Positron emission tomography combined with computed tomography (PET/CT) enables assessment of not only anatomical and structural but also metabolic changes in tumor mass. F-fluoroethyl tyrosine (F-FET) PET/CT is based on evaluation of transport of F-labeled tyrosine in tissues. We present a clinical case of a patient with a newly diagnosed brain tumor, demonstrating the capabilities ofF-FET PET/CT in assessing the reliable volume and degree of tumor anaplasia, which is important when choosing the treatment approach for a patient.
BackgroundThe purpose of the study to evaluate possibilities of CT-perfusion and PET methods with 18F–FDG and 18F–fluorocholine in the complex diagnosis of hepatocellular carcinoma. The study included the results of PET/CT with 18F–FDG, 18F–FCh and CT-perfusion of the liver in 18 patients with histologically confirmed diagnosis of hepatocellular carcinoma (HCC). Depending on the degree of tumor differentiation, all patients were divided into 3 groups - patients with highly differentiated (6 patients), moderately differentiated (4 patients), and low-differentiated HCC (8 patients).ResultsAverage values of maxSUV in the group of patients with highly differentiated HCC in PET/CT with 18F–FDG and 18F- fluorocholine in a solid component of tumor reached 3.51 and 18.24, respectively; in patients with moderately differentiated HCC - 3.91 and 12.32, respectively; in patients with low-differentiated HCC - 9.58 and 9.70, respectively. Average values of CT perfusion imaging in a solid component of the tumor in the group of patients with highly differentiated HCC were the following: BF - 55,33 ml/100 ml/min, BV - 13,71 ml/100 ml, ALP - 52,41 ml/100 ml/min, PVP - 10.81 ml/100 ml/min (p ≤ 0,05), in the group of patients with moderately differentiated HCC: BF - 52,78 ml/100 m /min, BV - 12,23 ml/100 ml, ALP - 47,26 ml/100 ml/min, PVP - 9,10 ml/100 ml/min (p ≤ 0.05), in the solid component of low-differentiated HCC: BF - 46,96 ml/100 ml/min, BV - 9,49 ml/100 ml, ALP - 40.54 ml/100 ml/min, PVP - 7,66 ml/100 ml/min (p ≤ 0,05).ConclusionsThe diagnostic capabilities of the complex of PET/CT techniques with 18F–FDG and 18F–FCh and CT perfusion in a single-scan mode for hepatocellular carcinoma were evaluated for the first time. The obtained data allow to assume that the integrated use of PET with 18F–FDG and 18F–FCh and CT perfusion in a single scan improves the differential diagnostic possibilities of PET/CT diagnostics, which can find application in planning and prognosis of the disease. Due to the small number of patients further study of the problem is required.
Primary hyperparathyroidism (PHPT) is caused by parathyroid malignant neoplasm in 1% of cases. The risk of the latter is higher in patients with symptomatic PHPT. The prognosis in this group of patients depends on the extent of the process and primary surgical intervention. In these cases, the differential diagnosis between secondary foci in the bones associated with parathyroid cancer and hyperparathyroid osteodystrophy is a challenging problem. This article describes two cases of severe PHPT accompanied by hyperparathyroid osteodystrophy suspected for metastatic parathyroid cancer. Positron emission tomography in combination with computed tomography (PET/CT) with 18F-fluorodeoxyglucose (18F-FDG) and/or 18F-fluorocholine was included in the examination algorithm. In both cases, pronounced bone changes similar to parathyroid metastases were observed. Accumulation of 18F-fluorocholine was also observed only in altered parathyroid gland. Histological examination of postoperative material verified benign parathyroid tumors, and characteristic lesions of bone tissue were regarded as areas of osteodystrophy. Therefore, accumulation of 18F-fluorocholine at the areas of bone destruction does not enable differentiation between hyperparathyroid osteodystrophy and metastatic lesions; further research is required to assess sensitivity and specificity of the method with respect to topical diagnosis of altered parathyroid gland.
e17518 Background:Long time the patients with high-differentiated thyroid cancer with distant metastases had only one type of treatment. It was radioiodine therapy courses and follow-up. In cases of revealed radioiodine (RAI) refractory process we did not have possibilities for treatment this category of patients. Results of trials DECISION and SELECT gave to oncologist new keys for successful treatment. We present our group of RAI refractory thyroid cancer patients, which was treated by Lenvatinib like routine clinical practice. Methods:We have on treatment 8 patients (3-male, 5-female). Histologically – papillary thyroid carcinoma. Provisions of national clinical recommendations were considered as criteria of a RAI-refractory status. Existence of a symptomatic progression of a tumor was main criterion. Results:Six patients received from 7 to 14 month courses of treatment. All these patients are revealed partial response of the tumor lesions by PET-FDG-CT and the dramatically decrease of thyroglobulin level is noted. Two patients stopped treatment after 1 month of therapy. One patient due to destructive pneumonia, other patient – death due to myocardial infarction. Adverse events not related with Lenvatinib. The adverse events were controllable. We noted the expressed arterial hypertension. Before correction of a dose of a drug increase of arterial pressure more than 160/100 mm Hg is noted. Arterial pressure managed to be corrected the combined scheme of therapy (amlodipin, bisoprolol, hydrochlorthiazide). Correction of a dose of lenvatinib is made at 3 patients to 20 mg daily, 2 patient – 14. Conclusions:Introduction of a lenvatinib clinical practice is very successful. But we noted of important accurate expert selection of patients for treatment after establishment of a condition of a RAI-refractory and revealed really symptomatic progression, adequate correction of the adverse effects (arterial hypertension) and well-timed correction of a dose of a lenvatinib.
BACKGROUND: Primary hyperparathyroidism (PHPT) is a widespread endocrine disease characterized by excessive production of parathyroid hormone (PTH) due to parathyroid gland hyperplasia (PGH) or tumor lesions (adenoma or cancer of the parathyroid gland (PG) in 80% and 15% of cases respectively). Choline kinase alpha (XK) overexpression is described in tumors of different localization, but there is no data on its expression in PG tumors. AIMS: To study the character of XK expression in PG neoplasms and its relationship with clinical, laboratory, and visualization characteristics (positron emission tomography combined with computed tomography (PET/CT) with 18Ffluorocholine (18FFC)). MATERIALS AND METHODS: The material for the study was based on tissue samples from 10 patients of 3470 years old (Me = 61.5; [48; 66]), with a laboratoryconfirmed diagnosis of PHT. An immunohistochemical study (IHC) was carried out on materials from 2 patients with hyperplasia of the main cells, from 5 patients with adenoma of PG, from 1 patient with atypical adenoma and 1 with carcinoma of PG; in 1 case the metastasis of cancer of the neck with lymph node was examined. RESULTS: The expression of XK is spotted in all types of PG cells (chief cells: active and inactive forms), transitional forms between the chief cells and oxyphil; oxyphil cells, but it was most intense in active chief cells. The expression of XK was observed in neoplasms of PG of various degrees of malignancy. In the most numerous group of PG formations with a favorable prognosis (11 samples from 7 patients), no statistically significant correlation (p 0.05) was obtained between the intensity expression of the XK, of the PTH and the proliferative activity index Ki67, the level of radiopharmaceutical accumulation in PET/CT with 18FFC (SUVmax) and laboratory data (PTH, Ca, Ca++). CONCLUSIONS: In the majority of investigated cases, moderate and intensive expression of the XK was detected in PG cells. A small amount of studied cases does not allow us to identify the connection between the intensity of XK expression and the malignant potential for the formation of PG.
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