PurposeThe observation that human meningioma cells strongly express somatostatin receptor (SSTR 2) was the rationale to analyze retrospectively in how far DOTATOC PET/CT is helpful to improve target volume delineation for intensity modulated radiotherapy (IMRT).Patients and MethodsIn 26 consecutive patients with preferentially skull base meningioma, diagnostic magnetic resonance imaging (MRI) and planning-computed tomography (CT) was complemented with data from [68Ga]-DOTA-D Phe1-Tyr3-Octreotide (DOTATOC)-PET/CT. Image fusion of PET/CT, diagnostic computed tomography, MRI and radiotherapy planning CT as well as target volume delineation was performed with OTP-Masterplan®. Initial gross tumor volume (GTV) definition was based on MRI data only and was secondarily complemented with DOTATOC-PET information. Irradiation was performed as EUD based IMRT, using the Hyperion Software package.ResultsThe integration of the DOTATOC data led to additional information concerning tumor extension in 17 of 26 patients (65%). There were major changes of the clinical target volume (CTV) which modify the PTV in 14 patients, minor changes were realized in 3 patients. Overall the GTV-MRI/CT was larger than the GTV-PET in 10 patients (38%), smaller in 13 patients (50%) and almost the same in 3 patients (12%). Most of the adaptations were performed in close vicinity to bony skull base structures or after complex surgery. Median GTV based on MRI was 18.1 cc, based on PET 25.3 cc and subsequently the CTV was 37.4 cc. Radiation planning and treatment of the DOTATOC-adapted volumes was feasible.ConclusionDOTATOC-PET/CT information may strongly complement patho-anatomical data from MRI and CT in cases with complex meningioma and is thus helpful for improved target volume delineation especially for skull base manifestations and recurrent disease after surgery.

Contrast-enhanced CT is superior compared with PET alone to predict the extent of PC. In our patient group, the combination of both modalities (contrast enhanced PET/CT) yielded the best results and proved to be a useful tool for selecting candidates for peritonectomy and HIPEC.

Sporadic primary hyperparathyroidism is the most common cause of hypercalcemia in the outpatient population, with a prevalence of one per 500 women and one per 2000 men over 40 years of age. Both increased cell proliferative activity and a decreased sensitivity of cells to secretory inhibition by calcium occur in hyperparathyroidism (1). The diagnosis of hyperparathyroidism is usually made by the demonstration of an inappropriately elevated parathyroid hormone level compared to the simultaneously measured serum calcium level (2). In 80% to 85% of patients, primary hyperparathyroidism is caused by one or more parathyroid adenomas, and in 15% to 20% of cases, it is the result of parathyroid hyperplasia. A rare cause of primary hyperparathyroidism, accounting for less than 1% of all cases, is parathyroid carcinoma. Persistent hyperparathyroidism occurs in 5% to 10% of all patients who undergo surgery for primary hyperparathyroidism, with a continuation of the pre-operative hypercalcemia in the immediate post-operative period. Hyperparathyroidism that presents after a period of more than six months of normocalcemia following surgery is called "recurrent hyperparathyroidism" and is commonly due to continuing growth of the remaining parathyroid glands (3). Secondary hyperparathyroidism is a compensatory hypertrophy of all parathyroid glands due to hypocalcemia, as occurs in renal failure or with vitamin D deficiency (4), whereas tertiary hyperparathyroidism describes the development of autonomous function of parathyroid tissue after longstanding secondary hyperparathyroidism (5-8).In most cases (80%-85%), parathyroid adenomas are found adjacent to the thyroid gland, which is the normal location for these adenomas. However, in up to 20% of cases, they are ectopically placed, e.g., in the anterosuperior, posterosuperior, or very rarely in the mid-lower mediastinum. Occasionally, parathyroid adenomas may be found within, or lateral to, the carotid sheath. Rarely, the lower parathyroid glands fail to migrate, remaining in the high neck anterior to the carotid bifurcation. Finally, 1.4% to 3.2% of all parathyroid adenomas are intrathyroidal, i.e., embedded completely within the thyroid gland (9).Among the several imaging procedures that have been developed for the detection and localization of parathyroid adenomas, dual-phase scintigraphy with Tc-99m sestamibi combined with ultrasonography is considered the imaging method of choice for pre-operatively localizing parathyroid adenomas. The overall accuracy of dual-phase scintigraphy combined with ultrasonography has been found to be superior to that of other scintigraphic or radiological techniques (10, 11). Studies comparing planar imaging and single photon emission computed tomography (SPECT) have shown significantly increased sensitivity for Tc-99m sestamibi SPECT, thus supporting its routine use prior to surgery (12-14). HEAD AND NECK IMAGING PURPOSETo compare the accuracy of planar scintigraphy, single photon emission computed tomography (SPECT), SPECT-CT, and positron...

Pre-therapeutic (68)Ga-DOTATOC tumor uptake as well as assumed uptake of (90)Y-DOTATOC are strongly associated with the results of subsequent PRRT. The defined cut-off values should be confirmed by prospective studies and may then provide the rationale for individual dosing and selecting patients with high likelihood of favorable treatment outcome.

Viable GS are FDG-avid. Using this metabolic information and morphologic CT criteria, combined FDG-PET/CT was more accurate in lesion detection than FDG-PET or CT alone. Changes in FDG uptake after therapy might be a useful additional parameter for therapy monitoring. Therefore, FDG-PET/CT appears to be a promising diagnostic and monitoring tool in the management of patients with GS.

In the absence of preoperative somatostatin receptor ( SST) scans, knowledge of immunohistochemical SST2 tumor expression may help predicting the success of somatostatin analogue-based follow-up studies and treatment of neuroendocrine tumors (NET). We studied the association between SST immunostaining and tracer uptake in [(111)In]-DTPA octreotide (DTPAOC) scintigraphy and [(68)Ga]-DOTA-D-Phe(1)-Tyr(3)-octreotide (DOTATOC) positron emission tomography (PET)/computed tomography (CT). Retrospective analy-sis of 36 NET patients was carried out. In 40 tumors, immunohistochemical SST2, SST3, and SST5 expressions were analyzed using a pathological scoring, applying monoclonal ( SST2) or polyclonal antibodies (SST3, SST5). In 14 lesions, [(111)In]-DTPAOC uptake was assessed by a semiquantitative score. In 26 tumors, [(68)Ga]-DOTATOC PET/CT was quantified using an uptake score and maximal standard uptake value (SUV(max)). Combined and separate qualitative analysis of SST scans revealed significant associations between increased tracer uptake and immunohistochemical SST2 detection (combined: rho=0.56, p=0.0002, [(111)In]-DTPAOC: rho=0.63, p=0.0152, and [(68)Ga]-DOTATOC: rho=0.52, p=0.0065, respectively). In contrast, SST3 and SST5 immunostaining was not associated with tracer uptake (all p>0.14). The semiquantitative immunohistochemical score for SST2 was associated with the [(68)Ga]-DOTATOC uptake score and SUV (max) values (rho=0.67, p=0.0002 and rho=0.63, p=0.0010, respectively), but not with the [(111)In]-DTPAOC uptake score (rho=0.24, p=0.4). In patients without preoperative SST scans, knowledge of immunohistochemical SST2 expression may help estimating the value of SST imaging in the clinical follow-up, in particular in those lesions with positive SST2 immunostaining. Negativity for SST2, however, does not rule out tracer uptake in some patients, with heterogeneous SST2 expression within the tumor as a potential explanation.

Multiphase CT data acquired with the use of highly concentrated CM can be used for qualitative assessment of liver lesions in torso FDG PET/CT. The influence on quantification of FDG uptake is small and negligible for most clinical applications.

A 51-yr-old male presented with a history of progressive lower back pain. Serum biochemistry revealed severe hypophosphatemia (0.5 mmol/liter; normal, 0.8 -1.5), increased alkaline phosphatase levels (297 U/liter; normal, 50 -136), and diminished 1,25-dihydroxyvitamin-D (15.6 pg/ ml; normal, 29.6 -65.1) and calcium (2.0 mmol/liter; normal, 2.2-2.75) levels. Serum levels of 25-hydroxyvitamin-D and intact PTH were normal. Renal phosphate clearance was markedly enhanced (55 ml/min; normal, 5.4 -16.2).99m Technetium-diphosphonate scintigraphy showed multiple regions of focally increased tracer uptake (Supplemental Fig. 1, published as supplemental data on The Endocrine Society's Journals Online web site at http://jcem. endojournals.org), indicating Looser's zones (pseudofractures) in the presence of histologically proven osteomalacia (Supplemental Fig. 2). Whole-body computed tomography (CT) and 111 Indium-diethylene-triamine-pentaacetate-acidoctreotide ( 111 In-DTPAOC)-scintigraphy proved negative. Treatment with oral phosphate and calcitriol was initiated, with only minor effect on serum phosphate levels. Two years later, the patient presented for the first time in our endocrine outpatient clinics. Serum levels of fibroblast growth factor-23 (FGF-23) were elevated (404 kilo resonance units/ liter; normal, 5-210), using a C-terminal FGF-23 assay, with normal renal function (serum creatinine, 0.9 mg/dl; normal,