Systemic Lupus Erythematosus Case Study #76 – Updated
Comprehensive Review with Expert Feedback
1. Relevance of Age and Gender
Already explained well. To expand: emphasize that
the patient’s early onset SLE fits the typical peak age (15–
45 years) and that female predominance is associated
with hormonal influences (estrogen modulates immune
response).
,2. Family History
Nicely covered. You could add that SLE is polygenic
and often overlaps with other autoimmune diseases in
family members due to shared HLA-DR2, HLA-DR3, and
complement pathway gene variants.
3. BMI / Weight
Good link to clinical manifestations. Expand by noting
that cachexia, poor appetite, renal involvement, and
medication side effects can contribute to underweight
status. Highlight malnutrition as a poor prognostic factor
in autoimmune diseases.
4. Hair Loss & ESR
Excellent pathophysiology explanation. To strengthen:
• Note that discoid lupus lesions can cause scarring
alopecia, which is permanent.
• Add that ESR is non-specific but correlates with
disease activity, while CRP is often normal unless
infection coexists (important teaching point).
5. Fatigue & Labs
Expand: Fatigue can be multifactorial. Consider thyroid
function testing (autoimmune thyroiditis is common in
,SLE). Add Ferritin/Iron studies if anemia of chronic
disease vs iron deficiency anemia is suspected.
6. Prednisone & Vasculitis
Strong answer. Expand by mentioning that prednisone
suppresses neutrophil migration, decreases capillary
permeability, and reduces cytokine expression (IL-1, IL-
6, TNF-alpha), all of which drive vasculitis.
7. CBC Abnormalities
Correct. Expand by naming the specific mechanism:
Type II hypersensitivity hemolytic anemia and immune-
mediated thrombocytopenia are well-documented in
SLE.
8. Jaundice
Well reasoned. Add: “Hemolytic anemia from
autoantibody-mediated RBC destruction leads to
unconjugated hyperbilirubinemia, explaining scleral
icterus/jaundice.”
9. Arthritis of Lupus vs RA
Perfect teaching point. Add: SLE arthritis is non-erosive,
unlike RA. Radiographs often remain normal despite joint
pain.
, 10. Pneumonia Concern
You nailed it. Add: Immunosuppressive therapies
(glucocorticoids, azathioprine, cyclophosphamide) also
further raise pneumonia risk.
11. Lymphadenopathy
Correct. Could expand with: “Generalized
lymphadenopathy in SLE may mimic lymphoma, making
biopsy sometimes necessary to rule out malignancy.”
12. Abnormal Labs
Good explanation. Add: “Severe leukopenia is a poor
prognostic factor and increases risk for opportunistic
infections.”
13. WBC Differential
Correct. Add: “Low lymphocyte counts (lymphopenia)
are most characteristic of SLE compared to other
autoimmune conditions.”
14. Labs + Lung + Cough
Correct. Could link to lupus pneumonitis or
secondary bacterial bronchitis/pneumonia triggered by
immunosuppression.
Comprehensive Review with Expert Feedback
1. Relevance of Age and Gender
Already explained well. To expand: emphasize that
the patient’s early onset SLE fits the typical peak age (15–
45 years) and that female predominance is associated
with hormonal influences (estrogen modulates immune
response).
,2. Family History
Nicely covered. You could add that SLE is polygenic
and often overlaps with other autoimmune diseases in
family members due to shared HLA-DR2, HLA-DR3, and
complement pathway gene variants.
3. BMI / Weight
Good link to clinical manifestations. Expand by noting
that cachexia, poor appetite, renal involvement, and
medication side effects can contribute to underweight
status. Highlight malnutrition as a poor prognostic factor
in autoimmune diseases.
4. Hair Loss & ESR
Excellent pathophysiology explanation. To strengthen:
• Note that discoid lupus lesions can cause scarring
alopecia, which is permanent.
• Add that ESR is non-specific but correlates with
disease activity, while CRP is often normal unless
infection coexists (important teaching point).
5. Fatigue & Labs
Expand: Fatigue can be multifactorial. Consider thyroid
function testing (autoimmune thyroiditis is common in
,SLE). Add Ferritin/Iron studies if anemia of chronic
disease vs iron deficiency anemia is suspected.
6. Prednisone & Vasculitis
Strong answer. Expand by mentioning that prednisone
suppresses neutrophil migration, decreases capillary
permeability, and reduces cytokine expression (IL-1, IL-
6, TNF-alpha), all of which drive vasculitis.
7. CBC Abnormalities
Correct. Expand by naming the specific mechanism:
Type II hypersensitivity hemolytic anemia and immune-
mediated thrombocytopenia are well-documented in
SLE.
8. Jaundice
Well reasoned. Add: “Hemolytic anemia from
autoantibody-mediated RBC destruction leads to
unconjugated hyperbilirubinemia, explaining scleral
icterus/jaundice.”
9. Arthritis of Lupus vs RA
Perfect teaching point. Add: SLE arthritis is non-erosive,
unlike RA. Radiographs often remain normal despite joint
pain.
, 10. Pneumonia Concern
You nailed it. Add: Immunosuppressive therapies
(glucocorticoids, azathioprine, cyclophosphamide) also
further raise pneumonia risk.
11. Lymphadenopathy
Correct. Could expand with: “Generalized
lymphadenopathy in SLE may mimic lymphoma, making
biopsy sometimes necessary to rule out malignancy.”
12. Abnormal Labs
Good explanation. Add: “Severe leukopenia is a poor
prognostic factor and increases risk for opportunistic
infections.”
13. WBC Differential
Correct. Add: “Low lymphocyte counts (lymphopenia)
are most characteristic of SLE compared to other
autoimmune conditions.”
14. Labs + Lung + Cough
Correct. Could link to lupus pneumonitis or
secondary bacterial bronchitis/pneumonia triggered by
immunosuppression.
