The modern role of corticosteroids in immune thrombotic thrombocytopenic purpura
Review Article

The modern role of corticosteroids in immune thrombotic thrombocytopenic purpura

Konstantine Halkidis ORCID logo

Division of Hematologic Malignancies and Cellular Therapeutics, Institute for Reproductive and Developmental Sciences, Department of Internal Medicine, University of Kansas Medical Center, Kansas, KS, USA

Correspondence to: Konstantine Halkidis, MD, PhD. Division of Hematologic Malignancies and Cellular Therapeutics, Institute for Reproductive and Developmental Sciences, Department of Internal Medicine, University of Kansas Medical Center, 3901 Rainbow Blvd, MS 3050, Kansas City, KS 66160, USA. Email: khalkidis@kumc.edu.

Abstract: Deficiency of ADAMTS13 caused by autoantibodies leads to the thrombotic microangiopathy immune thrombotic thrombocytopenic purpura (iTTP). Corticosteroids have long been utilized in the management of patients with iTTP, both in the acute setting and continued after clinical remission has been achieved, usually tapered over a period of weeks. However, with recent advances in the field, the landscape of steroid utilization is changing, particularly since the mid-2010s with the advent of caplacizumab and anti-cluster of differentiation 20 (CD20) directed therapy in iTTP. Though steroids are generally well tolerated, many patients are at risk of adverse events related to corticosteroid use, such as patients with diabetes mellitus, hypertension, and cardiovascular disease. There are no uniform guidelines regarding optimal steroid formulations, dosages, or duration of treatment. Modern treatment modalities target more specific aspects of the pathophysiology of iTTP, leading to speculation that steroid-free regimens may become the new standard of care. Despite this, because of the favorable adverse event profile of steroids and the modest benefit they provide, steroid use is still widespread for patients with iTTP. As such, there is a need for further studies regarding corticosteroid dosing; duration of treatment with corticosteroids; adverse events associated specifically with the use of corticosteroids; and whether, how, or in what context corticosteroids can safely be omitted or replaced with another treatment modality in the care of patients with iTTP. In this Mini-Review, we will explore the historical reasoning and data supporting the use of corticosteroids in iTTP and the shifting role of steroids in the modern era.

Keywords: Corticosteroids; immune thrombotic thrombocytopenic purpura (iTTP); thrombotic microangiopathy

Received: 30 May 2025; Accepted: 07 November 2025; Published online: 18 December 2025.

doi: 10.21037/aob-25-16

Introduction

Immune thrombotic thrombocytopenic purpura (iTTP) is a thrombotic microangiopathy caused by autoantibody-mediated reduction of the activity of the metalloprotease ADAMTS13 (1). In normal hemostasis, ADAMTS13 cleaves von Willebrand factor (VWF) multimers to prevent the accumulation of ultra-large VWF aggregates, which leads to thrombosis and end-organ damage. As it is an autoimmune disease, the treatment of iTTP has involved the utilization of immunosuppressive and immunomodulatory therapeutic interventions since the basic pathophysiology of the disease was elucidated over the last few decades (2-6). Corticosteroids, in particular, have been utilized to treat patients with iTTP for many years, dating as far back as the 1950s (6). However, heterogeneity exists amongst providers and in the literature as to the specific agent, dosage, and duration of steroid utilization for iTTP. Furthermore, as iTTP treatments have become more targeted, the role of steroids in iTTP care continues to evolve.

Pointedly, though corticosteroids are still considered part of the “standard of care” for patients with iTTP, there is no standard approach regarding dose, formulation, and/or duration of treatment with corticosteroids, suggesting that additional research is needed to help optimize the utilization of these agents in clinical practice. In this Mini-Review, we will explore the role of steroids in the care of iTTP patients in the modern era, with a brief overview of commonly utilized approaches and the rationale behind their use, in order to highlight the ongoing need for future studies to define the corticosteroid regimen(s) best suited to help in the management of these patients.

Methods

Literature was searched using PubMed from 1924 to 2025 using the following free text searches: (“thrombotic thrombocytopenic purpura”) AND (“treatment”); and (“corticosteroid”) AND (“mechanism”). We found 4,739 peer-reviewed articles and sorted through these for literature pertinent and relevant for the review. A total of 30 articles were included for review and the remainder were excluded.

The role of corticosteroids in acute iTTP management

The immediate goal of acute iTTP directed therapy is to improve ADAMTS13 activity to normal or near-normal levels and induce clinical remission. There exist a variety of definitions of clinical remission of iTTP, but essentially it is defined as a normal platelet count that persists after the completion of therapeutic plasma exchange (TPE) and/or VWF-directed therapy, i.e., caplacizumab (7). The rationale for the use of corticosteroids in iTTP is based on their mechanistic effects on gene transcription and inflammatory response mediators such as phospholipase A2, which in aggregate help reduce tissue damage in the presence of inflammation (8). Though corticosteroids had been used to help treat acute episodes of iTTP since the mid-20th century, it was not until the end of the 20th century that standard approaches were developed to care for these patients. TPE was established as the standard of care for iTTP in 1991 and remains the cornerstone of treatment for patients with the disease (3). However, at that time and since, corticosteroids have always been used alongside TPE, though studies to determine the optimal dose, formulations, and/or duration of steroid treatment are relatively low in number (Table 1). In fact, in that same year of 1991, one group utilized corticosteroid treatment alone for patients with limited signs and symptoms of end-organ damage and reported that 30/54 patients with those clinical characteristics responded to steroid monotherapy (9). Notably, the patient populations at this time were identified as having thrombotic thrombocytopenic (TTP) without the ability to confirm the diagnosis using modern methods, since ADAMTS13 had not yet been identified as the VWF-cleaving protease whose deficiency is responsible for the pathophysiology of the disease (1). Nonetheless, steroids clearly had a role in the treatment of iTTP.

Table 1

Evidence regarding the use of corticosteroids for the treatment of iTTP

Manuscript (PMID) Year of publication Notes on doses, other therapeutic interventions, and relevant study details Number of patients Selected outcomes
2062331 1991 Intervention #1: 200 mg oral prednisone daily if minimal symptoms and no hepatic dysfunction 108 total (54 initially receiving corticosteroids alone; 54 initially receiving corticosteroids plus TPE) Number of patients receiving corticosteroids alone who received oral vs. IV formulations not reported
Intervention #2: 200 mg IV prednisolone daily if minimal symptoms and hepatic dysfunction 2 deaths in initial corticosteroids alone but 24 patients in this group eventually also received TPE
Intervention #3: 200 mg IV prednisolone daily and TPE daily if moderate-to-severe symptoms Total of 78 patients received TPE at some point in treatment course with 8 deaths reported
Intervention #4: 200 mg IV prednisolone and TPE daily with infusion of packed RBCs if initial hematocrit below 0.20 All deaths occurred within 16 days of initial diagnosis
14982878 2004 All patients received plasma exchange and 23 received prednisone; no dose or duration reported 37 total One patient treated with TPE and prednisone alone remained in clinical remission (normalized platelet count and other parameters) for 18 months though still with ADAMTS13 activity <5% at end of study
20 with “idiopathic” TTP (TTP occurring with “no apparent pre-existing illness”), 16 of which had ADAMTS13 activity <5%
Number of patients treated with corticosteroids who had “idiopathic” TTP and/or ADAMTS13 <5% not reported
20033409 2010 TPE and aspirin (see citation for details) plus: Arm 1: methylprednisolone 1 mg/kg IV daily. Arm 2: 10 mg/kg IV daily for 3 days and subsequently 2.5 mg/kg IV daily 60 total, 30 per arm Arm 1 vs. Arm 2: primary outcome of “good response” at day 9: 43.4% vs. 23.4% (P=0.17). Death by day 23: 13.3% vs. 3.3% (P=0.35)
22547583 2012 Retrospective study that included 32 patients with iTTP diagnosed during pregnancy 32 29 of 32 patients who received “steroids” had “good” outcomes; 1 death; 1 with “neurologic sequellae”; 1 with “renal sequellae”
17 received “steroids”, with no dose, formulations, or duration reported 6 miscarriages
5 cases of intrauterine fetal death
6 “good” fetal outcomes
23263974 2013 Retrospective study of 12 pediatric acquired TTP cases 2 Both patients receiving corticosteroids achieved lasting remission from TTP
2 pediatric patients received prednisone (dose not reported) in relapse setting along with vincristine and rituximab
27878664 2016 Retrospective single center study of patients with “acute acquired TTP” from 2005–2015 60 All 3 patients treated with steroids alone died within 15 days of initial diagnosis
Corticosteroids administered in 54/69 “episodes”; no dose, formulations or duration reported Mortality improved comparing patients treated with or without steroids (4/37, 10.81% vs. 8/12, 66.67%) who also received either TPE or plasma infusion but no other intervention (P value not reported)
“Glucocorticoids” alone given to 3 patients at presentation
29296854 2017 All patients also received daily TPE plus: Arm 1: prednisone 1 mg/kg prednisone daily. Arm 2: cyclosporine 2 to 3 mg/kg divided into a twice-daily dose; patients receiving CSA were permitted to receive hydrocortisone as needed for hypersensitivity reactions to TPE 26 initially enrolled Non-significant decreased rate of exacerbation comparing patients receiving prednisone vs. cyclosporine (1/11, 9% vs. 3/11, 27%, P=0.3)
11 in each arm “evaluable for the primary end point of exacerbation”

All studies are prospective in nature unless otherwise noted. CSA, cyclosporine; iTTP, immune thrombotic thrombocytopenic purpura; IV, intravenous; RBCs, red blood cells; TPE, therapeutic plasma exchange; TTP, thrombotic thrombocytopenic purpura.

Subsequent studies comparing specific doses and regimens are surprisingly limited. As an example, the Italian TTP Study Group published the results of a multi-center study in 2010 comparing “standard dose” (1 mg/kg daily) vs. “high dose” (10 mg/kg daily for 3 days, followed by 2.5 mg/kg daily) methylprednisolone alongside TPE in each group (10). After 23 days, the patients receiving the higher dose of methylprednisolone were twice as likely to achieve clinical remission when compared to the patients receiving the lower dose. Notably, and to the point of this review, several aspects of the study protocol differ from the approach to TPE in other countries and institutions, and all patients with a platelet count >30×109/L received aspirin alongside gastric ulcer prophylaxis. Though intriguing, the utility of the results of this study and other small studies may be difficult to apply to the general iTTP population.

The International Society of Thrombosis and Haemostasis (ISTH) has published guidelines on the treatment of iTTP, and offers a “strong recommendation in the context of very low certainty of evidence” to use corticosteroids alongside TPE in iTTP patients experiencing a first acute event (11). The adverse event profile of corticosteroids is relatively mild, though caution should be observed for patients with hyperglycemic conditions, hypertension, cardiovascular disease, and other conditions that can be exacerbated or triggered by steroid use; similarly, most studies of patients with iTTP have not reported Grade 3 or higher adverse effects attributed specifically to the use of corticosteroids (12,13). Though these recommendations were initially published in 2020, no new prospective studies are available comparing dosage and duration of any given steroids, and no studies have ever been done comparing different corticosteroids to one another. Notably, the strong recommendation was made despite the lack of definitive evidence about whether TPE plus steroids was significantly better than TPE alone, though there was evidence of mortality benefit when steroids were added (Table 1) (14-17). Notably, the mortality benefit was observed in studies conducted before the widespread use of cluster of differentiation 20 (CD20)-directed therapy and caplacizumab, as will be discussed below. An updated version of the ISTH guidelines does not change recommendations as no significant data about the use of steroids in iTTP management has accumulated since the 2020 guidelines (18).

Corticosteroids after clinical remission

Most clinicians who treat iTTP patients will usually continue steroids in the early phases of clinical remission and taper the dose over a period of weeks. This is done in part to prevent clinical relapse and ADAMTS13 relapse, the latter of which manifests as a decrease in ADAMTS13 activity to levels below 20% with or without concomitant recurrent thrombocytopenia (7). A typical regimen utilized by providers is to give 1 mg/kg of prednisone or an equivalent dose of a different corticosteroid daily continued at least until normalization of platelets and subsequently taper the dose over a period of weeks. However, there is little to no data guiding choice of agent, dosage, and taper duration (9,19-23). Some providers will taper steroids over 2–3 weeks, while others will taper over 6–8 weeks, with variability amongst individual provider choices also factoring in disease severity and end-organ manifestations of iTTP for individual patients (X. Zheng, personal communication, 1/15/2024). As such, a great deal of heterogeneity in corticosteroid taper utilization persists in the field.

Data to support the utilization of extended corticosteroid administration and taper is also somewhat lacking. A study comparing cyclosporine to prednisone showed that anti-ADAMTS13 antibody titers decreased to a greater extent in the cohort using steroids, though beyond this study, very little data exists to support the hypothesis that corticosteroids may prevent relapses and exacerbations of iTTP by reducing pathogenic antibody levels and restoring ADAMTS13 activity (23). Since the 2010s, in fact, CD20-directed therapy with therapeutic agents such as rituximab, which target antibody-producing B cells, has proven more efficacious in preventing iTTP relapse than steroids alone (24-26). At our institution and most other centers, patients are treated with a course of CD20-directed therapy as primary and/or secondary prophylaxis against iTTP exacerbation and relapse as a standard approach in all patients diagnosed with iTTP barring patient-specific contraindications (19,27). Patients on steroids for more than 3 weeks are also routinely given prophylaxis against opportunistic infection, primarily to prevent Pneumocystis jirovecii pneumonia (PJP), which itself can be associated with adverse effects related to antimicrobial medications such as trimethoprim-sulfamethoxazole (28).

Steroids in the post-rituximab, caplacizumab, and rADAMTS13 era

Caplacizumab received approval for the treatment of iTTP from the European Medicines Agency (EMA) in 2018 and from the Food and Drug Administration (FDA) in 2019 (29). Since then, it has moved to the front line of iTTP treatment, as caplacizumab prevents aggregation of platelets in the vasculature by blocking the interaction of the A1 domain of VWF with the platelet GP1b receptor (11,30). A phase 3 clinical trial utilizing caplacizumab in the absence of TPE (MAYARI) has recently been completed (NCT05468320). The use of recombinant ADAMTS13 (rADAMTS13) for iTTP treatment is also in clinical trials (NCT03922308), with results reported at the time of this writing; rADAMTS13 promises to be yet another tool in the arsenal of providers caring for iTTP patients. Still, even in the modern iTTP treatment era, most providers still give steroids up front and through early remission as outlined in the ISTH guidelines given the relatively low risk profile of corticosteroids and the potential benefits they provide (11). Steroids in the form of either prednisone or prednisolone were given to all patients in the MAYARI trial, and intravenous methylprednisolone was given to patients in the rADAMTS13 trial (NCT03922308). Anecdotally, however, providers caring for iTTP patients have begun to shorten the steroid taper since caplacizumab should help prevent clinical relapse, and rituximab or similar agents usually help reduce antibody levels and prevent ADAMTS13 relapse (7). Since the rationale for the use of steroids is to prevent exacerbation and relapse and to help restore ADAMTS13 activity, it is now more common to offer steroid tapers over the course of 2–3 weeks rather than 6–8 weeks (S. Chaturvedi, personal communication, 2/16/2024). Rarely are patients continued on corticosteroids two or more months after an acute iTTP event, particularly in the caplacizumab era. Notably, there have been no new prospective studies comparing steroid regimens since 2019, when caplacizumab attained FDA approval for iTTP patients. In personal practice, with consideration of comorbid conditions such as diabetes mellitus and other possible contraindications, the author typically utilizes oral prednisone at an initial dose of 1 mg/kg continued until clinical remission with a short taper (2–3 weeks) and usually without PJP and/or other prophylactic interventions to mitigate the adverse effects of steroids due to the short course of the taper.

Conclusions

Corticosteroids have been a mainstay of the treatment of iTTP for many decades. Though evidence to support steroid utilization in iTTP remains scant to this day, adverse effects of treatment are usually mild and limited in the vast majority of patients, particularly since treatment courses are temporary. The therapeutic advantages appear to outweigh the risks in the care of iTTP patients, both in the acute setting and in early remission, but further evidence would be helpful in identifying specific populations that may continue to benefit from corticosteroids, the optimal doses to use, the most appropriate formulations, and the ideal corticosteroid treatment duration.

Acknowledgments

None.

Footnote

Peer Review File: Available at https://aob.amegroups.com/article/view/10.21037/aob-25-16/prf

Funding: K.H. is the recipient of a National Institutes of Health K08 award from the National Heart, Lung, and Blood Institute (HL163471) as well as a Career Development Award from the American Heart Association.

Conflicts of Interest: The author has completed the ICMJE uniform disclosure form (available at https://aob.amegroups.com/article/view/10.21037/aob-25-16/coif). K.H. serves as an unpaid editorial board member of Annals of Blood from August 2024 to July 2026. K.H. also reported a K08 award from the National Heart, Lung, and Blood Institute (NHLBI) and a Career Development Award from the American Heart Association. He received an honorarium for participating as an ad hoc member of a National Institutes of Health (NIH) study section (CHD) in June 2025. K.H. also served as an invited speaker at the annual Hemostasis & Thrombosis Research Society (HTRS) scientific meeting in March 2025 on his academic work on mechanisms of action of antibodies in immune thrombotic thrombocytopenic purpura and was awaiting payment of honorarium for this. The author has no other conflicts of interest to declare.

Ethical Statement: The author is accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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doi: 10.21037/aob-25-16
Cite this article as: Halkidis K. The modern role of corticosteroids in immune thrombotic thrombocytopenic purpura. Ann Blood 2025;10:26.

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