Things to know about lupus erythematosus
One of the most common autoimmune diseases that we know is lupus erythematosus (LE). It manifests in systemic and cutaneous forms.
The disease is known to be caused by a complicated interplay of genetics, environmental factors, hormones, and even the patient’s ethnicity.
The resultant morbidity and mortality of LE has a significant impact on the quality of life of patients suffering from this disease.
Females have a higher chance of getting cutaneous LE (CLE) and systemic LE (SLE) across all age levels and ethnic backgrounds.
More often, the incidence of LE is seen in mid-adulthood, but initial onset of the disease occurs later in life (Rees et al., 2017b; Vera-Recabarren et al., 2010).
In some areas, such as in Australia, the highest incidence of SLE is seen more in Indigenous Australians and Australians with a South-Asian background (Grennan and Bossingham, 1995; Segasothy and Phillips, 2001).
In Central Australia, Indigenous Australians are 3.8 times more likely to develop SLE than their Caucasian counterparts (Segasothy and Phillips, 2001).
Indigenous Australians may not that susceptible to CLE, but this may be due to difficulties of diagnosing the condition in patients with darker skin color (Segasothy and Phillips, 2001).
Moreover, LE is caused by dysfunction within the adaptive and innate immune system.
LE begins with a loss of self-tolerance in the adaptive immune system through the production of auto antibodies.
The antibodies inappropriately react to the self-antigens present in cellular debris after apoptosis, resulting in activation and alignment of T and B cells and production of immune complexes, which end up causing direct tissue injury or damage.
A number of pro-inflammatory signalling pathways are seen exhibiting increased response to stimuli, in patients with LE, which results in increased cytokine activity.
The innate immune and complement systems are also critical for pathogen clearance, recognition of foreign antigens, and removal of apoptotic cells.
The resulting dysfunction in these two systems further causing LE manifestations.
In addition to the roles of genetics and gender in the development of CLE, it is also known that a number of potential environmental triggers causing LE have been identified through the years, by medical experts.
Several common drugs have been linked to the development SLE and CLE in some patients.
Smoking is linked with increased risk of CLE and may lead to poorer response to antimalarial treatment (Bockle and Sepp, 2015; Chasset et al., 2015).
There is also a strong link between CLE activity and ultraviolet (UV) radiation, the kind of radiation coming from sunlight.
Exposure to UV light makes cutaneous lesions worsen and can increase the chances of the appearance of symptoms such as arthralgia and fatigue to appear in patients with systemic symptoms (Kuhn et al., 2005).
CLE has occasionally been associated to malignancy.
A Swedish study of 3,663 patients with CLE showed an increased risk of lymphoma, non-melanoma skin cancer, buccal cancer, and even lung cancer with an increased risk of malignancy overall (hazard ratio: 1.8; Gronhagen et al., 2012).
The diagnosis of LE should be done swiftly by a medical professional and should be done in timely manner to prevent complications and to keep the problem from getting worse.