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Perspective - (2023)Volume 8, Issue 5
Lupus, or more formally known as Systemic Lupus Erythematosus (SLE), is a complex autoimmune disease that affects millions of people worldwide. While SLE can manifest in various ways, including skin rashes, joint pain, and organ involvement, there is a distinct form of lupus known as Discoid Lupus Erythematosus (DLE) that deserves special attention.
Discoid Lupus Erythematosus is a subtype of lupus that primarily affects the skin. It is characterized by chronic inflammation that leads to distinct skin lesions, typically appearing as red, scaly, and raised patches. These lesions are often circular in shape, giving DLE its name, as "discoid" refers to a round or disk-like appearance. Unlike SLE, which can affect multiple organ systems, DLE primarily targets the skin.
Skin Lesions are the feature of DLE is the presence of skin lesions. These lesions can vary in size and location, most commonly appearing on the face, scalp, and neck. They may be red or purplish in color and covered in scales, leading to hair loss if they occur on the scalp. Individuals with DLE often experience increased sensitivity to sunlight, which can exacerbate skin symptoms. Sunscreen and protective clothing are crucial for managing this aspect of the condition. As DLE progresses, the affected skin can undergo scarring, potentially leading to permanent hair loss or disfigurement. Skin lesions can be painful and itchy, causing discomfort for those with DLE.
While DLE primarily affects the skin and SLE is a systemic condition that can involve multiple organs, there is a notable connection between the two. Discoid Lupus Erythematosus is often considered a subtype of SLE, and it can serve as an indicator of future Systemic Lupus Erythematosus development.
Both DLE and SLE can present with similar symptoms, such as skin rashes, joint pain, and photosensitivity. DLE is considered a milder, cutaneous form of lupus, while SLE can involve more severe and systemic manifestations. Approximately 5-10% of individuals with DLE eventually progress to develop Systemic Lupus Erythematosus. This transition may occur over a period of years, and it underscores the importance of close monitoring for individuals with DLE. The underlying causes of both DLE and SLE involve complex interactions between genetics and the immune system. Shared genetic and immunological factors are thought to contribute to the connection between these two conditions. Like SLE, DLE can also experience disease flares, where symptoms worsen and then improve. Managing these flares often involves similar treatments, such as corticosteroids and immunosuppressive drugs.
Diagnosing DLE and SLE typically involves a combination of clinical evaluation, medical history, and laboratory tests. A dermatologist or rheumatologist will assess the patient's symptoms and conduct a physical examination to identify skin lesions and other relevant clinical findings.
A detailed medical history is taken to understand the patient's symptoms and any family history of autoimmune diseases, as genetics can play a role in both DLE and SLE. Blood tests may be performed to detect specific antibodies associated with SLE, such as Anti-Nuclear Antibodies (ANA). Elevated ANA levels are common in SLE and may indicate the presence of systemic involvement. A skin biopsy is often performed to confirm the diagnosis of DLE. In this procedure, a small piece of affected skin is removed and examined under a microscope for characteristic changes. To diagnose SLE, doctors rely on established diagnostic criteria, such as the American College of Rheumatology (ACR) criteria, which require the presence of certain clinical and laboratory findings.
Both DLE and SLE are chronic conditions with no known cure, but there are treatment options available to manage their symptoms and prevent disease progression. Treatment for DLE include topical corticosteroids, these anti-inflammatory creams or ointments are commonly used to reduce skin inflammation in DLE. Topical calcineurin inhibitors, Drugs like tacrolimus or pimecrolimus may be prescribed to manage skin lesions in DLE.
Given the photosensitivity associated with DLE, sun protection measures, such as wearing sunscreen and protective clothing, are crucial. Intralesional steroid injections, for localized, stubborn lesions, doctors may administer steroid injections directly into the affected areas. Medications like hydroxychloroquine are used to control skin lesions and may help in preventing progression to SLE. Treatment for SLE include Nonsteroidal Anti- Inflammatory Drugs (NSAIDs), these are used to manage joint pain and inflammation in SLE. Corticosteroids like prednisone and similar drugs are prescribed to reduce inflammation and manage severe symptoms. Medications like azathioprine, mycophenolate mofetil, and methotrexate are used to suppress the overactive immune response in SLE. Hydroxychloroquine is often prescribed for its immunomodulatory effects and its role in preventing disease flares. In severe cases of SLE, biologic agents like belimumab may be considered to specifically target the immune system. Patients with SLE are encouraged to maintain a healthy lifestyle, including a balanced diet, regular exercise, and stress management. Discoid Lupus Erythematosus is a distinct subtype of lupus that primarily affects the skin, whereas Systemic Lupus Erythematosus is a more complex autoimmune disease that can impact multiple organ systems. However, the relationship between the two should not be underestimated. DLE can serve as a precursor to SLE, and shared symptoms, genetics, and immunological factors connect these conditions. It is crucial for individuals with DLE to be closely monitored by healthcare professionals and to adhere to treatment plans to manage their skin symptoms effectively and potentially prevent the progression to SLE. For those already diagnosed with SLE, early intervention and effective treatment are essential to improve the quality of life and reduce the risk of organ damage.
Citation: Digens M (2023) Discoid Lupus Erythematosus and its Correlation to Systemic Lupus Erythematosus. Lupus: Open Access. 8:261.
Received: 05-Oct-2023, Manuscript No. LOA-23-27844; Editor assigned: 09-Oct-2023, Pre QC No. LOA-23-27844; Reviewed: 23-Oct-2023, QC No. LOA-23-27844; Revised: 30-Oct-2023, Manuscript No. LOA-23-27844; Published: 06-Nov-2023 , DOI: 10.35248/2684-1630.23.8.261
Copyright: © 2023 Digens M. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.