What is lupus and what causes it?
Systemic lupus erythematosus is an autoimmune disease. We call autoimmune diseases those in which the body’s defense mechanisms designed to defend us from external aggressions, for reasons not well known, begin to target and attack the body itself. In the case of systemic lupus erythematosus we know that there is a hereditary basis to the disease as demonstrated by the familial aggregation of cases and the relationship between this disease and other autoimmune diseases, although we do not know the exact mechanisms by which this alteration is set in motion.
What are the symptoms?
The symptoms of the disease are very varied because these auto-antibodies, which are the products of the defense mechanisms that attack the organism, can target a multitude of organs and systems. In any case, the most common symptoms are skin lesions, especially photosensitivity of reactions to the sun, joint pain with arthralgias, arthritis, frequent myalgias, although a multitude of symptoms may appear such as inflammation of the serosae, pleura, pericardium, kidney involvement, neurological involvement, although all the more severe forms of the disease are much less frequent. The vast majority of patients have either skin lesions or skin lesions plus joint pain plus biological alterations.
What is the treatment and what is new?
When we diagnose a patient with systemic lupus erythematosus the first thing to say is whether or not they need treatment. Not all patients need treatment, but all patients should be monitored. There are patients for whom an annual follow-up visit is more than enough. Patients with very mild forms of the disease such as joint or skin lesions can do very well with a very old known and widely used drug which is hydroxychloroquine sometimes combined with small doses of corticosteroids or anti-inflammatory drugs at specific times. If the disease affects other organs and the risk of complication is a little higher, corticosteroids at higher doses can be added to hydroxychloroquine and sometimes we use immunosuppressants such as azatriopine. Currently, in more severe cases which, I repeat, are less frequent, we use corticosteroids at very high doses, sometimes immunosuppressants such as cyclophosphamine and sometimes monoclonal antibodies such as rituximab has been used recently. A new monoclonal antibody, belimumab, which is indicated for patients who have used azatriopine or mycophenolate, have not controlled the disease and have positive anti-DNA antibodies, i.e. a small specific group of patients who can benefit from the use of monoclonal antibodies, has recently been accepted by the Spanish drug agency.