肾上腺结节样增生性高血压的诊断与治疗(附31例报告)

目的探讨肾上腺结节样增生性高血压的诊断与治疗方法。方法回顾性分析31例肾上腺结节样增生性高血压患者的发病年龄、术前术后血压变化情况、影像学检查结果与术后病理的对应情况、术前术后实验室检查结果的变化情况。结果本组病例平均年龄38.8岁。CT检查阳性率达92.8%;术后血钾、24 h尿钾、血醛固酮均恢复正常,10例术前血皮质醇增高者8例降至正常,2例未完全恢复正常。术后1、3、6、12月的收缩压与舒张压与术前相比均明显下降。结论薄层CT扫描是诊断肾上腺结节样增生性高血压病的主要方法,实验室检查可作为辅助。腹腔镜患侧肾上腺全部切除术是肾上腺结节样增生性高血压病的有效治疗手段。     

肾上腺转移癌的诊断与治疗

目的总结肾上腺转移癌的诊断、治疗方法。方法回顾性分析2000～2011年收治的12例经病理检查证实的肾上腺转移癌患者的临床资料。结果术前B超检查诊断为肾上腺转移癌10例、肾上腺腺瘤1例、肾上腺增生1例,诊断正确率83.3%;术前CT检查诊断为肾上腺转移癌11例、肾上腺神经节细胞瘤1例,诊断正确率91.7%。8例行肾上腺及肿瘤切除术,术后生存0.5～11 a,平均33.2个月;3例行介入栓塞治疗,生存6～9个月,平均7.3个月;1例行放射治疗,生存6.5个月。手术切除肾上腺及肿瘤患者的生存时间明显长于介入栓塞治疗和放射治疗患者。结论 CT是诊断肾上腺转移癌的主要方法,手术切除是其主要治疗方法。     

腹膜后神经鞘瘤的诊断及治疗（附7例报告）

目的探讨腹膜后神经鞘瘤的诊断及治疗方法。方法对7例腹膜后神经鞘瘤患者的临床资料作回顾性分析。结果本组查体发现2例,腰腹部疼痛不适5例（其中3例查体可触及肿物）,肿瘤直径4.7~12 cm,6例位于肾上腺区、1例位于右后盆壁。5例经腹手术切除肿物,1例经腰手术切除肿物,1例行后腹腔镜肿瘤探查、切除术。术后病理检查证实为神经鞘瘤。结论腹膜后神经鞘瘤缺乏特异临床表现,术前诊断困难,确诊依赖病理学检查,手术切除是有效治疗方法。     

原发性醛固酮增多症的分型诊断

目的 探讨用于原发性醛固酮增多症(原醛症)分型诊断检查方法的价值.方法 收集本院近7年来57例临床确诊的原醛症患者[醛固酮瘤22例,特发性醛固酮增多症(特醛症)26例,原发性肾上腺增生9例],检测患者的血电解质、血浆肾素活性及血、尿醛固酮,将结果与19例原发性高血压患者对照.再通过肾上腺CT、体位激发试验及肾上腺静脉采血检查对原醛症患者分型并随访.结果 (1)醛固酮瘤患者血压及血、尿醛固酮较特醛症患者高,血钾及血浆肾素活性则低,而原发性肾上腺增生患者临床及生化改变介于两者之间.肾上腺CT检查在原醛症分型诊断中的符合率为醛固酮瘤86.4%,特醛症73.1%,原发性肾上腺增生22.2%;肾上腺静脉采血检查以两侧醛固酮之比作为判定标准时符合率为86.4%、80.8%和77.8%,以醛固酮与皮质醇之比为判定标准则符合率分别为95.5%、92.3%及100.0%.(2)醛固酮瘤及原发性肾上腺增生患者术后随访血醛固酮均下降,血压恢复正常者分别为22.7%及44.9%,血钾恢复正常者为83.3%及100.0%,而特醛症患者随访中各项测值无明显变化,另有33.3%诊断时血钾正常的患者随访中出现低血钾.结论 原醛症的分型诊断需依靠多种检查手段综合分析,单纯依赖影像学检查或体位激发试验并不可靠,肾上腺静脉采血检查可作为影像学检查的补充,用两侧醛固酮与皮质醇的比值分析较单纯比较两侧醛固酮之比更为可靠;醛固酮瘤及原发性肾上腺增生患者术后临床及生化测值均得以明显改善,而特醛症患者随访中无明显变化.     

隐匿性肾上腺肿瘤14例临床和病理分析

目的　分析隐匿性肾上腺肿瘤的临床特征和病理情况。方法　自 1995年 12月至1997年 4月经B超和CT诊断为隐匿性肾上腺瘤共 14例 ,全部患者均作了手术切除及病理检查。结果　 14例中 10例为无功能肿瘤 ,4例存在着隐性功能变化 ,病理检查发现 3例为嗜铬细胞瘤 ,5例发生肾上腺肿块内出血坏死 ,其瘤体较大 ,直径在 6～ 16cm。结论　隐匿性肾上腺瘤是肾上腺最常见的肿瘤。少数有激素分泌。若肿瘤 >3cm或进行性增大者 ,均应尽早手术治疗。     

肾上腺节细胞神经瘤的诊断与治疗（附8例报告）

目的总结肾上腺节细胞神经瘤的诊治经验。方法对8例肾上腺节细胞神经瘤患者的临床资料作回顾性分析。结果肾上腺节细胞神经瘤患者多无临床症状,CT多表现为形态规则的圆形或类圆形低密度影,边界光滑,质地均一,增强扫描强化不明显。术前诊断为肾上腺嗜铬细胞瘤6例,无功能腺瘤2例。均采用手术治疗。手术均获成功。术后病理检查证实为肾上腺节细胞神经瘤。随访0.5~2 a,患者肾功能无异常,未见肿瘤复发。结论肾上腺节细胞神经瘤临床表现不典型,易误诊。诊断主要靠影像学检查,确诊依赖病理检查。手术治疗预后良好。     

肾上腺皮髓质混合性病变19例临床分析

目的探讨肾上腺皮髓质混合性病变的临床特点及诊断、治疗方法。方法回顾性分析19例肾上腺皮髓质混合性病变患者的临床资料。结果19例患者中,16例术前均有高血压,2例表现为高血压和血浆皮质醇、尿香草扁桃酸增高,3例表现为高血压、低血钾和血浆醛固酮、尿香草扁桃酸增高。对CT扫描显示有影像学改变的一侧肾上腺在后腹腔镜下行切除术,术后病理检查证实为肾上腺皮髓质混合性病变。术后随访3—48个月,14例治愈,5例于术后1a内复发,其中3例再次行对侧肾上腺部分切除后治愈。19例中,病理诊断为肾上腺皮髓质同时增生18例,肾上腺皮质腺瘤并髓质增生1例。结论肾上腺皮髓质混合性病变临床表现多样,对于既有皮质醇增多症表现,又有儿茶酚胺症表现的患者,应考虑肾上腺皮髓质混合性病变的可能。患侧肾上腺全切或部分切除术是首选治疗方法。     

自发性肾上腺出血的诊断及治疗（附8例报告）

目的探讨自发性肾上腺出血的诊断及治疗方法。方法对8例自发性肾上腺出血患者的临床资料作回顾性分析。结果本组8例中B超检查发现肾上腺囊性肿物5例、低回声肿物3例。6例行CT检查,发现肾上腺囊性肿物5例、实性肿物1例,CT值34．7—85．0HU,增强CT扫描均无强化。行肾上腺及肿物切除术5例,部分肾上腺及肿物切除术3例。结果8例术后病理检查均诊断为肾上腺髓质内出血。结论自发性肾上腺出血术前诊断困难,B超、CT检查有助于诊断。双侧肾上腺出血、腰腹痛明显、单侧肾上腺出血但血肿〉5cm者应采取手术治疗。     

马尾肿瘤的MRI诊断

目的分析马尾肿瘤MRI的诊断特点。方法选择我院15例马尾肿瘤患者全部行MRI检查，其中男9例，女6例，14例经手术治疗。结果病理诊断15例马尾肿瘤中，神经纤维瘤8例，皮样囊肿和表皮样囊肿3例，脂肪瘤2例，室管膜瘤1例，转移瘤1例。术前MRI诊断与术后病理诊断基本相符。结论MRI对马尾肿瘤的诊断可靠，为，临床的手术治疗提供了正确的病变分析。     

高血压并发低血钾与肾上腺疾病15例临床分析

目的:总结我院15例高血压并低血钾患者的临床表现与诊治结果,提高继发性高血压的诊疗水平。方法:对15例患者的临床表现、激素水平、CT定位诊断及术后病理进行回顾分析。结果:15例患者中原发性醛固酮增多症13例(醛固酮瘤11例、双侧肾上腺增生2例),腺瘤型皮质醇增多症2例。结论:顽固性高血压并发低血钾应高度怀疑肾上腺疾病,诊断依靠临床表现及内分泌功能测定,定位诊断依靠CT,腺瘤型手术效果好。     

Predictive value of preoperative tests in discriminating bilateral adrenal hyperplasia from an aldosterone-producing adrenal adenoma

In primary hyperaldosteronism, discriminating bilateral adrenal hyperplasia (BAH) from an aldosterone-producing adenoma (APA) is important because adrenalectomy, which is usually curative in APA, is seldom effective in BAH. We analyzed the results from our most recent 7-yr series to evaluate the predictive value of preoperative noninvasive tests compared with adrenal vein sampling (AVS). Forty-eight patients with hypertensive hyperaldosteronism underwent bedside testing, computed tomography (CT) imaging, and AVS. Those in whom the results of AVS indicated APA underwent adrenalectomy. Twelve (30%) and 14 (34%) of 41 patients with APA had paradoxical falls with ambulation in plasma aldosterone concentration (PAC) and 18-hydroxycorticosterone (18-OH-B), respectively. Twenty-nine (70%) and 26 (65%) APA patients had a rise in PAC and 18-OH-B, respectively, as did all 8 BAH patients. Significant identifiers of BAH were supine PAC values less than 15 ng/dL (P: = 0.04), an increase greater than 60% (P: = 0.02) in PAC with ambulation, and supine 18-OH-B values less than 60 ng/dL (P: = 0.04). CT imaging alone was not predictive for BAH or APA. In our population, patients with a positive bedside test result (e.g. a fall in PAC and/or 18-OH-B) and a unilateral adrenal nodule on CT (10 of 41 patients) could have proceeded directly to adrenalectomy for APA. However, a positive bedside test result with a negative CT or a negative bedside test result regardless of CT findings required AVS to confirm the diagnosis and site of disease.     

Comparison of adrenal vein sampling and computed tomography in the differentiation of primary aldosteronism

Determination of the etiology of primary aldosteronism remains a diagnostic challenge. The most common types of primary aldosteronism are bilateral adrenal hyperplasia (BAH), aldosterone-producing adenomas (APA), and primary adrenal hyperplasia. Computed tomography (CT) and adrenal vein sampling (AVS) are the primary modalities used to differentiate these subtypes. The purpose of this study was to compare AVS and CT imaging of the adrenal glands in patients with hyperaldosteronism in whom CT imaging was normal or in whom focal unilateral or bilateral adrenal abnormalities were detected. The diagnosis of primary aldosteronism was made in 62 patients based on an elevated plasma aldosterone to PRA ratio and an elevated urinary aldosterone excretion rate. Thirty-eight patients had CT imaging and successful bilateral adrenal vein sampling and were included in the final analysis. AVS was considered the gold standard in determining the specific subtype of primary aldosteronism. There were 15 patients with APA, 21 patients with BAH, and 2 patients with primary adrenal hyperplasia. Plasma aldosterone was significantly higher in patients with APA (46.3 +/- 8.5 ng/dL; 1284 +/- 235 pmol/L) than in those with BAH (29.3 +/- 2.4 ng/dL; 813 +/- 11 pmol/L; P < 0.05). Plasma potassium was significantly lower in patients with APA (3.1 +/- 0.1 mmol/L) than in patients with BAH (3.5 +/- 0.1 mmol/L; P < 0.02). There was considerable overlap in the other biochemical indices (e.g. PRA and urinary aldosterone) in patients with the different subtypes. In patients with APA proven by AVS, eight had concordant findings with CT imaging, four had discordant findings, and three had normal CT imaging. In patients with BAH proven by AVS, four had concordant findings with CT imaging, eight had discordant findings, and nine had normal CT imaging. Compared with AVS, CT imaging was either inaccurate or provided no additional information in 68% of the patients with primary aldosteronism. We conclude that adrenal CT imaging is not a reliable method to differentiate primary aldosteronism. Adrenal vein sampling is essential to establish the correct diagnosis of primary aldosteronism.     

Collision/composite tumors of the adrenal gland: a pitfall of scintigraphy imaging and hormone assays in the detection of adrenal metastasis

CONTEXT: In patients with a history of extraadrenal tumor, incidental discovery of an adrenal mass necessitates excluding the possibility of metastatic malignancy. Detection of the malignant tissue is a difficult challenge when metastasis occurs in an adrenal adenoma, forming a collision/composite tumor. OBJECTIVE, DESIGN, AND SETTING: We report two patients with adrenal collision/composite tumors referred to two French university hospitals. PATIENTS AND RESULTS: Two patients with histories of mammary and sigmoid carcinomas, respectively, presented with adrenal mass discovered 8 and 3 yr after surgical removal of the primary tumor. In the two cases, computerized tomographic scan showed that the adrenal tumor contained two components with low and high attenuation values, respectively. Uptake of iodocholesterol by the adrenal tumor in case 1 and elevated plasma ACTH-stimulated 17-hydroxyprogesterone values in case 2 strongly argued for the diagnosis of primary adrenocortical tumors. Enlargement of the adrenal mass during follow-up in case 1 and association of the adrenal lesion with a hepatic mass in case 2 led to adrenalectomy. In both cases, histological examination of the tumor demonstrated the presence of metastatic carcinoma tissue in an adrenocortical adenoma, allowing classification of the neoplasia as a collision/composite tumor. CONCLUSION: These observations show that collision/composite tumors of the adrenal gland formed by carcinoma metastasis in benign adenomas are a pitfall of iodocholesterol scintigraphy and/or plasma steroid assays to exclude the diagnosis of adrenal metastasis. Conversely, computerized tomographic scan is a useful tool for the distinction between the benign and malignant tissues in adrenal collision/composite tumors.     

103例肾上腺肿瘤病例分析

目的 进一步提高肾上腺肿瘤的诊治水平。方法 对103例肾上腺肿瘤病例进行分析。结果 详细进行临床观察和内分泌生化检查以及B超、CT或MR等检查，能较准确地对肾上腺肿瘤进行定性定位诊断。结论 术前明确肾上腺肿瘤的性质是手术成功的前提。     

腹腔镜手术治疗肾上腺嗜铬细胞瘤(附24例报告)

目的评价腹腔镜手术治疗肾上腺嗜铬细胞瘤的安全性及临床价值。方法对24例肾上腺嗜铬细胞瘤患者采用腹腔镜经腹腔途径手术治疗。结果23例手术取得成功，1例因粘连严重、术中出血改行开放手术。肿瘤最大径2．5～8cm，平均4．2cm；手术时间30～150min，平均70min；术中出血量20～200ml，平均50ml，均未输血；术后住院5～10d，平均6．8d；术后病理检查证实均为肾上腺嗜铬细胞瘤。全部病例获得随访3～18个．月，平均10个月，患者血压正常，B超或CT复查均未见肿瘤复发。结论对于直径〈6cm的肾上腺嗜铬细胞瘤，腹腔镜手术具有手术时间短、出血少、损伤小、恢复快、安全性高、并发症少等优点，可替代开放手术。     

经腹腹腔镜肾上腺嗜铬细胞瘤切除术(附15例报告)

目的观察经腹腹腔镜肾上腺嗜铬细胞瘤切除术治疗肾上腺嗜铬细胞瘤的疗效。方法用经腹腹腔镜手术治疗肾上腺嗜铬细胞瘤15例。结果手术均成功。手术时间50-160 min,术中出血量40-220 ml。12例随访5-36个月,10例患者血压恢复正常,2例血压明显下降,均无局部复发。结论经腹腔腹腔镜肾上腺嗜铬细胞瘤切除术术中解剖标志清楚,手术安全性高,效果满意,可作为肾上腺嗜铬细胞瘤首选治疗方法。     

Laparoscopic resection of gastric gastrointestinal stromal tumors presenting as left adrenal tumors

Gastrointestinal stromal tumors (GISTs) are rare gastrointestinal malignancies. They are rarely seen near the urinary tract. In a literature review, only one case of GIST presenting as a left adrenal tumor was reported. We report two documented cases of gastric GISTs mimicking left adrenal tumors which were successfully treated with pure laparoscopic adrenalectomy and wedge resection of the stomach by excising the tumor from the stomach with serial firing of endoscopic gastrointestinal staplers. The surgical margins were clear, and the patients recovered smoothly. No adjuvant therapy with imatinib was prescribed. During the surveillance for 9 mo and 44 mo respectively, no tumor recurrence and metastasis were documented. Laparoscopic tumor excision, when adhering to the principles of surgical oncology, seems feasible and the prognosis is favorable for such tumors.     

21-hydroxylase deficiency associated with adrenal tumor: case report of two brothers

Described herein are two brothers with 21-hydroxylase deficiency (21-OHD) associated with adrenal tumors, and these possible mechanisms are discussed. A 34-year-old male was admitted on Jan. 9, 1984 because of an enlarged and tender left breast. Physical examination revealed short stature (152 cm, 76.5 kg), gynecomastia and shortening of metacarpal bone. His testes were small (2.6 X 1.6 X 1.9 cm). Urinary excretion of 17-OHCS was within normal range (5.9 mg/day), but those of 17-KS, 17-KGS and pregnanetriol were markedly increased (44.4, 110 and 22.6 mg/day, respectively). Plasma concentrations of progesterone and ACTH and urinary excretions of estrone, estradiol and estriol were also increased. Urinary excretions of 17-KS were decreased to 11.7 mg/day and 17-KGS to 22.3 mg/day after the ingestion of 2 mg/day dexamethasone for two days. The computed tomography and a scintigraphy with 131I-Adosterol revealed a tumor in the left adrenal gland, and the adrenal arteriography revealed a neovascularity and a tumor stain in the tumor. These data indicated that the patient was suffering from both 21-OHD and the left adrenal tumor. At this point, adenoma or adenocarcinoma of the adrenal gland was suspected. The left adrenal tumor (85 g) was resected on April 10, 1984, and the pathological diagnosis was adrenal adenoma. The patient's endocrinological abnormalities, however, did not improve after the operation. Urinary excretions of 17-KS and KGS were increased to 57.9 and 108.5 mg/day, respectively, in the patient's elder brother, and 63.3 and 127.9 mg/day, respectively, in his younger brother, indicating that they also had 21-OHD. Interestingly, an adrenal tumor was diagnosed by abdominal computed tomography in the elder brother who had the same HLA typing as the present case. The three brothers had 21-OHD, and two of them had both 21-OHD and adrenal tumor. To our knowledge, this is the first report documenting the co-existence of adrenal tumors in brothers with 21-OHD. This suggests that adenoma can be one of the complications of 21-OHD, probably due to the chronic stimulation by ACTH, and that a possible linkage to HLA may exist in such cases.     

Adrenal incidentaloma and patients with homozygous or heterozygous congenital adrenal hyperplasia.

Adrenal tumors are being detected more frequently in consequence of the wider application of increasingly sensitive radiological investigation techniques. According to the working hypothesis that more silent adenomas could develop from hyperplastic tissue areas under increased stimulation of the adrenal cortex, heterozygous and homozygous patients with congenital adrenal hyperplasia (CAH) were studied. A high incidence of adrenal masses, nearly 82% in homozygous and 45% in heterozygous patients, was found. There was no correlation between tumor size and serum 17-hydroxyprogesterone concentrations. These tumors are, therefore, probably silent adenomas. On the basis of these results, CAH should always be ruled out in the case of incidentally detected adrenal masses. Since CAH is a relatively frequent disease, and the adrenal carcinoma belongs to the rarest malignant tumors, a malignant transformation of these tumors seems to be unlikely.     

Bilateral adrenal hemorrhage associated with heparin induced thrombocytopenia

Heparin induced thrombocytopenia (HIT) is associated with serious and sometimes devastating thrombotic events. We report a case of bilateral adrenal hemorrhage (BAH) associated with HIT after prophylactic use of low molecular weight heparin. The vague presenting symptoms of acute adrenal insufficiency offers a diagnostic challenge, which if delayed may be life threatening. A high index of suspicion for adrenal hemorrhage is required in patients receiving any form of heparin therapy presenting with new onset thrombocytopenia, abdominal pain, and fevers.