三种栓塞方法治疗甲亢对照研究

近年来发现介入栓塞治疗甲亢安全简便，疗效可靠，但栓塞剂的种类较多，疗效、反应和费用不一。为选择一种疗效好、反应轻、费用低的甲状腺栓塞方法，我们应用聚乙烯醇微粒(PVA)、α-氰基丙烯酸正辛酯(TH胶)及平阳霉素碘油乳剂(PLE)分别栓塞动物甲状腺动脉并进行对照研究。现报告如下。     

PLE+GF栓塞治疗肝血管瘤

目的探讨平阳霉素碘油乳剂(PLE) 明胶海绵(GF)颗粒栓塞治疗肝血管瘤的疗效和价值.方法采用Seldinger技术经股动脉穿刺插管,超选择至血管瘤供血动脉,对15例肝海绵状血管瘤(CHL)注入PLE至血管瘤体完全充填,并用GF颗粒栓塞供血动脉.定期观察瘤腔碘油充填情况、疗效和并发症.结果PLE GF栓塞治疗后,碘油存积好,血管瘤体积明显缩小,无严重并发症.结论PLE GF栓塞治疗肝血管瘤具有疗效好、创伤小、并发症少等优点.     

介入栓塞甲状腺动脉与口服抑亢丸联合治疗Graves病

目的：观察抑亢丸与介入栓塞甲状腺动脉联合治疗甲状腺机能亢进症(Graves病)的临床疗效。方法：16例Graves病患均行介入栓塞甲状腺上、下动脉后，8例术后口服他巴唑或丙基硫氧嘧啶，8例患术后口服抑亢丸，观察比较抑亢丸的疗效。结果：介入术后口服抑亢丸与口服他巴唑或丙基硫氧嘧啶效果相同。结论：介入栓塞甲状腺动脉后口服中药抑亢丸与口服他巴唑或丙基硫氧嘧啶治疗Graves病疗效相同。     

介入栓塞治疗10例甲状腺功能亢进症的分析

目的探讨用介入栓塞治疗甲状腺功能亢进症(甲亢)的方法、临床疗效及安全性。方法10例反复复发的甲亢患者,经选择性插管至甲状腺双侧上动脉,使用明胶海绵糊进行栓塞治疗,观察栓塞后的临床症状、甲状腺功能及甲状腺大小的变化。结果10例患者均获临床治愈,随访12个月,术前TT32.5~3.5μg/L、TT4125.4~236.8μg/L,术后TT3降至1.3~2.0μg/L,TT4降至64.3~99.3μg/L。甲状腺明显缩小,无严重并发症。结论介入栓塞甲状腺上动脉,能使甲亢达到临床治愈,且安全、副作用少,是治疗甲亢的新方法。     

介入栓塞术治疗肝海绵状血管瘤8例报告

1999年4月～2002年2月，我们分别用无水酒精，碘油 明胶海绵，碘油乳化剂(PLE)栓塞治疗肝海绵状血管瘤(CHL)患者8例，现将其疗效、术后肝功变化及并发症分析报告如下。     

栓塞甲状腺动脉治疗Graves病的临床分析

目的 探讨难治性Graves病介入栓塞治疗的方法并观察疗效。方法 8例难治性Graves病患，采用Seldinger方法穿刺超选择插管至甲状腺动脉，使用PVA微球栓塞治疗，观察栓塞后临床症状及甲状腺大小的变化。结果 随访4个月—2年，临床症状缓解，并停用抗甲状腺药物。甲状腺明显缩小。无严重并发症。结论 介入栓塞治疗Graves病是一种安全、有效的新方法，为Graves病的治疗开辟了一种新的途径，但远期疗效尚需进一步观察。     

Fontan术后蛋白丢失性肠病的机制和治疗研究综述

蛋白丢失性肠病（PLE）是Fontan术后的并发症之一,Fontan术后出现PLE提示预后不良。目前无特异有效的治疗方法。本综述通过分析PLE的病理生理、肠系膜病理解剖、治疗有效病例的特征,探讨PLE发生的机制,分析Fontan术后出现PLE的危险因素并提出治疗建议。     

真丝线段栓塞甲状腺上动脉治疗难治性甲状腺功能亢进症

近年来 ,国内外一些学者相继报道用栓塞甲状腺上动脉的方法治疗临床上的难治性甲亢 ,均取得一定的疗效。本研究采用真丝线段血管内栓塞的方法 ,治疗了 6例患者 ,取得同样的效果 ,现报道如下。一、对象和方法6例甲亢患者均为我院内分泌科住院患者 ,入院前有不同程度的心悸、消瘦、怕热、多汗等症状 ,甲状腺Ⅱ Ⅲ度肿大 ,无结节 ,无压痛 ,不伴突眼 ,经查血Ｔ3 、Ｔ4、ＴＳＨ、ＦＴ3 、ＦＴ4、甲状腺球蛋白抗体 (ＴＧＡ)、甲状腺微粒体抗体 (ＴＭＡ) ,甲状腺ＥＣＴ ,甲状腺细针穿刺检查等明确诊断为Ｇｒａｖｅｓ病 ,其中 1例为13 1Ｉ治疗术后半…     

肝动脉化学栓塞后2例病人发生甲状腺功能减退

本文报告２例既往未曾接受过甲状腺疗法但在肝动脉化学栓塞后成为甲状腺功能减退的病人。例１ 女性,６６岁,患转移性类癌瘤。其血清甲状腺刺激激素(ＴＳＨ)水平为３．０ｍＩＵ/Ｌ(正常值:０．３~０．５ｍＩＵ/Ｌ),于３个月内进行了２次肝动脉化学检查疗法。于第１次化学栓塞后     

甲状腺功能减退症合并肺血栓栓塞症1例

正甲状腺功能减退症(简称甲减)是由于甲状腺激素合成和分泌减少或组织利用不足导致的全身代谢减低综合征,是一种常见的内分泌疾病。其临床表现复杂,缺乏特异性,甲减时激素水平下降可累及全身多脏器、参与心血管疾病、肺血管病等发展过程,严重者危及生命。甲状腺功能亢进症合并肺动脉高压、肺血栓栓塞症多见,而甲状腺功能减退症合并肺血栓栓塞症病例报道相对较少,临床工作中容易漏诊或误诊。本文报告甲减合并肺血栓栓塞症1例,通过对该例疾病分析及回顾,减少漏诊及误诊。报告如下。     

Decompression of the thoracic duct: A novel transcatheter approach

In patients with total cavopulmonary connections, elevated central venous pressures (CVP) have detrimental effects on the lymphatic system causing an imbalance in fluid production and drainage of the interstitium. This combination may result in life‐threatening lymphatic complications including plastic bronchitis (PB), protein losing enteropathy (PLE), chylothorax, and ascites. While embolization of the abnormal lymphatics has greatly improved outcomes from these complications, alternative treatment strategies have been proposed that would result in improved lymphatic drainage while leaving the lymphatic system intact. We report two novel transcatheter approaches for thoracic duct (TD) decompression in two patients who developed PLE after completion of the Fontan procedure as part of staged palliation for congenital heart disease. In addition, one patient had severe concurrent PB. In both patients, a connection was created between a left superior vena cava (LSVC) to the left atrium allowing for a nonsurgical method to decompress the TD. This procedure resulted in significant clinical and laboratory improvement of both patients' PLE and other symptoms of lymphatic dysfunction.     

Lymphatic Obstruction and Protein‐losing Enteropathy in Patients with Congenital Heart Disease

Objective. Protein‐losing enteropathy (PLE) is a known complication of surgical procedures for congenital heart disease. The pathogenesis and pathophysiology of PLE remain poorly understood. However, lymphatic insufficiency appears central to the disease process. We sought to investigate the role of lymphatic obstruction and central venous catheter‐related central venous thrombosis in patients with congenital heart disease and PLE. Design. A case‐control study design was constructed consisting of patients with congenital heart disease and PLE and 2:1 matched controls having undergone the same definitive surgical procedure. Obstruction to lymphatic return was considered present if the thoracic duct was ligated, or if there was complete central venous obstruction at the usual site of thoracic duct drainage. Results. Obstruction to lymphatic return was identified in 4 of 16 cases (25%) and 1 of 32 controls (4%), P = .06. There was no association between PLE and central venous catheter use or duration, and no discriminating characteristics between cases and controls with respect to anatomy, pre‐Fontan hemodynamic variables, operative or perioperative factors, or hemodynamic variables at the time of PLE diagnosis. Mortality for patients with PLE was 25% compared with 9% in controls (P = not significant). Long‐term resolution of PLE was obtained in six patients (38%). Conclusion. There is a high prevalence of apparent lymphatic obstruction in patients with congenital heart disease and PLE, suggesting that physical lymphatic obstruction may play an important, and previously unrecognized role in the development of PLE in patients with complex congenital heart disease.     

Portal vein embolization induces compensatory hypertrophy of remnant liver

AIM:To evaluate the effectiveness and safety ofdifferent portal vein branch embolization agents ininducing compensatory hypertrophy of the remnantliver and to offer a theoretic basis for clinical portal veinbranch embolization.METHODS:Forty-one adult dogs were included in theexperiment and divided into four groups.Five dogsserved as a control group,12 as a gelfoam group,12as a coil-gelfoam group and 12 as an absolute ethanolgroup.Left portal vein embolization was performed ineach group.The results from the embolization in eachgroup using different embolic agents were compared.The safety of portal vein embolization(PVE)wasevaluated by liver function test,computed tomography(CT)and digital subtraction angiography(DSA)ofliver and portal veins.Statistical test of variance wasperformed to analyze the results.RESULTS:Gelfoam used for PVE was inefficient inrecanalization of portal vein branch 4 wk after theprocedure.The liver volume in groups of coil-gelfoamand absolute ethanol increased 25.1% and 33.18%,respectively.There was no evidence of recanalization ofembolized portal vein,hepatic dysfunction,and portalhypertension in coil-gelfoam group and absolute ethanolgroup.CONCOUSION:Portal vein branch embolization usingabsolute ethanol and coil-gelfoam could induce atrophyof the embolized lobes and compensatory hypertrophy ofthe remnant liver.Gelfoam is an inefficient agent.     

复杂硬脑膜动静脉瘘的静脉途径栓塞治疗

目的探讨静脉途径栓塞治疗复杂性硬脑膜动静脉瘘的有效性和安全性。方法回顾分析6例复杂性硬脑膜动静脉瘘患者行经静脉途径栓塞治疗的临床效果。结果静脉途径栓塞治疗后,5例患者解剖性治愈(造瘘口消失),另1例患者症状好转。1例患者乙状窦栓塞后吞咽困难,1例患者海绵窦栓塞后外展不佳,经对症治疗均好转。结论静脉途径栓塞是治疗复杂性硬脑膜动静脉瘘较好的方法。     

经未显影静脉窦栓塞治疗硬脑膜动静脉瘘

目的探讨经未显影静脉窦栓塞治疗硬脑膜动静脉瘘（DAVF）的可行性、安全性及有效性。方法回顾性分析92例经未显影静脉窦栓塞治疗的DAVF患者的临床资料，其中病变位于海绵窦区91例，侧窦区1例。经颈内静脉的起始段探查未显影岩下窦，进入引流静脉窦内栓塞海绵窦区DAVF；通过颈内静脉探查未显影乙状窦，进入静脉窦栓塞侧窦区DAVF。首选可控纤毛弹簧圈进行栓塞，待血流减慢以后，用游离纤毛弹簧圈继续栓塞。若仍存在少量瘘口，通过静脉窦内注射液体栓塞剂（25％～33％Glubran或Onyx18），观察置管的成功率、安全性和栓塞的疗效。术后6个月通过电话、门诊或DSA随访。结果92例患者中，均未出现并发症，无死亡病例。1例海绵窦区DAVF患者置管失败；其余91例患者均顺利置管，并成功进行静脉栓塞。所有患者栓塞后即刻造影，均未见异常静脉窦早显，瘘口消失，达到了影像学上治愈。置管成功率及治愈率均为99％（91／92）。术后6个月对38例进行随访，无一例DAVF复发。对其余患者进行电话或门诊随访。所有患者临床症状好转或消失。结论经未显影静脉窦栓塞治疗DAVF，尤其对于海绵窦区DAVF，经未显影岩下窦超选择置管进行栓塞，具有较高的可行性、安全性及有效性，可作为海绵窦区DAVF的首选常规治疗方法。     

Mixed connective tissue disease associated with protein losing enteropathy: successful treatment with intravenous cyclophosphamide therapy.

A patient with mixed connective tissue disease who developed protein losing enteropathy (PLE) is described. The PLE and other symptoms improved dramatically after monthly intravenous administration of 700 mg/day cyclophosphamide three times combined with oral prednisolone, while they were ineffective to the treatment with intravenous methyl-prednisolone 500 mg per day for 3 days. The serum level of CA125 antigen paralleled the severity of symptoms, signs and laboratory data associated with PLE. Thus, pleural effusion, ascites, edema and hypoalbuminemia improved along with the decrease in the level of CA125, suggesting that CA125 might be a marker of the activity of PLE.     

Protein-losing enteropathy in systemic lupus erythematosus: analysis of the clinical features of fifteen patients.

OBJECTIVE: Protein-losing enteropathy (PLE) is an unusual manifestation of systemic lupus erythematosus (SLE), so its clinical manifestations and management are not well understood. In this study, we try to characterize the basic clinical features and the management of PLE by retrospectively analyzing the clinical data of 15 PLE patients and hope this study can improve the awareness of PLE in lupus patients with severe hypoalbuminemia that could not be explained by other causes. METHODS: The clinical data of 15 SLE patients with PLE hospitalized during November 2001 and April 2006 in Peking Union Medical College Hospital were retrospectively reviewed. The PLE was diagnosed by Tc-99m albumin scintigraphy (99mTc-HAS). The clinical characteristics, laboratory tests, response to treatment, and the outcome were studied. RESULTS: The mean age of PLE onset was 40.1 +/- 15.4 years (19-71 years). Twelve were female and 3 were male. 53.3% (8 of 15) patients had PLE as the initial presentation of SLE. All patients had different degree of peripheral pitting edema. Eleven had ascites, 9 had pleural effusion, and 7 had pericardial effusion. Only 6 patients presented with abdominal pain and diarrhea. Positive antinuclear antibodies (HEP-2) with a speckled pattern were found in all patients, but the antidsDNA antibody was negative in most cases. All patients had marked hypoalbuminemia, 80% had hypocomplementemia, 66.7% had hyperlipoproteinemia, and 40% had hypocalcemia. The liver function tests and the prothrombin time were in normal ranges. The 24-hours urine protein was less than 0.5 g in 60% (9 of 15) and more than 1.0 g in 20% (3 of 15) patients who were renal biopsied but only found to have very mild pathologic changes. Gastrointestinal endoscopy examination discovered generalized edema in the intestinal wall whereas the biopsy showed chronic inflammation only. Most cases had good response to corticosteroid and immunosuppressive therapies. The serum albumin level improved evidently in all patients after treatment and normal scintigraphic finding was found in 9 patients. CONCLUSION: PLE can be the initial presentation of SLE or can develop a very long time after the diagnosis of SLE. The prominent clinical presentations are caused by hypoalbuminemia. 99mTc-HAS is useful not only for the diagnosis of PLE but is also helpful for monitoring the efficacy of treatment. When a SLE patient presents with evident hypoalbuminemia without evidence of other causes, PLE should be considered. Early diagnosis and treatment may improve the prognosis.     

Protein‐losing Enteropathy after the Fontan Operation: Associations and Predictors of Clinical Outcome

Objective. We sought to define what clinical parameters were related to the ultimate outcome in Fontan patients who had developed protein‐losing enteropathy (PLE). Background. PLE is a serious complication of the Fontan operation. Several preoperative and perioperative findings are associated with later PLE. However, there is limited information regarding postoperative abnormalities contributing to or influencing outcome in PLE. Methods. We evaluated 44 consecutive Fontan patients with PLE. A matched control group of Fontan patients without PLE was used for comparison (matched‐pair analyses). Kaplan–Meier and Cox proportional hazard methods were used for survival analyses. Results. Median age was 18 years (range 4–48 years). Short‐axis and apical fractional area change (ΔFA) were less in PLE patients than in controls (50 vs. 57% [P < .0001] and 49 vs. 54% [P = .01]). Five and 10‐year actuarial survival rates for the PLE group were 49 ± 9% and 30 ± 11%. Deceleration time <120 milliseconds (hazard ratio [HR] = 9.2, P = .04), New York Heart Association classification III or IV (HR = 4.0, P = .01), and lower serum albumin (HR = 0.30, P = .04) were independent predictors of mortality in those with PLE. Conclusion. Mild reduction in ΔFA was the only late echocardiographic finding associated with development of PLE. However, short deceleration time, poor New York Heart Association (NYHA) class, and low serum albumin identify a group of patients at the greatest risk for death. Presence of these findings in a PLE patient should lead to aggressive management strategies and may warrant early consideration of transplantation.     

Simultaneous occurrence of gastric antral vascular ectasia and protein-losing enteropathy in chronic graft-versus-host disease

Gastric antral vascular ectasia (GAVE) leading to upper gastrointestinal bleeding is a heterogeneous disorder that is not commonly recognized in hematopoietic stem cell transplantation (HSCT). Protein-losing enteropathy (PLE) is noted as another gastrointestinal complication in the context of chronic graft-versus-host disease (GVHD) after HSCT. The possibility of a relationship between these two distinct gastrointestinal disorders, however, remains obscure. A 6-year-old boy with acute myelogenous leukemia developed severe hematemesis 4 months after myeloablative HSCT from a human leukocyte antigen-matched sibling donor. The diagnosis of GAVE was made by upper endoscopy and histological examination. The patient simultaneously developed frequent diarrhea and significant hypoproteinemia, consistent with a diagnosis of PLE. This co-occurrence of GAVE and PLE against a background of chronic GVHD was successfully treated with cyclosporin A and prednisolone. To our knowledge, this is the first report of GAVE concurrent with PLE following HSCT. The possible association of GAVE and PLE in chronic GVHD is discussed.