Evidence map›Paper›PMID 42613620›Full record

ArticleThrombosis journal2026

Severe immune thrombocytopenia induced by vancomycin in a critically ill patient: a case report and literature review.

Niloofar Khoshnam Rad, Fatemeh Ghasemi, Shahram Firouzbakhsh, Bita Rashidinejad

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Article in Thrombosis journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Niloofar Khoshnam RadThoracic Research Center, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0001-6700-3570
Fatemeh GhasemiThoracic Research Center, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran.
Shahram FirouzbakhshThoracic Research Center, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran.
Bita RashidinejadThoracic Research Center, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran. bita.rn299@gmail.com.ORCID http://orcid.org/0009-0001-9995-4482

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundVancomycin-induced immune thrombocytopenia (VIIT) is a rare but potentially life-threatening adverse drug reaction characterized by profound platelet destruction. Diagnosis is challenging in critically ill patients, and optimal management beyond drug cessation remains poorly defined. A 54-year-old female admitted to the ICU for severe community-acquired pneumonia developed profound, refractory thrombocytopenia 12 days after the initiation of vancomycin. Blood, sputum, and pleural fluid cultures were negative. Vancomycin was continued due to the severity of the pneumonia, a fluctuating clinical course with recurrent fevers and progressive infiltrates, a complicated parapneumonic effusion requiring drainage and surgical consultation, and infectious disease service recommendations. The patient presented with gross hematuria and a rapid decline in platelet count to 6,000/µL. Following the exclusion of alternative etiologies-including sepsis-associated coagulopathy and heparin-induced thrombocytopenia (HIT)-vancomycin was discontinued. The patient required intravenous immunoglobulin (IVIG) and corticosteroids in addition to drug cessation to achieve platelet recovery.

conclusionThis case underscores the critical importance of early recognition of VIIT. Our literature review reveals that while discontinuation of the offending agent is the cornerstone of therapy, severe cases (platelets < 20,000/µL) often require adjunctive immunomodulatory treatment. VIIT should remain a primary differential diagnosis in patients presenting with unexplained thrombocytopenia during vancomycin therapy.

Indexed as

Adverse drug reactionCase reportCritical careDrug-induced immune thrombocytopenia (DITP)Vancomycin

Identifiers

PMID42613620
PMCPMC13488012

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