Rapid Platelet Recovery With Cyclosporine and Romiplostim Enabled Gastric Cancer Surgery in Severe Aplastic Anemia

A 76-year-old woman with aplastic anemia and untreated gastric cancer has become the subject of a newly published case report describing how a carefully chosen drug combination allowed doctors to bridge a dangerous hematological gap. Her platelet count had fallen below 20,000 per microliter, far too low for surgeons to safely remove her stomach tumor.

Aplastic anemia is characterized by pancytopenia and a hypoplastic bone marrow, and the primary acquired form is largely an autoimmune bone marrow failure driven by cytotoxic T lymphocytes attacking hematopoietic stem cells. Standard treatment relies on immunosuppressive therapy, typically anti-thymocyte globulin combined with cyclosporine A. More recently, thrombopoietin receptor agonists such as eltrombopag and romiplostim have shown efficacy against aplastic anemia when combined with immunosuppressive therapy, expanding the therapeutic arsenal available to hematologists.

But the presence of an untreated malignancy complicates that standard approach in ways the authors of the report take pains to explain. There is some potential concern that immunosuppressive therapy increases the risk of cancer aggravation by suppressing the immune surveillance that normally keeps emerging tumors in check. Anti-thymocyte globulin is a particularly blunt instrument, because it suppresses T cells broadly rather than selectively. In most prospective clinical trials of immunosuppressive therapy for aplastic anemia, patients with concomitant malignancies were excluded, leaving clinicians with little direct evidence to guide decisions when the two diseases collide in the same patient.

The case began, as many do, with an unrelated complaint. The woman presented to hospital with a dry mouth and was diagnosed with Sjögren’s syndrome, an autoimmune condition, for which symptomatic treatment was started. Roughly one year later her anemia progressed, and endoscopy revealed gastric cancer. Thrombocytopenia worsened until she developed pancytopenia, the simultaneous deficiency of red cells, white cells and platelets. A bone marrow examination showed hypoplasia with decreased megakaryocytes, no significant dysplasia and no increase in blasts, and chromosomal analysis revealed a normal karyotype, findings that pointed away from a malignant marrow process.

Supporting laboratory evidence strengthened the diagnosis of immune-mediated aplastic anemia. Peripheral blood testing detected paroxysmal nocturnal hemoglobinuria-type granulocytes and erythrocytes, each at 0.007 percent, and her plasma thrombopoietin level measured 765 pg/mL. The presence of a minor PNH-type clone, the authors note, supported the immune-mediated nature of the disease and provided a rationale for immunosuppressive therapy, since such cells have been reported to serve as predictors of response and as useful markers for shaping treatment strategy. Her aplastic anemia was classified as severe according to the Camitta criteria, which would ordinarily prompt consideration of anti-thymocyte globulin.

That was precisely the option the team declined. Because her gastric cancer was untreated and surgery was already urgent, the physicians worried that broad T-cell depletion might accelerate tumor progression. Instead, they initiated cyclosporine A, with blood concentrations adjusted to a target C2 level of 600 ng/mL, together with romiplostim at 10 micrograms per kilogram per week. Following the initiation of treatment, the platelet count and reticulocyte count increased rapidly, eliminating the need for red blood cell transfusions. A partial hematological response was achieved one month after treatment began, and no deterioration in renal function was observed after cyclosporine was started, an important safety check given the drug’s known renal effects.

With platelet recovery established and no gastric cancer metastases detected during therapy, the surgical team proceeded. Laparoscopic pyloric gastrectomy was performed 63 days after the start of immunosuppressive therapy, and the authors report that no bleeding or thrombotic complications occurred. After the operation, the romiplostim dosage was reduced, and treatment with both cyclosporine A and romiplostim was continued. The sequence is the heart of the report: the drugs did not cure the cancer and were never intended to, but they bought the surgical window that thrombocytopenia had closed.

The choice of romiplostim over eltrombopag was grounded in prior trial evidence the authors cite. A phase II/III trial of cyclosporine A plus romiplostim in treatment-naive patients with aplastic anemia demonstrated an overall response rate of 23.1 percent at Week 14 and 46.2 percent at Week 27 among patients with severe disease. Several studies have also reported the efficacy of romiplostim in patients refractory to eltrombopag, and the authors suggest romiplostim may have a potent hematopoietic effect, although they caution that direct comparisons between the two agents are lacking. In this case, the combination was selected specifically to prioritize platelet recovery and enable timely surgical resection.

The report also engages honestly with the broader uncertainty around immunosuppressive therapy in patients with untreated cancer. Previous studies have reported that anti-thymocyte globulin-based therapy for aplastic anemia increases the long-term risk of several malignancies, and the authors’ own earlier work on aplastic anemia secondary to chemoradiotherapy found that two of four patients who received immunosuppressive therapy while not in complete remission of their original cancers showed cancer progression. Research on immunosuppressive therapy for aplastic anemia with untreated malignant tumors remains limited, and the risk-benefit balance, particularly for agents with pan T-cell suppressive effects, must be weighed case by case.

The authors are explicit about the limits of what a single patient can demonstrate. As this is a single case, the generalizability of the approach remains limited, and they call for further studies to clarify the optimal treatment strategy for aplastic anemia complicated by malignant tumors. They also note that close monitoring for gastric cancer recurrence is necessary in this patient. What the case does establish is narrower but still useful: in one carefully worked-up patient, cyclosporine A and romiplostim rapidly improved blood counts, made curative surgery feasible, and did so without the broad immunosuppression of anti-thymocyte globulin, suggesting a bridging strategy that deserves systematic evaluation rather than immediate generalization.

Subject of Research: A case report of cyclosporine A and romiplostim used as a bridging therapy to enable curative gastric cancer surgery in a patient with severe aplastic anemia.

Article Title: Cyclosporine A and Romiplostim as a Bridging Therapy to Curative Surgery in Aplastic Anemia Complicated by Gastric Cancer: A Case Report

Article References: Nakagawa, N., Yamazaki, M., & Hosokawa, K. (2026). Cyclosporine A and Romiplostim as a Bridging Therapy to Curative Surgery in Aplastic Anemia Complicated by Gastric Cancer: A Case Report. eJHaem, 7(5), Article e70440. https://doi.org/10.1002/jha2.70440

Image Credits: AI Generated

DOI: 10.1002/jha2.70440

Keywords: aplastic anemia, cyclosporine A, romiplostim, gastric cancer, thrombopoietin receptor agonist, immunosuppressive therapy, thrombocytopenia, case report, PNH-type clone, bone marrow failure, bridging therapy, Sjögren's syndrome