生长激素治疗对GHD患儿免疫功能的影响

对生长激素缺乏症（GHD）患儿生长激素（GH）治疗前后的免疫功能改变进行了观察。结果显示：（1）GHD患儿NK细胞活性明显降低，经GH治疗3个月后恢复到正常水平；（2）GHD患儿治疗前IL－1a和IL－2活性偏低，治疗后两者有逐渐增高的趋势；（3）治疗前后CD细胞亚群、sIL－2R和LPS诱生的TNFa含量均无明显变化。认为GH缺乏症患儿存在一定的免疫功能缺陷，而GH有调节其免疫功能的作用。     

Graves病患者血甲状旁腺激素、钙、磷、碱性磷酸酶基础值的观察

对照观察了28例Graves病患者及29名正常人血浆甲状旁腺激素、(PTH)血钙、血磷、碱性磷酸酶的基础值。Graves病组血碱性磷酸酶明显高于对照组,而PTH、钙、磷无显著差异。Graves病组血钙>2.75mmol/L者占21%,与某些文献大致相符。正常组血钙与PTH基础值间呈负相关,而Graves病组该两值间无相关,提示Graves病时血钙浓度的平衡调节中PTH以外的因素如甲状腺激素等可能对其影响较大。     

A case of polycythemia vera complicated by chronic renal failure under hemodialysis requiring parathyroidectomy for secondary hyperparathyroidisim

A case of polycythemia vera complicated by chronic renal failure under maintenance hemodialysis requiring parathyroidectory (PTH) for secondary hyperparathyroidism (2° HPT) is reported. A 62 year old female presented with 75000 white blood cells (WBC)/μl, 703×10⁴ red blood cells (RBC)/μl, 23×10⁴ platelets (PLT)/μl, hyperuricemia and hypertension in 1970 and the diagnosis of polycythemia vera was made. Hemodialysis was started in October 1974 for chronic renal failure. Blood cells in peripheral blood rapidly decreased in number after the beginning of dialysis, reaching the level of 10000∼20000 WBC/μl, and 150∼250×10⁴RBC/μl. In August 1988, marked bone resorption in X-ray picture and high serum alkaline phosphatase and parathyroid hormone (PTH) noted along with 17400 WBC/μl, 370×10⁴RBC/μl and 35.9×10⁴PLT/μl. After subtotal PTX removing 3.21g parathyroid gland, serum PTH rapidly fell. At 3 months after PTX, WBC rose to 23600/μl, RBC 372×10⁴/μl and PLT 94.0×10⁴/μl. At 6 months, WBC was to 31000/μl, RBC 429×10⁴/μl and PLT 78.0×10⁴/μl, suggesting an inhibitory action of PTH on not only RBC, but also WBC and PLT.     

血清保存方法对促甲状腺激素结果的影响观察

目的 :观察血清保存方法对促甲状腺激素 (TSH)结果的影响。方法 :将甲状腺功能正常、异常患者共 10份血清 ,采用不同血清量、不同条件分组保存后测定 TSH。结果 :保存方法对 TSH结果有一定的影响。结论 :用于 TSH血清的保存量要多、要密封管口、低温保存。     

生长激素在肝硬变门脉高压低蛋白血症手术前的应用研究

目的：研究生长激素（rhGH)对肝硬变门脉高压低蛋白血症患者手术前的治疗价值。方法：肝硬变门脉高压抑行脾切除、门奇静脉断流手术患者60例，Child分级B级，随机分为rhGH治疗组30例，对照组30例。rhGH组术前5d每天皮下注射rhGH 4IU，对照组给予安慰剂生理盐水。两组术前均行相同肠外营养支持。测定治疗前、治疗后3d、4d、5d血浆白蛋白、球蛋白、前白蛋白及空腹血糖。结果：rhGH组治疗后3d前白蛋白较治疗前及对照组明显升高（P＜0．05），治疗后4d、5d仍维持较高水平；治疗后5d白蛋白较治疗前及对照组明显升高（P＜0．05）。rhGH组患者一般情况改善，生活质量提高。对照组白蛋白、前白蛋白无明显变化。两组空腹血糖、球蛋白无明显改变。结论：rhGH联合肠外营养支持对纪正肝硬变门脉高压低蛋白血症患者术前低蛋白状态，改善生活质量有良好疗效，由于rhGH起效慢，应早期、足量、足疗程应用。     

Intermittent etidronate partially prevents bone loss in hirsute hyperandrogenic women treated with GnRH agonist

Treatment with gonadotropin-releasing hormone (GnRH) agonist leads to enhanced bone turnover and accelerated bone loss in premenopausal women with endometriosis, uterine leiomyomatomas and hirsutism. Sodium etidronate is a powerful inhibitor of bone resorption which has been proven efficacious in the prevention and treatment of postmenopausal osteoporosis. The objective of this study was to evaluate the skeletal effects of 6 months of therapy with the depot preparation of the GnRH agonist triptorelin (decapeptil 3.75 mg intramuscularly every 4 weeks) in 24 hirsute patients, aged 24–33 years, with hyperandrogenic chronic anovulation. Ten patients also received cyclical etidronate in an oral dose of 400 mg/day for 2 weeks, followed by an 11-week period of 500 mg/day elemental oral calcium (one cycle). The remaining 14 patients received 500 mg/day of elemental calcium continuously. After 6 months all treatments were discontinued for at least a further 6 months. Bone mineral density (BMD) at lumbar spine and hip (dual-energy X-ray absorptiometry, Sophos LXRA, France) and biochemical markers (serum alkaline phosphatase, osteocalcin, urinary N-telopeptide and hydroxyproline/creatinine ratio) were evaluated at baseline, 6 months and 12 months. In the group given GnRH agonist alone BMD fell significantly at all measured skeletal sites during the first 6 months. In the patients treated with etidronate a significant decrease in BMD was observed at lumbar spine but not in the femoral neck and trochanter, and the changes at lumbar spine and trochanter were significantly smaller than those in the control group. At 6 months bone turnover was also increased in patients treated with GnRH and calcium. Cyclical etidronate prevented the increase in biochemical markers of bone formation and resorption, with the exception of calcium/creatinine excretion, which was significantly increased in both groups. Six months after treatment withdrawal BMD did not recover in either group. Biochemical markers (N-telopeptide, serum alkaline phosphatase) remained increased in those patients previously treated with calcium alone while they remained close to baseline values in the patients treated with cyclical etidronate.Our study indicates that: (1) GnRH agonist therapy causes remarkable bone loss in young individuals with androgen excess who are expected to have increased bone mass; (2) this bone loss can be partially prevented by intermittent cyclical etidronate therapy.     

Growth hormone resistance in uremia

Growth retardation is a major complication in children with uremia. Protein restriction, calorie deficit, metabolic acidosis, renal osteodystrophy, and endocrinologic disturbances contribute to the growth failure. The effect of these factors on growth retardation can be attenuated in part by therapy with vitamin D metabolites, adequate nutrition, alkalization, and dialysis. Linear growth in children with uremia is markedly retarded despite normal or increased levels of circulating serum growth hormone. An increased growth hormone level in children with uremia is due to normal growth hormone secretion from the pituitary gland and impaired growth hormone clearance in the kidney. However, the elevated growth hormone level does not lead to a commensurate rise in serum insulin-like growth factor I (IGF-I); the serum IGF-I level is decreased or normal in relation to the degree of renal failure. This discrepancy suggests growth hormone resistance in the liver in uremia. Recent molecular techniques open a new era in studying the gene expression for growth hormone or IGF-I. There is no doubt today that growth hormone treatment has the beneficial effect of growth promotion in children with uremia, which also suggests endogenous growth hormone resistance in target organs or target cells in uremia.     

Postmenopausal HRT is not independent risk factor for dural sinus thrombosis

While a dural sinus thrombosis (DST), is a well-known consequence of the use of oral contraceptives, the role of hormone replacement therapy (HRT) in DST was not previously evaluated. We report two postmenopausal women, presenting with DST under HRT. Antiphospholipid antibodies in one case and borderline protein S deficiency in another were diagnosed. Only five cases of DST under HRT were previously reported and in two of them additional prothrombotic risk factors were found. According to these and previous cases, HRT is not an independent risk factor for DST.     

重组人生长激素对体外人结肠癌COLO-320细胞生长的影响

目的　探讨重组人生长激素 (rhGH)对体外人结肠癌COLO 3 2 0细胞生长的影响。方法　取对数生长期的人结肠癌细胞株COLO 3 2 0细胞 ,分别在有血清 (血清组 )和无血清 (无血清组 )条件下培养 ,以不同浓度的rhGH和(或 )羟基喜树碱 (CPT)培养COLO 3 2 0细胞 ,分别培养 2 4h、48h及 72h ,然后用四甲基偶氮唑蓝 (MTT)法测定结肠癌细胞生长抑制率。结果　不同浓度的rhGH作用不同时间对人结肠癌细胞株COLO 3 2 0细胞的生长均无明显影响 (P>0 .0 5 ) ;单用CPT或rhGH联合CPT使用时对该细胞生长的抑制率均明显高于单用rhGH(P<0 .0 1) ,但前两者间差异无统计学意义 (P>0 .0 5 )。结论　体外条件下rhGH对人结肠癌细胞株COLO 3 2 0细胞的生长既无促进作用 ,也无抑制作用 ,且不影响CPT对人结肠癌细胞株COLO 3 2 0细胞的抑制作用。