Abstract
Background
Aggressive chemoradiotherapy for limited-stage small cell lung cancer (SCLC) frequently causes severe hematologic toxicities, particularly chemotherapy-induced thrombocytopenia (CIT), which can compromise treatment efficacy. While thrombopoietin receptor agonists (TPO-RAs) are preferred for CIT management, refractory cases pose significant challenges.
Case presentation
A patient with stage IIIC (cT3N3M0) limited-stage SCLC achieved a durable partial response exceeding five years following etoposide/cisplatin chemotherapy and concurrent thoracic radiotherapy (60 Gy). However, severe, persistent, and refractory CIT developed, unresponsive to multiple interventions including recombinant human thrombopoietin (rhTPO), avatrombopag, eltrombopag, corticosteroids, thalidomide, tretinoin, and intermittent platelet transfusions. Bone marrow aspiration confirmed profound hypocellularity and megakaryocytic hypoplasia.
Intervention & outcome
Initiation of subcutaneous romiplostim successfully elevated and maintained platelet counts, enabling sustained disease control. Platelet counts declined rapidly below 100×10&xxx2079;/L upon extending the dosing interval beyond 3-4 weeks, indicating that platelet maintenance remained dependent on continued romiplostim administration.
Conclusion
This case demonstrates romiplostim’s efficacy in managing severe, refractory CIT following intensive SCLC therapy, facilitating long-term disease control in a sustained responder. It highlights the critical role of TPO-RAs in this setting but underscores challenges including ongoing dependence on continued romiplostim for platelet maintenance and the need for strategies to coordinate romiplostim with future systemic therapies should disease progression occur. The potential for loss of romiplostim response necessitates exploration of alternative approaches.
Keywords: chemotherapy-induced thrombocytopenia, refractory thrombocytopenia, romiplostim, small cell lung cancer, thrombopoietin receptor agonist
1. Introduction
Small cell lung cancer (SCLC) is an aggressive malignancy characterized by rapid growth and early metastasis, with over 70% of patients presenting with extensive-stage disease at diagnosis (1). For limited-stage SCLC, the cornerstone of first-line treatment is platinum-based chemotherapy (typically etoposide plus cisplatin, EP) combined with thoracic radiotherapy, an approach that has been further enhanced by the integration of immune checkpoint inhibitors like durvalumab (2, 3). However, the intensification of this multimodal therapy inevitably amplifies treatment-related toxicities, particularly hematological adverse events. Severe myelosuppression, including neutropenia and thrombocytopenia, occurs frequently, affecting more than 30% of patients receiving chemoradiotherapy, and represents a major cause of treatment delays or dose reductions that can compromise efficacy (4).
Chemotherapy-induced thrombocytopenia (CIT) poses a significant clinical challenge due to the risk of bleeding and the historical lack of broadly effective pharmacological interventions (5). While recombinant human granulocyte colony-stimulating factor (rhG-CSF) has improved the management of neutropenia, effective strategies for CIT have been more elusive. Interleukin-11 (IL-11) was previously explored but is no longer recommended due to significant drawbacks, including dose-dependent fluid retention, cardiotoxicity, arrhythmias, and critically, well-documented pro-oncogenic properties that may promote tumor growth, metastasis, and chemoresistance (6).
Thrombopoietin receptor agonists (TPO-RAs) have emerged as the preferred therapeutic class for managing CIT. These agents stimulate platelet production by activating the thrombopoietin receptor (c-Mpl) on megakaryocytes (7, 8). Recombinant human thrombopoietin (rhTPO) demonstrated efficacy but faced potential limitations like immunogenicity. Second-generation TPO-RAs, including the peptibody romiplostim and oral agents like avatrombopag (9), eltrombopag (10), and hetrombopag (11), offer distinct pharmacological profiles and administration routes (8). Romiplostim, administered subcutaneously, exhibits potent thrombopoietic activity through molecular targeting of c-Mpl, activating key signaling pathways (JAK2/STAT5, PI3K/Akt, ERK), and uniquely, beneficial immunomodulatory effects via TGF-β enhancement and potential Fc-mediated immune tolerance (12).
This report details the case of a patient with limited-stage SCLC (cT3N3M0, stage IIIC) who achieved a durable partial response (PR) exceeding five years following treatment with concurrent chemoradiotherapy (EP regimen plus 60 Gy radiotherapy). However, the patient developed severe, persistent, and refractory CIT, unresponsive to multiple therapeutic interventions including rhTPO, avatrombopag, eltrombopag, corticosteroids, thalidomide, tretinoin, and intermittent platelet transfusions. Bone marrow aspiration confirmed profound hypocellularity and megakaryocytic hypoplasia. Ultimately, romiplostim therapy successfully elevated and maintained platelet counts, enabling long-term disease control. This case highlights the critical role of TPO-RAs, specifically romiplostim, in managing refractory CIT within the context of aggressive SCLC therapy, while also underscoring the challenge of ongoing dependence on continued romiplostim for platelet maintenance and the need for strategies to coordinate CIT management with potential future systemic anticancer treatments should disease progression occur.
2. Case presentation
2.1. Chief complaint
A 55-year-old man, previously a farmer, presented with cough and expectoration for over one month. No headache, dizziness, nausea, or vomiting. No hoarseness, dysphagia, shortness of breath, or chest pain. No hemoptysis or limb weakness.
2.2. Past medical history
Previously healthy.
2.3. Personal history
Smoking history of 60 pack-years (1200 cigarette-years), quit approximately 1 month prior to diagnosis. Alcohol consumption history for over 30 years, equivalent to approximately 212 grams per day. Family history was unremarkable for malignancy. His past medical history is negative for any chronic diseases, previous surgeries, or severe trauma.
2.4. Physical examination
Zubrod performance status score of 1. Scattered skin petechiae present over the body, more pronounced on both lower limbs and back. No superficial lymphadenopathy detected. Lungs clear without rales or rhonchi. Heart rhythm regular; no pathological murmurs auscultated. Abdomen soft and flat, no tenderness or rebound tenderness. Liver and spleen not palpable below costal margins. No costovertebral angle tenderness. No abnormal abdominal masses palpated. No mucosal, gingival, nasal, conjunctival, or gastrointestinal bleeding was present.
2.5. Imaging studies
Contrast-enhanced Chest CT: A left hilar mass measuring approximately 5 × 7 cm, encasing the left upper lobe bronchus. Multiple enlarged lymph nodes noted in the mediastinum and left hilum; the largest, located anterior and right to the trachea, measured approximately 3.7 × 4.6 cm.
Bone Scan (ECT):No definite evidence of bone metastasis.
Contrast-enhanced Brain MRI: No evidence of intracranial metastasis.
Neck Ultrasound: No significant cervical lymphadenopathy detected.
2.6. Laboratory investigations
Final Diagnosis: Small cell lung cancer of the left lung (cT3N3M0 stage IIIC, limited stage). Metastases to bilateral mediastinal and bilateral hilar lymph nodes(Figure 1).
Figure 1.
Histopathological confirmation of small-cell lung cancer. (A) Haematoxylin–eosin staining shows small tumour cells with scant cytoplasm and finely granular chromatin. (B) Immunohistochemistry shows a high Ki-67 proliferation index.
2.7. Treatment course
Cycle 1-4: EP regimen (cisplatin 75 mg/m² on day 1 plus etoposide 100 mg/m² on days 1–3, every 21 days, per the CONVERT protocol (18)) for 4 cycles.
Cycle 5: Concurrent chemoradiotherapy with EP regimen.
Radiotherapy regimen: A total dose of 60 Gy in 30 fractions.
Cycle 6: EP regimen (Etoposide + Cisplatin) for 1 cycle.
2.8. Treatment response evaluation
Partial Response (PR)
Treatment response evaluations after cycles 2, 4, and 6: PR.
Re-evaluation at 90 days post-treatment completion: PR.(Figure 2)
Figure 2.
Serial contrast-enhanced chest CT. (A) Baseline; (B) after 2 cycles of chemotherapy; (C) after 4 cycles; (D) after concurrent chemoradiotherapy; (E) after 6 cycles; (F) 6 months after treatment completion. The tumour maintained a partial response throughout.
2.9. Treatment adverse effects
2.9.1. Neutropenia
Grade 3 neutropenia occurred during cycle 2 (WBC: 2.61×109/L, ANC: 0.65×109/L, Platelets: 235×109/L). Corrected after administration of G-CSF (6 mg). Subsequent cycles included prophylactic pegylated recombinant human G-CSF (6 mg) administered 24 hours post-chemotherapy, preventing further severe bone marrow suppression.
2.9.2. Severe neutropenia and thrombocytopenia
Post-Treatment: Grade 4 neutropenia developed after chemoradiotherapy completion (WBC: 0.59×109/L, ANC: 0.15×109/L, Hemoglobin: 94 g/L, Platelets: 27×109/L) accompanied by fever (peak temperature >40 °C) and scattered skin petechiae. Managed with G-CSF, antibiotics, IL-11 (interleukin-11), and cafaminol (coagulation stimulant). Neutropenia resolved; thrombocytopenia persisted.
2.9.3. Thrombocytopenia management summary
2.9.3.1. Phase 1
Treatment: Oral avatrombopag (20 mg once daily) or eltrombopag (25 mg once daily) (approximately 4–13 months after diagnosis; throughout, time points are expressed relative to the date of diagnosis).
Outcome: Ineffective; no significant platelet increase.
2.9.3.2. Phase 2
Treatment: Prednisone (1 mg/kg/day) + thalidomide (50 mg nightly) + tretinoin (all-trans retinoic acid, 10 mg twice daily) (approximately 13–15 months after diagnosis).
Outcome: Ineffective; no significant platelet increase.
2.9.3.3. Phase 3
Treatment: Prednisone (1 mg/kg/day) + thalidomide (50 mg nightly) + tretinoin (all-trans retinoic acid, 10 mg twice daily) + recombinant human thrombopoietin (rhTPO) 15000 units/day for 14 days (approximately 15–20 months after diagnosis).
Outcome: Ineffective; no significant platelet increase.
Perform a bone marrow aspiration test: (approximately 20 months after diagnosis)
The bone marrow cellularity is markedly decreased, nucleated cells are sparse, fat cells are significantly increased presenting a “desolate” sign; hematopoietic cells of three lineages are concurrently reduced, the proportion of erythroid precursors at all stages sharply decreases, precursor granulocytic cells and mature neutrophils are significantly reduced and a developmental “gap” can be seen, the number of megakaryocytes is markedly reduced, platelet production is extremely low;the morphology of residual cells is normal, no increase in blast cells, no dyshematopoiesis or malignant cell infiltration;non-hematopoietic components in the interstitium are relatively increased.(Figure 3)
Figure 3.
Bone marrow aspiration. (A) The aspirate smear shows severe hypocellularity, with markedly reduced nucleated cells and increased adipose tissue. (B) All three lineages are suppressed — scant erythroid precursors, granulocytic maturational arrest, and near-absent megakaryocytes; the residual cells are morphologically normal, with no blasts, dysplasia or malignant infiltration.
2.9.3.4. Phase 4
Treatment: Intermittent platelet transfusions (approximately monthly) plus rhTPO (from approximately 20 months onward).
Outcome: Ineffective. Platelet counts transiently increased post-transfusion but declined to <10×109/L within 3–4 weeks.
2.9.3.5. Phase 5
Treatment: Romiplostim 250 µg weekly (qw), later changed to Romiplostim 250 µg every 3 weeks (q3w) approximately 57 months after diagnosis [≈4.8 years] to present.
Outcome: Effective. Platelet counts increased significantly (up to 263×109/L) within 1 week of administration. However, counts decreased below 100×109/L upon extending the dosing interval.
2.10. For now
The patient maintains well-controlled cancer and has been in a partial response (PR) state for over 5 years. The patient receives romiplostim via subcutaneous injection every three to four weeks for thrombocytopenia. The all-treatment plan is showed in Figure 4 and Table 1.
Figure 4.
Longitudinal blood counts and treatment phases. Platelet (A), leukocyte (B), neutrophil (C), haemoglobin (D) and erythrocyte (E) counts across the six treatment phases (P1–P6, top ribbon). Romiplostim (dashed line, ~57 months after diagnosis) raised the platelet count to a peak of 263×109/L, which then declined when the dosing interval was extended.
Table 1.
Chronological summary of thrombocytopenia management, platelet response, and outcome.
| Phase | Period | Intervention (dose / duration) | Platelet (×109/L) | Response / outcome |
|---|---|---|---|---|
| P1 | Diagnosis to ~5 months | EP chemotherapy ×6 cycles (cisplatin 75 mg/m² d1 + etoposide 100 mg/m² d1–3, q21d) + concurrent thoracic radiotherapy 60 Gy/30 fractions; prophylactic PEG-G-CSF 6 mg from cycle 2 | Baseline 235 → post-treatment nadir 27 | Grade 4 neutropenia (WBC 0.59) and severe thrombocytopenia emerged; neutropenia resolved, thrombocytopenia persisted |
| P2 | ~5–13 months | Avatrombopag 20 mg once daily or eltrombopag 25 mg once daily (oral) | 1–27 (persistently low) | Ineffective; no significant platelet increase |
| P3 | ~13–15 months | Prednisone 1 mg/kg/day + thalidomide 50 mg nightly + tretinoin (ATRA) 10 mg twice daily | 3–7 | Ineffective |
| P4 | ~15–20 months | Prednisone 1 mg/kg/day + thalidomide 50 mg nightly + tretinoin 10 mg twice daily + rhTPO 15000 U/week | 1–10 | Ineffective |
| — | ~20 months after diagnosis | Bone marrow ASPIRATION (no biopsy / flow / cytogenetics / PNH / molecular performed) | — | Severe hypocellularity, trilineage suppression, markedly reduced megakaryocytes; no dysplasia or malignant infiltration |
| P5 | ~20–57 months | Intermittent platelet transfusion (~monthly) + rhTPO | 1–26 | Ineffective; transient post-transfusion rise, declined to <10 within 3–4 weeks |
| P6 | ~57 months to present | Romiplostim 250 µg subcutaneously, weekly (qw) → every 3 weeks (q3w) | 13 → peak 263; falls <100 when interval extended | Effective; platelet maintained, but maintenance dependent on continued romiplostim administration |
3. Discussion
Small cell lung cancer (SCLC) accounts for approximately 15% of lung cancers, and over 70% of patients present with extensive-stage disease (1, 13, 14). For limited-stage disease, platinum–etoposide chemotherapy combined with thoracic radiotherapy is the cornerstone of first-line treatment, and the addition of immune checkpoint inhibitors (e.g., the ADRIATIC trial) further improves survival (10, 15). This multimodal intensification, however, amplifies treatment-related toxicity — grade ≥3 neutropenia affects >30% of patients (16) — underscoring the need for strategies that limit toxicity while preserving efficacy (17).
Concurrent chemoradiotherapy significantly exacerbates myelotoxicity, particularly myelosuppression (15, 18). This manifests primarily as neutropenia, anemia, and thrombocytopenia. Although supportive care measures, including recombinant human granulocyte colony-stimulating factor (rhG-CSF), have substantially ameliorated chemotherapy-induced neutropenia, thrombocytopenia remains a persistent challenge. Thrombocytopenia is particularly problematic as it lacks broadly effective pharmacological interventions and represents a leading cause of chemotherapy dose delays or interruptions. Effective management of chemotherapy-induced thrombocytopenia (CIT) is therefore crucial for maintaining treatment intensity and optimizing outcomes in SCLC (19).
Historically, interleukin-11 (IL-11) was used as a thrombopoietic agent for CIT, promoting megakaryocyte maturation and platelet release through JAK-STAT signalling (20, 21). However, its use is now discouraged: beyond dose-dependent fluid retention and atrial arrhythmias, IL-11 has well-documented pro-oncogenic properties — persistent STAT3 activation promotes tumour proliferation and chemoresistance, and IL-11 derived from cancer-associated fibroblasts drives tumour growth and correlates with poor prognosis (22, 23). Given this toxicity and pro-tumorigenic potential, IL-11 is no longer recommended for CIT management.
Thrombopoietin receptor agonists (TPO-RAs) are now the preferred approach for CIT (24). A 2025 network meta-analysis (16 RCTs, n=1,746) confirmed that they significantly reduce chemotherapy delays or dose reductions (OR = 0.37) and grade 3/4 thrombocytopenia (OR = 0.50) (32). Recombinant human thrombopoietin (rhTPO), the first-generation agent, is effective but limited by immunogenicity and cost (24–26).
Among second-generation TPO-RAs, romiplostim — a subcutaneous peptibody that binds the native TPO-binding site and additionally exerts immunomodulatory effects — is the best supported for CIT (Table 2) (9–12, 27–30). In the phase 3 RECITE trial of 165 patients with persistent CIT, 84% of romiplostim-treated patients needed no CIT-related chemotherapy dose modification versus 36% with placebo (OR 10.16; 95% CI 4.44–23.72; P<0.001) (31); a real-world study likewise showed faster platelet recovery with romiplostim than rhTPO (9 vs. 12 days; P = 0.012) (33).
Table 2.
Comparison of the thrombopoietin receptor agonists relevant to this case (romiplostim and eltrombopag) and recombinant human thrombopoietin (rhTPO).
| Feature | Romiplostim | Eltrombopag | rhTPO |
|---|---|---|---|
| Type | Peptibody (Fc-fusion protein)(s.c.) | Small molecule (Oral) | Recombinant protein (s.c./i.v.) |
| Administration | Subcutaneous (Weekly) | Oral (Once daily) | Subcutaneous / Intravenous |
| Mechanism | Binds TPO-R (c-Mpl) | Binds transmembrane domain | Identical to endogenous TPO |
| Key Features | Long half-life, Immunomodulatory (Treg↑) | Hepatotoxicity risk | First-generation, similar to TPO |
| Main Indications (Beyond CIT Research) | ITP, CIT, Aplastic Anemia | ITP, Aplastic Anemia, CLD thrombocytopenia | Severe thrombocytopenia (e.g., post-chemo, Hep C) |
| Dosing Considerations | Weight-based (μg/kg/week) target-based adjustments | Strict: Empty stomach, avoid cations | Variable dose/frequency |
| Distinct Safety Notes | General TPO-RA risks | Hepatotoxicity, Cataracts (long-term), Strong DDIs | Potential immunogenicity |
The oral agents differ mainly in practical terms: eltrombopag requires an empty stomach and carries a higher hepatotoxicity risk (10), avatrombopag has minimal dietary restrictions (9), and hetrombopag is used mainly for adult ITP in China (11). Selection depends on the indication, patient factors, drug interactions and cost, and all require platelet monitoring.
A central question in this case concerns the precise nature of the underlying haematological disorder, and the therapeutic sequence followed the evolution of this diagnostic reasoning. Oral TPO-RAs were used first, consistent with their position as the preferred pharmacological class for CIT; when these failed, a corticosteroid-based immunomodulatory regimen was introduced on the suspicion of secondary, immune-mediated marrow failure; thalidomide and all-trans retinoic acid were selected for their immunomodulatory and megakaryopoiesis-promoting properties, a recognised second-line option for corticosteroid-refractory immune-mediated thrombocytopenia in China (36); rhTPO and, ultimately, romiplostim were added as thrombopoietic support was intensified. Although the bone marrow aspiration (performed at approximately 20 months after diagnosis) showed severe hypocellularity with trilineage suppression and markedly reduced megakaryocytes — morphologically resembling acquired aplastic anaemia (AA) — we regard this case as most consistent with persistent, treatment-related CIT rather than AA, for two reasons. First, a definitive diagnosis of AA could neither be confirmed nor therapeutically tested: the marrow assessment rested on aspiration morphology alone (the comprehensive marrow-failure work-up detailed below was not performed), and standard AA-directed immunosuppression, such as antithymocyte globulin plus ciclosporin, was never administered. Second, and most importantly, the cytopenias did not behave as in AA — the neutropenia and anaemia recovered spontaneously, without lineage-specific treatment, and have remained normal for years, leaving thrombocytopenia as the sole persistent abnormality. This selective, durable single-lineage deficit is more consistent with prolonged, treatment-related bone-marrow and megakaryocytic hypoplasia following high-dose platinum-based chemotherapy combined with 60 Gy thoracic irradiation than with a global stem-cell failure syndrome such as AA. Positioning this case within the broader spectrum of treatment-related bone-marrow failure, it is notable that romiplostim retains activity even when marrow hypoplasia predominates: in refractory AA unresponsive to eltrombopag or to multiple oral TPO-RAs, high-dose romiplostim (initial 20 µg/kg/week) has produced rapid multilineage responses, with some patients maintaining counts after drug discontinuation (34, 35).
Why this patient failed rhTPO yet responded to romiplostim cannot be established from a single case, but a closer look at how the two agents engage c-Mpl suggests several explanations. Activation of c-Mpl requires ligand-induced receptor homodimerisation, and both the efficiency and the duration of that dimerisation influence JAK2 transphosphorylation and the strength of downstream STAT5, PI3K–Akt and MAPK signalling. rhTPO is a recombinant protein carrying the native thrombopoietin sequence and engages the receptor as a single, native ligand molecule. Romiplostim, by contrast, is a peptibody in which four c-Mpl–binding peptides — sharing no sequence homology with endogenous TPO — are displayed on a single immunoglobulin Fc scaffold; this multivalent geometry cross-links receptors more efficiently and may generate a stronger, more complete signal than the native ligand.
Three consequences of this design are relevant here. First, signal duration: expansion and endomitotic maturation of megakaryocyte progenitors depend on sustained rather than pulsatile c-Mpl signalling over several days. FcRn-mediated recycling of the Fc domain gives romiplostim a long half-life, so that weekly injection maintains steady receptor occupancy, whereas rhTPO, even when given at the full standard dose (15000 units/day for 14 days), is rapidly cleared and delivers only intermittent stimulation — plausibly insufficient in a hypoplastic marrow containing few residual progenitors. Second, receptor-mediated clearance: endogenous TPO is removed largely by c-Mpl on platelets and megakaryocytes, so in severe thrombocytopenia with megakaryocytic hypoplasia this clearance pathway is lost and circulating TPO is already high; supplying additional native-sequence ligand may therefore add little, whereas a more potent agonist, or one with more sustained exposure, can still increase net receptor signalling. Third, immunogenicity: because rhTPO is homologous to endogenous TPO, it can elicit neutralising anti-TPO antibodies that abolish the response to further rhTPO — an effect documented chiefly for the early truncated recombinant TPO products, and one that romiplostim, built from non-homologous peptides, was expressly engineered to avoid. Neither anti-TPO antibodies nor TPO levels were measured in this patient, so these mechanisms remain hypotheses. The earlier failure of eltrombopag is separately explained by its distinct binding site (the transmembrane domain rather than the ligand-binding region) and its frequent dose-capping by hepatotoxicity; because it engages a different part of the receptor, its failure does not predict failure of romiplostim.
Several diagnostic limitations should be acknowledged. A comprehensive bone-marrow-failure work-up was not completed: bone-marrow biopsy, flow cytometry, cytogenetic analysis, PNH-clone testing, platelet-antibody testing and molecular studies were not performed. This working classification — most consistent with treatment-related, persistent CIT — therefore rests on the bone-marrow aspiration morphology, the exclusion of malignant infiltration and dysplasia, and the distinctive clinical course described above, rather than on a complete exclusionary panel. As a single-patient observation, this report also precludes mechanistic confirmation; immunophenotyping, cytokine profiling and functional immune assays were not undertaken, and the pharmacological explanations offered above therefore remain hypotheses.
Two issues will require proactive planning in this patient. First, should disease progression necessitate renewed chemotherapy, platelet support must be coordinated in advance, with close monitoring and dose titration before and throughout treatment to keep counts safe and minimise CIT-related delays. Second, should romiplostim lose effect over time, a multi-target approach — for example adding an oral TPO-RA such as avatrombopag, which engages a distinct receptor region — might be explored; this remains, however, a speculative hypothesis, as no clinical cohort or case series has shown that adding an oral TPO-RA after romiplostim failure restores response, and it should be considered only within a research setting (5, 9, 24).
Several practical lessons emerge from this case. First, when chemotherapy-induced thrombocytopenia persists — particularly beyond a few weeks of standard support — early bone-marrow evaluation is advisable to guide therapy, rather than empirically stacking successive agents; in this patient a prolonged refractory interval preceded the marrow assessment that ultimately informed effective treatment. Second, TPO-RA selection may benefit from marrow-guided stratification: patients with marked megakaryocytic hypoplasia and a long transfusion history, as here, may be reasonable candidates for earlier consideration of romiplostim. Third, long-term cancer survivors who develop chronic treatment-related cytopenias require dual, parallel management — ongoing oncological surveillance together with sustained management of treatment toxicity. Finally, dosing should be individualised to identify the minimum effective dose and interval that maintains a safe platelet count, balancing efficacy against patient burden and cost rather than adhering rigidly to a fixed schedule.
In summary, managing CIT within aggressive multimodal SCLC therapy requires strategies that restore platelets without adding toxicity or promoting tumour growth. Romiplostim exemplifies this balance, combining potent thrombopoietic activity with a favourable safety profile, and it enabled durable disease control in this patient. While oral TPO-RAs offer convenience, agent choice should be individualised, and biomarkers to predict CIT risk and guide TPO-RA selection remain an important goal.
Funding Statement
The author(s) declared that financial support was not received for this work and/or its publication.
Footnotes
Edited by: Priya Singh, Gandhi Institute of Technology and Management School of Pharmacy, India
Reviewed by: Asım Armağan Aydın, Antalya Training and Research Hospital, Turkey
Xijuan Lin, Chinese Academy of Medical Sciences and Peking Union Medical College, China
Ethics statement
Ethical approval was not required for the study involving humans in accordance with the local legislation and institutional requirements. Written informed consent to participate in this study was not required from the participants or the participants’ legal guardians/next of kin in accordance with the national legislation and the institutional requirements. Written informed consent was obtained from the individual(s) for the publication of any potentially identifiable images or data included in this article.
Author contributions
MW: Writing – original draft. PT: Writing – original draft. TH: Data curation, Writing – review & editing. KS: Software, Writing – review & editing. JL: Writing – review & editing. PW: Writing – original draft, Writing – review & editing.
Conflict of interest
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