Soru

Zorluk: Çok zorRheumatology and Immunology

Match each advanced biologic or targeted synthetic disease-modifying antirheumatic drug (DMARD) with its most characteristic severe adverse effect or specific clinical contraindication.

  • TocilizumabCarries an increased risk of lower gastrointestinal perforation; avoid in patients with a history of recurrent diverticulitis.
  • SecukinumabMay induce de novo onset or exacerbate preexisting inflammatory bowel disease; avoid in patients with Crohn disease.
  • RituximabHigh risk of progressive multifocal leukoencephalopathy and hepatitis B virus reactivation; rigorous screening is mandatory.
  • TofacitinibAssociated with an increased risk of venous thromboembolism, major adverse cardiovascular events, and herpes zoster reactivation.
  • AbataceptAssociated with an increased incidence of respiratory exacerbations and pneumonia in patients with underlying chronic obstructive pulmonary disease.

Cevap

Tocilizumab matches with increased risk of lower gastrointestinal perforation. Secukinumab matches with exacerbation of inflammatory bowel disease. Rituximab matches with PML and HBV reactivation. Tofacitinib matches with venous thromboembolism and herpes zoster risk. Abatacept matches with exacerbations in COPD.
Each targeted DMARD carries specific risks beyond general immunosuppression. Tocilizumab (IL-6 inhibitor) is uniquely associated with GI perforation, particularly in diverticular disease. Secukinumab (IL-17 inhibitor) can exacerbate or unmask IBD. Rituximab (anti-CD20) causes profound B-cell depletion, risking HBV reactivation and PML. Tofacitinib (JAK inhibitor) is associated with thrombosis, cardiovascular events, and shingles. Abatacept (T-cell costimulation modulator) worsens COPD symptoms.

Adım Adım Çözüm

1
Identify the mechanism of action for each targeted DMARD.
Tocilizumab (anti-IL-6), Secukinumab (anti-IL-17A), Rituximab (anti-CD20), Tofacitinib (JAK inhibitor), Abatacept (CTLA4-Ig).
Understanding the precise immunologic target is necessary to predict pathway-specific toxicities.
2
Correlate each mechanism of action with its pathway-specific clinical consequences and FDA warnings.
IL-6 blockade impairs bowel integrity (perforation). IL-17 blockade triggers gut inflammation (IBD). CD20 depletion risks severe viral reactivation (HBV, JC virus). JAK inhibition alters lipid metabolism and coagulation (MACE, VTE) and VZV immunity. CTLA4-Ig exacerbates existing lung disease (COPD).
Accurately matching the drug to its unique severe adverse effect is critical for safe prescribing in rheumatology.

Anahtar Kavram

Adverse effect profiles and specific contraindications of non-TNF biologic and targeted synthetic DMARDs.
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