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Rituximab-associated secondary antibody deficiency — SCE Rheumatology MCQ

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ModerateImmunologyRituximab-associated secondary antibody deficiencySCE Rheumatology

A 55-year-old woman with granulomatosis with polyangiitis has received 6-monthly rituximab maintenance for 3 years. Her vasculitis has been in glucocorticoid-free remission for 20 months. During the past year, she has had four antibiotic-treated lower respiratory tract infections, including two radiographically confirmed pneumonias and one hospital admission. Six months of azithromycin prophylaxis has not prevented a further pneumonia. Her serum IgG is 5.0 g/L, confirmed on repeat testing; IgA is 0.32 g/L and IgM is 0.18 g/L. Immunoglobulin concentrations were normal before rituximab. Urinalysis, serum electrophoresis and assessment for gastrointestinal protein loss are unremarkable. When clinically well, an immunology-supervised vaccine challenge produces less than a twofold rise in IgG antibody titres to both pneumococcal polysaccharide and tetanus toxoid antigens at 4 weeks. Circulating CD19-positive B cells remain undetectable. Which is the most appropriate immune-directed management?

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Correct answer: D — Commence immunoglobulin replacement therapy under clinical immunology supervision

Explanation lettering: D = shown as A · E = shown as C · C = shown as D · A = shown as E

This patient has clinically significant rituximab-associated secondary antibody deficiency: immunoglobulins were previously normal, alternative causes of antibody loss or immunoparesis have been excluded, and persistent B-cell depletion is present. More importantly, she has recurrent serious respiratory infections despite antimicrobial prophylaxis and proven specific antibody failure following both polysaccharide and polypeptide antigen challenge. Immunoglobulin replacement is therefore appropriate under clinical immunology supervision. A serum IgG below 4 g/L is not mandatory when severe or recurrent infections, ineffective antimicrobial treatment and proven specific antibody failure are present. A is inadequate because prophylactic antibiotics have already failed, including with breakthrough pneumonia. B would perpetuate B-cell depletion and should not precede reassessment of the maintenance strategy in a patient with sustained remission and clinically important immunodeficiency. D is unlikely to correct the established functional antibody defect while B cells remain depleted; the supervised challenge has already demonstrated inadequate responses. E incorrectly treats 4 g/L as an obligatory threshold. That threshold is an alternative laboratory criterion for replacement in secondary immunodeficiency, not a prerequisite when specific antibody failure has been demonstrated in the required clinical context.

Reference: Octagam 10% solution for infusion — Summary of Product Characteristics (8 May 2025) — https://www.medicines.org.uk/emc/product/4701/smpc