Biomedical subjects

Wolfgang Eschner

Publications and source records attributed to Wolfgang Eschner.

6 recordsLinked to original sources

PubMed2006

[Image reconstruction and quantification in emission tomography].

Radionuclide tomographic imaging has substantially benefited from the introduction of statistical image reconstruction. Although the main concepts of these iterative algorithms were published decades ago, their widespread use in clinical routine only became available with faster computers for image processing in the last few years. This article gives an overview of data acquisition and iterative reconstruction in emission tomography, deals with the popular maximum likelihood algorithm, and describes the basics of the maximum a posteriori reconstruction. Prerequisites and corrections necessary for quantification are discussed in the second part of the article on the basis of positron emission tomography. Improvements in technical equipment are expected to stimulate future research into image reconstruction.

Humans↗

PubMed2006

Incidence of postradioiodine immunogenic hyperthyroidism/Graves' disease in relation to a temporary increase in thyrotropin receptor antibodies after radioiodine therapy for autonomous thyroid disease.

BACKGROUND: The aim of the study was to analyze retrospectively the incidence of postradioiodine immunogenic hyperthyroidism/Graves' disease in relation to a temporary increase in TSH-receptor antibodies without overt hyperthyroidism after radioiodine therapy for autonomous thyroid disease. PATIENTS AND METHODS: Between May 2000 and May 2003 all patients (n = 1,357) who had undergone radioiodine therapy for autonomous thyroid disease were retrospectively analyzed for development of postradioiodine immunogenic hyperthyroidism. On pretreatment evaluation 565 of 1,357 patients (41.6%) had unifocal autonomous thyroid disease (UFA), 693 of 1,357 patients (51.1%) had multifocal autonomous thyroid disease (MFA), and 99 of 1,357 patients (7.3%) had diffuse thyroid disease (DISS). Free triiodothyronine (FT(3)), free thyroxine (FT(4)), thyrotropin (TSH), and thyroid antibodies were measured. Ultrasound examinations and thyroid scintigraphy were performed before and after radioiodine therapy. A sensitive assay with the human TSH receptor as antigen was chosen for measurement of the TSH receptor antibody and the study was limited to analysis of data obtained since introduction of this assay. RESULTS: Fifteen of 1,357 patients (1.1%) (UFA, 8/565 = 1.4%; MFA, 6/693 = 0.9%; DISS 1/99 = 1.0%) developed postradioiodine hyperthyroidism between 1 and 13 months after radioiodine therapy with clinically overt hyperthyroidism and an elevation of TSH receptor antibodies. Patients with elevated thyroid peroxidase (TPO) antibodies before radioiodine therapy had an almost 10-fold (6/57 patients =10.5%) higher risk of developing postradioiodine immunogenic hyperthyroidism. Thirteen of 999 patients (1.3%) with antibody measurements after radioiodine therapy (UFA, 2/421 = 0.5%; MFA, 9/494 = 1.8%, DISS, 2/84 = 2.4%) had increased levels of TSH receptor antibodies and, to some extent, TPO antibodies without development of clinically overt hyperthyroidism. CONCLUSIONS: There is an estimated 1.1% risk of developing postradioiodine immunogenic hyperthyroidism/Graves' disease in patients undergoing radioiodine therapy for autonomous thyroid disease and this increases approximately 10-fold when TPO antibody levels are elevated before radioiodine therapy. Furthermore, there is an estimated 1.3% risk of a temporary increase of TSH receptor antibodies after radioiodine therapy for autonomous thyroid disease without development of clinically overt hyperthyroidism.

Graves Disease↗

PubMed2005

Treatment of refractory Hodgkin's lymphoma patients with an iodine-131-labeled murine anti-CD30 monoclonal antibody.

PURPOSE: Hodgkin's lymphoma (HL) has been demonstrated to be a good target for immunotherapy since lymphocyte activation markers such as CD30 are expressed in high numbers on the malignant cells. Thus, we developed a new radioimmunoconjugate consisting of the murine anti-CD30 monoclonal antibody (MAb) Ki-4 labeled with iodine-131 ((131)I). PATIENTS AND METHODS: The biodistribution of (131)I-Ki-4 was assessed via dosimetry after preinfusion of 5 mg native Ki-4 followed by 250 to 300 MBq (131)I-labeled Ki-4. Whole-body scintigraphy was performed 1 hour, 24 hours, 48 hours, 72 hours, and 6 days after the infusion. Dosimetry was calculated using the programs NucliDose ICON-IDL (version 5.0.2; Siemens, Erlanger, Germany) and MIRDOSE (version 3.1; Oak Ridge National Laboratories; Oak Ridge, TN). The therapeutic dose was given on day 8 after preinfusion of unlabeled Ki-4. RESULTS: We treated 22 patients with relapsed or refractory CD30-positive HL. Preinfusion of 5 mg native Ki-4 was sufficient to bind the soluble CD30. Imaging demonstrated localization of involved areas measuring 5 cm in diameter or more in four patients and 2.5 cm in one patient. Patients received total body doses of 0.035 Gy to 0.99 Gy. Acute toxicity was mild with grade 1 fatigue in 19 of 22 assessable patients. Seven patients experienced grade 4 degrees hematotoxicity 4 to 8 weeks after treatment. Response included one complete remission, five partial remissions, and three minor responses. CONCLUSION: Treatment with (131)I-Ki-4 is effective but can be associated with severe hematotoxicity.

Adolescent↗

PubMed2005

Imaging of central nervous system lymphomas with iodine-123 labeled rituximab.

Most patients with primary central nervous system (CNS) lymphoma (PCNSL) relapse after initial response to chemotherapy or the combination of chemotherapy and irradiation. Thus, novel treatment regimens for relapsed PCNSL are needed. As the majority of PCNSL are B-cell neoplasms expressing the CD20 antigen, treatment with the chimeric monoclonal antibody (MAb) rituximab might be reasonable. Nevertheless, the potential efficacy of intravenous rituximab in PCNSL seems to be limited as MAbs are high molecular weight proteins, which might be unable to pass the blood brain barrier. Thus, we performed dosimetric measurements with iodine-123 (123I)-rituximab to evaluate rituximab uptake in PCNSL after systemic intravenous administration. We analyzed four patients with PCNSL receiving a preinfusion of 250 mg/m2 rituximab followed by 200-500 MBq of the gamma-emitter 123I-rituximab. Single photon emission computed tomography (SPECT) was performed 1, 24 and 48 h after administration of the radio-immunoconstruct. Only one patient showed a very weak or questionable uptake of 123I-rituximab into tumor tissue which was ninefold lower compared with the blood-pool accumulation. These data suggest that systemic MAb-based radio-immunotherapy is not feasible in patients with PCNSL because a sufficient activity in the tumor will be associated with severe hematotoxicity. If an uptake of therapeutic rituximab doses into PCNSL can be achieved remains questionable.

Adult↗

PubMed2004

[Calibration of a whole body counter using Monte Carlo methods].

Radioactive substances in the human body can be identified and quantified by gamma spectroscopy using whole body counters. Counting efficiencies needed for calculation of incorporated activities are generally determined from measurements of phantoms simulating shape and density of a human and filled with known activity concentrations. The Cologne whole body counter setup was simulated using the EGSnrc Monte Carlo code system. The simulations did reproduce the spectra and efficiencies from phantom measurements (within +/- 2% for K-40). Variations of the phantom position alongside the stretcher resulted in parabola-shaped courses with efficiency changes of up to 5%. Nuclides which are inaccessible to phantom measurements can be quantified by weighted summation of efficiencies generatedfrom simulation offictitious monoenergetic gamma emitters. For I-131, a strong dependence upon the activity distribution inside the body was observed in simulations with a simplified model of the human body Inclusion of the skeleton in the model had a rather small effect. The efficiency decreases linearly with body length by up to 6% when body mass is kept constant. This has to be taken into account when the activity needs to be determined with high precision. For in vivo counting in the context of radiation protection, however, efficiencies can be deduced with sufficient accuracy from measurements or simulations of simple phantoms.

Calibration↗

PubMed2002

Direct comparison of spatially normalized PET and SPECT scans in Alzheimer's disease.

UNLABELLED: Hexamethylpropyleneamine oxime (HMPAO) SPECT and 18F-FDG PET depict similar aspects of perfusion and metabolic abnormalities in Alzheimer's disease (AD), but the correspondence between them is not known in detail. We therefore used statistical parametric mapping to detect and compare abnormal brain areas objectively and quantitatively. METHODS: Twenty-six patients with probable AD (mean age +/- SD, 66 +/- 9 y; mean Mini-Mental State Examination score, 22.5 +/- 4.2) and 6 nondemented healthy volunteers (mean age, 63 +/- 11 y) were studied with HMPAO SPECT and 18F-FDG PET. All images underwent the same processing steps, including 12-mm gaussian smoothing, spatial normalization, and z transformation with respect to normal average and SD. Thresholding of z maps was used to detect abnormal voxels. RESULTS: The overall correlation between PET and SPECT across the entire brain was significant but not close (average r = 0.43). The best correspondence was found in the temporoparietal and posterior cingulate association cortices. There, the number of abnormal voxels for PET correlated strongly with the number for SPECT (r = 0.90 at a z threshold of -2.25), but tracer uptake reductions were significantly more pronounced for PET than for SPECT. Discordant findings were most frequently seen in the temporobasal and orbitofrontal areas (PET low, SPECT high) and in the cerebellum, parahippocampal cortex, and midcingulate cortex (PET high, SPECT low). The correlation between dementia severity and the number of abnormal voxels was closer for PET than for SPECT. Separation of patients from healthy volunteers by counting the number of abnormal voxels was possible over a much wider range of z thresholds with PET than with SPECT. CONCLUSION: Correspondence between 18F-FDG PET and HMPAO SPECT is limited to the main finding of temporoparietal and posterior cingulate functional impairment in mild to moderate AD. The distinction between healthy volunteers and patients is less sensitive to threshold selection with PET than with SPECT, and findings in the frontal, temporobasal, and temporomesial cortices and in the cerebellum may differ between the 2 techniques.

Aged↗