A range of autoimmune skin conditions known as cutaneous lupus erythematosus (CLE) are typified by interface dermatitis and immune complex deposition. CLE can develop as a symptom of systemic lupus erythematosus (SLE) or as a separate cutaneous condition. Because of the disease's chronicity, scarring, photosensitivity, and esthetic deformity, quality of life is greatly impacted [1-2].

In general, there are three types of CLE: acute, subacute, and chronic. The most common subtype of chronic CLE is Discoid Lupus Erythematosus (DLE). While many patients only have skin-related symptoms, a small percentage acquire systemic involvement, which calls for close observation and multidisciplinary treatment [3].

With an emphasis on the value of early diagnosis and interdisciplinary cooperation, this study attempts to assess the clinical patterns, systemic connections, and therapy approaches in CLE patients [4]. Since cutaneous symptoms commonly precede or coexist with systemic disease, dermatologists are frequently the first professionals to diagnose SLE. CLE is not uncommon; its frequency (about 70 per 100,000) and incidence (3 to 4 per 100,000) are similar to those of SLE.1 Dermatologists play a crucial role in early diagnosis and risk stratification, as up to 29% of patients with SLE initially present with skin abnormalities [5–8].

Beyond its diagnostic significance, CLE can be crippling, resulting in significant emotional anguish, discomfort, pruritus, and scarring. Controlling disease activity and preventing persistent scarring, especially in chronic types like discoid lupus, requires prompt diagnosis and therapy. Crucially, CLE is not always restricted to the skin; 10 to 25% of individuals who are first diagnosed with CLE go on to develop SLE, requiring continuous systemic assessment [9]. Early identification of systemic symptoms. Early detection of systemic symptoms such as fever, arthritis, nephritis, or serositis can facilitate timely rheumatologic referral and prevent irreversible organ damage.

An observational study was conducted at Sukhsagar Medical College, Jabalpur for 01 Year with consent of 100 patients.

Study Population

• Sample size: 100 patients
• Inclusion criteria:
• Clinically and/or histopathologically confirmed CLE
• Age ≥12 years
• Exclusion criteria:
• Drug-induced lupus
• Isolated systemic lupus without cutaneous manifestations

Data Collection

Patient records were reviewed for:

• Demographic data
• Clinical subtype of CLE
• Distribution and morphology of skin lesions
• Laboratory investigations (ANA, anti-dsDNA, complement levels)
• Systemic involvement (based on ACR/EULAR criteria)
• Treatment modalities and specialist referrals

Statistical Analysis

Data were analyzed using descriptive statistics. Results are expressed as percentages and frequencies.

Table 1: Demographic Profile of Patients (n = 100)

Table 2: Distribution of Cutaneous Lupus Subtypes

DLE predominantly involved the face and scalp, with scarring alopecia noted in 18% of cases.

Table 3: Systemic Involvement and Immunological Profile

Systemic involvement was more frequent in ACLE and SCLE compared to DLE. The clinical and immunological features of the study population. Overall, 34% of patients exhibited some form of systemic involvement. Musculoskeletal manifestations were the most common, occurring in 22% of cases, followed by renal involvement in 14% and hematological involvement in 12%. Regarding immunological findings, antinuclear antibody (ANA) positivity was observed in 68% of patients, while anti–double-stranded DNA (anti-dsDNA) antibodies were present in 36%. Low complement levels were detected in 29% of the cohort.

Table 4: Treatment Modalities and Specialist Involvement

The treatment modalities and referral patterns among the study population. Topical corticosteroids were the most frequently used therapy, administered to 92% of patients. Antimalarial therapy with hydroxychloroquine was prescribed in 74% of cases. Systemic corticosteroids were used in 38% of patients, while 26% received additional immunosuppressive agents. Regarding specialist care, 34% of patients were referred to rheumatology and 14% to nephrology services. Overall, 41% of patients required multidisciplinary management

This study highlights the heterogeneous nature of CLE, with DLE being the most common presentation, consistent with existing literature. The female predominance reflects the known autoimmune predisposition in women of reproductive age.

Approximately one-third of patients exhibited systemic involvement, emphasizing the need for routine screening for SLE in CLE patients. ANA positivity was observed in over two-thirds of patients, supporting its role as a useful screening tool, though not disease-specific[10].

Management of CLE requires a stepwise and individualized approach, beginning with photoprotection and topical therapy, progressing to systemic agents in resistant or systemic cases. The substantial proportion of patients requiring multidisciplinary care underscores the importance of collaboration between dermatologists, rheumatologists, nephrologists, and pathologists[11].

Early diagnosis, patient education regarding sun avoidance, and regular follow-up play pivotal roles in preventing disease progression and improving quality of life. Among LE non-specific, skin lesions non-scarring diffuse alopecia was more frequent (86.67%) as compared to 57% noted by Wysenbeek and 82% by Malaviya[12]. Oral ulcers were seen in this study in 56.67% of the cases as compared to 9.1% and 64% reported by Dubois and Malaviya, respectively. Raynaud’s phenomenon is a less common skin lesion in SLE. In this study, we had seen this in 6.67% of the cases, whereas Malaviya, et al. from north India and Vaidya, et al. from Western India noted[13].

Raynaud’s phenomenon in 32% and 15.5% of the cases, respectively. This variation may be attributable to the climatic condition of that particular region. We had noted two cases of pyoderma gangrenosum in the patients; it is a rare skin lesion, and may be the initial presentation of the disease. Urticaria-like skin lesions are very unusual in patients suffering from SLE but we had noted such lesions in 6.67% of the cases[14]. Dubois mentioned that development of urticaria in a patient with SLE should lead the physician to carefully evaluate that patient for active systemic disease. Bullous lesions are rare blistering conditions occurring in less than 5% of patients with SLE in isolation or in combination with other skin lesions but in this study, 10% of the patients had such lesions[15].

Bluish discoloration of the nails as noticed commonly by Kapadia, et al. was not seen in this study. Livedo reticularis, sclerodactyly, and lichen planus were not observed in this study, which also closely matched the results of the study by Watson, et al.

In some cases, skin lesions may be associated with the involvement of other organs. Vasculitic skin lesions in some cases are associated with neuropsychiatric manifestations of lupus but in this study, patients having such lesions were devoid of any overt neuropsychiatric features[16]. In this study, patients having bullous skin lesions had systemic flares that were also reported previously by Malcangi, et al.  An association between concomittant lupus nephritis and bullous lesions had been documented by Ng, et al. but no such association has been documented in this study.

Cutaneous Lupus Erythematosus presents with diverse clinical patterns and variable systemic associations. DLE remains the most prevalent subtype, while systemic involvement is more common in acute and subacute forms. Comprehensive evaluation and multidisciplinary management are essential for optimal outcomes. Regular monitoring for systemic disease should be an integral part of CLE management protocols.

Limitations

• Retrospective design
• Single-center study
• Lack of long-term follow-up data

1. Fredeau L, Courvoisier DS, Ait Mehdi R, et al. Riskfactors of progression from discoid lupus to severe systemic lupus erythematosus: a registry-based cohort study of 164 patients. J Am Acad Dermatol. 2023;88(3):551-559.
2. Yung S, Chan TM. Anti-dsDNA antibodies and resident renal cells - their putative roles in pathogenesis of renal lesions in lupus nephritis. Clin Immunol. 2017;185:40-50.
3. Liang E, Taylor M, McMahon M. Utility of the AVISE Connective Tissue Disease test in predicting lupus diagnosis and progression. Lupus Sci Med. 2020;7(1):e000345.
4. Graham RR, Ortmann W, Rodine P, et al. Speci­c combinations of HLA-DR2 and DR3 class II haplotypes contribute graded risk for disease susceptibility and autoantibodies in human SLE. Eur J Hum Genet. 2007;15(8):823-830.
5. Chen HW, Barber G, Chong BF. The genetic landscape of cutaneous lupus erythematosus. Front Med (Lausanne). 2022;9:916011.
6. Jarvinen TM, Hellquist A, Koskenmies S, et al. Polymorphisms of the ITGAM gene confer higher risk of discoid cutaneous than of systemic lupus erythematosus. PLoS One. 2010;5(12):e14212.
7. Zhu JL, O'Brien JC, Barber G, Saxena R, Chong BF, et al. Elevated serum levels of C-X-C motif chemokine ligand 10 can distinguish systemic lupus erythematosus patients from cutaneous lupus erythematosus patients. J Am Acad Dermatol. 2021;85(4):1051-1054.
8. Postal M, Vivaldo JF, Fernandez-Ruiz R, Paredes JL, Appenzeller S, Niewold TB, et al. Type I interferon in the pathogenesis of systemic lupus erythematosus. Curr Opin Immunol. 2020;67:87-94.
9. Tarazi M, Ganey RG, Kushner CJ, et al. Cutaneous lupus erythematosus patients with a negative antinuclear antibody meeting the American College of Rheumatology and/or Systemic Lupus International Collaborating Clinics criteria for systemic lupus erythematosus. Arthritis Care Res (Hoboken). 2019;71(11):1404-1409.
10. Black SM, Walocko F, Li X, Chong BF. Development of systemic lupus in patients with cutaneous lupus using the 2012 Systemic Lupus International Collaborating Clinics (SLICC) classi­cation criteria for systemic lupus erythematosus. J Am Acad Dermatol. 2021;85(1):200–202.
11. Lu Q, Long H, Chow S, et al. Guideline for the diagnosis, treatment and long-term management of cutaneous lupus erythematosus. J Autoimmun. 2021;123:102707.
12. Meroni PL, Schur PH. ANA screening: an old test with new recommendations. Ann Rheum Dis. 2010;69(8):1420-1422.
13. Tonutti E, Bizzaro N, Morozzi G, et al. The ANAre ex test as a model for improving clinical appropriateness in autoimmune diagnostics. Auto Immun Highlights. 2016;7(1):9.
14. Littlejohn E, Marder W, Lewis E, et al. The ratio of erythrocyte sedimentation rate to C-reactive protein is useful in distinguishing infection from are in systemic lupus erythematosus patients presenting with fever. Lupus. 2018;27(7):1123-9.
15. Malcangi G, Brandozzi G, Giangiacomi M, Zampetti M, Danieli MG. Bullous SLE: Response to methrotreate and relationship with disease activity. Lupus 2003;12:63-6.
16. Ng YY, Chang IT, Chen TW, Liou HN, Yang AH, Yang WC. Concomitten lupus nephritis and bullous eruption in SLE. Nephrol Dial Transplant 1999;4:1739-43.