International Journal of Clinical Case Reports 2018, Vol.8, No.

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Research Report Open Access

Systemic Lupus Erythematosus: A Case Report
S.L. Chavan , Yash Merchant, R.S. Deshmukh
Bharati Vidyapeeth Dental College and Hospital, Pune, Maharashtra, India
Corresponding author email: surekhachavan16@gmail.com
International Journal of Clinical Case Reports 2018, Vol.8, No.2 doi: 10.5376/ijccr.2018.08.0002
Received: 24 Jan., 2018
Accepted: 22 Feb., 2018
Published: 23 Mar., 2018
Copyright © 2018 Chavan et al., This is an open access article published under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Preferred citation for this article:
Chavan S.L., Merchant Y., and Deshmukh R.S., 2018, Systemic lupus erythematosus: a case report, International Journal of Clinical Case Reports, 8(2):
5-9 (doi: 10.5376/ijccr.2018.08.0002)

Abstract Systemic lupus erythematosus is an immunologically mediated condition. It is also called as connective tissue disease.
With more than 1.5 million people affected, it may exhibit any one of several clinicopathological forms. This condition is
characterized by the presence of abnormal antibodies and immune complex. SLE has a wide range of symptoms like joint pain, skin
rash, fever, and can affect the kidneys, lungs and nervous system. Symptoms have remission and exacerbation. Lupus is a Latin word
for ―wolf‖ and erythematosus is from the Greek word for ―red‖ and refers to the color of the rash.
Keywords Lupus erythematosus; Autoimmune disease; Collagen disorder

Background
Lupus erythematosus (L.E) is a chronic autoimmune disease in which auto-antibodies bind to components of the
cell surface, cytoplasm and nucleus, including nucleic acids and nucleoprotein particles. This antibody binding
prompts an inflammatory reaction, which leads to cell and tissue destruction (Louis and Fernandes, 2001).

L.E occurs most commonly in young women and ranges from mild cutaneous lesions and ⁄ or arthritis to renal
failure or intense nervous, cardiac and hematological disturbances (Neville et al., 2009).

L.E can manifest as different clinical forms: systemic lupus erythematosus (SLE), chronic cutaneous lupus
erythematosus and subacute cutaneous lupus erythematosus (Burge et al., 1989).

A wide spectrum of oral mucosal lesions is found in cutaneous and systemic forms of LE: cheilitis, erythematous
patches, ‗honeycomb‘ plaques, discoid lesions, lichen planus (LP)-like lesions and discrete ulcers have been
described. In established disease, reported prevalence rates range from 9% to 45% of cases (Jonsson et al., 1984;
Rowell and Goodfield, 1998) although the true figure may be nearer to 20% (Lever et al., 1983).

1 Case Report
A 33 year old female patient came to the department of Oral Patholgoy and Microbiology, Bharati Vidyapeeth
Dental College, with the chief complaint of ulcers and burning sensation in the oral cavity since last 6 months.
She also complained of pain in the joints of the lower limbs. Extra oral examination and facial appearance
appeared normal (Figure 1).

Figure 1 Frontal view

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Intraoral examination revealed reddish ulcers on the buccal mucosa, tongue, soft and hard palate (Figure 2, Figure
3, Figure 4 and Figure 5). Patient had visited a private dentist for the same and was prescribed mouthwash and
anti-inflammatory drugs with vitamins supplements but the lesion was not responding to any drug. Our
differential diagnosis was Lupus Erythematosus and Lichen Planus. Patient was advised investigations like routine
hemogram, Xray of the bone, and biopsy with anti-nuclear antibody (A.N.A) testing immuno-fluoroscence.

Figure 2 Lesion on the left buccal mucosa Figure 3 Ulcer on the ventral surface of tongue

Figure 4 Ulcers on the hard and soft palate Figure 5 Shallow ulcer on Ventral surface of the tongue

A biopsy of the representative lesion was taken under Local anesthesia under antibiotic coverage. Hemotoxylin
and Eosin (H.E) stain section showed stratified squamous epithelium with hyperkeratosis and acanthosis (Figure
6), perivascular cuffing, liquefaction degeneration of basal cell layer (Figure 7) and chronic inflammatory cells as
well as sub-epithelial vesicles (Figure 8). ANA and immune-fluroscence tests were positive (Figure 9 and Figure
10). Patient was referred to the general physician for further investigation opinion and treatment.

Figure 6 (40x) H&E showing Figure 7 (10x) H&E showing Figure 8 (4x) H&E showing
hyperkeratosis perivascular cuffing & liquefaction inflammatory cells
degeneration of basal cell layer

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Figure 9 Immunofluorescence showing mesangial deposits of IgG and C3

Figure 10 Immunofluorescence showing granular deposits of IgG

2 Discussion
SLE has a complex etiopathogenesis including genetic factors, drug induced, viral infection, sun exposure and
estrogen. Clinical features of SLE are diverse as it affects joints, lungs, nervous system, kidneys and skin. The
initial complaint starts with fever, malaise, joint pain, muscle pain and fatigue. While SLE is more common in
females than males, the symptoms associated with each sex are different. Females tend to have greater relapses,
decreased WBCs, Raynaud‘s phenomena, arthritis and psychiatric symptoms while males have kidney diseases,
serositis, skin rash and peripheral neuropathy (Long et al., 1998).

Inflammation caused by SLE may affect many parts of the body. Anemia is a common complication along with
problems in bleeding and clotting time and vasculitis. Patients with SLE are more susceptible to inflammation of
the lung. Many people with lupus complain of headache, dizziness, behavioural change and memory problems.
Kidney damage is a common complication and may lead to death. The risk of cardiovascular diseases and heart
attack is more common in SLE patients. Many studies suggested increased risk of cancer in SLE patients. Women
with lupus have increased risk of miscarriage. In the oral cavity, long term use of medication to control lupus can
cause root canal calcification, delayed tooth eruption, dilacerations of root, gingival enlargement with bleeding
and viral infections (Burnham et al., 1963).

The main differential diagnoses are Lichen Planus (L.P) and oral leucoplakia, but distinguishing between oral LE,
LP and leucoplakia can be difficult, both clinically and histologically, even when established histopathological
criteria are used (Bottomley and Goodfield, 1995).

The American College of Rheumatology has published criteria for the classification of patients as having SLE
(Figure 11). If a patient has, at any time in his or her medical history, 4 of the 11 criteria documented, the
diagnosis of SLE can be made with approximately 95% specificity and 85% sensitivity.

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Figure 11 1982 revised SLE Classification Criteria

Note: The proposed classification is based on 11 criteria. For the purpose of identifying patients in clinical studies, a person shall be
said to have SLE if any four or more of the 11 criteria are present, serially or simultaneously, during any interval of observation.

Treatment is aimed at symptom control. There are very few large, controlled studies that describe the management
of this chronic disease comprehensively. The efficacy of methotrexate (Ruzicka and Goerz, 1981), dapsone
(Edwards and Gayford, 1977) and gold (Gardner-Medwin and Powell, 1994) is described in isolated cases and
small series.

Thalidomide should be of benefit on theoretical grounds (Cojocaru et al., 2011). Antimalarials

(hydroxychloroquine and mepacrine) and azathioprine in patients with oral manifestations of LE, LP and lichen
sclerosus, and have found to be of significant benefit.

Expression of immunofluorescence in almost all cases emphasizes the importance of the direct
immunofluorescence, differentiating LE with other diseases as oral lichen planus. However, as some cases were
negative to any immunological marker, diagnosis should not be relying on immunofluorescence results alone.
Clinical, histopathological and immunopathological correlation is imperative in order to accomplish a correct
diagnosis (Berbert and Mantese, 2005).

Authors’ contributions
S.L. collected records, observations, investigations and diagnosis, Y.M. edited reading and checked references and R.S. drafted
manuscript. There was no conflict of interest. All authors read and approved the final manuscript.

Acknowledgments
The authors wish to acknowledge the contribution of Dr. Swapnil Karnik (M.D) Onco and Renal Histopathologist, (Megavision Labs,
Pune, Maharashtra, India) for the immunofluorescent studies. Authors disclose that no financial funding or support was provided by
any agency/institute for the the compilation of the case report or manuscript.

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