Thrombocytopenia & Immune Thrombocytopenia (ITP)

Meet the patient

A 28-year-old teacher notices bruises on her shins for two weeks, two heavy periods, and a nosebleed that took an hour to stop. She is otherwise completely well — no fevers, no weight loss, no rash, no joint pain, no new drugs.^[1]

Her full blood count shows platelets 12, haemoglobin 132, white cells 6.4, film unremarkable apart from large young platelets. She has no splenomegaly and no lymphadenopathy. The registrar reaches for steroids — and that is probably right — but the consultant's first question is the one that decides everything: is this ITP, or is this TTP? Because the treatment of one can kill the patient with the other.^[2]

A low platelet count is a mechanism problem, not a number

A platelet count is the commonest abnormal result on a full blood count, and the number alone tells you almost nothing. Platelets live 7 to 10 days, made by marrow megakaryocytes and cleared mainly by the spleen — so a low count means one of five things has happened. Memorise them once as PRODS and every thrombocytopenia becomes a five-second triage:^[2]

The bleeding risk tracks the count, and severity grading frames urgency — but the dangerous causes do not obey the count, which is why TTP at a platelet count of 20 is a one-hour emergency while ITP at 20 may go home.^[1]

ITP — the diagnosis you build by exclusion

Immune thrombocytopenia (ITP) is an acquired autoimmune disorder defined by isolated thrombocytopenia (platelets under 100), an otherwise normal full blood count, a normal marrow with normal or increased megakaryocytes, and no other identifiable cause. It is the commonest cause of isolated severe thrombocytopenia in adults and children, and the past decade has rewritten its management around TPO receptor agonists and a safe-count target rather than a cure.^[1][3]

Classification — by mechanism first, then by duration

Enlarge

Run every low platelet count through the mechanism framework before you anchor on ITP — that is the single most rewarding organising principle in a viva or long case:^[2]

• Decreased production — marrow failure (aplastic), marrow infiltration (acute leukaemia, MDS, myelofibrosis, lymphoma, metastases), chemotherapy and radiotherapy, megaloblastic anaemia (B12 or folate), alcohol, and viral marrow suppression (HIV, parvovirus B19, dengue, EBV, CMV). The marrow is abnormal and there is often pancytopenia.
• Increased destruction — immune: primary ITP, and secondary ITP (SLE, antiphospholipid syndrome, HIV, hepatitis C, common variable immunodeficiency, drugs, post-vaccination).
• Increased destruction — non-immune, microangiopathic: TTP, haemolytic-uraemic syndrome, DIC, HELLP, pre-eclampsia, malignant hypertension, giant haemangioma (Kasabach-Merritt). The film shows schistocytes — a finding that must never be missed, because the response (plasma exchange) is the opposite of ITP's.
• Sequestration — hypersplenism; roughly a third of the platelet mass is normally pooled in the spleen, rising to 90 percent when the spleen is massive.
• Dilutional — massive transfusion dilutes viable platelets.
• Spurious — EDTA-dependent platelet clumping; recheck in citrate and on the film.^[1]

ITP itself is then sliced by duration — a treatment-decision frame, not just taxonomy: newly diagnosed (under 3 months), persistent (3 to 12 months), chronic (over 12 months, roughly 60 percent of adults). And by aetiology: primary (idiopathic) versus secondary (HIV, hepatitis C, H. pylori, SLE, drugs, common variable immunodeficiency, vaccination). The International Working Group fixed these terms in 2007 to retire the misleading "acute or chronic" labels.^[1]

Epidemiology — two peaks and a childhood mirror-image

Adult ITP has an incidence of about 3 to 5 per 100,000 per year and a bimodal age curve — a peak in young women (often with other autoimmunity) and a larger, slower peak in older adults, in whom disease is more often chronic, harder to treat, and bleeds more at any count.^[1]

Childhood ITP is its mirror image: about 5 per 100,000 per year, peaks at age 2 to 5, equal sex ratio, classically acute and post-viral one to four weeks after a respiratory or GI infection or MMR, with 70 to 80 percent recovering spontaneously within 6 months.^[6]

The classic traps live in the secondary causes and the artefacts. H. pylori earns its line because eradication can produce lasting remission in high-prevalence regions (India, Japan, Latin America). EDTA-dependent pseudothrombocytopenia affects 0.1 to 0.2 percent of samples — treating it with steroids or splenectomy is an avoidable catastrophe. Gestational thrombocytopenia complicates 5 to 8 percent of pregnancies (benign); neonatal alloimmune thrombocytopenia (NAIT) affects 1 to 2 per 1000 births and can cause devastating neonatal intracranial haemorrhage.^[1]

Pathophysiology — ITP is destruction plus under-production

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Everyone was taught ITP is autoantibody-mediated platelet destruction. That is half the story, and the half you forget is why some treatments disappoint. ITP is a combined defect:^[1]

1. Autoantibody formation — polyclonal IgG against platelet glycoproteins, mainly GPIIb/IIIa and GPIb/IX, produced largely in the spleen and lymph nodes by T-cell-driven autoreactive B cells.
2. Opsonisation and destruction — antibody-coated platelets are phagocytosed by splenic macrophage Fc-gamma receptors, shortening survival from 7 to 10 days to hours. The liver also clears platelets coated with anti-GPIb antibodies — which is why splenectomy is not universally curative.
3. Impaired production — the same antibodies and cytotoxic CD8+ T cells damage megakaryocytes, so the marrow shows increased but dysfunctional megakaryocytes: present in number, unable to compensate.
4. Inappropriately normal thrombopoietin — unlike other cytopenias, TPO does not rise in ITP (it is constitutively produced by the liver and cleared by platelets), which is exactly the rationale for TPO receptor agonists.^[1]

The dangerous destructive thrombocytopenias — four mechanisms, four different rescues

The exam favourite is the differential of a low platelet count with schistocytes or thrombosis, because each mimic has a diametrically opposed treatment:^[2]

The mechanism one-liners: TTP is severe ADAMTS13 deficiency leaving ultra-large von Willebrand multimers uncleaved on endothelium, generating platelet-rich microvascular thrombi. HUS is Shiga-toxin endothelial injury (enterohaemorrhagic E. coli O157:H7) in children, renal-predominant. DIC is uncontrolled coagulation activation consuming platelets and factors at once. HIT is IgG against the PF4-heparin complex cross-linking platelet Fc receptors — the patient presents with thrombosis, not bleeding.^[1]

Clinical presentation — the site of bleeding predicts the defect

Typical ITP shows mucocutaneous (platelet-type) bleeding, and the pattern is the key clue:^[1]

• Petechiae — 1 to 2 mm, non-blanching pin-point haemorrhages in dependent areas and pressure points; the hallmark of platelet-type bleeding.
• Purpura and ecchymoses — larger spontaneous bruises, often overnight, no remembered trauma.
• Wet purpura — haemorrhagic blood blisters on the buccal mucosa; a high-risk marker for serious bleeding.
• Mucosal bleeding — epistaxis, gum bleeding, menorrhagia, GI bleeding, haematuria.^[1]

The discriminator examiners love: petechiae and mucocutaneous bleeding = a platelet problem (number or function); deep bleeding into joints and muscles (haemarthrosis, compartment bleeding) = a coagulation-factor problem (haemophilia, von Willebrand disease). The site predicts the defect.^[1]

Many adults are asymptomatic — picked up on a routine FBC — and fatigue, disproportionate to the count, is now recognised as part of ITP and a real driver of impaired quality of life. Intracranial haemorrhage is rare overall (under 1 percent) but is the feared, fatal complication, concentrated at platelets under 10 and in elderly patients and those with wet purpura or active bleeding.^[1]

Differential diagnosis — run every count through PRODS

Every low platelet count must pass through the mechanism framework, anchored by three decisive tests: the blood film (schistocytes, blasts, parasites), the coagulation screen, and, when indicated, the bone marrow. Anchoring on ITP before excluding the dangerous mimics is the commonest viva trap.^[2]

Inherited thrombocytopenias are rare but examine the family and the platelet size: Wiskott-Aldrich (small platelets, eczema, immunodeficiency, X-linked), Bernard-Soulier (giant platelets, GPIb deficiency, autosomal recessive), MYH9-related disease (giant platelets, Dohle-like bodies, nephritis, deafness, cataracts), and CAMT. The mean platelet volume on the FBC is a cheap clue: small points to Wiskott-Aldrich, giant to Bernard-Soulier or MYH9.^[1]

Clinical and bedside assessment

A focused history defines the bleeding phenotype and hunts a cause: bleeding pattern, onset and tempo, drug history (prescription, over-the-counter, herbal, quinine in tonic water), recent infection or vaccination (MMR, COVID-19), pregnancy, systemic features of SLE (malar rash, arthritis, photosensitivity, oral ulcers) or infection, alcohol, and family history of low platelets or bleeding.^[2]

Quantify bleeding with the ISTH Bleeding Assessment Tool or the WHO bleeding scale (grades 0 to 4) — a high score predicts worse outcomes and justifies treatment beyond the count: a well patient at 25 is managed differently from one with wet purpura at 25.^[1]

Examination is decisive. Skin and mucous membranes for petechiae in dependent distribution and wet purpura (a danger sign); abdomen for splenomegaly (which excludes primary ITP and points to sequestration, infiltration, portal hypertension, or myeloproliferative disease); lymph nodes (lymphoma, HIV); and systemic clues (malar rash of SLE, jaundice and chronic liver disease, fever and sepsis focus, pregnancy, malignancy). The cardinal message: isolated thrombocytopenia in an otherwise well patient with no splenomegaly and no lymphadenopathy is ITP until proven otherwise — splenomegaly or extra cytopenias demand another diagnosis and a marrow.^[1]

Investigations — ITP is a diagnosis of exclusion

ITP is a diagnosis of exclusion: investigations confirm the criteria and, more importantly, exclude the dangerous mimics. The goal is not to "prove" ITP but to exclude everything else.^[1][3]

First-line tests, every patient:^[1]

• Full blood count — isolated thrombocytopenia; haemoglobin, MCV and white cells normal. Pancytopenia or macrocytosis demands another diagnosis.
• Blood film (essential) — confirms true thrombocytopenia (excludes EDTA clumping), looks for large or giant platelets (peripheral destruction), schistocytes (do not miss TTP, HUS, DIC), blasts (leukaemia), malarial parasites, Dohle-like bodies (MYH9), leucoerythroblastic features.
• Repeat platelet count in a citrate tube — to exclude EDTA-dependent pseudothrombocytopenia.
• Coagulation screen (PT, APTT, fibrinogen, D-dimer) — normal in ITP. Prolonged PT and APTT with low fibrinogen and high D-dimer = DIC.
• Blood group (ABO and Rh), renal and liver function, LDH, haptoglobin, direct antiglobulin test — to assess haemolysis and plan anti-D therapy.^[1]

Bone marrow aspirate and trephine shows normal or increased megakaryocytes. It is indicated for atypical features (extra cytopenias, macrocytosis, abnormal film), age over 60, before splenectomy, or refractory disease. It is not required in a typical young adult or child with isolated thrombocytopenia and a normal film — routine marrow here is over-investigation.^[1]

Secondary-cause screen in all newly diagnosed adults: HIV and hepatitis C serology (mandatory — they change management), H. pylori testing (higher yield in high-prevalence regions), antinuclear antibody and anti-dsDNA, beta-HCG, thyroid function, quantitative immunoglobulins (CVID), and a pregnancy test in women of childbearing age.^[2]

Tests NOT routinely useful: platelet-associated antibody (low specificity), anti-GPIIb/IIIa assays (research only), routine TPO level. ADAMTS13 is sent only when TTP is suspected (under 10 percent is diagnostic) — never as a blanket test.^[1]

Management — resuscitation

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ABCDE first. The single most important triage question is "is this ITP, or is this TTP, DIC or HIT?", because the treatments diverge completely — HIT and the thrombotic microangiopathies are among the causes that need emergency hospitalization, while ITP without bleeding often does not.^[9] Life-threatening bleeding or suspected intracranial haemorrhage in ITP is treated with corticosteroids plus IVIg; corticosteroids are the standard initial treatment for newly diagnosed ITP, and IVIg is an established ITP therapy.^[2][6] Prophylactic platelet transfusion is NOT given in ITP — transfusion may be considered for a platelet count below 50 × 10^9/L before an intervention or operation, but never as routine prophylaxis.^[10]

In ITP, transfused platelets are rapidly destroyed (survival in hours), so they are given with IVIg and steroids only for active life-threatening bleeding or before an emergency procedure — not prophylactically, and not to raise the number alone. General haemostatic measures: avoid intramuscular injections, NSAIDs and antiplatelets, control hypertension, suppress menses, and give tranexamic acid for mucosal bleeding when there is no thrombotic contraindication and no haematuria (clots can obstruct the renal tract).^[1]

Management — definitive and stepwise

The guiding principle, repeated until it is reflexive: aim for a SAFE platelet count (haemostatic, generally over 30), not a normal count. Asymptomatic patients over 20 to 30 may be observed. Treat the bleeding patient, not the number.^[3]

First-line therapy:^[1][3]

• Prednisone 1 mg/kg per day from days 0 to 28 — the standard-dose corticosteroid regimen, compared head-to-head with the dexamethasone pulse in a randomised trial of newly diagnosed adults.^[8]
• High-dose dexamethasone 40 mg per day for 4 days, repeated every 14 days for up to three consecutive courses — the alternative first-line pulse regimen.^[8]
• IVIg (intravenous immunoglobulin) — an established ITP therapy, listed alongside corticosteroids and splenectomy among prior treatments in the romiplostim paediatric licensing trials; a treatment goal is to resolve bleeding events and prevent severe bleeding.^[6][2]

Second-line therapy (chronic, persistent, refractory, or steroid-dependent):^[1][3]

• TPO receptor agonists — eltrombopag 50 mg once daily is the regimen used in the RAISE phase 3 trial: adults with previously treated chronic ITP (platelets under 30 × 10^9/L) received standard care plus 50 mg eltrombopag or placebo once daily for 6 months, with dose modifications made on the basis of platelet response.^[7] Romiplostim is a once-weekly subcutaneous injection, FDA-approved for children 1 year and older with ITP of over 6 months' duration and insufficient response to corticosteroids, immunoglobulins or splenectomy.^[6]
• Rituximab — the standard dose is 375 mg/m2 (low-dose 100 mg regimens also studied); a meta-analysis of 12 trials in 869 adults found rituximab increased complete and overall response rates versus control.^[14]
• Splenectomy — in a 20-year single-centre series of 174 adults, 72.4 percent achieved a complete response and a further 16.1 percent a response; 20.8 percent of responders relapsed (median 24 months). It carries overwhelming post-splenectomy infection risk — see the vaccination and antibiotic-prophylaxis requirements below.^[16][18]
• Fostamatinib — the first spleen tyrosine kinase (Syk) inhibitor approved for chronic ITP in adults with an insufficient response to previous treatment; in the placebo-controlled phase 3 FIT1 and FIT2 trials, 24 weeks of oral fostamatinib increased platelet counts in previously treated adults.^[15]
• Rilzabrutinib — an oral BTK inhibitor with dual mechanisms (decreased macrophage Fcγ-receptor-mediated platelet destruction and reduced production of pathogenic autoantibodies), showing platelet responses in previously treated ITP in a phase 1-2 trial.^[5]

Second-line selection is individualised — no rigid ladder — and combination therapy (TPO-RA plus rituximab) is increasingly used.^[4]

Specific subtypes and scenarios

• Childhood ITP — in children ITP is usually a self-limiting and benign disorder; management is observation-first when bleeding is absent or mild, because robust randomised trials are lacking and much paediatric guidance rests on expert opinion. The Italian AIEOP consensus conference stresses that treatment varies widely in practice and should be reserved for significant bleeding.^[12]
• Pregnancy — thrombocytopenia occurs in about 10 percent of pregnancies and is dominated by gestational thrombocytopenia (over 75 percent of cases): it typically appears in the last trimester, requires no exploration or specific treatment, and corrects itself spontaneously after delivery. ITP is the other main immune cause and may appear as early as the first trimester; the obstetric emergencies — pre-eclampsia and HELLP — are treated with resuscitative and symptomatic measures and delivery.^[13][9]
• Secondary ITP — treat the underlying cause. H. pylori eradication produces a significant platelet response in chronic ITP — a Middle East meta-analysis of seven studies (228 infected patients) found an odds ratio of 8.83 for platelet response with eradication versus no eradication.^[17] For drug-induced and immune-mediated cases, treatment can include discontinuation of precipitating drugs, immunosuppressive drugs, or TPO receptor agonists.^[10]
• Heparin-induced thrombocytopenia (HIT) — an adverse drug reaction of platelet-activating antibodies against platelet factor 4–heparin complexes, carrying a markedly increased risk of thromboembolism — thrombosis, not bleeding. Diagnose with the 4Ts score (strongly recommended over gestalt assessment); stop all heparin and treat with a non-heparin anticoagulant — argatroban, bivalirudin, danaparoid, fondaparinux or a direct oral anticoagulant.^[11]

Complications and pitfalls

Disease complications: severe mucosal or GI bleeding; menorrhagia (iron deficiency, hormonal suppression); intracranial haemorrhage — rare overall but catastrophic, concentrated under 10 and in the elderly and those with wet purpura. Fatigue and impaired quality of life are common and independent of the count.^[1]

Treatment-related complications:^[1]

• Corticosteroids — diabetes, hypertension, osteoporosis, peptic ulcer, infection, mood disturbance, weight gain, avascular necrosis, myopathy; why long courses are avoided and TPO-RA deployed earlier in older patients.
• IVIg — infusion reactions, headache (including aseptic meningitis), thromboembolism (stroke, MI, DVT — important in older or vascular patients), renal impairment, haemolytic anaemia (especially non-O blood groups), transfusion-related acute lung injury.
• Splenectomy — OPSI from encapsulated organisms, portal vein thrombosis, operative risk; requires pre-op vaccination, lifelong penicillin V, a medical alert, and a standing instruction to present with any febrile illness.
• TPO receptor agonists — thrombosis (when counts overshoot), hepatotoxicity (eltrombopag — monitor LFTs), rebound thrombocytopenia on abrupt cessation, marrow reticulin fibrosis with long-term use.
• Rituximab — infusion reactions, hepatitis B reactivation (screen first), late-onset neutropenia, hypogammaglobulinaemia.^[1]

The classic pitfalls: missing TTP (fatal — never transfuse platelets); missing leukaemia or marrow failure (marrow if atypical features, age over 60, or refractory); over-treating the number (a well patient over 30 needs observation, not escalating immunosuppression); failing to vaccinate before splenectomy; missing secondary causes (HIV, HCV, H. pylori); diagnosing EDTA pseudothrombocytopenia as true disease (always check a citrate tube and the film); and confusing HIT (thrombosis, stop heparin) with other drug-induced thrombocytopenias (bleeding, stop the drug).^[1]

Prognosis and disposition

• Childhood ITP — 70 to 80 percent spontaneous remission within 6 months; only 20 to 25 percent become chronic; mortality from intracranial haemorrhage is very low (under 1 percent).^[6]
• Adult ITP — usually chronic; only 10 to 30 percent achieve lasting remission; overall mortality is low but intracranial haemorrhage is catastrophic when it occurs, in elderly patients with counts under 10 and active bleeding. Treatment aims for a safe count and preserved quality of life, not cure.^[1]
• Disposition — outpatient if no or mild bleeding and platelets over 20 to 30; admit for active bleeding, wet purpura, platelets under 10 to 20, or to initiate urgent therapy.
• Splenectomy achieves a durable response in about two-thirds, but is now used far less because of TPO-RA efficacy and the permanent OPSI risk.^[1]

Special populations

• Children — childhood ITP is usually self-limiting and benign; observe without treatment when bleeding is absent or mild, and reserve therapy for significant bleeding.^[12]
• Pregnancy — distinguish benign gestational thrombocytopenia (over 75 percent of pregnancy thrombocytopenia; last trimester; resolves spontaneously postpartum) from ITP, which may present as early as the first trimester; watch for the obstetric emergencies pre-eclampsia and HELLP.^[13]
• Anticoagulated patient with new thrombocytopenia — if HIT is possible, stop heparin first and switch to a non-heparin anticoagulant (argatroban, bivalirudin, danaparoid, fondaparinux or a DOAC), guided by the 4Ts score.^[11]

Evidence, guidelines and regional differences

• The international consensus report (Provan 2019, Blood Advances) is the global reference for primary ITP — diagnosis, first- and second-line therapy, emergency management.^[1]
• The ASH 2019 guidelines (Neunert) agreed 21 recommendations covering the management of ITP in adults and children; the 2022 review confirmed they map to recommendations 1-9 for adults and 10-21 for children after re-reviewing 193 studies published to July 2022.^[3][4]
• The RAISE trial (Cheng 2011, Lancet) established eltrombopag as durable 6-month second-line therapy for chronic ITP — the landmark that shifted TPO-RA from rescue to mainstream long-term therapy.^[7]
• Romiplostim for paediatric ITP and TPO-RA broadly have transformed second-line therapy and reduced the need for splenectomy.^[6]
• Rilzabrutinib, an oral BTK inhibitor, demonstrated response in refractory ITP, expanding the targeted armamentarium alongside fostamatinib (SYK).^[5]
• Beyond the guidelines. A randomised trial defines the two first-line corticosteroid regimens (prednisone 1 mg/kg daily vs high-dose dexamethasone 40 mg daily for 4 days);^[8] a splenectomy series of 174 adults reports 72.4 percent complete response at long-term follow-up;^[16] a rituximab dosing meta-analysis confirms 375 mg/m2 as the standard dose;^[14] and H. pylori eradication shows a significant platelet response in Middle East cohorts.^[17]

The mantra

Treat the patient, not the number — aim safe (over 30), exclude TTP before steroids, and never platelet-transfuse TTP.^[1]

Ward-round test

Stem 1 — the rapid responderShowHide

A 30-year-old woman, platelets 8, widespread petechiae and epistaxis, otherwise well, normal film and coagulation. What is the first-line treatment, and when would you reach for IVIg?^[1]

AnswerShowHide

Prednisone 1 mg/kg per day from days 0 to 28, or high-dose dexamethasone 40 mg per day for 4 days (repeated every 14 days for up to three courses), is first-line — the two regimens compared head-to-head in a randomised trial of newly diagnosed adults.^[8] IVIg is the alternative immunoglobulin option when corticosteroids are unsuitable, and the goal of therapy is to resolve bleeding events and prevent severe bleeding, not to normalise the count.^[6][2]

Stem 2 — the mimic that killsShowHide

A 35-year-old man, platelets 15, confusion and headache, creatinine rising, film shows schistocytes. The registrar suggests IVIg and platelets. What do you do?^[2]

AnswerShowHide

Stop. This is TTP until proven otherwise — not ITP. Start urgent plasma exchange within 4 to 8 hours plus corticosteroids and caplacizumab if available. Do NOT give platelets (they fuel microvascular thrombosis) and do NOT wait for the ADAMTS13 result — treat on clinical suspicion. A normal ADAMTS13 later lets you step back; a delayed plasma exchange kills.^[2]

Stem 3 — the splenectomy trapShowHide

A 52-year-old with chronic ITP is listed for laparoscopic splenectomy. Name the two non-negotiable pre-operative steps and the lifelong prescription.^[1]

AnswerShowHide

Two non-negotiables: immunisation and antibiotic prophylaxis. Post-splenectomy sepsis carries very high mortality and is partly preventable by immunizations and prophylactic or early use of antibiotics — so vaccinate before surgery, prescribe standing antibiotic prophylaxis, give a medical alert, and instruct the patient to present urgently with any febrile illness.^[18]

Stem 4 — the artefactShowHide

A well 45-year-old has platelets 25 on a routine FBC, no bleeding, no splenomegaly. The lab flags clumping. What is the next step before any treatment?^[1]

AnswerShowHide

Exclude EDTA-dependent pseudothrombocytopenia: recheck the platelet count in a citrate tube and confirm on the blood film. If the citrate count is normal, the patient has no disease — treating with steroids or splenectomy would be an avoidable catastrophe.^[1]

References18ShowHide

1. [1]Provan D, Arnold DM, Bussel JB, et al. Updated international consensus report on the investigation and management of primary immune thrombocytopenia Blood Adv, 2019.PMID 31770441
2. [2]Anat GG Current approaches for the diagnosis and management of immune thrombocytopenia Eur J Intern Med, 2023.PMID 36424271
3. [3]Neunert C, Terrell DR, Arnold DM, et al. American Society of Hematology 2019 guidelines for immune thrombocytopenia Blood Adv, 2019.PMID 31794604
4. [4]Neunert CE, Arnold DM, Grace RF, et al. The 2022 review of the 2019 American Society of Hematology guidelines on immune thrombocytopenia Blood Adv, 2024.PMID 38608258
5. [5]Kuter DJ, Efraim M, Mayer J, et al. Rilzabrutinib, an Oral BTK Inhibitor, in Immune Thrombocytopenia N Engl J Med, 2022.PMID 35417637
6. [6]Neunert CE, Rose MJ Romiplostim for the management of pediatric immune thrombocytopenia: drug development and current practice Blood Adv, 2019.PMID 31239245
7. [7]Cheng G, Saleh MN, Marcher C, et al. Eltrombopag for management of chronic immune thrombocytopenia (RAISE): a 6-month, randomised, phase 3 study Lancet, 2011.PMID 20739054
8. [8]Mazzucconi MG, Rodeghiero F, Avvisati G, et al. Prednisone vs high-dose dexamethasone in newly diagnosed adult primary immune thrombocytopenia: a randomized trial Blood Adv, 2024.PMID 38231017
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11. [11]Cuker A, Arepally GM, Chong BH, et al. American Society of Hematology 2018 guidelines for management of venous thromboembolism: heparin-induced thrombocytopenia Blood Adv, 2018.PMID 30482768
12. [12]Russo G, Parodi E, Farruggia P, et al. Recommendations for the management of acute immune thrombocytopenia in children. A Consensus Conference from the Italian Association of Pediatric Hematology and Oncology Blood Transfus, 2024.PMID 37677093
13. [13]Khellaf M, Loustau V, Bierling P, et al. Thrombocytopenia and pregnancy Rev Med Interne, 2012.PMID 22742709
14. [14]Dong Y, Yue M, Hu M The Efficacy and Safety of Different Dosages of Rituximab for Adults with Immune Thrombocytopenia: A Systematic Review and Meta-Analysis Biomed Res Int, 2021.PMID 34660807
15. [15]Paik J Fostamatinib: A Review in Chronic Immune Thrombocytopenia Drugs, 2021.PMID 33970459
16. [16]Guan Y, Wang S, Xue F, et al. Long-term results of splenectomy in adult chronic immune thrombocytopenia Eur J Haematol, 2017.PMID 27753191
17. [17]Pezeshki SMS, Saki N, Ghandali MV, et al. Effect of Helicobacter Pylori eradication on patients with ITP: a meta-analysis of studies conducted in the Middle East Blood Res, 2021.PMID 33707351
18. [18]Lammers AJ, van der Maas N, Peters EJ Prevention of severe infections in patients with hyposplenism or asplenia Ned Tijdschr Geneeskd, 2012.PMID 23114171