Emerging role of 18F-FDG PET/CT in Castleman disease: a review

Benjamin Koa, Austin J Borja, Mahmoud Aly, Sayuri Padmanabhan, Joseph Tran, Vincent Zhang, Chaitanya Rojulpote, Sheila K Pierson, Mark-Avery Tamakloe, Johnson S Khor, Thomas J Werner, David C Fajgenbaum, Abass Alavi, Mona-Elisabeth Revheim, Benjamin Koa, Austin J Borja, Mahmoud Aly, Sayuri Padmanabhan, Joseph Tran, Vincent Zhang, Chaitanya Rojulpote, Sheila K Pierson, Mark-Avery Tamakloe, Johnson S Khor, Thomas J Werner, David C Fajgenbaum, Abass Alavi, Mona-Elisabeth Revheim

Abstract

Castleman disease (CD) describes a group of rare hematologic conditions involving lymphadenopathy with characteristic histopathology and a spectrum of clinical abnormalities. CD is divided into localized or unicentric CD (UCD) and multicentric CD (MCD) by imaging. MCD is further divided based on etiological driver into human herpesvirus-8-associated MCD, POEMS-associated MCD, and idiopathic MCD. There is notable heterogeneity across MCD, but increased level of pro-inflammatory cytokines, particularly interleukin-6, is an established disease driver in a portion of patients. FDG-PET/CT can help determine UCD versus MCD, evaluate for neoplastic conditions that can mimic MCD clinico-pathologically, and monitor therapy responses. CD requires more robust characterization, earlier diagnosis, and an accurate tool for both monitoring and treatment response evaluation; FDG-PET/CT is particularly suited for this. Moving forward, future prospective studies should further characterize the use of FDG-PET/CT in CD and specifically explore the utility of global disease assessment and dual time point imaging.Trial registration ClinicalTrials.gov, NCT02817997, Registered 29 June 2016, https://ichgcp.net/clinical-trials-registry/NCT02817997.

Keywords: Castleman disease; Fluorodeoxyglucose F18; HIV; Interleukin-6; Positron emission tomography/computed tomography.

Conflict of interest statement

DCF has received research funding from EUSA Pharma for the ACCELERATE Registry (formerly sponsored by Janssen Pharmaceuticals). The rest of the authors declare no conflicts of interest.

Figures

Fig. 1
Fig. 1
Summary of the main types of Castleman disease [–22]. UCD, unicentric Castleman disease; MCD, multicentric Castleman disease; HHV-8, human herpesvirus-8; iMCD, idiopathic multicentric Castleman disease; POEMS, polyneuropathy, organomegaly, endocrinopathy, monoclonal protein, skin changes
Fig. 2
Fig. 2
a displays the PET scan of a subject with multicentric Castleman disease (MCD) in the coronal view. Enlarged axillary and cervical lymph nodes and an enlarged spleen are seen in a, demonstrating the systemic nature of MCD. b–d display the CT, PET, and PET/CT cross-sectional scans of the subject’s thorax, respectively. d displays high uptake of lymph nodes in the right and left axillary regions as shown in a
Fig. 3
Fig. 3
a–c consist of the CT, PET, and PET/CT scans, respectively, of a subject with multicentric Castleman Disease (MCD). High FDG uptake of lymph nodes can be visualized in the neck in b and c. d–f were taken 8 months after (a–c) and demonstrate decreased FDG-uptake in the same neck region, indicating that the subject’s Castleman disease treatment has been successful
Fig. 4
Fig. 4
FDG-PET images of a multicentric Castleman disease (MCD) subject over 8 months. a and b demonstrate cervical, axillary, and pelvic lesions, while c and d show decrease in FDG-uptake in accordance to treatment. Total lesion glycolysis (TLG) was calculated to be 934.7, 1001.7, 17.5, and 16.4 for a–d respectively. TLG was calculated by multiplying the metabolic volume with FDG uptake segmented by fixed threshold methods at 41% of maximum SUV in the volume of interest (VOI) [75] by the mean standardized uptake value (SUVmean) and them summing all the intensity-volume product values from all lesions
Fig. 5
Fig. 5
A subject with multicentric Castleman disease (MCD) with lesions in the axillary, neck, and abdomen is shown over the course of 10 months. a indicated the initial lesions seen in PET before treatment. b was taken after 4 months from the initial scan, and a decrease of lesions in the axillary, neck, and abdomen is seen. However, the disease seemed to reappear in the axillary and cervical lesions despite treatment as visualized in c, which was taken 6 months after the scan for b. Total lesion glycolysis (TLG) was calculated to be 365.9, 204.5, and 601.6 for a–c, respectively. TLG was calculated by multiplying the metabolic volume with FDG uptake segmented by fixed threshold methods at 41% of maximum SUV in the volume of interest (VOI) [75] by the mean standardized uptake value (SUVmean) and then summing all the intensity-volume product values from all lesions

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