肾上腺肿瘤及增生27例诊治经验

27例肾上腺肿瘤及增生中皮质醇症8例、嗜铬细胞瘤16例、原发性醛固酮增多症、髓质增生症及无功能性肿瘤各1例。定位诊断主要为CT检查及腹膜后注气造影。皮质醇症术前应有效地控制血糖;嗜铬细胞瘤术前使用皮质激素有助于患者顺利地度过手术关。本组患者以手术治疗为主,并阐述了手术治疗的经验。     

Effect of Tripterygium Vilfordii on Adrenal Cortex in Rat with Adjuvant Arthritis

(张明敏)(刘沛霖)(叶望云)ＥｆｆｅｃｔｏｆＴｒｉｐｔｅｒｙｇｉｕｍＶｉｌｆｏｒｄｉｉｏｎＡｄｒｅｎａｌＣｏｒｔｅｘｉｎＲａｔｗｉｔｈＡｄｊｕｖａｎｔＡｒｔｈｒｉｔｉｓ￥ＺＨＡＮＧＭｉｎｇ－ｍｉｎ；ＬＩＵＰｅｉ－ｌｉｎ；ＹＥＷａｎｇ－ｙｕｎ（Ｔｏｎｇｊｉ...     

Differential Stimulation of Noradrenaline Release by Reversal of the Na+/Ca2+ Exchanger and Depolarization in Chromaffin Cells

We compared the effectiveness of Ca²⁺ entering by Na⁺/Ca²⁺ exchange with that of Ca²⁺ entering by channels produced by membrane depolarization with K⁺ in inducing catecholamine release from bovine adrenal chromaffin cells. The Ca²⁺ influx through the Na⁺/Ca²⁺ exchanger was promoted by reversing the normal inward gradient of Na⁺ by preincubating the cells with ouabain to increase the intracellular Na⁺ and then removing Na⁺ from the external medium. In this way we were able to increase the cytosolic free Ca²⁺ concentration ([Ca²⁺]_c) by Na⁺/Ca²⁺ exchange to 325 ± 14 nM, which was similar to the rise in [Ca²⁺]_c observed upon depolarization with 35 mM K⁺ of cells not treated with ouabain. After incubating the cells with ouabain, K⁺ depolarization raised the [Ca²⁺]_c to 398 ± 31 nM, and the recovery of [Ca²⁺]_c to resting levels was significantly slower. Reversal of the Na⁺ gradient caused an −6-fold increase in the release of noradrenaline or adrenaline, whereas K⁺ depolarization induced a 12-fold increase in noradrenaline release but only a 9-fold increase in adrenaline release. The ratio of noradrenaline to adrenaline release was 1.24 ± 0.23 upon reversal of the Na⁺/Ca²⁺ exchange, whereas it was 1.83 ± 0.19 for K⁺ depolarization. Reversal of the Na⁺/Ca²⁺ exchange appeared to be as efficient as membrane depolarization in inducing adrenaline release, in that the relation of [Ca²⁺]_c to adrenaline release was the same in both cases. In contrast, we found that for the same average [Ca²⁺]_c, the Ca²⁺ influx through voltage-gated channels was much more efficient than the Ca²⁺ entering through the Na⁺/Ca²⁺ exchanger in inducing noradrenaline release from chromaffin ceils. This greater effectiveness of membrane depolarization in stimulating noradrenaline release suggests that there is a pool of noradrenaline vesicles which is more accessible to Ca²⁺ entering through voltage-gated Ca²⁺ channels than to Ca²⁺ entering through the Na⁺/Ca²⁺ exchanger, whereas the adrenaline vesicles do not distinguish between the source of Ca²⁺.     

Long-term survival after bilateral adrenalectomy for metachronous adrenocortical cancer

We report the case of a female patient with bilateral metachronous adrenocortical cancer who survived long-term after adrenalectomy. In 1991, the patient underwent left adrenalectomy to remove a huge adrenal mass (10 x 9 cm) displaying no hormonal abnormality. Histological diagnosis was adrenocortical cancer. A right adrenal mass (7 x 6 cm) was found 4 years after left adrenalectomy. Right adrenalectomy was performed, and histological diagnosis was again adrenocortical cancer. The patient remains alive with no evidence of disease 8 years after last surgery.     

腹腔镜肾上腺肿瘤切除术75例报告

目的探讨腹腔镜下肾上腺肿瘤切除的方法和临床应用价值.方法1999年1月～2004年6月75例患者行腹腔镜肾上腺肿瘤切除术,其中采用经腹腔途径51例和经腹膜后途径24例.结果手术时间平均为(170.16±33.81)min,术中的出血量平均为(70.82±37.15)ml.术后平均住院时间为(5.87±1.01)d.中转开放手术2例(2.67%).发生并发症4例(5.33%),分别为膈肌损伤、胰腺损伤、肠道损伤、皮下血肿各1例.结论腹腔镜下行肾上腺肿瘤切除术具有创伤小,术中出血少,术后恢复快等优点,已经成为现代治疗肾上腺肿瘤的金标准.     

原发性醛固酮增多症的定位诊断与手术径路选择的初步研究——附10例报告

收治10例原发性醛固酮增多症。所有病例术前均经B超、CT扫描、血管造影及取肾上腺静脉血测醛固酮浓度4种定位方法检查。CT扫描和取肾上腺静脉血样分别获得75％和71.4％的肾上腺腺瘤诊断准确率。综合上述4种方法,7侧术前做出腺瘤定位诊断,其中5例获得术中和病理组织学证实,定位准确率为71.4％。并对手术入路的选择进行讨论,单侧腰切口仍然不能代替经腹切口。     

强磁场对幼年大鼠生长发育的影响

将幼年Ｗｉｓｔａｒ大鼠分别于１０日龄和２０日龄时两次暴露于１０Ｔ稳态磁场中，每次３０ｍｉｎ，观察强磁场对幼年大鼠生长发育的影响。与对照组相比，４０日龄时强磁场组的生长体重无明显差异，心、肝、脾、肾、脑、垂体、性腺的重量亦无明显差异，但肾上腺重量显著增加。提示稳态１０Ｔ磁场可引起应激反应，但对生长发育无明显影响。     

Urinary 17α-hydroxyprogesterone in management of 21 -hydroxylase deficiency

Objectives: The study was designed to assess the reliability of measurement of 24-hour urinary 17α-hydroxyprogesterone (17-OHP) by radio-immunoassay (RIA) as an alternative biochemical assessment for monitoring the treatment of congenital adrenal hyperplasia (CAH) due to 21 -hydroxylase deficiency (21 -OHD) and to assess the need for sample purification by column chromatography to improve assay specificity.
Methodology: Morning serum 17-OHP was measured using RIA and 24-hour urinary pregnanetriol using gas chromatography. Twenty-four-hour urinary 17-OHP was measured in samples from 17 prepubertal patients with CAH due to 21 -OHD, and 20 normal prepubertal children as controls. In 24 urine samples, RIA of 17-OHP was performed with and without column chromatography.
Results: There was a good correlation between 24-hour urinary 17-OHP and 24-hour urinary pregnanetriol (r = 0.962, P <0.01) and between 24-hour urinary 17-OHP and morning serum 17-OHP ( r = 0.955, P <0.01). There was no significant difference in the RIA of the urine samples with and without purification by column chromatography.
Conclusions: The measurement of 24-hour urinary 17-OHP is a reliable alternative for the biochemical monitoring of 21-OHD, and RIA specificity is unaffected by omission of column chromatography.     

大白鼠肾上腺的血管构筑

本实验采用血管铸型扫描电镜,注射明胶卡红组织切片显微镜下观察和注射铅丹乳胶追踪血管来源三种方法对14只健康大白鼠肾上腺血管构筑进行了研究。大白鼠肾上腺动脉发自腹主动脉和肾动脉。它们在行程中发出分支至腺体表面,再次分支穿入囊内,逐级分支至毛细血管。皮质动脉发自囊内血管,它们在皮质中分支分布。球状带的毛细血管与囊的毛细血管相连,毛细血管在球状带围绕细胞团形成网眼状;在束状带呈放射状排列;在网状带吻合增多形成网状。髓质动脉亦发自囊的血管,它们在皮质中不发分支直抵髓质,在髓质分成毛细血管。网状带的毛细血管越向髓质口径越粗,它们在皮髓交界处互相吻合形成更粗的静脉,这些静脉逐级吻合,最后形成一主干——中央静脉,它穿出皮质出现于肾上腺门处。左侧的中央静脉注入在肾静脉,右侧的注入下腔静脉。     

Hypothalamic-pituitary adrenal function in end-stage non-alcoholic liver disease

Abstract Patients with end-stage liver disease have significant mortality often associated with intercurrent episodes of bleeding or sepsis. Intact adrenal function is essential in such situations. In order to test the hypothesis that adrenal insufficiency might be present in severe liver disease, hypothalamic-pituitary adrenal function was evaluated in patients with end-stage liver disease awaiting transplantation. The study had a prospective, open comparative design with patients restricted to those having non-alcoholic liver disease in order to avoid the confounding direct effects of alcohol on adrenocortical function. Fifty-one consecutive patients with end-stage, non-alcoholic liver disease undergoing evaluation for liver transplantation and 40 healthy controls were studied. Patients who had used corticosteroids (n= 8) or who were unable to complete the investigations (n= 5) were excluded leaving 38 patients eligible for analysis. Adrenal function was evaluated under basal conditions by single morning measurements of plasma total and free cortisol, corticosteroid-binding globulin, dehydroepiandrosterone sulfate and by adrenal stimulation indirectly using insulin-induced (0.1 U/kg, i.v.) hypoglycaemia and/or directly by adrenocorticotrophic hormone (ACTH); 250 μg tetracosactrin, i.v.) stimulation. Compared with healthy controls, patients with liver disease had a 64% reduction in maximal increments of plasma cortisol to indirect adrenal stimulation via insulin-induced hypoglycaemia and a 39% reduction to direct adrenal stimulation by ACTH (all P < 0.001). There was a significant negative correlation between the severity of underlying liver disease as assessed by Child-Pugh scores and peak control responses to ACTH (r= -0.647, P < 0.0001) and insulin-induced hypoglycaemia (r= -0.597, P < 0.0001). Patients with liver disease also exhibited significantly blunted and delayed hypoglycaemic responses to insulin (0.1 U/kg), brisker growth hormone responses of reduced magnitude and decreased corticosteroid-binding globulin levels. Baseline morning cortisol, free cortisol and dehydroepiandrosterone sulfate levels were unchanged compared with healthy controls. Patients on spironolactone had lower basal and peak cortisol responses to ACTH and hypoglycaemia, but the reductions were unrelated to spironolactone dose. Although insulin resistance and spironolactone therapy are confounding factors, it can be concluded that hypothalamic-pituitary regulation of adrenal function is defective in end-stage non-alcoholic liver disease. It is therefore possible that functional central adrenal insufficiency might contribute to the mortality of patients with end-stage liver disease and raises the question of the need for controlled studies of adrenocortical replacement therapy during acute deteriorations (sepsis and haemorrhage) in severe hepatic disease.