative side affects of long-term usage?

Risks and benefits of Corticosteroid Therapy

Systemic corticosteroids are important tools that are used by dermatologists to treat a large number of diseases. In dispensing this, care is taken to ensure that potential benefits are balanced against the risks, (Fessel, 1975).

Physicians and patients take care by considering both their rate of occurrence and degree of harm. These include disclosing information and discussing the risks of the therapy.

Before initiating any therapy, physicians and patients compare the inherent risk of the disease with the potential risks of the therapy. Disclosure also involve explaining the proposed treatment including prescription, monitoring and duration of therapy.

Dosing Considerations

Single-dose therapy reduces normal diurnal cortical secretion while still providing clinical efficacy. Except for osteoporosis and posterior sub capsular cataract formation, many of the common side effects associated with corticosteroid therapy are reduced or eliminated with alternate dose therapy (Gladman et al, 1980).


It is estimated that 11% to 20% of patients treated for more than one year with a dose of prednisone between 7.5 and 10 mg per day will develop skeletal fractures. Persons at greater risk include those older than 50 years of age or younger than 15, postmenopausal women, and patients who already have had fractures after minimal trauma. Patients with amenorrhea, immobilization, chronic obstructive pulmonary disease, inflammatory bowel disease, or hypogonadism (in men), or who have undergone organ transplantation are also considered to be at high risk.

An intensive prevention program that includes selecting the lowest possible steroid dose should be initiated in patients on long-term corticosteroid therapy. Calcium as well as vitamin D enhancing, sex hormone substitution, as well as burden-bearing practice program are considered first line precautionary procedures. In patients who develop hypercalciuria associated with glucocorticoid use, thiazide diuretics in conjunction with sodium restriction are recommended. For patients who are unable to take sex hormone replacement, have established osteoporosis, or continue to show deterioration in bone mineral density despite appropriate preventive therapies, other agents such as bisphosphonates or calcitonin are indicated, (Gladman et al, 1980).

Avascular Necrosis (Osteonecrosis)

Osteonecrosis is a serious complication of corticosteroid therapy. Although the risk of osteonecrosis is greater with prolonged (months to years) high-dose therapy, there have been reports of osteonecrosis with short-term, very-high-dose therapy. Intra-articular injection and topical application of corticosteroid have also been associated with the development of osteonecrosis. Most reported cases have been in patients receiving corticosteroids for noncutaneous conditions, such as inflammatory bowel disease and systemic lupus erythematosus. Bone pain is usually the first symptom of osteonecrosis and precedes radiological signs by up to six months, (Bernardine and Roberts1975).

MRI is a specific and sensitive method for early diagnosis. Treatment of early-stage disease usually involves medical management and surgical core decompression; advanced osteonecrosis commonly requires total hip replacement.

Avoidance of other risk factors for osteonecrosis, such as alcohol and tobacco, and prevention of trauma are recommended for patients on long-term corticosteroid therapy. MRI testing may help in the early diagnosis of patients who develop bone pain.

Ophthalmological Complications: Cataracts and Glaucoma

Cataracts: Development of posterior sub capsular cataracts is not rare, occurring in approximately 40% of patients with rheumatoid arthritis treated with corticosteroids. Patients at greater risk include children and those taking 10 mg or more of prednisone per day for one year or more. Alternate-day schedules do not appear to reduce the risk of cataract development. A slit-lamp examination at baseline and every 6 to 12 months thereafter is recommended for patients on long-term glucocorticoid therapy.


Increased intraocular pressure may develop in patients using oral glucocorticoids, especially those with a personal or family history of glaucoma, diabetes mellitus, or myopia.


Because corticosteroids are immunosuppressive, it has been thought that patients on long-term corticosteroid therapy may have an increased susceptibility to many bacterial, fungal, viral, and parasitic infections, (Ginzlerand Berg, 1992).

However, studies of large groups of patients receiving low-dose chronic therapy have not demonstrated a significantly increased risk. Further, the risk of developing active tuberculosis while taking glucocorticoids is lower than previously suspected. Nevertheless, it is recommended that adult patients who are severely immunocompromised (those taking large amounts of corticosteroids) should receive routine immunization with the following vaccines: tetanus/diphtheria (Td), Haemophilus influenzae B (Hib), pneumococcus, and influenza.

If healthy household members or other close contacts of severely immunocompromised patients have been immunized against polio, the patient should be given inactivated polio vaccine to avoid spread of live oral polio virus. Live-virus vaccine should not be given until three months after discontinuation of high-dose corticosteroid therapy.

Corticosteroid therapy is not considered to result in significant immunosuppression when it is given short term (less than two weeks), in low to moderate doses (less than 1 mg/kg per day of prednisone or equivalent), or as alternate-day treatment with short-acting preparations, as maintenance therapy at physiologic doses, or when it is administered topically or by intra-particular, bursal, or tendon injection.


The use of long term corticosteroids therapy in the treatment of lupus has both risks and benefits. However, when compared, the risks outweigh the benefits. These calls for further research in the field of corticosteroids therapy to find alternatives that could minimize the risks and bring a balance, (Bernardine and Roberts1975). The answer therefore, to the question whether the benefits of long-term use of corticosteroids outweigh the risks in systemic lupus autoimmune disease is yes.


It is very important for patients undergoing corticosteroid therapy to get thorough information from their physician both before and during the therapy. It is imperative for the patients to talk with the doctors to avoid dangerous scenarios that might arise later. Since knowledge is power, an informed patient is in a good position to get details about the available treatments.


  1. Ginzler, E and Berg, A (1992). Mortality in systemic lupus erythematosus. 3(14), 218–228
  2. Bernardine, HB and Roberts, WC (1975). The heart in systemic lupus erythematosus and the change induced in it by corticosteroid therapy. 2(58), 243–284
  3. Gladman D, et al (1980). Guidelines for the management of systemic lupus erythematosus in adults. 4(60), 74-90.
  4. Fessel, WJ (1975). Systemic lupus erythematosus in the community. Incidence, prevalence, outcome, and first symptoms; the high prevalence in black women.1 (34), 102-120.
  5. Scopelitis, E 3rd ed. (1992). Systemic lupus erythematosus. In: Hurst JW, ed. Medicine for the practicing physician. Boston: Butterworth-Heinemann.

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