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Zorluk: ZorRheumatology and Immunology

A 65-year-old man presents to the clinic with a 3-week history of progressively worsening shortness of breath and swelling in his legs. He reports waking up in the middle of the night gasping for air and now requires three pillows to sleep comfortably. His medical history is significant for severe, erosive rheumatoid arthritis, chronic obstructive pulmonary disease, and hypertension. His medications include methotrexate, lisinopril, tiotropium, and acetaminophen. Three months ago, his rheumatologist added etanercept due to inadequately controlled joint symptoms. He has a 40-pack-year smoking history but quit 5 years ago. Vital signs show a temperature of 37.0°C (98.6°F), blood pressure of 145/85 mmHg, pulse of 96/min, and respiratory rate of 22/min. Pulse oximetry shows 94% on room air. Physical examination reveals distended jugular veins, bibasilar lung crackles, and 3+ bilateral pitting edema up to the knees. Cardiac auscultation reveals a regular rhythm with an S3 gallop. Joint examination shows chronic deformities but no acute inflammation. Which of the following is the most likely cause of this patient's current presentation?

  1. Toxic effect of a biologic agent on ventricular functionCevap
  2. B
    Acute exacerbation of chronic obstructive pulmonary disease
  3. C
    Inflammatory interstitial pulmonary fibrosis
  4. D
    Opportunistic bacterial pneumonia
  5. E
    Idiosyncratic pulmonary reaction to methotrexate

Cevap

Toxic effect of a biologic agent on ventricular function
The patient's presentation of progressive dyspnea, orthopnea, paroxysmal nocturnal dyspnea, jugular venous distension, bibasilar crackles, an S3 gallop, and lower extremity edema is the classic clinical picture of acute decompensated heart failure (ADHF). Tumor necrosis factor (TNF)-alpha inhibitors, such as etanercept, infliximab, and adalimumab, are biologic disease-modifying antirheumatic drugs (DMARDs) used for severe rheumatoid arthritis. A well-documented and highly tested adverse effect of TNF-alpha inhibitors is the development of new-onset heart failure or the exacerbation of underlying heart failure. Therefore, these agents should be used with extreme caution or completely avoided in patients with moderate to severe heart failure. The addition of etanercept three months ago is the most likely culprit for his sudden ventricular dysfunction and subsequent volume overload.

Adım Adım Çözüm

1
Analyze the clinical presentation and physical examination findings.
The patient presents with orthopnea, paroxysmal nocturnal dyspnea, jugular venous distension, bibasilar crackles, an S3 gallop, and severe pitting edema.
To establish the primary physiologic syndrome, which is acute decompensated heart failure characterized by profound volume overload.
2
Review the patient's medical history and recent medication changes.
The patient has a history of severe rheumatoid arthritis and recently started etanercept three months ago.
To identify potential triggers, etiologies, or iatrogenic causes for the new-onset heart failure.
3
Connect the medication profile to the clinical syndrome.
Etanercept is a TNF-alpha inhibitor, a class of drugs known to cause or worsen heart failure.
Recognizing this adverse effect identifies the most likely cause of the patient's acute decompensation, as TNF-alpha inhibitors are strictly contraindicated in moderate-to-severe heart failure.

Anahtar Kavram

Tumor necrosis factor (TNF)-alpha inhibitors (e.g., etanercept, infliximab, adalimumab) can cause new-onset heart failure or exacerbate underlying heart failure, and their use is contraindicated in patients with moderate to severe ventricular dysfunction.
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Rheumatology and Immunology

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