131I-MIBG肾上腺髓质显像胆囊显影二例

例1　患者女,32岁,因反复头晕、胸闷、心悸、消瘦、腹痛6个月,加重1个月余入院。患者于2003年3月20日在外院住院后血压呈阵发性升高,发作时血压>160110mmHg(1mmHg=0.133kPa),立基丁试验阳性,予以对症、支持治疗。4月24日在本科行131I间碘苄胍(MIBG)肾上腺髓质断层 同机CT融合显像,示双肾上腺阴性,胆囊放射性明显浓集。临床拟诊“异位嗜铬细胞瘤”。入院后血压在100～11065～85mmHg波动,有时无诱因出现腹痛、呕吐,发作时血压140105mmHg,服苯苄胺控制不佳。患者24h尿香草基扁桃酸(VMA)正常,血压升高时查5h尿VMA肌酐(Cr)比值轻度升高。…     

肥厚性心肌病患者201Tl和123I-MIBG心肌SPECT显像

目的：探讨肥厚性心肌病的肥厚心肌与非肥厚心肌交感神经活性。方法选择１８例肥厚性心肌病（ＨＣＭ）患和６例对照（Ｎ组）。根据超声心动图将ＨＣＭ组分为心尖部肥厚性心肌病（ＡＰＭ）５例，非对称性心室间隔肥厚性心肌病（ＡＳＨ）７例，弥漫性肥厚性心肌病（ＤＰＭ）６列。所有患均进行超声心动图（Ｍ型和Ｂ型）检查＾２０１Ｔｌ和＾１２３Ｉ－间碘苄胍（ＭＩＢＧ）显像。结果ＨＣＭ组＾１２３Ｉ－ＭＩＢＧ显像与Ｎ组相     

131I-间位碘代苄胍SPECT/CT显像诊断肾上腺皮髓质增生1例

1 病例简介患者男,43岁,因“间断高血压伴头痛、心悸1年”入院.病史:1年前饮酒后出现双下肢无力,血压248/1 30mmHg,当时无心悸、胸闷、面色苍白、出汗、恶心、呕吐、恐惧焦虑、乏力等症状,休息后无减轻.1年来上述症状反复出现,考虑“高血压、糖尿病”给予口服降压药、降血糖药物治疗,症状时有发作,后来我院就诊.体格检查:血压160/105mmHg,其余未见阳性体征.     

双核素显像诊断右侧巨大嗜铬细胞瘤

双核素显像诊断右侧巨大嗜铬细胞瘤张锦明田嘉禾１资料与方法患者，女，６３岁。主诉头痛１年，发现阵发性高血压近２个月，每日发作２～３次。平时血压２４／１３．３ｋＰａ，发作时３０／１７．３ｋＰａ，尿ＶＭＡ为１４３．５～２３９．２μｍｏｌ／２４ｈ，尿儿茶酚胺...     

肾上腺髓质增生4例临床报告

肾上腺髓质增生为继发性高血压的少见类型 ,解放军总医院近 8年来收治了 4例肾上腺髓质增生患者 ,其临床表现、生化检查与嗜铬细胞瘤相似 ,13 1I 间碘苄胍扫描和CT影像有助于鉴别诊断。本文结合文献对肾上腺髓质增生的病因、诊断和治疗进行了探讨     

冠心病患者血浆肾上腺髓质素浓度的变化

本文测定46例冠心病(CHD)患者血浆肾上腺髓质素[ADM(13~52)]的放免活性,结果示31例急性心肌梗塞(AMl)患者发病后即刻血浆ADM(13~52)水平升高达峰值(118.4±9.49ng/L),峰值较对照组(46.63±3.55ng/L)增加1.5倍(P<0.001),第3天开始逐渐下降,至第28天恢复至对照组水平;即刻血浆ADM(13~52)与内皮素(ET)水平呈正相关(r=0.9003,P<0.001);5例心绞痛(AP)患者AP发作时ADM(13~52)明显升高(101.7±10.15ng/L),其值较对照组增加1.2倍(P<0.001),AP缓解后在第3天恢复至对照组水平;10例病情稳定的陈旧性心肌梗塞(OMl)患者ADM(13~52)轻度增高(58.67±6.40ng/L,P>0.05);实验性心梗大鼠血浆ADM(13~52)水平明显升高(P<0.001).以上提示在血管壁及内皮细胞受损或/和被激活后,多种血管活性肽的合成释放及降解的平衡关系失衡,ADM(13~52)释放增加,对维持机体循环的自身调节是一种有益的保护作用.     

131I-MIBG与化疗联合治疗神经母细胞瘤的研究现状

神经母细胞瘤是一种侵犯儿童、恶性程度高、对射线敏感的肿瘤,近年来主要用131I-问碘苄胍(131I-MIBG)与化疗进行联合治疗,获得了良好的效果.主要综述131I-MIBG与化疗、免疫治疗等联合治疗神经母细胞瘤的几个不同方法和路径,并讨论了联合治疗的机制.     

肾上腺髓质脂肪瘤的超声诊断

目的探讨肾上腺髓质脂肪瘤的超声表现,以提高其诊断准确性。方法回顾性分析总结经病理证实的7例肾上腺髓质脂肪瘤,所有病例术前均接受超声检查,将超声结果和病理进行对照分析。结果7例肾上腺髓质脂肪瘤的声像图特点均为边界清晰,形态基本规则,内部呈均匀中等强回声或中等强回声与低回声相间,肿瘤内部未见无回声区,内部未测及血流信号。结论肾上腺髓质脂肪瘤是一种少见的良性无功能性肿瘤,具有特征性的声像图表现,超声检查可作出正确诊断,最后确诊仍依靠病理学检查。     

Cardiac sympathetic activity pre and post resynchronization therapy evaluated by 123I-MIBG myocardial scintigraphy

Background Imaging with ¹²³I-metalodobenzylguanidine (MIBG) is used for the assessment of cardiac sympathetic activity (CSA). We analyzed CSA before and after cardiac resynchronization therapy (CRT), and correlated these data with CRT response. Methods and Results Thirty patients with chronic heart failure and classic indications for CRT were prospectively studied before and at least 3 months after CRT. The variables analyzed were: QRS width, left-ventricular ejection fraction (LVEF), left-ventricular end-diastolic diameter (LVEDD), heart/mediastinum MIBG uptake ratio (H/M), and washout rate (WR). After CRT, patients were divided into two groups: group 1 (21 patients), responders improving to functional class (FC) I or II; and group 2 (9 patients), nonresponders remaining in FC III or IV. After CRT, only group I showed favorable changes in QRS width (P=.003), LVEF (P=.01), LVEDD (P=.04), and H/M ratio (P=.003). The H/M ratio and WR were associated with CRT response (P=.005 and P=.04, respectively). The H/M ratio was the only independent predictor of CRT response (P=.01). Receiver operating characteristic curves showed that the optimal H/M ratio cutoff point was 1.36 (sensitivity, 75%; specificity, 71%). Conclusions Improvement in CSA correlated with a positive CRT response. Lower MIBG uptake before therapy was associated with CRT nonresponse. The H/M ratio could be helpful in selecting patients for CRT.     

Clinical experience with the adrenal scanning agents iodine 131-19-iodocholesterol and selenium 75-6-selenomethylcholesterol

Adrenocortical scintigraphy with iodine 13119-iodocholesterol or selenium 75-6-selenomethylcholesterol was performed in 94 patients with proven or suspected adrenal disease. According to the final diagnosis, 36 patients suffered from primary aldosteronism, 33 from Cushing's syndrome, 8 from low renin hypertension, 6 from nonfunctioning adrenal tumour, 4 from simple obesity, 3 from adrenal metastases, 1 from congenital adrenal hyperplasia, 1 from virilizing adrenal adenoma, 1 from extraadrenal phaeochromocytoma, 1 from ganglioneuroma. Surgical confirmation of the diagnosis was obtained in most cases. With a few exceptions, the scintigraphy results were consistent with the final diagnosis. The two tracers were equally effective adrenal scanning agents. Tracer concentration was measured in a number of surgical specimens, mostly from patients given selenocholesterol. This measurement in surgical samples has not been reported in previous studies with this agent. The results provided a direct validation of uptake measurements in vivo. The data, collected over a 17-year period, demonstrate that despite the advent of new imaging techniques, adrenal scintigraphy that gives both functional and morphologic information still has an important role in the diagnosis of adrenal disease.Offprint requests to: E. Reschini     

99Tcm-HTOC和131I-MIBG显像诊断嗜铬细胞瘤的比较

目的 比较和评价^99Tc^m-奥曲肽（HTOC）和^131 I-间碘苄胍（MIBG）显像诊断嗜铬细胞瘤的临床价值。方法 28例临床疑嗜铬细胞瘤患者先后进行^99Tc^m-HTOC和^131 I-MIBG全身显像，如全身显像发现异位病灶则加做同机CT融合检查。结果 28例中最终证实为嗜铬细胞瘤者19例，18例经手术或活组织病理检查证实，1例经生化和其他影像学检查证实。28例患者中9例^99Tc^m-HTOC的^131 I-MIBG显像均阳性，病灶位于心脏1例、腹主动脉旁3例、肾上腺3例，恶性多发病灶2例；恶性多发患者^99Tc^m-HTOC显像发现的病灶多于^131 I-MIBG。^99Tc^m-HTOC显像阳性而^131 I-MIBG显像阴性患者共5例，病灶位于心脏3例，恶性多发病灶2例。^99Tc^m-HTOC显像阴性而^131 I-MIBG显像阳性4例，病灶均位于肾上腺。两种显像均阴性10例，1例为嗜铬细胞瘤伴囊性变，其他9例均除外嗜铬细胞瘤。”^99Tc^m-HTOC和^131 I-MIBG显像的灵敏度、特异性、准确性分别为73．7％、100％、82．1％和68．4％、100％、78．5％。^99Tc^m-HTOC显像对异位于心脏的嗜铬细胞瘤和恶性多发病灶的诊断明显优于^131 I-MIBG，但对。肾上腺来源的嗜铬细胞瘤的检出不如^131 I-MIBG。结论 ^131 I-MIBG显像仍是诊断嗜铬细胞瘤的首选检查，但结果阴性时需进行^99Tc^m-HTOC显像。     

Contemporary adrenal scintigraphy

Introduction High-resolution computed tomography (CT) and magnetic resonance (MR) imaging have replaced scintigraphy as primary imaging modalities for the evaluation of adrenal diseases. Discussion Thin-slice CT, CT contrast washout studies and MR pulse sequences specifically designed to identify adrenal lipid content have radically changed the approach to anatomic imaging and provide unique insight into the physical characteristics of the adrenals. With a confirmed biochemical diagnosis, further evaluation is often unnecessary, especially in diagnostic localization of diseases of the adrenal cortex. However, despite the exquisite detail afforded by anatomy-based imaging, there are not infrequently clinical situations in which the functional insight provided by scintigraphy is crucial to identify adrenal dysfunction and to assist in localization of adrenocortical and adrenomedullary disease. The introduction of hybrid PET/CT and SPECT/CT, modalities that directly integrate anatomic and functional information, redefine the radiotracer principle in the larger context of high-resolution anatomic imaging. Instead of becoming obsolete, scintigraphy is an element of a device that combines it with CT or MR to allow a direct correlation between function and anatomy, whereby the combination creates a more powerful diagnostic tool than the separate component modalities.     

Computed tomography and 131I-MIBG scintigraphy in the diagnosis of pheochromocytoma

In order to evaluate the usefulness of computed tomography (CT) and 131I meta-iodobenzylguanidine (131I-MIBG) scintigraphy for the localization of pheochromocytoma, a prospective study was undertaken in 23 patients with possible pheochromocytoma. Seventeen tumors were identified in 13 patients. Two tumors were extra-adrenal. CT was superior for locating tumors in the adrenal glands while 131I-MIBG scintigraphy was more useful in the detection of extra-adrenal pheochromocytoma. Together with adrenal and extra-adrenal pheochromocytoma, the sensitivity for locating the tumor was calculated as 82 per cent (14/17) for CT and 76 per cent (13/17) for 131I-MIBG scintigraphy, respectively. One adrenal tumor (1 cm in size) only was missed by both methods. No false positive CT scans of 131I-MIBG scintigraphy were obtained in the remaining 10 patients who had possible pheochromocytoma but were excluded. These results indicated that CT and 131I-MIBG scintigraphy were both useful tools for detecting pheochromocytoma.     

Complementary roles of CT and 131I-MIBG scintigraphy in diagnosing pheochromocytoma

Recently 131I-MIBG (metaiodobenzylguanidine), an adrenergic tissue-localizing radiopharmaceutical, has been used for diagnosis of pheochromocytoma. In a retrospective study of 32 patients with pathologically proved primary, metastatic, or recurrent pheochromocytoma, the roles of 131I-MIBG scintigraphy and computed tomography (CT) in pheochromocytoma detection were compared. The two methods were equally accurate in the identification of primary and recurrent pheochromocytoma. 131I-MIBG scanning was more accurate as the initial examination in patients with extraadrenal tumors. In patients with metastatic disease, scintigraphy was preferable to CT because of its nontomographic nature, which permitted imaging of the entire body. Although a positive MIBG scan is diagnostic of pheochromocytoma, CT of extraadrenal tumors (particularly in the chest) has been very useful in planning appropriate surgical intervention. Furthermore, the roles of 131I-MIBG scintigraphy and CT in the detection of pheochromocytoma are complementary because each method has certain limitations.     

Serial change in123I-MIBG myocardial scintigraphy in non-insulin-dependent diabetes mellitus

PURPOSE: We performed 123I-MIBG (MIBG) myocardial scintigraphy twice in patients with non-insulin-dependent diabetes mellitus (NIDDM) to investigate whether MIBG distribution was improved by pertinent clinical control. To determine the influential factors for MIBG distribution, we investigated the association between various clinical parameters and the serial change in MIBG uptake parameters. PATIENTS AND METHODS: Twenty NIDDM patients with no cardiac disorders were evaluated. Planar images were taken at 30 minutes (early) and 3 hours (delayed) after MIBG injection. The heart-to-upper-mediastinum uptake ratio (H/M) and washout ratio (WR) were calculated as parameters for estimating cardiac sympathetic function. Patients were divided into two groups, eight in the improved group and twelve in the unimproved group, according to the serial change in H/M. The mean interval between the baseline and the follow up study was 2.1 +/- 0.6 year. Differences between the means of the laboratory data in patients in both groups were compared for the baseline and the follow up study by using the paired t-test. As a means of determining the influential factors for a serial change of MIBG uptake, Fisher's exact test was performed to evaluate the association between the serial change in cardiac MIBG parameters and changes in other clinical parameters, such as blood sugar (BS) control, BS control method (insulin therapy), serum cholesterol control, and severity of diabetic complications. We also analyzed the association between the changes in CV(R-R) (coefficient variance of R-R intervals at rest ECG) or NCV (velocity of posterior tibial nerve) and those of other clinical parameters. Associations among these neurological parameters (MIBG parameters, CV(R-R) and NCV) were also analyzed. RESULTS: Paired t-tests showed a significant decrease in fasting blood sugar and fructosamine in the improved group in the follow up study compared to those in the baseline study. Nevertheless, Fisher's exact test showed no significant association between FBS, HbA1C, fructosamine and the improvement in cardiac MIBG uptake. The only significant association was observed between the serial change in H/M and the BS-control method (insulin therapy). Within the neurological parameters, a significant association was noted between the serial changes in H/M and CV(R-R). CONCLUSION: Although BS control was likely to be an important factor, it did not always ameliorate cardiac MIBG uptake. Based on the significant association between the BS-control method (insulin therapy) and MIBG uptake change, the severity of diabetes mellitus was likely to be a more influential factor. It was suggested that cardiac MIBG uptake could improve within the mild stage if controlled by diet therapy or an oral hypoglycemic agent in NIDDM.