Tc-99m sestamibi parathyroid imaging was performed in 28 patients with chronic renal failure to localize abnormal parathyroid glands in patients receiving hemodialysis, and compared the localization with ultrasonography and magnetic resonance (MR) imaging. Methods: We imaged 28 patients with secondary hyperparathyroidism using Tc-99m sestamibi (about 600 MBq) at 10 min and 2–3 h following radiotracer injection. In addition, mediastinal images were recorded at approximately 1 h following injection to identify ectopic parathyroid glands. All patients also were evaluated with ultrasonography and MR imaging. Results: Tc-99m sestamibi scans demonstrated focal uptake in 60 glands of the 28 patients, and was categorized as slight uptake in 71.7% (43/60), and intense uptake in 28.3% (17/60). Seventeen of the 28 patients underwent parathyroidectomy. A total of 64 glands were resected. Sestamibi imaging was more sensitive for localizing abnormal parathyroid glands than ultrasonography or MR imaging. Histologic evaluation of 27 resected parathyroid glands revealed that the number of oxyphil or chief cells was not proportional to sestamibi uptake. Conclusion: Our data indicate that Tc-99m sestamibi imaging should be used initially to localize abnormal parathyroid glands in hemodialysis patients with secondary hyperparathyroidism, prior to MR imaging or ultrasonography. Sestamibi uptake in parathyroid glands may not correlate with the degree of hypercellularity of oxyphil cells.

The aim of the study was to compare the accuracy of technetium-99m sestamibi imaging for localization of ectopic parathyroid glands in patients with hyperparathyroidism with that of magnetic resonance (MR) and computed tomographic (CT) imaging. Eleven patients with primary (n=3) or secondary (n=8) hyperparathyroidism were studied with 99mTc sestamibi parathyroid imaging CT and MR imaging. Images of the neck were acquired at 10 min and 2-3 after tracer injection. The three patients with primary hyperparathyroidism and five patients with secondary hyperparathyroidism underwent parathyroidectomy. The ectopic glands were confirmed by histopathological examination of the resected specimens. In respect of 20 parathyroid glands in the eight patients explored surgically, the sensitivity and specificity of sestamibi imaging were 70% (14/20) and 88%, respectively, those of CT, 40% (8/20) and 88%, and those of MR imaging, 60% (12/20) and 88%. Of these patients, three had parathyroid adenomas while five had hyperplasia (17 glands). Sestamibi imaging localized eight ectopic parathyroid glands, which were surgically confirmed (six were located in the thymus and two in the mediastinum). In one patient explored surgically, the ectopic gland was located outside the field of the MR coil. Although the remaining three cases of secondary hyperparathyroidism were not confirmed surgically, these patients demonstrated sestamibi uptake in five parathyroid glands, including three ectopic glands. MR images demonstrated abnormal parathyroid glands in the same regions as sestamibi imaging. Our data indicate that 99mTc-sestamibi imaging should be used initially to localize the ectopic parathyroid glands in patients with hyperparathyroidism for anatomical guidance prior to MR or CT imaging.

Abstract. To determine the usefulness of parathyroid scintigraphy in histological estimation for secondary hyperparathyroidism (2HPT) using Tc-99m sestamibi or Tc-99m tetrofosmin. Tc-99m sestamibi (MIBI) and Tc-99m tetrofosmin (Tetro) parathyroid imaging following double-phase study, magnetic resonance imaging (MRI), and ultrasound were performed on 14 patients with 2HPT. All patients underwent parathyroidectomy. The uptake of two tracers in parathyroid areas was compared with the histopathologic findings. Forty-nine parathyroid glands were surgically explored and histologically proven to be hyperplastic. Of these, 42 were diagnosed with nodular type (N-type) hyperplasia, and 7 with diffuse type (D-type) hyperplasia. MIBI and Tetro parathyroid imagings detected 34 and 35 parathyroid glands, respectively. The sensitivity of MIBI was determined to be 76.2% (32/42) for N-type, and 28.6% (2/7) for D-type. The sensitivity of Tetro was determined to be 78.6% (33/42) for N-type and 28.6% (2/7) for D-type. The sensitivity of both MIBI and Tetro was significantly higher for N-type than for D-type, 76.2% (32/42) vs. 28.6% (2/7) in MIBI, P = 0.022; 78.6% (33/42) vs. 28.6% (2/7) in Tetro, P = 0.015. The sensitivity of MRI was determined to be 76.2% (32/42) for N-type and 42.9% (3/7) for D-type, and the sensitivity of ultrasound was 71.4% (30/42) for N-type and 71.4% (5/7) for D-type. There was no significant difference in the sensitivity of MRI or ultrasound between N-type and D-type. The uptake ratios of MIBI and Tetro were also greater for N-type than for D-type. The detectability of both MIBI and Tetro was greater for N-type than for D-type. Tc-99m MIBI or Tc-99m Tetro parathyroid scintigraphy therefore may be used clinically to distinguish N-type from D-type parathyroid gland hyperplasia.

These results support the notion that indoxyl sulfate and TGF-beta1 may be involved in the progression of CRF, and that the oral adsorbent AST-120 may suppress the progression, at least in part, by reducing overproduction of TGF-beta1.

SummaryInfiltration by circulating inflammatory cells is a prominent local inflammatory feature of ulcerative colitis (UC). Several trials have suggested that leukocytapheresis by filtration can benefit patients with active UC. We investigated how this therapy might modulate the inflammatory response. Patients with active UC who were beginning repeated filtration leukocytapheresis were studied. Mononuclear cell preparations were obtained from blood before and after the first treatment, and expression of cytokine signalling components and the cell-proliferative response were analysed in vitro . Leukocytapheresis reduced lipopolysaccharide-induced production of proinflammatory cytokines (interleukin-1, -6, -8 and tumour necrosis factor-a a a a , P < < < < 0·05 for all) and activation of intracellular signalling components (nuclear factor-k k k k B, mitogen-activated protein kinases, and signal transducer and activator of transcription-3), as well as surface expression of toll-like receptor-4 ( P < < < < 0·05) in mononuclear cells. The therapy also reduced the cell-proliferative response by mononuclear cells stimulated with sonicated bacterial preparations from autologous intestine ( P < < < < 0·05). These results indicate that activated mononuclear cells in the peripheral blood of patients with active UC are removed by leukocytapheresis and replaced by cells with a lower activation status. This replacement may partly explain the therapeutic benefit.