Introduction: The aim of our study was to determine whether treatment with a long-acting somatostatin-receptor analogue is effective in patients with (131)I-negative but somatostatin-receptor-positive metastases from dedifferentiated and anaplastic thyroid cancer.
Materials and methods: Twelve patients were screened for the study. All of them showed progressive disease confirmed by radiologic evaluation, increasing serum thyroglobulin (Tg), and negative diagnostic or posttherapeutic (131)I whole-body scans (WBS). Eight of 12 patients (4 males and 4 females; age range, 57-89 years; 1 papillary thyroid cancer; 4 poorly differentiated follicular thyroid cancer; 1 follicular and anaplastic thyroid cancer; 2 anaplastic thyroid cancer) showed positive somatosatin-receptor expression in Tc-99m depreotide WBS/SPECT (Tc-99m Dep.WBS). Initially, in all patients fluorine-18 2-fluoro-2- D-glucose-positron emission tomography-computed tomography ((18)F-FDG-PET-CT), Tc-99m Dep.WBS, and Tg measurements were performed. In the case of positive receptor scintigraphy, patients were treated with 20mg Sandostatin LAR (Novartis Pharmaceuticals, Basel, Switzerland) once per month intramuscularly over a period of 6 months followed by repeated (18)F-FDG-PET-CT, Tc-99m Dep.WBS, and Tg measurement to determine metabolic activity and tumor size. In case of tumor progression, the dose was increased to 30mg of Sandostatin LAR once per month.
Results: Only 3 patients were able to undergo long-term treatment. Two patients were treated with octreotide long-acting release (LAR) for 1 year and 1 patient for 1(1/2) years. All patients showed progressive disease during the treatment: an increase of serum Tg on one hand and an increase in the number of lesions and extent in tumor size visible on FDG-PET-CT and Tc-99m Dep.WBS on the other. During the treatment there was no change in receptor expression, nevertheless, clear tumor progression under therapy with a somatostatin analogue was visible in FDG-PET-CT and in Tc-99m Dep.WBS.
Conclusion: Our data demonstrate that all of our patients treated with a somatostatin analogue showed clinical progression and that our attempt to achieve a stabilization of the disease failed.