Nuclear Medicine Review 1/2015-Diagnostic value of 18F-FDG-PET/CT for monitoring myelofibrosis after allogeneic stem cell transplantation

Case report

Diagnostic value of 18F-FDG-PET/CT for monitoring myelofibrosis after allogeneic stem cell transplantation

Thorsten Derlin1, Guntram Büsche2; Nicolaus Kröger3

1Department of Diagnostic and Interventional Radiology, University Medical Center, Hamburg-Eppendorf, Hamburg, Germany

2Institute of Pathology, Hannover Medical School, Hannover, Germany

3Department of Stem Cell Transplantation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany

Conflicts of interest and source of funding: none declared

[Received 04 II 2014; Accepted 12 XII 2014]


Myelofibrosis is a rare hematopoietic stem cell neoplasm leading to marked bone marrow fibrosis and ineffective hematopoiesis. We report a case highlighting the potential role of 18F fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) for therapy monitoring. A 62-year-old man with myelofibrosis underwent FDG-PET/CT for evaluation of the extent of disease before and after allogeneic stem cell transplantation (SCT). PET after SCT demonstrated complete normalization of initially increased bone marrow tracer uptake, consistent with bone marrow biopsy showing complete remission. 18F-FDG-PET/CT may become a valuable diagnostic tool in myelofibrosis, enabling both sensitive initial staging and therapy monitoring.

KEY words: myelofibrosis, bone marrow, stem cell transplantation, therapy monitoring, FDG, PET/CT

Nuclear Med Rev 2015; 18, 1: 35-36

Case report

Primary myelofibrosis (PMF) and the clinically indistinguishable secondary forms of myelofibrosis (post-essential thrombocythemia and post-polycythemia vera myelofibrosis) are BCR-ABL1-negative hematopoietic stem cell neoplasms leading to marked bone marrow fibrosis and inefficient bone marrow blood formation [1, 2]. PMF is a rare disease with a reported incidence of 1.5 per 100,000 per year [3]. Patients with myelofibrosis may present with various symptoms including marked hepatosplenomegaly, severe anemia, thrombotic events, fatigue and night sweats. PMF is associated with reactive bone marrow fibrosis due to abnormal deposition of collagen and proliferation of hyperactive bone marrow fibroblasts, replacing normal myelopoiesis and causing cytopenias [2]. Patients with symptomatic forms of PMF have a median survival of less than 5 years [4]. The only curative treatment approach in PMF is currently allogeneic hematopoietic stem cell transplantation leading to 5-year survival rates between 51% and 61% [4]. Bone marrow fibrosis shows rapid regression after stem cell transplantation. An imaging-derived surrogate parameter for bone marrow fibrosis would be desirable not only for initial staging of the extent of disease, but also for therapy monitoring and potential adjustment of therapy, given that sampling errors on bone marrow biopsies are a frequently encountered problem since fibrosis may be an inhomogeneous process with variable distribution [2].

We herein present the case of a 62-year-old man with a history of JAK2-V617F-negative primary myelofibrosis who underwent whole-body 18F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) for evaluation of the extent of disease 1 week before and 12 months after allogeneic stem cell transplantation (Figure 1). PMF had been diagnosed 6 months before the first PET/CT, and he presented with anemia and thrombocytopenia. He received an allogeneic stem cell transplantation from a related donor without major complications. Complete histo-hematological remission was achieved at the time of the follow-up PET/CT

Figure 1. Whole-body maximum intensity projection (MIP) FDG-PET image before stem cell transplantation (A) demonstrating inhomogeneous tracer uptake in the bone marrow of the axial skeleton (SUVmax 3.5) and the long bones (arrows). Corresponding transversal PET (B) image showing marked bilateral tracer uptake in femoral bone marrow (arrows). Corresponding bone marrow biopsy microphotograph (C) demonstrating marked bone marrow fibrosis (Gomori’s silver impregnation, x250). Whole-body MIP FDG-PET image after allogeneic stem cell transplantation (D) showing complete resolution of abnormal bone marrow uptake. Corresponding transversal PET (E) image demonstrating unremarkable femoral bone marrow tracer accumulation. Corresponding bone marrow biopsy microphotograph (F) showing hypoplastic bone marrow without residual fibrosis (Giemsa stain, x250)

This report highlights the potential usefulness of 18F-FDG-PET/CT to visualize the extent and activity of bone marrow fibrosis in PMF, and – more importantly – to monitor normalization of tracer uptake after successful stem cell therapy. In recent years, PET/CT using tracers like 18F-FDG or 18F fluorodeoxythymidine (FLT) has been increasingly used as a morphofunctional imaging modality for both initial evaluation and therapy monitoring in various hematologic malignancies including several types of lymphoma and leukemia [5-9].

Apart from malignant diseases including lymphoma [5], increased bone marrow 18F-FDG uptake has been reported in a variety of benign conditions, e.g. after administration of granulocyte colony stimulating factor (G-CSF) or following erythropoietin therapy, which may cause false-positive results [10, 11]. Hyperplastic bone marrow is usually advocated as the main mechanism to explain tracer uptake in these patients. In contrast, myelofibrosis is characterized by marked inflammation of the bone marrow compartment [12] and uptake is likely caused by active inflammatory cells. Although quantitative values for normal bone marrow uptake have been published [13] they are not used in clinical routine because Standardized Uptake Values (SUVs) may be incalculably influenced by a variety of technical and biological factors [14]. Bone marrow FDG uptake has to be regarded as pathologic if there is non-homogeneous focal uptake [15], or a bone marrow metabolism pattern which is not to be expected in the patient’s age group like in the present patient who demonstrated atypical bone marrow expansion into the tibial bones.

This is a case of primary myelofibrosis with marked pre-therapeutic and absent post-therapeutic tracer uptake on 18F-FDG-PET/CT


  1. Tefferi A. Pathogenesis of myelofibrosis with myeloid metaplasia. J Clin Oncol 2005; 23: 8520-8530.
  2. Wolf BC, Neiman RS. Myelofibrosis with myeloid metaplasia: pathophysiologic implications of the correlation between bone marrow changes and progression of splenomegaly. Blood 1985; 65: 803-809.
  3. Mesa RA, Silverstein MN, Jacobsen SJ, Wollan PC, Tefferi A. Population-based incidence and survival figures in essential thrombocythemia and agnogenic myeloid metaplasia: an Olmsted County Study, 1976-1995. Am J Hematol 1999; 61: 10-15.
  4. Kroger N, Holler E, Kobbe G et al. Allogeneic stem cell transplantation after reduced-intensity conditioning in patients with myelofibrosis: a prospective, multicenter study of the Chronic Leukemia Working Party of the European Group for Blood and Marrow Transplantation. Blood 2009; 114: 5264-5270.
  5. Engert A, Haverkamp H, Kobe C et al. Reduced-intensity chemotherapy and PET-guided radiotherapy in patients with advanced stage Hodgkin’s lymphoma (HD15 trial): a randomised, open-label, phase 3 non-inferiority trial. Lancet 2012; 379: 1791-1799.
  6. Jang SJ, Lee KH, Lee JY et al. (11)C-methionine PET/CT and MRI of primary central nervous system diffuse large B-cell lymphoma before and after high-dose methotrexate. Clin Nucl Med 2012; 37: e241-244.
  7. Buck AK, Bommer M, Juweid ME et al. First demonstration of leukemia imaging with the proliferation marker 18F-fluorodeoxythymidine. J Nucl Med 2008; 49: 1756-1762.
  8. Schollaert P, Loosen C, André M, Chatelain B, Krug BM. An atypical relapse of acute myeloid leukemia diagnosed by 18F-FDG-PET/CT Clin Nucl Med 2012; 37: 1018-1021.
  9. Derlin T Weber C, Habermann CR et al. 18F-FDG-PET/CT for detection and localization of residual or recurrent disease in patients with multiple myeloma after stem cell transplantation. Eur J Nucl Med Mol Imaging 2012; 39: 493-500.
  10. Plantade A, Montravers F, Selle F, Izrael V, Talbot JN. Diffusely increased 18F- FDG uptake in bone marrow in a patient with acute anemia and recent erythropoietin therapy. Clin Nucl Med. 2003; 28: 771-772.
  11. Kazama T Swanston N, Podoloff DA, Macapinlac HA. Effect of colony-stimulating factor and conventional- or high-dose chemotherapy on FDG uptake in bone marrow. Eur J Nucl Med Mol Imaging 2005; 32: 1406-1411.
  12. Hasselbalch HC. Chronic inflammation as a promotor of mutagenesis in essential thrombocythemia, polycythemia vera and myelofibrosis. A human inflammation model for cancer development? Leuk Res. 2013; 37: 214-220
  13. Ramos CD, Erdi YE, Gonen M et al. FDG-PET standardized uptake values in normal anatomical structures using iterative reconstruction segmented attenuation correction and filtered back-projection. Eur J Nucl Med 2001; 28: 155-164.
  14. Boellaard R. Standards for PET image acquisition and quantitative data analysis. J Nucl Med. 2009; 50 Suppl. 1: 11S-20S.
  15. Berthet L, Cochet A, Kanoun S et al. In newly diagnosed diffuse large B-cell lymphoma, determination of bone marrow involvement with 18F-FDG-PET/CT provides better diagnostic performance and prognostic stratification than does biopsy. J Nucl Med 2013; 54 :1244-1250.

Correspondence to:
Thorsten Derlin, MD
University Medical Center Hamburg-Eppendorf
Department of Diagnostic and Interventional Radiology
Martinistraße 52, D-20246 Hamburg, Germany
Phone: +49-40-7410-56146 Fax: +49-40-7410-55181


Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

By "Via Medica sp. z o.o." sp.k., Świętokrzyska 73 street, 80–180 Gdańsk, Poland

tel.:+48 58 320 94 94, faks:+48 58 320 94 60, e-mail: