A 34-year-old man with history of Hodgkin lymphoma presented 7 months after allogeneic stem cell transplantation with an unexplained severe musculoskeletal pain syndrome. A 99mTc-MDP bone SPECTCT showed multiple foci with moderate to intense bone uptake across the axial and appendicular skeleton consistent with periostitis. The patient had been on voriconazole daily for 4 months to treat an Aspergillus pneumonia, and in the absence of other causes, a drug-induced periostitis was suspected. Voriconazole was changed to posaconazole with complete resolution of the musculoskeletal symptoms within 3 weeks.

Background Metal artefact reduction (MAR) techniques still are in limited use in positron emission tomography/computed tomography (PET/CT). This study aimed to investigate the effect of Smart MAR on quantitative PET analysis in the vicinity of hip prostheses. Materials and methods Activities were measured on PET/CT images in 6 sources with tenfold activity concentration contrast to background, attached to the head, neck and the major trochanter of a human cadaveric femur, and in the same sources in similar locations after a hip prosthesis (titanium cup, ceramic head, chrome-cobalt stem) had been inserted into the femur. Measurements were compared between PET attenuation corrected using either conventional or MAR CT. In 38 patients harbouring 49 hip prostheses, standardized uptake values (SUV) in 6 periprosthetic regions and the bladder were compared between PET attenuation corrected with either conventional or MAR CT. Results Using conventional CT, measured activity decreased with 2 to 13% when the prosthesis was inserted. Use of MAR CT increased measured activity by up to 11% compared with conventional CT and reduced the relative difference with the reference values to under 5% in all sources. In all regions, to the exception of the prosthesis shaft, SUVmean increased significantly (p < 0.001) by use of MAR CT. Median (interquartile range) percentual increases of SUVmean were 1.4 (0.0–4.2), 4.0 (1.8–7.8), 7.8 (4.1–12.4), 1.5 (0.0–3.2), 1.4 (0.8–2.8) in acetabulum, lateral neck, medial neck, lateral diaphysis and medial diaphysis, respectively. Except for the shaft, the coefficient of variation did not increase significantly. Except for the erratic changes in the prosthesis shaft, decreases in SUVmean were rare and small. Bladder SUVmean increased by 0.9% in patients with unilateral prosthesis and by 4.1% in patients with bilateral prosthesis. Conclusions In a realistic hip prosthesis phantom, Smart MAR restores quantitative accuracy by recovering counts in underestimated sources. In patient studies, Smart MAR increases SUV in all areas surrounding the prosthesis, most markedly in the femoral neck region. This proves that underestimation of activity in the PET image is the most prevalent effect due to metal artefacts in the CT image in patients with hip prostheses. Smart MAR increases SUV in the urinary bladder, indicating effects at a distance from the prosthesis.

No abstract

Background Hypercalcemia of malignancy is not uncommon in patients with advanced stage cancer. In rare cases the cause of the hypercalcemia is excessive production of calcitriol, the active form of vitamin D. Although inappropriate tumoral secretion of calcitriol is typically associated with lymphomas and some ovarian germ cell tumors, we present a case of calcitriol overproduction-induced hypercalcemia due to a pancreatic neuroendocrine tumor. The high expression of somatostatin receptors on this neuroendocrine neoplasm opened up the opportunity to treat the patient with radiolabelled somatostatin analogs, which successfully controlled the refractory hypercalcaemia and calcitriol levels. This case documents a rare finding of refractory hypercalcaemia of underlying malignancy due to a calcitriol-producing pancreatic neuroendocrine tumor, responding to peptide receptor radionuclide therapy (PRRT). Case presentation A 57 years-old patient presented with back pain, general discomfort, polydipsia, polyuria, fatigue and recent weight loss of 10 kg. Clinical examination was normal and there was no relevant medical history. Biochemical evaluation showed hypercalcemia with markedly increased calcitriol levels. CT-thorax-abdomen and ultrasound guided biopsy revealed a pancreatic neuroendocrine tumor with multifocal liver metastases, suggesting that excessive overproduction of calcitriol by this neuroendocrine tumor was the cause of the refractory hypercalcemia. The patient was eligible for PRRT. Four cycles of 177Lu-DOTATATE PRRT resulted in a morphological response and a normalization of serum calcium levels, confirming the hypothesis of a calcitriol producing pancreatic neuroendocrine tumor. Progression of liver metastases warranted further therapy and temozolomide-capecitabine was started with morphological and biochemical (serum calcium, calcitriol) stabilization. Conclusion Although up to 30–40% of gastroenteropancreatic neuroendocrine tumors are known to be functional (i.e. producing symptoms associated with the predominant hormone/peptide secreted), calcitriol secreting pancreatic neuroendocrine tumors are very rare. However, treatment with PRRT resulted in normalization of calcium and calcitriol levels, strongly supporting the hypothesis of a calcitriol-producing pancreatic neuroendocrine tumor.