Low-dose oral propranolol could reduce brown adipose tissue F-18 FDG uptake in patients undergoing PET scans.

UNLABELLED: Fluorine-18 fluoro-2-deoxy-D-glucose (FDG) uptake in brown adipose tissue (BAT) may generate FDG-PET scan misinterpretation. Recent studies have shown reduced FDG uptake in BAT in rats treated with high doses of the beta-blocker propranolol. The aim of this observational study was to present a cohort of patients with high FDG uptake in BAT who underwent a second scan after receiving a low dose of propranolol, to determine whether the use of this premedication could improve the diagnostic confidence of FDG-PET scans by inhibition FDG uptake in BAT, and also whether administration of this drug affects tracer uptake in tumors. METHODS: Twenty-six cancer patients, presenting with increased BAT FDG uptake, were selected prospectively. On a different day, patients were given propranolol 20 mg orally 60 minutes prior to FDG administration 185-277.5 MBq (5-7.5 mCi) and were scanned again. Basal and postpropranolol BAT SUVmax, and tumor SUVmax (when present) were measured. RESULTS: Mean basal BAT SUVmax was 5.52+/-2.3. Mean postpropranolol SUVmax was 1.39+/-0.42 (P<0.0001). In 11 patients, the basal mean tumor SUVmax was 8.07+/-6.4, and 7.88+/-5.9 in postpropranolol scans (P=0.53). Nine patients showed mediastinal FDG uptake in the basal scan, affecting image interpretation. This was not observed in postpropranolol scans. No adverse effects due to propranolol were encountered. CONCLUSIONS: In this patient cohort, there was significant reduction of FDG uptake in BAT following propranolol administration, allowing for adequate interpretation of FDG-PET and software-fused FDG-PET with CT images, particularly in the mediastinal area, without affecting tumor tracer uptake.

Ectopic growth hormone-releasing hormone secretion by a metastatic bronchial carcinoid tumor: a case with a non hypophysial intracranial tumor that shrank during long acting octreotide treatment.

Ectopic acromegaly represents less than 1% of the reported cases of acromegaly. Although clinical improvement is common after treatment with somatostatin (SMS) analogs, the biochemical response and tumor size of the growth hormone-releasing hormone (GHRH)-producing tumor and its metastases are less predictable. Subject A 36-year-old male was referred because of a 3-year history of acromegaly related symptoms. He had undergone lung surgery in 1987 for a "benign" carcinoid tumor. Endocrine evaluation confirmed acromegaly Plasma IGF-1: 984 ng/ml (63-380), GH: 49.8 ng/ml (<5). MRI showed a large mass in the left cerebellopontine angle and diffuse pituitary hyperplasia. Pulmonary, liver and bone metastases were shown by chest and abdominal CT scans. Ectopic GHRH secretion was suspected. Methods Measurement of circulating GHRH levels by fluorescence immunoassay levels and immunohistochemical study of the primary lung tumor and metastatic tissue with anti-GHRH and anti-somatostatin receptor type 2 (sst2A) antibodies. Results Basal plasma GHRH: 4654 pg/ml (<100). Pathological study of liver and bone biopsy material and lung tissue removed 19 years earlier was consistent with an atypical carcinoid producing GHRH and exhibiting sst2A receptor expression. Treatment with octreotide LAR 20-40 mg q. month resulted in normalization of plasma IGF-1 levels. Circulating GHRH levels decreased dramatically. The size of the left prepontine cistern mass, with SMS receptors shown by a radiolabeled pentetreotide scan, decreased by 80% after 18 months of therapy. Total regression of pituitary enlargement was also observed. No changes were observed in lung and liver metastases. After 24 months of therapy the patient is asymptomatic and living a full and active life.