The aim of this study was to evaluate the clinical use of fluorine-18 fluorodeoxyglucose positron emission tomography (FDG-PET) in acute and chronic osteomyelitis and inflammatory spondylitis. The study population comprised 21 patients suspected of having acute or chronic osteomyelitis or inflammatory spondylitis. Fifteen of these patients subsequently underwent surgery. FDG-PET results were correlated with histopathological findings. The remaining six patients, who underwent conservative therapy, were excluded from any further evaluation due to the lack of histopathological data. The histopathological findings revealed osteomyelitis or inflammatory spondylitis in all 15 patients: seven patients had acute osteomyelitis and eight patients had chronic osteomyelitis or inflammatory spondylitis. FDG-PET yielded 15 true-positive results. The tracer uptake correlated with the histopathological findings in each case. Bone scintigraphy performed in 11 patients yielded ten true-positive results and one false-negative result. Follow-up carried out on two patients revealed normal or clearly reduced tracer uptake, which correlated with a normalisation of clinical data. In early postoperative follow-up it was impossible to differentiate between postsurgical reactive changes and further infection using FDG-PET. It is concluded that acute and chronic osteomyelitis of the peripheral as well as the central skeleton can be detected using FDG-PET. Osteomyelitis can be differentiated from soft tissue infection surrounding the bone. Unlike computed tomography and magnetic resonance imaging, FDG-PET is not affected by metal implants used for fixing fractures. FDG-PET demonstrated promising initial results with respect to treatment monitoring. Nevertheless, in the early postoperative phase FDG-PET seems to be of limited value owing to unspecific tracer uptake.

The aim of this study was to determine the maximum tolerated dose of rhenium-188 hydroxyethylidene diphosphonate (HEDP) in prostate cancer patients with osseous metastases who are suffering from bone pain. Twenty-two patients received a single injection of escalating doses of carrier-added 188Re-HEDP [1.3 GBq (35 mCi), 2.6 GBq (70 mCi), 3.3 GBq (90 mCi) and 4.4 GBq (120 mCi)]. Blood counts and biochemical parameters were measured weekly over a period of 8 weeks. Haematological toxicity (WHO grading) of grade 3 or 4 was considered unacceptable. Clinical follow-up studies including methods of pain documentation (medication, pain diary) were performed for 6 months after treatment. In the 1.3-GBq group, no haematological toxicity was observed. First haematotoxic results were noted in those patients with a dose of 2.6 GBq 188Re-HEDP. In the 3.3-GBq group, one patient showed a reversible thrombopenia of grade 1, one a reversible thrombopenia of grade 2 and three a reversible leukopenia of grade 1. In the 4.4-GBq group, thrombopenia of grades 3 and 4 was observed in one and two patients (baseline thrombocyte count <200x10(9)/l), respectively, and leukopenia of grade 3 was documented in one patient. The overall nadir of thrombopenia was at week 4. The individual, maximum percentage decrease in thrombocytes in the 1.3-, 2.6-, 3.3- and 4.4-GBq groups was 17%, 40%, 60% and 86%, respectively. In two patients, a transient increase in serum creatinine was observed (max. 1.6 mg/dl). Pain palliation was reported by 64% of patients, with a mean duration of 7.5 weeks. The response rate seemed to increase with higher doses, reaching 75% in the 4.4-GBq group. It is concluded that in prostate cancer patients, the maximum tolerated dose of 188Re-HEDP is 3.3 GBq if the baseline thrombocyte count is below 200x10(9)/l. In patients with thrombocyte counts significantly above 200x10(9)/l, a dose of 4.4 GBq might be tolerable. Thrombo- and leukopenia are the most important side-effects. Pain palliation can be achieved in 60%-75% of patients receiving a dose of 2.6 GBq or more of 188Re-HEDP. Studies in a larger patient population are warranted to evaluate further the palliative effect of 188Re-HEDP.

IntroductionThe diagnosis of spine infections can be difficult, because the patient's history, subjective symptoms and physical findings are often inconclusive, particularly in the early stages. Nuclear medicine procedures, which identify pathophysiological reactions preceding morphological changes, can play a useful role in the diagnosis of spondylodiscitis. Specific tracers are used in infectious bone disease: Ga-67, Tc-99m nanocolloid, Tc-99m-HMPAO-and In-111-labeled leukocytes, Tc-99m and In-111 polyclonal human immunoglobulin, and Tc-99m-labeled monoclonal antibodies [10]. However, for diagnosing spine infections, these procedures are still not optimal [10,19]. On white cell imaging, up to 50% of all patients with spondylodiscitis show photopoenic defects, which are not specific for infection [12].Fluorine-18 fluorodeoxyglucose positron emission tomography (FDG-PET) is increasingly playing an important role in the diagnosis, staging and monitoring of malignant tumours [3,5,15]. Not only tumours but also infections show an increased uptake of FDG. The FDG uptake depends on the increased glucose metabolism in activated inflammatory cells such as leukocytes, granulocytes and macrophages [20]. In detecting osteomyelitis with FDG-PET, first studies reported a sensitivity of up to 100% [6,7,9,18]. However, there are limited experiences Abstract Nuclear medicine procedures can be helpful in diagnosing spine infections. The purpose of the study was to evaluate the findings of positron emission tomography with fluorine-18 fluorodeoxyglucose (FGD-PET) in the detection of spondylodiscitis. We performed FDG-PET in 16 patients with suspected spondylodiscitis. All the patients were operated and underwent histopathological examination. The FDG-PET findings were graded and evaluated by two independent nuclear medicine physicians. Of the 16 patients, 12 had a histopathologically confirmed spondylodiscitis. In all these 12 patients, FDG-PET was true-positive. In the four patients without spondylodiscitis, FDG-PET showed three true-negative and one false-positive result. In spondylodiscitis, the mean standard uptake value (SUV) of FDG was 7.5 (SD± 3.8). The PET scans depicted the paravertebral soft tissue involvement in cases of spondylodiscitis. Our first results showed that FDG-PET is a very sensitive imaging procedure in the detection of spondylodiscitis. Compared to other nuclear medicine procedures, PET enables a rapid imaging with acceptable radiation dose and high spatial resolution.

The aim of this study was to evaluate the clinical use of fluorine-18 fluorodeoxyglucose positron emission tomography (FDG-PET) in medullary thyroid cancer (MTC) on the basis of comparison with findings obtained using indium-111 pentetreotide (SMS), pentavalent technetium-99m dimercaptosuccinic acid (DMSA), technetium-99m sestamibi (MIBI), computed tomography (CT) and magnetic resonance imaging (MRI). One hundred FDG-PET examinations in 85 patients (40 males, 45 females) with elevated tumour marker levels and/or pathological findings on other imaging methods were evaluated retrospectively. Eighty-two patients were examined after total thyroidectomy, and the remaining three patients prior to surgery. Overall, 181 lesions could be identified with at least one of the imaging techniques. Fifty-five lesions were confirmed histologically. FDG-PET detected 123 of 181 sites, which is a lesion detection probability of 68%. In the 55 cases with histological confirmation, we found 32 true positive, 3 false positive, 11 true negative and 9 false negative lesions using FDG-PET, resulting in a sensitivity of 78% and a specificity of 79%. Sensitivity and specificity were, respectively, 25% and 92% for SMS, 33% and 78% for DMSA, 25% and 100% for MIBI, 50% and 20% for CT and 82% and 67% for MRI. Compared with morphological techniques and functional imaging methods with single-photon emitters, FDG-PET showed the highest lesion detection probability for MTC tissue, with a high sensitivity and specificity. It is concluded that FDG-PET is a useful method in the staging and follow-up of MTC.