Abstract
Background:
New bone pain and destructive skeletal lesions after allogeneic hematopoietic stem cell transplantation (allo-HSCT) raise concern for malignant relapse or infection. Synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) syndrome is an uncommon inflammatory disorder that may produce overlapping imaging findings.
Case presentation:
A 19-year-old man with acute myeloid leukemia underwent haploidentical allo-HSCT in second complete remission. Thirteen months later, while measurable residual disease remained undetectable, he developed severe thoracolumbar pain and extensive inflammatory acneiform eruptions. Magnetic resonance imaging showed abnormal thoracic vertebral marrow and paravertebral signals, initially raising suspicion of osseous leukemic relapse. C-reactive protein and erythrocyte sedimentation rate were elevated, whereas bone marrow examination confirmed continued remission. Computed tomography and technetium-99 m methylene diphosphonate bone scintigraphy with single-photon emission computed tomography/computed tomography demonstrated lesions involving the sternum, bilateral clavicles, and T6–T9 costovertebral joints. Computed tomography-guided sternal biopsy showed collagenized fibrous tissue with myxoid change, focal chondroid differentiation, a small amount of newly formed bone, and mild inflammatory-cell infiltration, without morphologic evidence of leukemic involvement. The combination of severe acne and osteitis in a characteristic distribution, after clinical evaluation for malignancy and infection, supported a diagnosis of SAPHO syndrome. Serum interleukin-6 elevation and altered peripheral immune-cell subsets were considered exploratory single-time-point observations. Symptoms improved after methylprednisolone followed by celecoxib, methotrexate, and dermatologic treatment.
Conclusion:
SAPHO syndrome should be considered when post-transplant bone lesions coexist with compatible skin manifestations. Multimodal imaging and targeted biopsy helped avoid inappropriate treatment for presumed AML relapse. The observed immune abnormalities are hypothesis-generating and do not establish a causal relationship between allo-HSCT and SAPHO syndrome.
Introduction
SAPHO syndrome is an uncommon inflammatory disorder characterized by variable combinations of osteitis, hyperostosis, synovitis, severe acne, and palmoplantar pustulosis (, ). The anterior chest wall is the most frequently affected site; the spine, sacroiliac joints, and long bones may also be involved (). No single laboratory test is diagnostic. Diagnosis therefore rests on the clinical pattern, imaging findings, and reasonable exclusion of infection and malignancy, with biopsy often required for atypical or destructive lesions (–).
New focal bone pain after allo-HSCT presents a high-stakes differential diagnosis. Malignant relapse, bacterial or fungal osteomyelitis, treatment-related injury, graft-vs.-host disease (GVHD)-associated musculoskeletal manifestations, and noninfectious inflammatory disease may overlap clinically and radiologically. Magnetic resonance imaging (MRI) is sensitive to marrow abnormalities but is not disease-specific (). In a patient transplanted for acute myeloid leukemia (AML), destructive vertebral lesions may therefore prompt treatment for relapse before their cause has been established.
Autoimmune and inflammatory disorders may arise during immune reconstitution after allo-HSCT (–), but a temporal association does not establish that transplantation caused a subsequent inflammatory disease. To assess the novelty of this presentation, PubMed/MEDLINE and Google Scholar were searched from inception through 30 June 2026 using combinations of “SAPHO” or “synovitis acne pustulosis hyperostosis osteitis” with “allogeneic hematopoietic stem cell transplantation,” “hematopoietic stem cell transplantation,” “bone marrow transplantation,” “acute myeloid leukemia,” “leukemia,” “malignancy,” and “cancer.” No previous report of SAPHO arising after allo-HSCT was identified. The closest oncologic precedent was the case reported by Kubo et al., in which SAPHO mimicked bone metastases during pembrolizumab treatment for non-small cell lung cancer (). We report a case that presented 13 months after haploidentical allo-HSCT and initially mimicked osseous AML relapse. The case is reported in accordance with the CARE guideline ().
Case description
A 19-year-old man was diagnosed with AML in August 2024 (Figure 1). Bone marrow aspirate contained 79.5% myeloblasts. Molecular testing (CEBPA transcript NM_004364.4) identified c.934_936dupCAG (p.Gln312dup; VAF, 43.7%), an in-frame duplication in the bZIP region, and c.125dupC (p.Pro43fs; VAF, 40.6%), a frameshift variant outside the bZIP region. Variant phasing was not performed; therefore, whether the two CEBPA variants were in trans could not be determined. Additional variants involved STAT5B (VAF, 45.1%), TET2 (VAF, 49.0%), and WT1 (VAFs, 82.7% and 2.7%). He received idarubicin plus cytarabine induction and high-dose cytarabine-based consolidation. Hematologic relapse occurred in February 2025, with 8% marrow blasts and flow-cytometric measurable residual disease (MRD) of 3.24%. Salvage therapy with idarubicin, cytarabine, and venetoclax induced a second complete remission.
Figure 1
In April 2025, he underwent myeloablative haploidentical allo-HSCT from his father (HLA 5/10 matched; donor blood group B positive and recipient AB positive). Conditioning comprised cytarabine, busulfan, cyclophosphamide, and semustine. GVHD prophylaxis comprised antithymocyte globulin, cyclosporine, mycophenolate mofetil, and short-course methotrexate. Neutrophil and platelet engraftment occurred on days +19 and +24, respectively. Cyclosporine was tapered and discontinued in October 2025. He developed no clinically significant acute or chronic GVHD. Two cycles of azacitidine maintenance were administered in December 2025 and March 2026. Serial marrow examinations showed continued morphologic remission with undetectable MRD. He had no history of acne, palmoplantar pustulosis, inflammatory arthritis, or chronic bone pain before AML.
There was no relevant family history of hematologic malignancy, inflammatory bone disease, severe acne, or psoriasis. He did not smoke or drink alcohol and worked in the catering industry. No clinically relevant psychosocial or mental-health concerns were reported.
In May 2026, 13 months after allo-HSCT, the patient developed progressively severe thoracolumbar pain that limited daily activities. At approximately the same time, inflammatory papules and pustules appeared extensively on the face (Figure 2). His white blood cell count was 9.34 × 109/L, neutrophil count 6.97 × 109/L, hemoglobin 124 g/L, and platelet count 210 × 109/L. C-reactive protein was 82.95 mg/L and erythrocyte sedimentation rate was 121 mm/h. Renal and hepatic biochemical tests were unremarkable. HLA-B27, rheumatoid factor, and anti-cyclic citrullinated peptide antibodies were negative; anti-PM-Scl was equivocal.
Figure 2
Serum (, )-β-D-glucan and galactomannan assays, plasma Epstein–Barr virus DNA, and T-SPOT.TB were negative. No bloodstream pathogen was identified. Culture of material from an acne pustule grew Serratia marcescens. Because no bacteremia or systemic infectious syndrome was present, this superficial culture was not considered sufficient evidence of S. marcescens osteomyelitis. The result was interpreted in conjunction with imaging, pathology, and the clinical course. The biopsy was performed primarily to evaluate suspected osseous AML relapse; because the patient had no fever, bacteremia, or systemic infectious syndrome at the time of sampling, allocation of fresh tissue for microbiological culture or molecular testing was not prospectively planned. This was an important diagnostic limitation in an allo-HSCT recipient, and an indolent bone infection could not be completely excluded.
Spinal MRI demonstrated abnormal marrow signals in the T6–T9 vertebral bodies with adjacent paravertebral soft-tissue signal abnormalities, raising concern for leukemic infiltration or infection (Figure 3A). Bone marrow aspirate showed continued morphologic remission and MRD remained undetectable; these findings reduced but did not independently exclude an isolated osseous relapse. Thoracic computed tomography (CT) showed destructive changes involving the thoracic vertebrae and abnormalities around both sternoclavicular joints (Figure 3B).
Figure 3
Whole-body technetium-99 m methylene diphosphonate (99mTc-MDP) bone scintigraphy demonstrated abnormally increased radiotracer uptake in the bilateral clavicles, sternum, and approximately T6-T9 levels. Regional SPECT/CT further localized the increased uptake to the sternal ends of both clavicles, the sternum, and the bilateral T6-T9 costovertebral joints, with greater uptake on the right. Quantitative SPECT standardized uptake values and a prespecified semi-quantitative uptake score were not acquired; interpretation was therefore qualitative. Representative SPECT, low-dose CT, and fused SPECT/CT images demonstrated prominent uptake centered on the anterior chest wall (Figure 3C). The nuclear medicine interpretation favored inflammatory skeletal lesions and recommended follow-up imaging. In conjunction with the characteristic anterior chest-wall involvement and inflammatory acneiform eruptions, these findings raised clinical suspicion of SAPHO syndrome.
Given the patient's AML history and the destructive osseous changes, the sternal lesion was selected for CT-guided core biopsy. Histopathologic examination revealed proliferative fibrous tissue with collagenization and myxoid change, accompanied by focal chondroid differentiation and a small amount of newly formed bone (Figures 4A,B). Proliferation of thin-walled small vessels was observed, with focal mild infiltration by lymphocytes and eosinophils; a small focus of stratified squamous epithelium was also present (Figure 4C). No morphologic evidence of leukemic infiltration was identified in the submitted tissue. Because bone tissue was not submitted for microbiological culture or broad-range 16S rRNA sequencing, an indolent infectious process could not be completely excluded microbiologically.
Figure 4
The patient fulfilled commonly used diagnostic criteria for SAPHO syndrome through the association of severe acne with osteitis in a characteristic distribution, after reasonable clinical exclusion of malignancy and active infection (, ). Chronic nonbacterial osteomyelitis, infectious osteomyelitis, axial spondyloarthritis, chronic GVHD, and osseous AML relapse were considered. The patient's age and multifocal osteitis overlapped with chronic nonbacterial osteomyelitis; however, the combination of severe acne and characteristic anterior chest-wall involvement favored the SAPHO spectrum (, ). The absence of sacroiliitis and negative HLA-B27 testing did not support axial spondyloarthritis. The absence of prior GVHD and of characteristic cutaneous, oral, hepatic, or pulmonary GVHD manifestations made chronic GVHD less likely.
A multiplex serum cytokine panel obtained during active symptoms showed elevated IL-6 (18.99 pg/mL; laboratory reference interval, 0-5.4 pg/mL). The other 11 measured cytokines (IL-5, IFN-α, IL-2, IL-1β, IL-10, IFN-γ, IL-8, IL-17, IL-4, IL-12p, and TNF-α) were within their respective laboratory reference intervals (Supplementary Table S1). Flow cytometry showed a CD4 + effector T-cell proportion of 7.09% (reference interval, 0.44%–6.06%), regulatory T cells of 5.94%, CD8 + CD27- cells of 66.32%, CD8 + CD28- cells of 86.43%, and CD8 + central memory T cells of 2.10%. Myeloid dendritic-cell subsets were reported as MDC1 71.79% and MDC2 15.38%. Absolute counts were not available; all immune-cell results are therefore presented as proportions only.
These results were generated from a single sample without a pre-symptom specimen, post-treatment sample, or matched allo-HSCT control. The laboratory reference intervals were derived from non-transplant adults. The findings therefore describe immune status at presentation but cannot distinguish SAPHO-associated changes from the effects of conditioning, antithymocyte globulin, prior immunosuppression, infection exposure, or post-transplant immune reconstitution.
Intravenous methylprednisolone 40 mg/day was initiated on 5 June 2026 and produced rapid improvement in pain and inflammatory symptoms. Oral methylprednisolone 20 mg/day was started on 9 June 2026, reduced by 4 mg every 7 days (20 mg/day on 9-15 June, 16 mg/day on 16-22 June, and 12 mg/day on 23-29 June), then maintained at 8 mg/day from 30 June through 29 July and reduced to 4 mg/day from 30 July. The patient was still receiving 4 mg/day at the last follow-up. Celecoxib 200 mg/day and methotrexate 10 mg/week were prescribed for ongoing musculoskeletal disease. Minocycline 100 mg/day and topical metronidazole twice daily were used for the facial eruption. At the last evaluation on 6 August 2026, 62 days after initiation of SAPHO-directed therapy, the pain score had improved to 1 on a 0-10 numerical rating scale and CRP had decreased from 82.95 to 15.6 mg/L; ESR was not repeated. Facial skin inflammation was clinically documented as improved, although no standardized dermatologic score or follow-up photograph was available. No repeat MRI, CT, bone scintigraphy, or SPECT/CT was performed. Medication adherence was good, treatment was tolerated, and no adverse events were reported. AML remained in morphologic remission with undetectable MRD.
Discussion
This case illustrates a diagnostically important mimic of post-transplant AML relapse. The diagnosis did not depend on MRI alone. Continued marrow remission, the combination of severe acne and anterior chest-wall osteitis, the distribution on bone scintigraphy and SPECT/CT, and the absence of malignant cells in a targeted bone biopsy collectively supported SAPHO syndrome. Tissue sampling was particularly important because isolated extramedullary relapse may occur despite a negative marrow examination.
Kubo et al. similarly described SAPHO mimicking malignant skeletal disease during pembrolizumab therapy for non-small cell lung cancer (). Both cases illustrate how inflammatory osteitis can be mistaken for malignant bone involvement; however, the present case arose after allo-HSCT and mimicked osseous AML relapse, a post-transplant setting not identified in our literature search.
SAPHO lesions commonly involve the sternoclavicular region and sternum, and spinal disease may manifest as vertebral marrow edema, endplate abnormalities, paravertebral inflammation, osteitis, or hyperostosis (, , ). These findings can resemble infection, spondyloarthritis, or malignancy. The classic “bull's head” appearance on bone scintigraphy is suggestive when present but is neither invariably present nor sufficient to establish the diagnosis (). Histopathology is also not pathognomonic; its appearance varies with disease stage and may range from acute inflammation to chronic fibro-osseous change (, ). In this patient, the biopsy was used primarily to assess leukemic involvement and characterize the lesion rather than as a stand-alone positive test for SAPHO syndrome.
The isolation of S. marcescens from an acne pustule requires cautious interpretation. Cutaneous lesions may be colonized or secondarily infected, whereas SAPHO-associated osteitis is generally considered noninfectious. Factors arguing against an invasive bone infection included the absence of bacteremia or systemic infectious manifestations, the characteristic clinicoradiologic distribution, and clinical improvement without prolonged pathogen-directed antimicrobial therapy. Nevertheless, because bone tissue was not cultured or analyzed by molecular microbiological methods, an indolent infection cannot be excluded with absolute certainty. This limitation is especially relevant in a recipient of allo-HSCT.
The temporal relationship between allo-HSCT and SAPHO syndrome is notable but does not prove that transplantation triggered the disease. Immune recovery after allo-HSCT is prolonged and nonuniform. Early expansion of mature donor T cells, delayed thymus-dependent production of naïve T cells, conditioning-related tissue injury, infections, and immunosuppressive therapy may all influence T-cell composition (, , ). CD28-negative and CD27-negative CD8 + populations may expand after repeated antigenic stimulation and during post-transplant immune remodeling; they should not automatically be interpreted as pathogenic senescent cells without functional assays (). Likewise, IL-6 is a nonspecific inflammatory mediator that has been reported in SAPHO syndrome and other inflammatory states ().
The immune findings in this case are therefore hypothesis-generating. They are compatible with post-transplant immune remodeling during an inflammatory episode, but they cannot demonstrate that IL-6, CD8 + differentiation, or dendritic-cell alterations caused SAPHO syndrome. Longitudinal sampling before and after clinical improvement, absolute cell counts, complete assay definitions, and comparison with allo-HSCT controls would be required to evaluate such a mechanism. A single patient's values cannot define a transplant-specific SAPHO immune signature.
Evidence guiding SAPHO treatment is based predominantly on observational studies. Nonsteroidal anti-inflammatory drugs are commonly used initially; glucocorticoids, conventional disease-modifying antirheumatic drugs, bisphosphonates, and targeted biologic agents have been used for refractory disease (, ). In a transplant recipient, management must also account for infection risk, marrow function, drug interactions, and relapse surveillance. The favorable early response in this patient supports the working diagnosis but does not establish comparative treatment efficacy.
This report has several strengths. It documents a clinically important mimic of post-transplant AML relapse; integrates cutaneous findings, marrow assessment, MRI, CT, bone scintigraphy/SPECT/CT, and targeted histopathology; and presents the differential diagnosis and uncertainty explicitly. Targeted biopsy helped prevent premature attribution of destructive skeletal lesions to leukemia and potentially inappropriate salvage therapy. The report also avoids inferring causality from the temporal association between allo-HSCT and SAPHO syndrome. Limitations include the single-patient design and short follow-up; the absence of serial immune measurements, absolute immune-cell counts, and an allo-HSCT comparator; use of non-transplant adult reference intervals; and lack of quantitative SPECT metrics or follow-up imaging. Bone tissue was not submitted for culture or molecular microbiological testing, so indolent infection cannot be completely excluded. The immune findings are therefore descriptive and hypothesis-generating, and the early clinical response cannot establish comparative treatment efficacy.
Conclusion
SAPHO syndrome is a relevant differential diagnosis when inflammatory acne is accompanied by destructive or metabolically active bone lesions after allo-HSCT. In this patient, multimodal imaging identified a characteristic distribution and targeted biopsy found no leukemic infiltration, allowing anti-inflammatory treatment rather than salvage chemotherapy. The single-time-point cytokine and immune-cell abnormalities should be treated as exploratory observations. Additional cases with longitudinal and controlled immune profiling are required before a causal relationship between post-transplant immune reconstitution and SAPHO syndrome can be proposed.
Patient perspective
The severe back pain and facial skin lesions substantially affected my daily activities and caused considerable anxiety. Because of my previous acute myeloid leukemia, I was particularly concerned that the bone abnormalities represented disease relapse. The diagnostic process, including multiple imaging examinations and the bone biopsy, was stressful, but I understood that these investigations were necessary to determine the cause of the lesions. I felt relieved when the biopsy showed no evidence of leukemic involvement and the diagnosis of SAPHO syndrome was made. My back pain and skin inflammation improved markedly after treatment, and I gradually resumed my usual daily activities. I hope that sharing my experience may help clinicians and other patients recognize that new bone lesions after transplantation do not always indicate leukemia relapse.
Statements
Data availability statement
The original contributions presented in the study are included in the article/Supplementary Material, further inquiries can be directed to the corresponding authors.
Ethics statement
The studies involving humans were approved by the Ethics Committee of the Affiliated Hospital of Qingdao University. The studies were conducted in accordance with the local legislation and institutional requirements. The participants provided their written informed consent to participate in this study. 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
WZ: Conceptualization, Data curation, Funding acquisition, Investigation, Visualization, Writing – original draft. XM: Data curation, Investigation, Validation, Writing – review & editing. XiaolL: Investigation, Resources, Visualization, Writing – review & editing. CZ: Data curation, Investigation, Writing – review & editing. HF: Data curation, Investigation, Writing – review & editing. XS: Data curation, Investigation, Writing – review & editing. WW: Data curation, Investigation, Writing – review & editing. XuL: Conceptualization, Supervision, Validation, Writing – review & editing. XiaodL: Conceptualization, Funding acquisition, Project administration, Supervision, Validation, Writing – review & editing.
Funding
The author(s) declared that financial support was received for this work and/or its publication. This work was supported by the Natural Science Foundation of Shandong Province (Grant Number: ZR2024QH613), the National Natural Science Foundation of China (Grant Number: 81300386), the China Postdoctoral Science Foundation (Grant Number: 2020M672006) and Fund of the Affiliated Hospital of Qingdao University.
Conflict of interest
The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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Supplementary material
The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fmed.2026.1936597/full#supplementary-material
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Summary
Keywords
acute myeloid leukemia, allogeneic hematopoietic stem cell transplantation, immune reconstitution, osseous relapse, osteitis, SAPHO syndrome
Citation
Zhang W, Ma X, Liu X, Zhao C, Fei H, Shi X, Wang W, Li X and Liu X (2026) Case Report: SAPHO syndrome mimicking osseous relapse after haploidentical allogeneic hematopoietic stem cell transplantation for acute myeloid leukemia. Front. Med. 13:1936597. doi: 10.3389/fmed.2026.1936597
Received
13 July 2026
Revised
01 September 2026
Accepted
02 September 2026
Published
28 September 2026
Volume
13 - 2026
Edited by
Matteo Colina, Santa Maria della Scaletta Hospital, Italy
Reviewed by
Şengül Çağlayan, Antalya Eğitim ve Araştırma Hastanesi, Türkiye
Ahmad Alshomrani, Umm al-Qura University, Saudi Arabia
Updates
Copyright
© 2026 Zhang, Ma, Liu, Zhao, Fei, Shi, Wang, Li and Liu.
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*Correspondence: Xiaodan Liu liuxiaodan8711@163.com Xuewei Li lixuewei1@qdu.edu.cn
ORCID Xiaodan Liu orcid.org/0000-0002-4459-8927
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.