Red blood cells labelling with 99mTc-HM-PAO.
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Biomedical subjects
Publications and source records attributed to A Catafau.
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A patient with AA amyloidosis secondary to ankylosing spondylitis showed intense liver uptake of Tc-99m MDP on bone imaging. The biopsy showed hepatic amyloid deposition. A repeat bone scan with Tc-99m MDP 1 year later was negative, although the clinical signs and liver function tests of the patient had not changed. A mechanism might exist, other than the affinity of amyloid to calcium, which would explain the extraosseous uptake of pyrophosphates and diphosphonates in organs and soft tissues affected by systemic amyloidosis.
Uptake of Tc-99m DISIDA in a bone metastasis from a hepatoma located at the humeral head is reported. Previous literature has only shown extrahepatic uptake of hepatobiliary agents in cases of lung metastases from hepatocellular carcinoma. The use of imaging with biliary tracers can increase the diagnostic specificity when bone metastases from hepatoma are suspected.
Thirty patients diagnosed as having systemic amyloidosis (six with primary amyloidosis and 24 with secondary amyloidosis) were given bone scans with 99Tcm-methylene diphosphonate in order to evaluate the skeletal and extra-osseous uptake and their clinical-scintigraphic correlation. Extra-osseous uptake appeared in nine instances, more frequently in primary (5/6) than in secondary (4/24) amyloidosis. Fourteen patients had clinical and echocardiographic suspicion of cardiac amyloidosis but only one showed cardiac uptake. Six patients had probable hepatic involvement but in only two cases was hepatic uptake seen. The extra-osseous uptake suggests the presence of amyloid deposits in the organs and soft tissues which take up the bone tracer. The absence of any uptake does not rule out amyloid infiltration.
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BACKGROUND: Sinus bradycardia in trained athletes is predominantly a manifestation of increased vagal tone, but it is not known whether an alteration in the cardiac sympathetic system can contribute to blunted chronotropic response. This study assessed the integrity of the sympathetic system in trained athletes with sinus bradycardia by means of the iodine-123-metaiodobenzylguanidine (123I-MIBG) procedure. METHODS AND RESULTS: Fourteen athletes with sinus bradycardia and 8 athletes with a normal heart rate were explored by means of planar and single photon emission computed tomography MIBG studies. The heart/mediastinum ratio, regional myocardial distribution, and percent of regional myocardial MIBG uptake were evaluated. The heart/mediastinum ratio in athletes with sinus bradycardia was 1.87+/-0.10, and in athletes with a normal heart rate, the heart/mediastinum ratio was 1.86+/-0.16 (P = not significant). In athletes with sinus bradycardia, the regional distribution of MIBG showed an inferior and apical uptake defect in 8 athletes, an inferior, apical, and septal defect in 3 athletes, an inferior defect in 1 athlete, and normal distribution in 2 athletes (14%). In athletes with a normal heart rate, the regional distribution of MIBG showed an apical uptake defect in 3 athletes and normal distribution in 5 athletes (63%). The percent of regional MIBG uptake in the inferior region was significantly reduced in athletes with sinus bradycardia (44%+/-13% vs. 72%+/-11%, P<.01). CONCLUSION: These results show severely reduced myocardial MIBG distribution in the inferior region in athletes with sinus bradycardia, suggesting selective inferior myocardial wall sympathetic denervation, which may be related to increased vagal tone.
The relationship between psychopathology and Wisconsin Card Sorting Test (WCST) performance was evaluated in 25 unmedicated young acute schizophrenic female patients (14 neuroleptic-naive and 11 neuroleptic-free) and 15 female controls. The schizophrenic patients (especially the neuroleptic-free) performed more poorly than controls in the WCST. In addition, WCST impairment correlated with both negative and positive symptoms. The results suggest that the neuropsychological dysfunction in schizophrenia is present at the onset of the illness, and is neither secondary to previous neuroleptic treatment nor to chronicity of the illness.