Background

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the loss of self-tolerance and development of nuclear autoantigens and immune complexes which resulted in the inflammation in multiple organs.

More commonly it is known a lupus.

SLE triggered inflammation may disturb several body vital organs and systems including joints, skin, kidneys, brain, heart and lungs.

SLE is one of the most heterogeneous illness and a systemic autoimmune disease for treatment by a physicians.

Due to underlying heterogeneity, there is big challenges in diagnosis, treatment, and therapeutic progresses in SLE.

Despite of different hurdles, the survival rate of SLE patients has significantly improved from 50% in the pre-corticosteroid era to 85–95% in the modern era.

SLE is most common in women compared to men.

Monozygotic twins have a 20%–40% higher danger of developing SLE, whereas there is only 2%–5% higher risk in heterozygous individuals.

One can read the most recent research article “Novel paradigms in systemic lupus erythematosus” for better the understanding about SLE which gor published in journal, Lancet.

Systemic lupus erythematosus symptoms

Some of the common systemic lupus erythematosus symptoms and signs are fatigue, fever, joint pain, stiffness and swelling, Skin lesions which get worsen with sun exposure i.e due to photosensitivity.

One of the most characteristic symptoms of systemic lupus erythematosus is a facial rash that look like the wings of a butterfly unfolding across both cheeks and bridge of the nose.

SLE Pathogenesis

SLE has long been recognized to have a heritable component, environmental component and sometimes physiological component such as hormone.

Environmental factors (such as UV exposure, smoking, medications, viruses, low vitamin D levels and environmental pollutants) and epigenetic modification play significant role in SLE pathogenesis. Some of the common factor associated to SLE includes;

  • Non-exclusive genetic association with HLA-DR3 and HLA-DR15 heterozygosity and other risk alleles such as PTPN22.
  • Myeloid lineage cells such as dendritic cells, plasmacytoid dendritic cells and lymphoid lineage cells such as T cells, plasma and B-cell subsets
  • Imbalances in proinflammatory versus anti-inflammatory cytokines and chemokines
  • Heterogeneity in the frequency and functionality of regulatory T- and B –cells

Treatments for systemic lupus erythematosus

Therapeutic approaches predominantly involve immunomodulation and immunosuppression. 

Some of the common option for treatment of systemic lupus erythematosus are usage of; Anti-inflammatory drugs (such as Acetaminophen, Aspirin, Ibuprofen and Naproxen), Antimalarial drugs such as Hydroxychloroquine (they might help with skin rashes, mouth sores, and joint pain), Corticosteroids such as (they work fast to ease swelling, warmth, and soreness in joints which is caused by inflammation and this way prevent long-term organ damage).

Some of the commonly used Immunosuppressants for treatment systemic lupus erythematosus includes; azathioprine, mycophenolate mofetil and cyclophosphamide.

Each of these options have their own advantage and disadvantages.

Since, B cells are at the center of SLE pathogenesis, so the agents which target B-cells will be a better immune cell targeted therapies.

Some of the known this targeted molecules for Systemic lupus erythematosus treatment are the monoclonal antibodies rituximab, veltuzumumab (anti-CD20), epratuzumab (anti-CD22) and belimumab (anti-BAFF).  

Avoidance of UV-light is also systemic lupus erythematosus treatments strategy.

Disclaimer: This content including advice provides a general information only. It is in no way a substitute for trained medical practitioner opinion. Always consult a specialist or your own doctor for more information. We does not claim obligation for this information.

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