CASE REPORT
Giampiero Giovacchini1,*, Andrea Ciarmiello2
1 Institute of Radiology and Nuclear Medicine, Stadtspital Triemli, Zurich, Switzerland
2 Nuclear Medicine Department, S. Andrea Hospital, La Spezia, Italy
Abstract
We report the case of a 72-yr-old prostate cancer patient with biochemical failure (PSA = 2.8 ng/mL) after radical prostatectomy in whom both bone scintigraphy and 11C-choline PET/CT detected an isolated focal pathological activity in the proximal diaphysis of the left tibia. Surgery was performed and histological analysis revealed enchondroma. The finding is discussed on the basis of the specificity of radiolabeled choline for prostate cancer vs. other tumors or inflammation processes. Particularly, proliferation or concomitant inflammatory processes associated with bone remodeling in enchondroma are discussed and related to 11C-choline uptake.
Keywords: 11C-choline PET/CT; enchondroma; prostate cancer
Introduction
A 72-yr-old prostate cancer patient with biochemical failure was referred to bone scintigraphy because of a biochemical recurrence (prostate-specific antigen, PSA = 2.8 ng/mL). The patient had been treated with radical prostatectomy five years earlier owing to prostate cancer (pT2 pN0 cM0, Gleason 3 + 3 = 6). Bone scan revealed an isolated hot spot in the proximal diaphysis of the left tibia (Figure 1).
Figure 1. Anterior (right) and posterior (left) view of whole body bone scintigraphy. Increased 99mTc-methylenediphoshonate activity is observed in the proximal diaphysis of the left tibia.
No lesions were visible in the pelvis or in the spine, which made the isolated finding in the tibia unlikely to be related to prostate cancer. The traditional whole body 11C-choline PET/CT, conducted from the cranial basis to the midthigh, did not reveal any pathological uptake site of 11C-choline (Figure 2).
Figure 2. Coronal view of fused 11C-choline PET/CT showing physiological distribution of the tracer. No pathological 11C-choline uptake sites could be detected.
However, since the sensitivity of 11C-choline positron emission tomography/computed tomography (PET/CT) is higher in comparison to bone scintigraphy and also because of the capability of PET/CT to investigate local recurrence and lymph node metastases, the patient underwent subsequent 11C-choline PET/CT to further exclude macroscopic disease. Physiological uptake was seen in the right axillary vein, in the liver, in the spleen, in both kidneys, in the small bowel and in the bladder. In the additional static acquisition centered on the knees, a pathological increase of 11C-choline uptake was seen in the proximal diaphysis of the left tibia which corresponded to the scintigraphic finding (Figure 3A).
Figure 3A. Coronal view of PET (A) of the inferior limb of at knee height. There is a region of increased uptake of 11C-choline in the area of bone thickening evident in the CT scan.
The CT component of the PET/CT revealed an area of sclerosis (Figure 3B).
Figure 3B. Coronal view of CT (B, bone window), of the inferior limb at knee height. There is a region of increased uptake of 11C-choline in the area of bone thickening evident in the CT scan.
Fusion imaging demonstrates that the increased metabolic activity localizes to the sclerotic area (Figure 3C).
Figure 3C. Coronal view of and fused 11C-choline PET/CT images (C) of the inferior limb at knee height. There is a region of increased uptake of 11C-choline in the area of bone thickening evident in the CT scan.
The patient decided to undergo surgery. Histological analysis revealed enchondroma (Figure 4A and Figure 4B).
Figure 4A. Typical enchondroma: hypocellular tumor with abundant hyaline cartilage matrix without necrosis and mitosis (e.e. 20x).
Figure 4B. Chondrocytes with finely granular eosinophilic cytoplasm is often vacuolated with small nuclei (e.e. 20x).
Discussion
Enchondroma is a benign bone tumor, which results from the continued growth of residual benign cartilaginous rests that are displaced from the growth plate. The tumor growth occurs in the medullary cavity of bone [1]. Overall, they are particularly frequent in the phalanges and commonly in the pediatric and young adult age groups, but may also occur in the diaphysis of femur and tibia. This is being recognized in 1.7% of femura at autopsy [2,3]. Enchondromas usually present as a painless bony mass, and radiographically often ovoid in shape with endosteal scalloping; displaying occasionally chondroid type matrix mineralization and do not induce periosteal reactions [4,5]. Bone scintigraphy shows a variable increase of tracer uptake in the skeletal phase whilst the perfusion phase and the blood pool phase are normal [1,2,4]. Malignant transformation into chondrosarcoma is rare but may occur, especially in the diffuse form of multiple enchondromatosis [5,6].
PET/CT with 11C-choline is frequently used for restaging prostate cancer in patients with biochemical failure. Several studies have shown that recurrent disease can be imaged for low PSA values [7–9], that PET/CT with radiolabeled choline might be more accurate than conventional imaging for the detection of lymph node and skeletal metastases [8,10–12], and that several clinical and pathological factors can be used to identify patients who have a higher risk of positive PET/CT [13–15].
Studies indicated that radiolabeled choline accumulates in several malignancies other than prostate cancer or physiological variants, including lung cancer, brain tumors, bladder cancer, meningiomas, as well as inflammatory arthritis disease, Paget’s disease, thymus hyperplasia, benign prostate hyperplasia [16–22]. Increased 11C-choline uptake has also been observed in the pelvic and retroperitoneal lymph nodes of prostate cancer patients with biochemical failure and no histological evidence of disease. This was attributed to lymph node hyperplasia [23]. A simple diffusion mechanism, in addition to an energy-dependent specific transport, regulates the uptake of choline in mammalian cells [24]. Therefore, it is possible that, at least in some of these cases, nonspecific uptake might represent the cause of the false positive.
An alternative hypothesis is that uptake of 11C-choline reflects increased proliferation of cell membranes or of some of their components [25]. It is unknown whether 11C-choline uptake in enchondroma reflects cell proliferation or a concomitant inflammatory process associated with bone remodeling and/or inflammation [26]. The relation between tracer uptake and cellular proliferation is however complex. In humans, the extent of uptake of [11C]choline in the prostate tumor is not related to the cell proliferation rate, as estimated by Ki67 [27].
Nevertheless, in various tumor cells, there was a significant correlation between choline uptake and cell proliferation, as reflected by the incorporation of [3H]methyl-thymidine into DNA [28]. Al-Saeedi et al. found that the concentration of the water-soluble product phosphocholine was higher in breast cancer MCF-7 cells than in control cells [29]. In the same cells, methyl-[3H]choline incorporation was found to be related to the fraction of cells in the S-phase as well as to the incorporation of [methyl-3H]thymidine into DNA [30].
Conclusion
In summary, this case report highlights the necessity of keeping in mind enchondroma in the differential diagnosis of 11C-choline uptake in the skeleton of patients undergoing [11C]choline PET/CT.
Conflict of interest
The authors confirm that this article content has no conflict of interest.
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Article information
Corresponding author: Giampiero Giovacchini.
Copyright: © 2016 Giovacchini G, Ciarmiello A. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are cited.
How to cite: Giovacchini G, Ciarmiello A. Solitary Increase of 11C-Choline Uptake in an Enchondroma Patient with Biochemical Recurrence of Prostate Cancer. J. Diagn. Imaging Ther. 2016; 3(1): 55-58 (https://dx.doi.org/10.17229/jdit.2016-0906-024).
Article history: Received 15 August 2016; Revised 01 September 2016; Accepted 02 September 2016; Published online 06 September 2016.
Archive link: JDIT-2016-0906-024
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