The Differential Diagnosis of Thromobocytopenia

Background: Thrombocytopenia is defined as a platelet count below 150 000/μL. It increases the risk of bleeding, often due to an existing underlying condition. A meticulous diagnostic evaluation is needed so that specific treatment can be initiated and complications avoided.

Methods: This review is based on clinical studies up to June 2025 that were retrieved by a selective search with pertinent key words in the MEDLINE/PubMed database, and on current guidelines.

Results: Thrombocytopenia often arises in association with pregnancy (7–10 %), immune-mediated diseases such as idiopathic thrombocytopenic purpura (ITP), certain drugs (e.g., heparin-induced thrombocytopenia [HIT] in as many as 1% of patients treated with unfractionated heparin), infections, and systemic and hematologic diseases. The diagnostic evaluation is by an algorithm involving the clinical history, a complete blood count, and other, specific tests. Emergencies such as thrombotic microangiopathy (TMA) and disseminated intravascular coagulation require rapid therapeutic intervention. The treatment depends on the cause and severity of thrombocytopenia; it can include the discontinuation of precipitating drugs, the use of immunosuppressive drugs or thrombopoietin receptor agonists in immune-mediated cases, and specific measures against infection, TMA, or malignant diseases. Prophylactic platelet transfusion can be considered if the platelet count drops below 10 000–20 000/μL, or below 50 000/μL before an intervention or operation, but not in cases of ITP or thrombotic thrombocytopenic purpura (TTP).

Conclusions: The treatment depends on the clinical manifestations, platelet count, and underlying cause.

Cite this as: Miesbach W, Stratmann J, Alesci RS, Chromik J, Bakchoul T, Wendt R: The differential diagnosis of thrombocytopenia. Dtsch Arztebl Int 2025; 122: 588–96. DOI: 10.3238/arztebl.m2025.0160

Thrombocytopenia, defined as a reduction in platelet count to less than 150 000/µL, is a common coagulation disorder with major clinical implications.

Thrombocytopenia plays an important role in medical care, as it can lead to an increased tendency to bleed and serve as an indicator of various underlying diseases. Its relevance stems from the increased risk of spontaneous bleeding, especially when the platelet count is below 50 000/μL, and the need for cautious consideration of medical interventions (1).

Learning objectives

This article is intended to enable readers to:

• classify the main causes of thrombocytopenia systematically and assess their clinical relevance;
• carry out a structured diagnostic evaluation of a patient with thrombocytopenia, with appropriate choice of diagnostic tests; and
• recognize medical emergencies associated with thrombocytopenia—such as thrombotic thrombocytopenic purpura [TTP], heparin-induced thrombocytopenia [HIT], and disseminated intravascular coagulation [DIC])—at an early stage and assess the need for immediate treatment.

The varieties and importance of thrombocytopenia

The prevalence of thrombocytopenia (Table 1) varies depending on the cause and population. Approximately 90% of cases have an identifiable cause, e.g., immune-mediated disease, infection, induction by a drug, or pregnancy. In some cases, the origin of thrombocytopenia remains unknown; these are to be distinguished from the entity called idiopathic thrombocytopenic purpura (ITP), which is of unknown etiology but has a specific pathogenetic mechanism involving autoantibodies against platelets (1). Diagnostic techniques for the evaluation of thrombocytopenia are listed in Table 2. The differential diagnosis of thrombocytopenia is highly important in everyday clinical practice, because its symptoms are often nonspecific and it can be a manifestation of a wide variety of underlying diseases. Differential diagnosis also serves to identify potential emergencies such as thrombotic microangiopathy (TMA) and HIT.

Table 1

Prevalence of the main types of thrombocytopenia

Table 2

Diagnostic methods for the evaluation of thrombocytopenia

Thrombocytopenia places a considerable burden on the healthcare system, as it requires frequent visits to the doctor, hospitalizations, and costly treatments.

Methods

This review is based on selected clinical studies retrieved from the MEDLINE/PubMed database with pertinent keywords (including “thrombocytopenia”), supplemented by information from recent presentations at scientific meetings, with an emphasis on fully published studies, phase 3 trials, and comparative trials of two or more treatments. The reliability of the available data is limited by the rarity of the condition and the small number of cases in many studies.

Causes of Thrombocytopenia

Pregnancy

Gestational thrombocytopenia arises in 5–10% of pregnancies and accounts for approximately 75% of cases of thrombocytopenia during pregnancy (12, 13). A systematic, stepwise diagnostic evaluation is recommended by the German Association for Obstetrics and Gynecology (Arbeitsgemeinschaft für Geburtshilfe und Gynäkologie, AGG): once pseudothrombocytopenia has been ruled out by testing with different anticoagulants (EDTA versus citrate), the ensuing steps of the differential-diagnostic algorithm depend on the platelet count (<150 000/μL), trimester of pregnancy, and clinical manifestations (14). Pseudothrombocytopenia is a common laboratory artifact (1–3 per 1000 blood samples, [2]) in which EDTA-dependent autoantibodies cause platelet aggregation in vitro. Automatic cell counters do not detect these aggregates correctly, resulting in a misdiagnosis of thrombocytopenia. Patients with pseudothrombocytopenia have no signs of bleeding and no increased bleeding tendency.

Gestational thrombocytopenia is a diagnosis of exclusion supported by a platelet count ≥ 70 000/μL and the absence of signs of bleeding (14).

Idiopathic thrombocytopenic purpura

Idiopathic thrombocytopenic purpura (ITP) is a common acquired autoimmune disease with a prevalence of 9.5 per 100 000 adults and an incidence of 1.9–8.8 per 100 000 children (4). Approximately 80% of cases are primary ITP (15). IgG autoantibodies against glycoprotein (GP)IIb/IIIa or GPIb/IX lead to increased phagocytosis in the spleen, liver, and bone marrow; megakaryopoiesis is reactively increased (16). The main clinical signs are petechiae, mucosal bleeding, and fatigue; severe bleeding is rare (less than 1%). ITP that is triggered by a viral infection tends to resolve spontaneously, while ITP with gradual onset in adults becomes chronic in 60–70% of cases (16). ITP is still a diagnosis of exclusion; bone marrow puncture is needed only for patients aged 60 and above, or in case of atypical findings (16, 17). Treatment is based on the risk of bleeding, not just on the platelet count. Corticosteroids and intravenous immunoglobulins (IVIG, 0.4 g/kg body weight daily for two to five days) are the first line of treatment; for chronic ITP, thrombopoietin (TPO) receptor agonists, rituximab, or splenectomy can be considered. The largest randomized controlled trial (n = 192) compared high-dose dexamethasone (HD-DXM) with prednisolone and showed higher initial response rates (82.1% versus 67.4%, p = 0.044) with HD-DXM (18). A meta-analysis (n = 533) confirmed a superior platelet response after 2 weeks of dexamethasone (79% versus 59%, P = 0.048) with fewer side effects. IVIG yields response rates up to 85% with an earlier onset of action (1–3 days) (19).

Drug-induced thrombocytopenia

Drug-induced thrombocytopenia may or may not be immune-mediated (20). The non-immune-mediated form is caused by a direct toxic effect on platelets and megakaryocytes. The varieties of immune-mediated thrombocytopenia included drug-induced immune thrombocytopenia (DITP), characterized by a tendency to bleed, and immune complex-induced thrombocytopenia, characterized by a thrombotic tendency (e.g., HIT, VITT).

Approximately 300 drugs can cause DITP (20). Among commonly used drugs, paracetamol (acetaminophen) and pantoprazole very rarely cause thrombotic complications (< 1/10 000); the most important precipitating drugs are heparin (3–5% for unfractionated versus 0.2% for low-molecular-weight heparin), quinine/quinidine, antibiotics such as vancomycin and trimethoprim-sulfamethoxazole, and antiepileptic drugs such as carbamazepine (21).

The treatment must begin with the immediate discontinuation of the suspect drug. In patients taking multiple drugs, all of the drugs that have been started in the last 5–10 days should be discontinued. The platelet count typically begins to rise after 4–5 half-lives of the responsible drug and usually normalizes within a week. In cases of severe thrombocytopenia with bleeding, high-dose intravenous immunoglobulins (1 g/kg body weight) can be used to accelerate recovery (22). This recommendation is mainly based on case reports and experimental data. In a mouse model, IVIG partially prevented DITP antibody-mediated platelet clearance. Randomized trials of IVIG for DITP have not yet been performed (23). Platelet transfusions are usually ineffective against DIPT if the drug or its metabolites are still circulating in the plasma (22).

Heparin-induced thrombocytopenia

HIT type I is a harmless, non-immune-mediated early form that arises 1–5 days after heparin administration and is characterized by mild thrombocytopenia (usually >100 000/µL) that resolves spontaneously (24, 25). HIT type II, on the other hand, is very dangerous because of a paradoxical thrombotic tendency despite thrombocytopenia. Changes in the complex behavior of platelets and PF4 (platelet factor 4) lead to marked platelet activation and paradoxical thrombocytopenia, while at the same time potentially activating the coagulation cascade, leading to thromboembolic complications (24). In recent studies, the thrombosis rate in patients with type II HIT was 20–64% (26). The detection of thromboembolic disturbances in HIT is especially challenging because they occur even before the platelet count drops in as many as 20% of cases.

The platelet count drops five to ten days after an exposure to heparin, typically by 50–60% of the baseline value. The platelet count rarely drops below 20 000/µL, with a median of approximately 60 000/µL (24). HIT rarely occurs more than 10 days after heparin administration. The risk of HIT is about 10 times lower with low-molecular-weight heparin (LMWH) than with unfractionated heparin (UFH) (27). Important considerations in the differential diagnosis of thrombocytopenia include its severity, time course, and accompanying clinical features: A marked drop (<20 000/µL) with bleeding more strongly suggests drug-induced immune thrombocytopenia, such as DITP, while a moderate drop (50–80 000/µL) and thromboembolic complications more strongly suggest HIT type II. HIT type I shows a mild, transient decrease of the platelet count in the first 48 hours, normalizes even with continued heparin therapy. HIT-like manifestations can also arise without exposure to heparin, fe.g., in the setting of vaccine-induced immune thrombotic thrombocytopenia (VITT) after COVID-19 vaccination, or in spontaneous, autoimmune-mediated HIT-like syndromes. HIT antibody testing be performed only if there is sufficient clinical suspicion (4T score: >3). The 4T score (also available as an online tool) comprises the four most important clinical criteria: thrombocytopenia, characteristic timing, thrombosis, and the absence of any other known cause. In a systematic review and meta-analysis of 13 studies involving a total of 3068 patients (27), the sensitivity of the 4T score at a cut-off of ≥4 (medium and high probability combined) was 99% [95% confidence interval: 86; 100], and its specificity was 54% [43; 66]. The specific negative predictive value (NPV) of a low 4T score (≤3) is 0.998 [0.970; 1.000]): this means that a low 4T score rules out HIT with near certainty. Antigen tests for the detection of HIT antibodies have a high negative predictive value (e.g., ELISA), but the detection of anti-PF4/heparin antibodies in the antigen test is not, in itself, conclusive evidence of HIT (28). The diagnosis is confirmed by a positive functional test (heparin-induced platelet activation test [HIPA test]), which checks whether platelet activation occurs in the patient’s serum when heparin is added in excess (28). If the 4T score is 4 points or above or HIT is confirmed, heparin must be discontinued and, depending on the degree of thrombocytopenia and clinical manifestations, a compatible anticoagulant (e.g., argatroban) must be started immediately (24). In a Bayesian network meta-analysis (n = 4338), argatroban was found to be associated with the lowest mortality (LOR: −1.16) and lowest bleeding rate of all anticoagulants tested (29). Argatroban and danaparoid have been approved for the treatment of acute HIT; fondaparinux and direct oral anticoagulants (DOACs) may be used as well.

Infection

Viral infection is a common cause of (transient) thrombocytopenia; many cases presumably remain undetected and unreported. The pathogenesis is complex (30). Severe or chronic viral infections (e.g., dengue, hepatitis C) can cause long-lasting thrombocytopenia (31, 32, 33). Autoimmune processes also play a role in thrombocytopenia due to cytomegalovirus (CMV), Epstein-Barr virus (EBV), varicella-zoster virus (VZV), and human immunodeficiency virus (HIV) (30, 34). Viral hemorrhagic fevers (Ebola, Marburg) are very rare in Germany; these often have severe general clinical manifestations, including shock and markedly impaired coagulation (35). COVID-19 can cause thrombocytopenia through coagulation activation, inflammation, and endothelial damage (36, 37, 38, 39). Vaccination with adenovirus-vectorized vaccines can also cause thrombocytopenia, possibly through autoimmune mechanisms (40, e1).

The detection of the underlying viral infection, or a history of vaccination that can cause thrombocytopenia, is the key to establishing the diagnosis. As for treatment COVID-19-associated thrombocytopenia is treated according to the guidelines for ITP: In cases of mild thrombocytopenia without signs of bleeding, a watch-and-wait approach is indicated (e2). For severe thrombocytopenia (<20 000/μL) or bleeding, corticosteroids (dexamethasone 40 mg for 4 days) and intravenous immunoglobulins (IVIG 1 g/kg for 1–2 days) are recommended as first-line therapy. Thrombosis prophylaxis with low-molecular-weight heparin should also be continued in patients with COVID-19 and ITP with platelet counts > 30 000/μL.

Systemic diseases

Thrombocytopenia accompanies a variety of systemic diseases, with common pathophysiological mechanisms including autoimmune reactions against platelets and their precursors, immune-mediated destruction, and impaired thrombocytopoiesis in the bone marrow (e3).

HELLP syndrome is a severe complication of preeclampsia, involving hemolysis; it arises in 0.1–0.2% of all pregnant women (e4). The diagnosis is made by the detection of hemolysis (fragmentocytes, a more than twofold increase in lactate dehydrogenase [LDH]), elevated liver values (more than twofold increase in GOT/GPT), and thrombocytopenia below 100 000/µL. Immediate delivery is indicated in pregnancies at or beyond 34 weeks of gestation or in cases with severe complications (DIC, hepatic or renal failure). Specialist care by obstetricians is essential.

Antiphospholipid antibody syndrome (APS) is an autoimmune disease with thrombophilic properties and occurs in familial, idiopathic, and secondary forms, e.g., in systemic lupus erythematosus. Thromboembolic events on the arterial and/or venous side, as well as complications of pregnancy, are typical manifestations. The diagnosis is made according to the 2023 ACR/EULAR criteria, with evidence of persistent antiphospholipid antibodies (lupus anticoagulant, anticardiolipin or anti-β2-glycoprotein I antibodies) and clinical manifestations (e5). APS-associated thrombocytopenia is usually mild (70–120 000/μL) and often does not need any specific treatment. If the thrombocytopenia is severe, the treatment is similar to that of ITP; with corticosteroids and IVIG; TPO agonists are contraindicated, however, because of the increased risk of thrombosis. In patients with APS and thrombocytopenia, careful consideration must be given to the necessary anticoagulation and the risk of bleeding. Anticoagulation, usually with vitamin K antagonists, should be continued in the setting of mild thrombocytopenia and paused only in case of severe thrombocytopenia or bleeding. Specialized consultation of a rheumatologist is recommended.

Evans syndrome is an autoimmune disease of unknown etiology characterized by simultaneous autoimmune hemolysis and immune thrombocytopenia. Its diagnosis is based on the detection of direct antiglobulin-positive autoimmune hemolysis and immune thrombocytopenia. First-line therapy for both cytopenias is with corticosteroids (prednisolone 1 mg/kg/day). Rituximab (375 mg/m²/week for four weeks) has become established as the most effective second-line treatment (e6). Because of the complexity of the disease and the associated mortality, specialist care by a hematologist is essential.

Chronic liver diseases

In patients with chronic liver disease, and especially in the setting of acute-on-chronic liver failure (ACLF), impaired coagulation with pronounced thrombocytopenia is often a component of complex multi-organ failure and has a major effect on the clinical outcome (e7). the prevalence of thrombocytopenia is only 6% among patients with chronic hepatitis are affected, but 65%-84% among those with cirrhosis (e8, e9).

Patients with cirrhosis are also at risk of thrombosis because of an imbalance in coagulation factors, despite the prolongation of global coagulation tests. Thrombocytopenia can also cause upregulation of platelet activation. TPO agonists can be used in cases of severe thrombocytopenia and bleeding: avatrombopag and lusutrombopag are the two TPO receptor agonists that have been approved for patients with cirrhosis. A randomized controlled trial with 435 subjects yielded response rates of 66–69% versus 23–35% (P<0.001) for avatrombopag versus placebo in patients with lower baseline platelet counts, and 88% versus 33–38% in patients with higher baseline platelet counts (e10).

Disseminated intravascular coagulation (DIC)

Many conditions including severe sepsis, systemic inflammatory states, trauma, and cancer activate the coagulation system. Marked activation can cause consumption coagulopathy, which manifests itself in prolonged coagulation test times and progressive thrombocytopenia. The extreme form of systemic activation of the coagulation system is disseminated intravascular coagulation (DIC), characterized by widespread blood clot formation, which, in turn, impairs organ perfusion, causing organ failure.

The prevalence of DIC is 30–50% among patients with sepsis and ca. 10% among patients with solid tumors, trauma, or obstetric complications. Its overall prevalence is estimated at 1% among hospitalized patients and 8.5–34% among critically ill patients in intensive care (e11).

The leading features of the three main DIC scoring systems are compared in the eTable. The ISTH score is highly specific, while the JAAM score is more sensitive for early DIC. The SIC score has the highest sensitivity, but very low specificity.

eTable

Features of the three DIC scoring systems

DIC is treated according to the evidence-based guidelines issued by the International Society on Thrombosis and Haemostasis (ISTH) (e11). The focus is on treating the underlying disease. Platelet transfusions are indicated only in cases of active bleeding and platelet counts <50 000/μL, or before an invasive procedure (e11, e12). Fresh frozen plasma (FFP) is recommended to treat bleeding in patients with prolonged PT/aPTT (initial dose, 15 mL/kg), although prothrombin complex concentrates can be used alternatively in patients with volume overload. In cases of severe hypofibrinogenemia (<1 g/L), fibrinogen concentrate or cryoprecipitate may be administered. Prophylactic anticoagulation with unfractionated or low-molecular-weight heparin is recommended for thrombosis prophylaxis in critically ill, non-bleeding patients with DIC.

Thrombotic microangiopathies

Thrombocytopenia is a key factor in thrombotic microangiopathies (TMA), which are rare multisystem diseases caused by dysfunction of the microvasculature. TMA are characterized by organ dysfunction, thrombocytopenia, microangiopathic hemolysis, and fragmentocytes.

The main types of TMA are:

• thrombotic thrombocytopenic purpura (TTP)
• HUS caused by higatoxin-producing pathogens (STEC-HUS)
• atypical hemolytic uremic syndrome (aHUS)
• STEC-HUS is caused by an almost always symptomatic infection with EHEC strains, with primarily gastrointestinal symptoms (diarrhea). The diagnosis is made by the detection of toxin in the stool with the polymerase chain reaction.

TTP is caused by ADAMTS13 deficiency and requires immediate treatment: if left untreated, its mortality is as high as 90%. The PLASMIC score, based on seven variables, can be used to estimate the probability of severe ADAMTS13 deficiency with high predictive power (C statistic 0.96, [0.92; 0.98]) (e17).

In TTP cases without ADAMTS13 antibodies, a hereditary form (hTTP) should be considered (e18).

TTP and aHUS can be clinically distinguished (e19):

• TTP: lower platelet counts (mean 17.4 GPT/L), milder kidney damage (mean serum creatinine 114 µmol/L)
• atypical HUS (aHUS): higher platelet counts (mean 66.6 GPT/L), more pronounced kidney damage (mean serum creatinine 454 µmol/L)

Neurological abnormalities (headaches, confusion, stroke) are characteristic of TTP, while signs of renal insufficiency such as oliguria, hypertension, and peripheral edema are more prominent in aHUS.

aHUS remains a diagnosis of exclusion, with a main focus on the search for TMA triggers such as infection, cancer, precipitating drugs, pregnancy, autoimmune disease, or other inflammatory conditions . Depending on the severity of an underlying predisposition (e.g., mutations in complement-regulating genes), these conditions can trigger the clinical picture of aHUS (e20).

In cases of Coombs-negative hemolytic anemia with thrombocytopenia, TMA must always be considered, and a blood smear must be performed (even during night shifts). This is one of the few emergencies that require immediate treatment. Testing for ADAMTS-13 activity serves to confirm the diagnosis. In an emergency, the clinical symptoms, organ dysfunction, and the detection of fragmentocytes are decisive.

If TMA is suspected, ADAMTS13 should be tested for immediately, before plasmapheresis is begun. TTP is treated with plasma exchange and immunosuppression. Caplacizumab (Cablivi®) is also used. This humanized monoclonal antibody inhibits the binding of von Willebrand factor to platelets, thereby preventing thrombus formation. Plasmapheresis-free treatment protocols involving this drug have already been used successfully (e21, e22). Regular FFP substitution is necessary for hereditary TTP, although the recently approved therapy with recombinant ADAMTS13 will improve treatment in the future (e23).

The treatment of aHUS is based on complement inhibition with eculizumab or ravulizumab. Plasmapheresis is indicated only in exceptional cases (e.g., if factor H antibodies are detected). Eculizumab is given intravenously every two weeks, while ravulizumab is given at eight-week intervals because of its longer half-life. The duration of therapy ranges from a few weeks to lifelong, depending on various factors (e.g., complement mutation status) (e24).

STEC-HUS is treated with purely supportive measures (e.g., volume therapy, renal replacement therapy as needed).

Bone marrow diseases

Bone marrow diseases can lead to inadequate formation of the cellular components of the blood, including low platelet counts. Possible causes include (e25, e26):

• clonal cytopenia of undetermined significance (CCUS)
• myelodysplastic syndrome (MDS)
• primary/secondary myelofibrosis
• chronic and acute leukemias
• lymphoma infiltration
• Less commonly, solid tumors

A manual differential blood count can provide initial evidence of bone marrow disease. Bone marrow puncture with flow cytometry and cytogenetic and molecular genetic analysis is the key to diagnosis and should be performed by a hematologist. Hypoplastic bone marrow (cellularity < 25%) may indicate aplastic anemia, possibly associated with paroxysmal nocturnal hemoglobinuria (PNH). This must be distinguished from other acquired or hereditary bone marrow failure syndromes. If a bone marrow disease is suspected, a specialized center should be consulted (e27).

Discussion

Patients with thrombocytopenia should be counseled on the basis of their platelet count, with fewer restrictions for higher counts (above 50 000/µL) and restrictions on activities and sports for lower counts. Platelet targets and measures to prevent and treat bleeding should also be considered before any invasive procedure. For any patient with a platelet count below 100 000/μL, blood should be sampled repeatedly with a special collecting system (e.g., Thromboexact) to avoid pseudothrombocytopenia, and blood smears should be performed (Box). Platelet counts below 50 000/μL or signs of bleeding call for prompt evaluation by a specialist (hematology or hemostaseology), while counts between 10 000/μL and 50 000/μL with relevant signs of bleeding or red flags indicate evaluation in a hospital emergency room. The clinical manifestations indicate the degree of urgency of further evaluation (Table 3). Red flags indicating the need for immediate intervention include persistent bleeding despite local compression, hematuria, hematemesis, or new-onset headaches and focal neurological deficits that could indicate DIC or intracranial hemorrhage. Laboratory warning signs include platelet counts below 10 000/μL, fragmentocytes, elevated LDH with elevated D-dimers and decreased fibrinogen concentration in DIC, or a greater than 50% drop in the platelet count after heparin in HIT.

Box

Case Illustration

Table 3

Symptom constellations, diseases, treatments, and urgency of medical measures in thrombocytopenia

The diagnostic evaluation of thrombocytopenia is a complex matter. We recommend a structured diagnostic algorithm based on our personal experience (Figure). Once pseudothrombocytopenia has been ruled out, the history, physical examination, and basic laboratory tests are used to differentiate among possible causes such as infection, drug effects, hematologic diseases, or autoimmune processes. Further tests, such as bone marrow biopsy, special laboratory or coagulation tests, and imaging studies, are indicated if the findings are unclear or if a serious underlying cause is suspected. The proper treatment for thrombocytopenia depends on the type and severity of the underlying disease, the severity of the bleeding tendency, the platelet count, and the patient’s overall state of health. In general, a restrictive transfusion strategy is justified in thrombocytopenia; the indication for transfusion is determined not solely by a platelet count below 10 000/µL, but also by the individual clinical risk constellation for bleeding. Platelet transfusions are contraindicated in some situations, such as TTP or ITP, unless the condition is life-threatening.

Figure

Algorithm for the evaluation of thrombocytopenia

Conflict of interest statement

RW has received lecture honoraria from, and has served as a paid consultant for, Sanofi, Alexion, and Takeda.

WM has received lecture honoraria from, and has served as a paid consultant for, Sanofi, Takeda, and Alexion.

RSA has received lecture honoraria from, and has served as a paid consultant for, Sanofi, SOBI, Amgen, Grifols, and Novartis. She has received payment for presentations from SOBI, Amgen, Novartis, and Grifols. She has received reimbursement of travel expenses from Grifols and SOBI. She has received writing support from Novartis further non-financial support from SOBI, Amgen, Grifols, and Octapharma.

Moreover, RW, TB, and WM are involved in the development of the German AWMF S3 guideline for TTP, and RSA is involved in the development of the Onkopedia guideline for ITP.

The remaining authors state that they have no conflict of interest.

Manuscript submitted on 31 December 2024, revised version accepted on 5 September 2025.

Translated from the German original by Ethan Taub, M.D.

Corresponding author
Prof. Dr. med. Wolfgang Miesbach

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