Immune Thrombocytopenic Purpura Secondary to Cytomegalovirus Infection: A Case Report.

Bessy S Flores-Chang,Sorab Gupta,Nicoleta Stoicea,Carlos E Arias-Morales,Francis G Wadskier

doi:10.3389/fmed.2015.00079

Abstract

Immune thrombocytopenic purpura (ITP) is defined as an acquired thrombocytopenia with antibodies detected against platelet surface antigens, and it is the most common form of thrombocytopenia in otherwise asymptomatic adults. ITP secondary to an underlying condition is a diagnosis of exclusion that is essential to establish for treatment efficacy. Secondary thrombocytopenia caused by cytomegalovirus (CMV) is common; however, case reports associated with diagnosis in immunocompetent adults are rare, and to the best of our knowledge only 20 publications have been associated with this diagnosis. Our report is based on a clinical presentation of a 37-year-old female complaining of petechiae, heavy menses, shortness of breath, and a platelet count of 1 × 109/L. Treatment with IVIG and steroids failed to improve platelet count. Subsequently, an infectious laboratory workup was performed, detecting CMV infection, and treatment with antiviral agents was initiated, causing platelet count to increase as viral load decreased.

Highlights

Immune thrombocytopenic purpura (ITP) is a form of acquired thrombocytopenia triggered by anti-platelet antibodies that destroy platelets peripherally, damage megakaryocytes, and inhibits platelet production in the marrow [1]
We present a case of a 37-year-old female patient with a history of petechia, heavy menstrual bleed, and low platelets (1 × 109/L) after a CMV infection
The use of thrombopoeitin receptor (TPO-R) agonists such as romiplostin (Nplate®) has been studied, and literature has shown that these agents are effective in refractory ITP compared to placebo [14,15,16]

Summary

INTRODUCTION

Immune thrombocytopenic purpura (ITP) is a form of acquired thrombocytopenia triggered by anti-platelet antibodies that destroy platelets peripherally, damage megakaryocytes, and inhibits platelet production in the marrow [1]. Agents such as CMV, hepatitis C, Epstein–Barr virus, and Parvovirus B19, among others, have been identified as the culprits behind this form of ITP [2]. CMV can cause disease in immunocompromised patients either via a primary CMV infection or reactivation of a latent CMV infection. It is characterized by malaise, myalgia, headache, sore throat, and fever. Treatment of the primary infection is imperative because standard therapies for ITP regain their efficacy once the infection is resolved [3]

CASE PRESENTATION

DISCUSSION

CONCLUSION