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CP-154 Acute coronary syndrome in a patient receiving romiplostim
  1. E Legaria,
  2. P Tejedor,
  3. N Rubio,
  4. D Suarez,
  5. M Pulido,
  6. FJ Hidalgo,
  7. B García
  1. Hospital Universitario Severo Ochoa, Pharmacy, Madrid, Spain


Background Idiopathic thrombocytopenic purpura (ITP) is an autoimmune disease caused by antibodies against platelet glycoproteins.

Glucocorticoids are the first treatment choice. Splenectomy and other alternatives (rituximab, cyclophosphamide or azathioprine) are used if there is no response or relapse.

Severe bleeding is treated with immunoglobulins achieving rapid but transient increases in platelets.

Romiplostim and eltrombopag, novel thrombopoietin receptor agonists, induce platelet proliferation and differentiation. They are indicated in splenectomised patients with chronic refractory ITP. Their adverse effects include gastrointestinal disorders, heart disease and thromboembolic events.

Purpose The case of a patient with refractory ITP under treatment with romiplostim, who presented with a severe episode of acute coronary syndrome (NSTE ACS).

Material and methods A 32-year-old man, diagnosed with ITP (2007), was initially treated with corticosteroids. 5 years later the patient was splenectomised for developing dependency and tolerance.

However, he underwent an episode of severe thrombocytopenia (10 000 platelets/µL) with bleeding diathesis. He was treated with intravenous immunoglobulin and prednisone.

Eltrombopag (Revolade) was requested for compassionate use (October 2013), 50 mg/day orally, achieving a rapid increase in platelet count.

A month later, the dose was reduced to 25–50 mg on alternate days due to significant fatigue and headache not controlled with painkillers but platelet count dropped. Therefore, the treatment was changed to romiplostim (Nplate) at doses between 125 and 200 µg/week (January 2014).

After 1 year, he developed severe thrombocytopenia (4000 platelets/µL) and respiratory infection. He received a 4 day cycle of intravenous immunoglobulin (40 g/24 h) and 500 µg of romiplostin, reaching values of 115 000 platelets/µL.

3 days later he came to hospital due to several episodes of 10–15 min of centre-thoracic oppression related to effort and respiratory movements. He was diagnosed with NSTE ACS, showing 487 000 platelets/µL and elevated troponin (132 ng/dl). Catheterisation was performed 24 h later. A month later, the patient came back due to 1 h of precordial pain at rest and changes in intensity. It was diagnosed as NSTEMI. A new catheterisation was performed and a conventional stent was placed.

Results The patient recovered. This adverse reaction was assessed as likely by the Karl-Lasagna algorithm and was notified to the Regional Pharmacovigilance Centre.

Conclusion Romiplostim could have been the cause of ACS in this patient.

No conflict of interest.

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