Journal of Hematology & Thromboembolic Diseases
Open Access

Post-Transfusion Purpura (PTP) and Heparin-Induced Thrombocytopenia (HIT) in the Thrombocytopenic Disorders

Masataka Banshodani^{* *}Correspondence: Masataka Banshodani, Department of Hematology, University of Aconcagua, Mendoza, Argentina, Email:

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Description

Distinguishing between Post-Transfusion Purpura (PTP) and Heparin-Induced Thrombocytopenia (HIT) poses a considerable challenge during the early stages of thrombocytopenia, given the striking similarities in their initial clinical presentations. This diagnostic complexity is underscored by the examination of four patients who were initially suspected, based on clinical manifestations, of suffering from HIT [1]. In each of these cases, the patients had recently undergone blood transfusions and exhibited the presence of platelet alloantibodies. However, upon further investigation, the conclusive diagnosis shifted towards PTP rather than HIT. Notably, two of the four patients experienced severe complications, including a lethal gastrointestinal hemorrhage and a retroperitoneal hemorrhage. Adding to the peculiarity of these cases, one patient stood out as male, and an unusual finding emerged in the detection of two distinct platelet alloantibodies in his serum. In another patient, not only were platelet alloantibodies present, but so too were HIT antibodies. These intricacies highlight the intricate nature of the differential diagnosis process and emphasize the need for nuanced consideration in similar clinical scenarios.

The urgency of arriving at an accurate diagnosis is paramount due to the markedly different treatment modalities required for PTP and HIT. Immediate initiation of the appropriate treatment is crucial for patient outcomes. The researchers suggest a pragmatic approach when HIT is suspected–the exploration of additional information. Specifically, if clinical features align more with PTP, such as a recent blood transfusion or a substantial drop in platelet count below 15 Gpt/L, parallel testing for platelet alloantibodies is recommended to effectively rule out PTP [2]. This recommendation stems from the recognition that the clinical presentations of PTP and HIT, though initially resembling each other, harbor distinct underlying mechanisms and necessitate changes in therapeutic interventions. By advocating for a comprehensive diagnostic approach that considers both clinical features and laboratory findings, the authors underscore the importance of precision in distinguishing between these two syndromes. In essence, this approach not only ensures the swift initiation of appropriate treatment but also contributes to enhanced patient care and outcomes in the complicated field of thrombocytopenic disorders.

In this study, we explore a case involving a 47-year-old female with a medical history of systemic lupus erythematosus who underwent major spinal surgery on day 1. During the procedure, the patient received several units of packed red cells, and routine postoperative thrombosis prophylaxis was initiated with subcutaneous heparin [3]. Notably, on day 10 post-surgery, a significant decline in platelet count occurred, dropping from 90 Gpt/L to 12.5 Gpt/L. Despite interventions such as plasma exchange on day 11 and subsequent platelet transfusions in the following days, there was no substantial improvement in the platelet count. The diagnostic investigation involved the use of patient serum and EDTA-anticoagulated blood, and samples were sent to our laboratory for analysis after the tentative clinical diagnosis of Heparin-Induced Thrombocytopenia (HIT) had been proposed.

To provide a comprehensive understanding of the clinical scenario, we retrospectively collected clinical data by reviewing the patient's records. The cases presented in this study underscore the inherent challenge in differentiating between HIT and Post-Transfusion Purpura (PTP) solely based on clinical grounds, particularly when there is isolated thrombocytopenia in the initial stages. The difficulty in distinguishing between these two syndromes is further emphasized by the commonality of surgical procedures that necessitate blood transfusions, coupled with the subsequent administration of heparin. This clinical context often complicates the timing of a drop in platelet count, making it challenging to definitively differentiate between HIT and PTP [4]. The study highlights the intricate diagnostic environment surrounding thrombocytopenic disorders and underscores the need for a nuanced approach that integrates clinical, laboratory, and temporal considerations to facilitate accurate and timely diagnoses. Consequently, the temporal relationship between the decline in platelet count and clinical events often fails to provide a clear distinction between the two syndromes.

Conclusion

In conclusion, the presented cases and the broader study illuminate the formidable challenge posed by the intricate diagnostic environment of Post-Transfusion Purpura (PTP) and Heparin-Induced Thrombocytopenia (HIT). The early stages of thrombocytopenia manifest with clinical presentations so strikingly similar that distinguishing between the two syndromes based solely on clinical grounds becomes a formidable task. This nuanced strategy ensures not only the swift initiation of appropriate treatment but also contributes to enhanced patient care and outcomes in the complex field of thrombocytopenic disorders. In essence, the study underscores the imperative for precision in the differential diagnosis of PTP and HIT, thereby paving the way for improved patient management in clinical scenarios characterized by isolated thrombocytopenia and overlapping clinical presentations.

References

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