肢端肥大症的药物治疗进展

垂体肿瘤分泌过多生长激素（GH）是导致肢端肥大症的最主要的原因，其治疗手段包括手术、药物和放疗。对于垂体微腺瘤者，外科手术仍然是首选的治疗方式，药物仅起辅助作用；对垂体大腺瘤而言，药物治疗，尤其是生长抑素类似和新近开发的GH受体拮抗剂的应用具有更加重要的地位。     

治疗肢端肥大症的新进展——Sandostatin

本文着重介绍生长抑素八肽类似物SMS治疗肢端肥大症的现状。包括临床疗效、抑制生长激素分泌效应等。并对长期治疗中的反应及停药后复发问题提出看法。     

培维索孟治疗肢端肥大症

生长激素(Growth Hormone,GH)分泌过多,在骨骺尚未闭合时期不断促进长骨生长,使患者身高不断增长,称为巨人症;在骨骺已经闭合以后则促进扁骨等膜化骨增宽增厚,导致面容变形,手足增大,肢端变粗,称为肢端肥大症;如起病时骨骺尚未闭合而就诊时已闭合,则兼备二者的临床表现,称为肢端肥大性巨人症.     

Sandostatin 治疗肢端肥大症的疗效

本文报道用生长抑素八肽类似物(Sandostatin, SMS201—995)治疗10例活动性肢端肥大症20.3±7.5个月的结果。治疗剂量为300～1500μg/d,分3次,每8小时皮下注射1次。结合临床及血清GH及SMC值评定,在用药期间,2例控制正常,4例显效,3例有效,1例无效。5例新诊断患者用药6个月后1例的微腺瘤消失,4例大腺瘤高度由12.4±4.9mm降至9.8±4.4mm。8例患者有短暂的胃肠道反应,8例胆囊收缩功能减弱,4例糖耐量变坏。指出SMS201-995对肢端肥大症有疗效,但其治疗价值尚待进一步研究。     

奥曲肽治疗肢端肥大症

用奥曲肽治疗５例活动性肢端肥大症，疗程６个月。奥曲肽剂量４５０－１５００μｇ／日，分次皮下注射。结果提示奥曲肽能有效地降低血清ＧＨ水平，改善临床症状。对药物的副作用应作进一步观察。     

对长期用生长抑素激动剂治疗肢端肥大症停药后生长激素分泌和胆…

为了探索克服长效生长抑素激动剂ＳＭＳ２０１－９９５治疗肢端肥大症（肢大）引起胆囊结石的方法，我们前瞻性地观察了１４例经ＳＭＳ治疗的肢大患者于停用ＳＭＳ后生长激素分泌轴系变化及胆囊病变的恢复情况。结果：停用ＳＭＳ后第１周，周围血中生长激素基础值及５小时生长激素谱中生长激素平均水平均显著低于用药前水平，分别为用药前生长激素水平的３６％和２４％。在停药后２周末，则生长激素基础值和５小时生长激素谱平均水平     

肢端肥大症的并发症

肢端肥大症可合并多种并发症,本文简要介绍肢端肥大症合并心血管系统疾病、糖代谢异常、骨关节病变等并发症,以及经手术、放疗等治疗后这些并发症的转归。     

肢端肥大症的内科治疗新进展

1 简介 肢端肥大症（以下简称“肢大”）是由于过度的生长激素（GH）分泌导致的一组疾病，其病因绝大多数是由于垂体GH分泌型肿瘤导致。传统的治疗方法通常是以手术作为首选治疗，对于残留肿瘤给予放射治疗。近年来，随着神经内分泌学和垂体细胞生物学的发展，使得该领域的药物发展突飞猛进，生长抑素类似物的应用对手术作为首选治疗方法的传统治疗模式形成了巨大的挑战，它使得几乎所有肢大患者术前的临床症状和生化指标得到了明显快速的改善。肢大患者生化缓解的重要意义是生化达标可以明显降低患者的病死率。目前，临床上肢端肥大症的治疗模式正在发生着变化，对于肢大这种临床治疗上较为棘手的疾病，药物的应用有可能明显改善患者的预后。     

肢端肥大症的内科治疗新进展

1简介肢端肥大症(以下简称“肢大”)是由于过度的生长激素(GH)分泌导致的一组疾病,其病因绝大多数是由于垂体GH分泌型肿瘤导致。传统的治疗方法通常是以手术作为首选治疗,对于残留肿瘤给予放射治疗。近年来,随着神经内分泌学和垂体细胞生物学的发展,使得该领域的药物发展突飞猛     

华法林个体化用药影响因素的研究进展

华法林等维生素K拮抗剂是目前临床上应用最广泛的抗凝药物,主要用于预防心脏瓣膜置换、心房颤动等疾病血栓事件的发生.但影响其临床疗效的因素较多,不同个体的华法林有效剂量差异较大.随着对华法林的药物基因组学的深入研究,华法林个体化用药逐渐成为可能,但目前基因指导华法林用药的有效性仍存在争议.本文拟对影响华法林剂量的非遗传因素...     

Estrogen treatment for acromegaly

Estrogens have been used in patients with acromegaly since the 1930?C1940s, suppressing plasma IGF-1 levels and improving clinical signs and symptoms of acromegaly. Estrogens antagonize GH function at the post-receptor level, inhibiting GH signaling, thus decreasing GH-induced hepatic IGF-1 synthesis. We report our experience with four female patients with active acromegaly, na?ve to medical treatment or inadequately controlled by somatostatin receptor ligands (SRLs) or the GH-receptor antagonist. Adding estrogen treatment (contraceptive pills or transdermal estrogen patches) to their ongoing medical treatment, suppressed IGF-1 significantly in all patients, achieving hormonal remission in three of them. We review the available data on the use of estrogens and selective estrogen receptor modulators in acromegaly, and their mechanisms of action. Estrogens could be an alternative, inexpensive adjuvant treatment for females with active acromegaly, who are only partially responding to SRLs or to the GH-receptor antagonist.     

Somatostatin agonists for treatment of acromegaly

The discovery of somatotropin-release inhibitory factor (SRIF) in hypothalamic extract in 1970 led to the synthesis of the first somatostatin analog octreotide, discovery of five somatostatin receptor subtypes, and development of additional somatostatin receptor ligands (SRL) as pharmacotherapy for acromegaly and other neuroendocrine tumors. Long-acting formulations of SRL (octreotide LAR Depot, lanreotide SR and lanreotide autogel) assure improved patient compliance with weekly up to monthly injections, and are commonly used as primary or adjuvant treatment of acromegaly. We review SRL currently available, emphasizing long-acting compounds and their efficacy in controlling acromegaly. Disease control is evaluated by biochemical markers, tumor shrinkage, and disease-symptom improvement balanced against drug-related side effects.     

Bromocriptine treatment of acromegaly

Bromocriptine at a dose of 7.5-30 mg/day was given to 12 acromegalics for 6 mo. Mean serum growth hormone (GH) levels during a glucose tolerance test (GTT) were significantly lowered by the drug. In four patients the serum GH response during a GTT was suppressed to normal (i.e. less than or equal to 5 mlU/liter). If bromocriptine had not brought the serum GH response to a GTT to normal at a dose of 20 mg/day, this effect was not achieved by raising the dose to 30 mg/day. Bromocriptine was effective for the duration of treatment. On discontinuing therapy there was an increase in serum GH levels. No obvious clinical changes in the acromegalic features were noted. One patient with impaired glucose tolerance and one with established diabetes had normal glucose tolerance while on bromocriptine and another two patients with impaired glucose tolerance showed no obvious changes while on the drug. Side effects were minor. X-rays of the pituitary fossa before starting and at the end of treatment showed no significant change. We conclude that although bromocriptine is the most promising form of medical treatment for acromegaly to date, it is fully effective only in a minority of patients.