能谱CT鉴别诊断大肠腺癌和腺瘤的应用价值

目的:探讨能谱CT鉴别诊断大肠腺癌和腺瘤的临床应用价值。方法:回顾性分析在我院接受治疗并经病理证实的65例大肠肿瘤患者（腺癌34例,腺瘤31例）的临床资料,所有患者治疗前均接受腹部能谱CT检查,观察并记录动脉期及静脉期增强扫描的CT参数:混合能量CT值和碘（水）浓度值、40~60 keV单能量CT值和能谱曲线斜率,并应用ROC对差异显著的CT参数进行诊断效能分析。结果:腺癌在动脉期的能谱曲线斜率以及碘（水）浓度值明显高于腺瘤,差异有统计学意义（P＜0.05）;腺癌在动脉期的40 keV及50 keV单能量CT值明显高于腺瘤,差异有统计学意义（P＜0.05）;以动脉期的碘（水）浓度值对腺癌和腺瘤进行鉴别诊断时,曲线下面积（AUC）为0.835,临界值21.585 mg/cm3,敏感度79.4%,特异度90.3%。结论:能谱CT为大肠腺癌和腺瘤的鉴别诊断提供了一种全新方法,其动脉期的CT参数诊断效能较优,具有一定临床应用价值。     

能谱CT多参数定量分析对肺癌病理类型的鉴别诊断价值

目的 分析能谱CT对肺癌病理类型的鉴别诊断价值。方法 回顾性收集82例肺癌患者临床资料,所有患者均经手术病理检查确诊,将患者分为腺癌组(44例)和鳞癌组(38例),统计2组影像学特征,比较2组能谱CT多参数、动脉期、静脉期不同keV下CT值、K值,采用ROC曲线分析能谱CT多参数对肺癌病理类型的鉴别诊断价值。结果鳞癌组胸膜凹陷征、磨玻璃密度患者占比(36.84%、31.58%)低于腺癌组(65.91%、54.55%),P<0.05。鳞癌组标准化碘浓度、能谱曲线斜率、碘-水含量低于腺癌组,动脉期70、100 keV下K值高于腺癌组(P<0.05)。能谱CT多参数鉴别肺癌病理类型的敏感度比较,标准化碘浓度低于能谱曲线斜率、动脉期碘-水含量、动脉期70 keV下K值(P<0.05),能谱曲线斜率、动脉期碘-水含量、动脉期100 keV下K值低于动脉期70 keV下K值(P<0.05);特异度比较,标准化碘浓度高于能谱曲线斜率、动脉期碘-水含量、动脉期70 keV下K值、动脉期100 keV下K值(P<0.05),能谱曲线斜率高于动脉期70 keV下K值,动脉期7...     

典型与不典型肾上腺嗜铬细胞瘤MS CT表现对比分析

目的：评价多层螺旋CT（multi-slice spiral CT,MSCT）扫描对不典型肾上腺嗜铬细胞瘤的诊断价值。方法回顾性分析30例经手术病理证实的肾上腺嗜铬细胞瘤病例,其中有典型临床表现22例,无典型临床表现8例。对两组MSCT图像进行对比分析。结果8例不典型肾上腺嗜铬细胞瘤中肿块最大长径为（6．94±2．38）cm,变性7例;肿瘤实质成分平扫、动脉期和门脉期平均CT值分别为43．5 HU （35．7～51．5 HU）、95．2 HU（80．5～120．2 HU）和89．0 HU（75．7～103．8 HU）。22例典型肾上腺嗜铬细胞瘤中肿块最大长径为（6．34±1．35）cm,变性22例;肿瘤实质成分平扫、动脉期和门脉期平均CT值分别为43.0 HU（34．3～52．6 HU）、97．9 HU（78．3～122．8 HU）、90．2 HU（75．5～105．2 HU）。不典型肾上腺嗜铬细胞瘤与典型肾上腺嗜铬细胞瘤比较在肿块最大长径、变性比例以及肿瘤强化程度方面差异均无统计学意义（均P＞0．05）。结论典型与不典型肾上腺嗜铬细胞瘤的MSCT表现具有一致性。     

^131I—MIBG诊断和治疗神经母细胞瘤1例

１３１Ｉ－ＭＩＢＧ（１３１Ｉ－ｍｅｔａｉｏｄｏｂｅｎｚｙｌｇｕａｎｉｄｉｎｅ，１３１Ｉ－间位碘代苄胍）已有效地应用于嗜铬细胞瘤的定位诊断［１～３］及对恶性嗜铬细胞瘤的治疗［４，５］。它是浓集在嗜铬细胞的神经分泌贮存颗粒之中［６］。其它肿瘤如来自神经嵴...     

腹部嗜铬细胞瘤的临床及螺旋CT多期扫描表现

目的 评价螺旋CT多期扫描在腹部嗜铬细胞瘤诊断和鉴别诊断中的价值.方法 回顾性分析70例患者的79个经病理证实为肾上腺嗜铬细胞瘤及腹内异位嗜铬细胞瘤的螺旋CT多期扫描表现.结果 70例患者中,有与嗜铬细胞瘤有关的内分泌症状者41例,隐匿型嗜铬细胞瘤15例,无功能嗜铬细胞瘤14例.单发63例,多发7例,共有79个病灶.肾上腺嗜铬细胞瘤60例,异位嗜铬细胞瘤8例,肾上腺嗜铬细胞瘤合并异位嗜铬细胞瘤2例.良性60例,恶性或术后复发10例.79个肿瘤病灶中,肿瘤均呈圆形或类圆形,长径2～15 cm,平均5.8 cm.6个长径≤4 cm的肿瘤病灶在扫描各时相均较均匀,25个肿瘤病灶有明显的血窦形成,48个肿瘤病灶有不同程度的出血、坏死和囊变灶,其中9个可见液-液平面.65个肿瘤为富血供,14个为中等血供.结论 约40%的腹部嗜铬细胞瘤无相关的内分泌症状,但腹部嗜铬细胞瘤多有较为特征性的CT表现:小的肿瘤较均匀而富血供;较大的肿瘤有不同程度的出血、坏死和囊变灶,为富血供或中等血供,约50%的病灶内可见血窦或液-液平面,有助于与其他疾病相鉴别.     

嗜铬素A和突触素在肾上腺肿瘤中的表达及其临床意义

目的探讨嗜铬素A（CgA）和突触素（Syn）在各型肾上腺肿瘤中的表达及其临床意义。方法对69例肾上腺肿瘤和4例正常肾上腺组织运用免疫组化方法进行组织染色,研究C外和Syn的表达,并采用x^2检验进行统计学分析。结果在正常肾上腺组织,CgA和Syn主要表达于髓质。CgA在全部25例嗜铬细胞瘤中均呈阳性表达,而在肾上腺皮质肿瘤中极少表达;Syn在肾上腺皮质腺瘤、皮质癌、嗜铬细胞瘤及肾上腺转移癌的阳性表达率分别为96．4％（27／28）、87．5％（7／8）、96．0％（24／25）和75．0％（6／8）。结论CgA在肾上腺皮质与髓质肿瘤间、嗜铬细胞瘤与恶性嗜铬细胞瘤间的表达率差异有统计学意义。CgA、Syn可作为标志物对各型肾上腺肿瘤进行鉴别诊断。     

肾上腺皮质腺瘤影像学诊断现状及进展

肾上腺皮质腺瘤是最常见肾上腺良性肿瘤，实际发病率尚不明确，但尸检发现率达1．4％～89％，患病率随年龄增长而增加［1］。典型肾上腺皮质腺瘤肉眼观表现为边界清晰的封闭型实性肿块，横断面往往呈黄色，与肿瘤内丰富的脂肪有关；不典型者横断面呈深褐色或黑色，即黑色肾上腺皮质腺瘤，此外，少数肿瘤内可伴有出血或囊性变。肿瘤的病理切片可见肿瘤细胞胞质内含有丰富的脂肪，肿瘤组织内含有丰富血管［2］。多数肾上腺皮质腺瘤内含有丰富脂肪，但也有约10％～40％肿瘤内含脂肪较少［3］。肾上腺皮质腺瘤特点是肿瘤内含有丰富脂肪及血管，结合临床及影像学往往不难诊断。但是肾上腺皮质腺瘤有时与肾上腺嗜铬细胞瘤及一些含有脂肪组织及丰富血管的肾上腺转移瘤（来源于肝细胞肝癌、肾透明细胞癌、肾颗粒细胞癌）的鉴别诊断比较困难，容易造成误诊。     

CT能谱成像对胃癌诊断价值的初步探讨

目的:探讨CT能谱扫描对胃癌诊断的价值。 方法:对40例胃腺癌患者行CT能谱增强扫描。在能谱单能量图像上测量和计算不同能量水平下病灶和正常胃壁的CT值、标准差、碘水浓度、病灶-胃壁的对比噪声比（contrast-to-noise ratio,CNR）、病灶能谱曲线斜率和标准化碘（水）浓度,对正常胃壁组和腺癌组间数据进行检验,对双期NIC行ROC工作曲线分析。结果:胃癌双期的最佳单能量水平以60 keV为中心上下浮动,双期最佳的CNR分别为4.13±2.75、6.81±5.10。两组在双期不同能量水平下的CT值和不同能量区间下的曲线斜率有统计学差异（P<0.05）。胃癌组和胃壁组双期标准化碘浓度有统计学意义（P<0.05）,动脉期胃癌NIC诊断效能灵敏度和特异度为65%和70%,门脉期NIC诊断效能灵敏度和特异度为70%和65%。结论:CT能谱的多项参数有助于增加对胃癌的诊断信心。     

肾上腺嗜铬细胞瘤53例临床及病理分析

目的探讨肾上腺嗜铬细胞瘤组织形态、免疫组织化学及生物学行为特征.方法采用回顾性分析的方法,对53例肾上腺嗜铬细胞瘤进行临床、病理形态学分析及免疫组织化学检测CgA、Syn抗原标记物在肿瘤中的表达情况,并行临床资料分析及跟踪随访.结果46例有阵发性高血压,4例有持续性高血压,4例无自觉症状.50例细胞分化成熟,4例有周围组织浸润.免疫组化染色:CgA(+);Syn(-).结论CgA在嗜铬细胞瘤呈阳性表达,可用于鉴别肾上腺皮质腺瘤和嗜铬细胞瘤.嗜铬细胞瘤的良、恶性鉴别诊断主要依据是否有转移.     

肾上腺肿瘤的CT临床鉴别诊断

目的探讨肾上腺肿瘤CT表现及鉴别诊断要点.方法回顾性分析27例经手术及病理证实的肾上腺肿瘤CT资料.结果 27例肾上腺肿瘤中腺瘤15例,嗜铬细胞瘤4例,皮质腺癌2例,转移瘤3例,神经纤维瘤、节神经瘤及髓性脂肪瘤各1例.结论 CT对肾上腺肿瘤的检出率较高,在定性诊断上也具有重要的价值.     

Adrenal Myelolipoma

A case of adrenal myelolipoma demonstrated by ultrasound and computed tomography is presented with a discussion of the aetiology and review of literature. Ultrasound and CT proved to be invaluable in the pre-operative diagnosis of adrenal myeldipoma.     

Adrenal insufficiency

Adrenocortical insufficiency may arise through primary failure of the adrenal glands or due to lack of ACTH stimulation as a result of pituitary or hypothalamic dysfunction. Prolonged administration of exogenous steroids will suppress the hypothalamic-pituitary-adrenal axis, and hence cortisol secretion. We review briefly the causes, investigation, and treatment of adrenal insufficiency, and highlight aspects of particular relevance to patients with adrenal tumors. J. Surg. Oncol. 2012; 106:595-599. ? 2012 Wiley Periodicals, Inc.     

Adrenal incidentaloma

Adrenal incidentalomas are incidentally discovered adrenal masses greater than 1 cm in diameter that appear to be clinically nonfunctioning. They are detected during imaging procedures of the abdomen and chest (CT, MRI, and ultrasonography) for an unrelated condition or symptom complex. With the widespread escalation in the use of these imaging modalities and marked improvements in image resolution, the probability of finding an incidentaloma on cross-section imaging is rapidly approaching the 6% prevalence of previously reported autopsy studies. All incidentalomas greater than 1 cm should be evaluated for hormonal activity, including a 1-mg overnight dexamethasone suppression test, total 24-hour urinary metanephrines and fractionated catecholamines, and, in the hypertensive patient, a serum potassium level and plasma aldosterone concentration to plasma renin activity ratio. All hormonally active tumors should be removed. Hormonally inactive tumors are resected based on size, imaging phenotype, and interval growth. Percutaneous biopsies are generally unwarranted and are potentially dangerous. Laparoscopic adrenalectomy has become the surgical procedure of choice for most benign functioning and nonfunctioning tumors of the adrenal gland. Subclinical metabolic abnormalities associated with adrenal incidentalomas remain an area of intense clinical research.     

Adrenal carcinosarcoma

The clinical and pathologic features of a case of adrenal carcinosarcoma are reported. Although synchronous malignancy of the adrenal gland has been described, no case of an adrenal tumor combining both carcinomatous and sarcomatous elements has been previously documented. This neoplasm is extremely aggressive with distant metastasis arising from the sarcomatous component, and rapid progression despite multimodal therapy.     

Giant Bilateral Symptomatic Adrenal Myelolipomas Associated with Congenital Adrenal Hyperplasia

Adrenal myelolipoma is an uncommon, benign, biochemically non-functioning and endocrinologically inactive tumor composed of variable amounts of mature adipose tissue and scattered islands of haemopoietic elements, including erythroid, myeloid and lymphoid series, as well as megakaryocytes. Diagnosis of myelolipomas is based on imaging, with ultrasonography, CT and MRI being effective in more than 90% of cases. Differential diagnosis includes other containing fat adrenal masses such as teratoma, lipoma and liposarcoma. The optimal treatment depends on the size and symptoms of the myelolipoma. For incidentally discovered, asymptomatic adrenal myelolipomas smaller than 4 cm surveillance seems to be enough while symptomatic, complicated, hormonally active and larger than 7 cm myelolipomas, should be surgically removed. We present a case of giant bilateral symptomatic adrenal myelolipomas associated with congenital adrenal hyperplasia. A 34 year old female, with congenital adrenal hyperplasia because of 21-hydroxylase deficiency, presented with diffuse abdominal pain and vomiting. Physical examination revealed hirsutism, pronounced virilization and palpable masses both on the right and left abdominal area. The abdominal CT demonstrated bilateral large masses in the anatomical position of the adrenal glands with densities indicating adipose tissue. The differential diagnosis was between myelolipoma and liposarcoma. For diagnostic and also therapeutical reasons, as the masses were large and symptomatic and causing pressure to the surrounding structures, the patient was submitted to laparotomy for bilateral excision. Histopathological examination established the diagnosis of adrenal myelolipoma.     

Adrenal incidentalomas.

The term adrenal incidentaloma refers to an adrenal mass occasionally and unexpectedly discovered by an abdominal imaging procedure performed for reasons a priori unrelated to adrenal dysfunction. The prevalence of adrenal incidentalomas as discovered by computed tomographic scan examination is estimated to be between 1% and 4%. The vast majority of these lesions are of adrenocortical origin, most often adenomas. Identification of steroid or catecholamine-secreting tumors is important but usually solved with appropriate endocrinologic investigations. A difficult problem, however, is to distinguish between benign and malignant primary or secondary tumors. Size less than 4 cm and an unenhanced computed tomographic attenuation under 10 Hounsfield Units (HU) are findings in favor of a benign adrenocortical adenoma, as is a positive NP 59 scintigraphic examination. The pathogenesis of adrenal tumors is not well understood. However, alterations of the cyclic AMP signalling pathway have recently been observed in benign adrenocortical lesions and molecular defects associated with insulin-like growth factor-II overexpression in malignant adrenocortical tumors.     

Adrenal cortical carcinoma

Opinion statement Adrenal cortical carcinoma is a rare endocrine tumor, and complete surgical resection is the only potentially curative treatment. Accurate preoperative biochemical and radiographic evaluation of the patient who presents with an adrenal mass optimizes patient management and facilitates a complete margin-negative resection of the primary tumor—the most important prognostic variable for long-term survival. Response to mitotane or chemotherapy is modest in patients with advanced disease. It is hoped that an improved understanding of the molecular pathogenesis of this challenging tumor will lead to the development of novel treatment strategies.     

Adrenal cortical carcinoma

The records of 110 patients (58 females and 52 males) with histologically proven adrenal cortical carcinoma were studied. Fifty-six of 110 (50.9%) patients had abdominal symptoms and 33 (30.0%) had a palpable abdominal mass. Surgery for localized and regional disease was associated with a disease-free survival time of at least 2 years in 28 of the 50 (56%) patients. Abdominal radiotherapy, systemic chemotherapy, and 1,1 dichloro-2 (O-chlorophenyl)-2 (P-chlorophenyl) ethane (OPDDD) were effective in three of 19 (15.8%) patients, three of 31 (9.7%) patients, and 21 of 72 (29.2%) patients, respectively. Combined radiotherapy and OPDDD did not confer any additional benefit over OPDDD alone. Six of seven patients who received OPDDD as adjuvant treatment are still alive at 1 to 4 years. Distant metastases occurred most commonly in the lungs, liver, peritoneum, lymph nodes, and bones. Only 23% of the patients survived 5 years or more. We conclude that early diagnosis and complete surgical excision offer the best prospects for long-term survival and that the efficacy of adjuvant OPDDD needs to be evaluated further.     

Metomidate-Based Imaging of Adrenal Masses

Due to broader use of conventional imaging techniques, adrenal tumors are detected with increasing frequency comprising a wide variety of different tumor entities. Despite improved conventional imaging techniques, a significant number of adrenal lesions remain that cannot be easily determined. A particular diagnostic challenge are lesions in patients with known extra-adrenal malignancy because these patients frequently harbor adrenal metastases. Furthermore, adrenal masses with low fat content and no detectable hormone excess are difficult to diagnose properly. Fine needle biopsy is invasive, often unsuccessful, and puts patients at risk, e. g., in cases of pheochromocytoma or adrenal cancer. Noninvasive characterization using radiotracers has therefore been established in recent years. (18)F-FDG PET helps to differentiate benign from malignant lesions. However, it does not distinguish between adrenocortical or nonadrenocortical lesions (e.g., metastases or adrenocortical carcinoma). More recently, enzyme inhibitors have been developed as tracers for adrenal imaging. Metomidate is most widely used. It binds with high specificity and affinity to CYP11B enzymes of the adrenal cortex. As these enzymes are exclusively expressed in adrenocortical cells, uptake of labeled metomidate tracers has been shown to be highly specific for adrenocortical neoplasia. (11)C-metomidate PET and (123)I-iodometomidate SPECT imaging has been introduced into clinical use. Both tracers not only distinguish between adrenocortical and nonadrenocortical lesions but are also able to visualize metastases of adrenocortical carcinoma. The very specific uptake has recently led to first application of (131)I-iodometomidate for radiotherapy in ACC. In conclusion, metomidate-based imaging is an important complementary tool to diagnose adrenal lesions that cannot be determined by other methods.