A new radioguided procedure for localization and surgical treatment of neck node metastasis of papillary thyroid cancer.

AIM OF THE STUDY: We intended to use a radioguided technique for pre-operative localization of neck node recurrences in patients with papillary thyroid cancer (PTC) already submitted to thyroidectomy and radioiodine treatment. PATIENTS AND METHODS: We selected 20 patients affected by PTC with evidence of neck nodes recurrences at ultrasound examination. Our method has been derived from the Radioguided Occult Lesion Localization technique used for pre-operative localization of occult breast lesions. The technique involves the inoculation of human albumin macroaggregates labeled with radioactive technetium (0.4 mCi in a volume of 0.05 ml) directly in the suspicious lesion, under ultrasound guidance. The persistence of the radioactive tracer in the nodes is confirmed by a scintigraphy performed 2 h after injection. During surgery, a gamma detecting probe is used to locate the suspicious lesions as "hot spots". RESULTS: Fifty lymph-nodes were injected with the tracer. All radiolabeled lymph-nodes were located and removed during surgery. At histology, metastasis of PTC was confirmed in 38/50 (76%) lymph-nodes. At least one metastatic lymph-node per patient was removed. In 8/20 (40%) patients, reactive lymphoid hyperplasia was found in 12/50 (24%) lymph-nodes. CONCLUSIONS: This radioguided technique has been highly effective for localization and surgical treatment of suspicious lymph-node detected at neck ultrasound and may play a valuable role in case of node metastases of thyroid cancer that show no radioiodine uptake.

Effect of trimetazidine on 99Tcm-tetrofosmin uptake in patients with coronary artery disease.

Myocardial uptake of 99Tcm-tetrofosmin in vivo is determined by a combination of flow and metabolic status of myocytes. The accumulation of tetrofosmin in the mitochondria is related to their ability to transduce metabolic energy into electronegative membrane potential. Trimetazidine (TMZ), an anti-ischaemic drug, appears to have a metabolic cytoprotective effect related to mitochondrial function, since it does not induce systemic or coronary haemodynamic changes. In this study, we evaluated the effects of TMZ on tetrofosmin uptake in hypoperfused myocardial regions in patients with coronary artery disease (CAD). Twenty-two patients, 14 with previous myocardial infarction (group A) and eight with a history of angina (group B), with angiographically documented CAD were studied. All patients underwent two tetrofosmin SPET studies at rest, before (baseline) and 1 week after TMZ administration (post-TMZ). On quantitative analysis, 131 segments showed less tetrofosmin uptake at baseline. In these segments, tetrofosmin uptake was 51 +/- 13% at baseline and 55 +/- 15% post-TMZ (P < 0.001 vs control). In the 86 hypoperfused segments of group A, tetrofosmin uptake was 48 +/- 14% at baseline and 52 +/- 17% post-TMZ (P < 0.001 vs control). In the 45 hypoperfused segments of group B, tetrofosmin uptake was 56 +/- 9% at baseline and 60 +/- 10% post-TMZ (P < 0.001 vs control). In the remaining 309 segments, no significant difference in tetrofosmin uptake before and after TMZ was observed. In conclusion, our results suggest that TMZ administration may increase myocardial uptake of tetrofosmin in hypoperfused regions at rest in patients with CAD, based on its metabolic effect.

Circulating somatostatin concentrations in healthy and cirrhotic subjects.

Plasma insulin, glucagon, somatostatin, and glucose concentrations were measured in the fasting state as well as after mixed meals (breakfast, lunch, and dinner) in 10 cirrhotic patients and 10 control subjects during a 24-hour period. Cirrhotic patients had fasting glucose values higher than controls (at -15 min: 5.2 +/- 0.2 mmol/L v 3.9 +/- 0.5 mmol/L, P less than 0.05; at 0 min: 5.5 +/- 0.3 mmol/L v 4.3 +/- 0.5 mmol/L, P less than 0.01). After meals blood glucose values remained higher in cirrhotics than in controls. Insulin levels did not differ between the groups in the fasting state, but cirrhotics showed a lower response to meals. Corresponding glucagon concentrations were greater in cirrhotics than in controls before and after meals throughout the 24-hour period (from -15 min to 24 hour: P less than 0.01). BAsal plasma somatostatin levels in the cirrhotic group were significantly higher than in control subjects (at -15 min and at 0 min: P less than 0.05) and further increased after meals. Plasma somatostatin was heterogeneous in normal and cirrhotic group, but the increase in its concentrations in patients with chronic liver disease was for the most part a consequence of elevations in the 1600 and 3500 molecular weight components. The half-life of exogenously infused somatostatin in cirrhotics was comparable to that of controls. These results indicate that in liver cirrhosis elevated levels of circulating somatostatin are associated with hyperglucagonemia and impaired insulin release. The high plasma somatostatin levels observed in cirrhotic patients are the result of hypersecretion of the D cell rather than impaired removal of the peptide.

The relationship between glycosylated haemoglobin levels and various degrees of glucose intolerance.

To assess the use of glycosylated haemoglobin to discriminate between various degrees of glucose intolerance, glycosylated haemoglobin levels were determined in 107 subjects (48 males and 59 females, age range 18-80 years). Following a 75 g oral glucose tolerance test and according to World Health Organization criteria, subjects were classified as normal (n = 32), diabetic (n = 46) or as having impaired glucose tolerance (n = 29). Mean glycosylated haemoglobin levels were 5.8 +/- 1.3% (range 4%-9%) in normal subjects, 7.1 +/- 1.7% in subjects with impaired glucose tolerance (range 4.1%-10.1%) and 10.1 +/- 2.6% (range 4.7%-18.8%) in diabetic patients. The difference between the groups was highly significant (p less than 0.01). Twelve per cent of normal subjects exceeded and 52% of subjects with impaired glucose tolerance fell below 7.4% (mean +/- 2SD, considered as the upper limit of normal values). A significant correlation was observed between glycosylated haemoglobin values and fasting blood glucose (r = 0.68, p less than 0.01). These results provide evidence that glycosylated haemoglobin levels are influenced by slightly reduced carbohydrate tolerance. Glycosylated haemoglobin may be a useful test to improve the specificity of the oral glucose load to select and to follow-up subjects with impaired glucose tolerance.