SLE and Autoimmune Disorders MCQ — NEET PG Practice Question | NEETPGAI
SLE and Autoimmune Disorders
medium
microscope Pathology
A 28-year-old woman from Mumbai presents with a 6-month history of arthralgia in her hands and knees, morning stiffness lasting 2 hours, and a photosensitive malar rash. She reports recurrent oral ulcers and has noticed hair loss over the past 3 months. Laboratory investigations show: ANA 1:640 (homogeneous pattern), anti-dsDNA antibodies positive (180 IU/mL), anti-Smith antibodies positive, complement C3 level 45 mg/dL (normal 90–180), and urinalysis shows 2+ proteinuria with RBC casts. What is the most likely diagnosis?
A. Mixed connective tissue disease
B. Drug-induced lupus erythematosus
C. Rheumatoid arthritis with secondary Sjögren syndrome
D. Systemic lupus erythematosus with lupus nephritis
Explanation
Clinical Diagnosis: Systemic Lupus Erythematosus with Lupus Nephritis
Key Clinical Features Present
Key Point
This patient meets ≥4 of the 2019 EULAR/ACR SLE classification criteria:
1.
Malar rash (photosensitive)
2.
Oral ulcers
3.
Arthralgia/arthritis (hands, knees)
4.
Alopecia
5.
Serology: ANA positive, anti-dsDNA positive, anti-Smith positive
6.
Low complement (C3 45 mg/dL)
7.
Renal involvement (proteinuria + RBC casts = active glomerulonephritis)
Serological Signature of SLE
Table
Marker
Significance
Patient's Status
ANA (homogeneous)
Present in >95% of SLE; high sensitivity
Positive 1:640
Anti-dsDNA
Highly specific for SLE; associated with nephritis
Positive (180 IU/mL)
Anti-Smith (Sm)
Highly specific for SLE; never seen in other diseases
Positive
Low C3/C4
Indicates active disease, lupus nephritis
C3 = 45 (↓)
High-YieldNEET PG
The combination of anti-dsDNA + anti-Sm + low complement + active urinary findings is pathognomonic for SLE with active glomerulonephritis.
Renal Involvement (Lupus Nephritis)
Clinical Pearl
RBC casts + proteinuria + low complement indicates proliferative lupus nephritis (WHO Class III or IV). This requires immediate immunosuppressive therapy to prevent progression to ESRD.
Pathophysiology
1.
Immune complex deposition: Anti-dsDNA antibodies form circulating immune complexes that deposit in glomeruli
2.
Complement activation: Leads to C3/C4 consumption (explaining low levels)
3.
Glomerular injury: Type III hypersensitivity reaction → inflammation, RBC leakage, proteinuria
4.
Systemic manifestations: ANA-driven B and T cell activation → multi-organ involvement
