Systemic Lupus Erythematosus (SLE) is a chronic autoimmune condition where the immune system mistakenly attacks healthy tissues throughout the body, causing widespread inflammation. Asthma is a chronic inflammatory disease specific to the airways, characterized by narrowing and hyper-responsiveness of the bronchial tubes. Although SLE does not directly cause asthma attacks, a strong clinical and biological association exists between the two conditions. This overlap stems from shared genetic predispositions, common environmental triggers, and underlying similarities in immune system dysfunction.
Statistical Links and Shared Risk Factors
Epidemiological studies consistently show a higher prevalence of asthma among people living with SLE compared to the general population. Individuals with lupus are more than twice as likely to be diagnosed with asthma. While asthma affects less than 10% of the general adult population in the United States, nearly 20% of lupus patients report having asthma.
This suggests both conditions share risk factors. Genetic factors play a role, as certain human leukocyte antigen (HLA) genes are associated with both autoimmune and allergic conditions. Environmental triggers, such as exposure to smoking or air pollutants, can also influence the development and severity of both diseases.
This increased risk is bidirectional: people with asthma also have a greater chance of developing lupus later in life. Common coexisting conditions like allergic rhinitis and chronic sinusitis are frequently observed in both patient groups.
Overlapping Immunological Mechanisms
The connection between lupus and asthma is rooted in shared inflammatory pathways and T-helper cell imbalances within the immune system. Lupus is a disease of systemic inflammation, and the constant activity of the immune response can influence the development of localized inflammation in the airways. Both conditions feature dysregulation of T helper cells, which coordinate the immune response.
Asthma is often driven by a Type 2 immune response, characterized by the activation of T helper 2 (Th2) cells and the release of cytokines like interleukin (IL)-4, IL-5, and IL-13. These signaling molecules promote allergic inflammation, IgE production, and the recruitment of eosinophils to the airways. Lupus involves more complex Th cell activity, but elevated levels of Th2-associated cytokines, including IL-4 and IL-5, have also been observed in lupus patients.
The systemic inflammation characteristic of lupus also involves other pro-inflammatory cytokines, such as IL-6, IL-17, and Tumor Necrosis Factor-alpha (TNF-alpha), which are increased in lupus patients. These molecules contribute to the overall inflammatory state and can indirectly enhance the hyper-responsiveness seen in asthmatic airways. The systemic immune hyperactivity, including B-cell overactivity and autoantibody production seen in SLE, can potentially trigger or amplify allergic-type inflammation in the lungs.
The overlap suggests that the underlying biological mechanisms are not entirely separate but represent different manifestations of broad immune system dysregulation. The persistent inflammatory state from lupus may lower the threshold for airway inflammation, making the individual more susceptible to developing clinical asthma.
Lupus-Related Lung Conditions That Mimic Asthma
A significant clinical challenge is that several lupus manifestations in the lungs can produce symptoms—such as shortness of breath, cough, and chest tightness—that are easily mistaken for asthma exacerbations. One of the most common issues is pleuritis, which is the inflammation of the pleura, the double-layered membrane surrounding the lungs. This condition causes sharp chest pain that worsens with deep breaths or coughing due to the inflamed membranes rubbing against each other.
Lupus can also cause acute lupus pneumonitis, an acute inflammation of the lung tissue itself, which occurs in a small percentage of patients. Symptoms include severe shortness of breath, cough, and sometimes coughing up blood, requiring immediate treatment. A less common, but serious, complication is Shrinking Lung Syndrome (SLS), which involves reduced lung volume due to weakness or dysfunction of the diaphragm muscle. SLS causes progressive shortness of breath and a restrictive pattern on pulmonary function tests. The treatment for these lupus-specific complications, which involves high-dose corticosteroids or other immunosuppressive agents, is distinct from the bronchodilators and inhaled steroids used for standard asthma. Correct diagnosis is important to ensure the appropriate course of therapy is initiated.
Management Strategies for Coexisting Conditions
Managing a patient with both SLE and asthma requires a coordinated approach between rheumatologists and pulmonologists to address both the systemic autoimmunity and the airway inflammation. The treatment plans often intersect, as many medications used to control lupus activity also target the underlying inflammation common to both diseases. Systemic immunosuppressive therapies, such as corticosteroids, mycophenolate mofetil, and cyclophosphamide, are used to treat lupus flares and lung involvement like pneumonitis.
These lupus-focused treatments can reduce the systemic and localized inflammation that contributes to asthma symptoms. For instance, corticosteroids used for lupus can simultaneously dampen the inflammatory response in the airways. Conversely, some asthma treatments, such as the biologic medication omalizumab (which targets immunoglobulin E), have shown potential in improving lupus activity in some patients. Careful selection of asthma medications is necessary to ensure they do not complicate lupus treatment or disease activity. The goal is to control airway inflammation and hyper-responsiveness with standard asthma therapies while managing the systemic autoimmune activity of lupus.