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Objective:To evaluate the ability of 68Ga-Pentixafor (nuclide ligand imaging agents for chemokine receptor 4) PET/CT to differentiate between aldosterone-producing adenoma (APA) and adrenal nonfunctional adenoma (NFA), and to assess how well this imaging method correlates with clinical features and postoperative outcomes. Methods:This was a cross-sectional study involving 73 APA and 12 NFA patients who received 68Ga-Pentixafor PET/CT imaging at Peking Union Medical College Hospital from August 2018 to October 2021. The receiver operating characteristic (ROC) curve was used to evaluate the differential value of visual analysis and the maximum standard uptake value (SUV max) of the focus on APA and NFA. The related factors of SUV max, and its predictive effect on postoperative outcomes were analyzed using Pearson or Spearman analysis and χ2 text. Results:68Ga-Pentixafor PET/CT imaging was positive in 64 APA patients (sensitivity=87.7%) and negative in all 12 NFA patients (specificity=100%). The area under the ROC curve with SUV max differentiating APA and NFA was 0.932 ( P<0.001). When the SUV max cut-off point was 6.23, the sensitivity was 80.8% and the specificity was 100%. The SUV max correlated positively with lesion size ( r=0.598) and aldosterone/renin activity ratio ( r=0.313) and correlated negatively with potassium level ( r=-0.286), renin activity ( r=-0.240) and age of diagnosis ( r=-0.273) (all P<0.05). Of the patients who underwent adrenalectomy and received more than 6 months of post-surgical follow-up, the clinical complete remission rate was higher for 68Ga-Pentixafor PET/CT imaging-positive patients than imaging-negative patients (24/39 vs. 0/4, P=0.031). Conclusions:68Ga-Pentixafor PET/CT is effective at differentiating between APA and NFA. The SUV max of 68Ga-Pentixafor PET/CT correlates with age at onset, lesion size, and the severity of clinical manifestations, and is able to predict postoperative outcomes.
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A 22-year-old female has complained of hirsutism, acanthosis nigricans, enlarged clitoris, and menstrual disorders since puberty. Laboratory examinations revealed hyperandrogenemia. Severe insulin resistance and diabetes were found during hospitalization in our hospital. She was diagnosed with type A insulin resistance syndrome finally. After treatment with metformin, the acanthosis nigricans was significantly relieved, blood glucose was controlled satisfactorily, and the menstrual cycle was restored.
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Objective:To analyze KCNJ5 mutation of adenomas in patients with aldosterone-producing adenoma (APA) companying with hypokalemia, and to compare the clinical characteristics of patients with and without KCNJ 5 mutations.Methods:Clinical data of 144 APA patients were retrospectively analyzed. DNA were extracted from adenoma tissues, and amplified and sequenced for KCNJ5 gene. The serum potassium level and cardiac complications in patients with and without KCNJ5 gene mutation were compared.Results:Among 144 tumors, 131 tumors (91%) had KCNJ5 mutation, including 68 tumors with G151R, 56 tumors with L168R, 5 tumors with E145Q, and two tumors with novel mutations, V156_K160delITE and G151delinsVR. Compared with patients without KCNJ5 mutation, patients with KCNJ5 mutation had lower preoperative serum potassium levels, more cardiac complications, lower postoperative systolic blood pressure, and better postoperative hypertension relief. There were no statistical differences in age, gender, blood pressure, serum potassium level, plasma renin activity or plasma aldosterone concertration.Conclusion:91% adenomas in patients with APA and hypokalemia had KCNJ5 mutation, suggesting that KCNJ5 mutation is the main cause in these patients.
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Objective To investigate the potential effects of simvastatin on angiotensin Ⅱ-stimulated secretion and proliferation of adrenocortical carcinoma H295R cells.Methods The H295R cells were divided into control group, Angiotensin Ⅱgroup, simvastatin group and Angiotensin Ⅱ plus simvastatin group.Cortisol in medium was determined by chemiluminescent method , and aldosterone was determined by radioimmunoassay .The mRNA expression of 11 beta-hydroxylase ( CYP11B1 ) and aldosterone synthase ( CYP11B2 ) were examined by RT-qPCR.Cell proliferation was detected by MTS method.Results Compared with control group, angiotensin Ⅱincreased the secretion of cortisol and aldosterone, and the expression of CYP11B1 and CYP11B2.Simvastatin decreased cortisol secretion and CYP11B1 mRNA expression ( P<0.05 ) .Simvastatin also inhibited angiotensinⅡ-induced the secretion of cortisol and aldosterone , and the expression of CYP 11 B1 and CYP11 B2 compared with Angiotensin Ⅱgroup ( P<0.05 ) .Angiotensin Ⅱhad no effect on cell proliferation , while simvastatin significantly inhibited cell proliferation .The inhibitory effect of simvastatin on proliferation was enhanced when simvastatin was prescribed with angiotensin Ⅱ( P<0.05 ) .Conclusions Simvastatin inhibits angiotensin Ⅱ-induced secretion of cortisol and aldosterone in H295R cells.Simvastatin inhibits cell proliferation, which could be enhanced by angio-tensin Ⅱ.