睡眠性呼吸困难与活动期肢端肥大症

目前,对睡眠性呼吸困难综合症(SAS)的研究已普遍开展。一些报道说明睡眠性呼吸困难(SA)与肢端肥大症有关。认为肢端肥大症主要临床表现为上呼吸道软组织增生引起上呼吸道狭窄,以至睡眠时气流阻塞。也有人认为可能与中枢性通气控制失调有关,也可能与上呼吸道阻塞有关。     

肢端肥大症患者尿生长激素的生物活性

人类生长激素(hGH)具有不均一性,最近有人用PAGE和等电聚焦电泳技术发现hGH也存在不同大小的分子形式,其中以22K的分子形式为主,作者用Nb_2细胞生物分析法和IM-9受体调节分析法(IM-9RMA)对尿hGH的生物活性进行了测定,并用高度敏感和特异的酶免疫分析法(EIA)对其分子大小的不均一性做了进一步研究。     

生长介素对肢端肥大症患者垂体瘤生长激素分泌影响的体外研究

作者在8例肢端肥大症体外培养的垂体GH瘤细胞上探讨IGF-1对GH分泌的反馈调节作用。10~(-7)mol IGF-1使3例垂体GH瘤细胞GH基础分泌抑制到对照的44.6％～52.4％(P<0.05),1例GH分泌增加134.9％(P<0.05),4例GH基础分泌没有明显改变,表明体外培养的垂体GH瘤有一半以上对IGF-1 3小的·的急性作用失去正常的GH分泌抑制反应。3例对IGF-1失去GH分泌抑制反应的垂体GH瘤细胞同时伴有GH对GHRH_(1-44)及(或)生长抑素激动剂SMS_(201-995)反应消失,提示部分垂体GH瘤细胞的IGF-1和某些下丘脑激素受体或受体后有异常。     

特发性垂体性侏儒和肢端肥大症病人的GHRH分泌

目前有关内源性GHRH释放机制或其病生理作用所知甚少。本文作者检验了GH分泌紊乱患者基础状态和对各种试验应答的GHRH血浆水平,以     

肢端肥大症病人生长激素释放因子对生长激素分泌的影响

肢端肥大症病人生长激素(GH)分泌的动力学不正常,包括口服葡萄糖后GH不完全被抑制或反常性升高,给予左旋多巴或促甲状腺素释放激素(TRH)刺激后GH反而下降。目前有人从人胰腺肿瘤中鉴定并合成了生长激素释放因子(GRFs),它具有生长激素释放激素(GHRH)所必须具有的1～29有生物活性作用的氨基酸,而GRFs的作用也与GHRH相同。本文着重研究GRFs对GH的刺激试验是否可作为肢端肥大症的诊断依据。 29例肢端肥大症患者,年龄20～72岁。其中8例未经治疗,2例为经蝶手术者,5例经放射治疗,9例放疗加手术治疗,1例手术加服溴隐亭,1例单服     

伴肢端肥大症垂体腺瘤患者的免疫组化研究

作者应用免疫组织化学方法测定了30例伴有肢端肥大症垂体腺瘤患者的HGH、PRL及ACTH激素抗血清染色,结果27例HGH阳性,其中HGH和PRL混合阳性8例,HGH、PRL和ACTH混合阳性2例。本文对垂俸腺癌组织病理与激素组织定位和临床症状的关系进行了探讨,阐明了免疫组化对于垂体腺瘤功能分类的意义。     

女性肢端肥大症患者治疗前后的性腺功能

肢端肥大症为罕见疾病,发病隐匿,常至中年方获诊断,因而目前对该病女性患者中性腺功能障碍的发生率及原因所知甚少.完全或部分性促性腺激素缺乏可能与肿瘤占位效应(大腺瘤)及(或)高催乳素血症有关.     

肢端肥大症病人选择性垂体腺瘤切除术前后血泌乳素的分泌

某些肢端肥大症病人,血泌乳素(PRL)与生长激素(hGH)同样升高,为了解 PRL 产生机制,本文研究手术前、后肢端肥大症病人血 PRL 的分泌。研究对象为13例肢端肥大症病人,术前 hGH 基     

1例肢端肥大症患者的不常见表现

病例患者男，于２２岁首次就医前无明显的病史。主诉从１６岁时起胸廓逐渐畸形，并出现渐增加的前额头痛、背部和关节痛，多汗，心悸。进而其颌部、两手、足增大。查体：血压１８．６６／１２ｋＰａ（１４０／９０ｍｍＨｇ），脉搏８０次／分。肢端肥大，甲状腺增大为正常...     

无症状性肢端肥大症患者的心脏肥厚和功能

肢端肥大症常常引起心脏病变,而且是死亡的一个重要原因。它可能与心脏肥厚、心肌缺血有关,是生长激素对心肌细胞的特殊作用。左室肥厚和功能减退最常见。本文应用多普勒超声心动图评价肢端肥大症患者的亚临床心脏受累情况。对象与方法:选择无症状性肢端肥大症病人15例(男6例、女9例),年龄20～69岁(平均48±13岁),其中6例有高血压病史,时间10±7年,使用β-阻滞剂3例、利尿剂1例、钙阻滞剂1例,血管紧张素转换酶抑制剂1例。所有病人肾功能正常,无心力衰竭征象。应用多普勒超声心动图记录,连续3     

Attenuated pulse size, disorderly growth hormone and prolactin secretion with preserved nyctohemeral rhythm distinguish irradiated from surgically treated acromegaly patients

BACKGROUND: Radiation induces time-dependent loss of anterior pituitary function, attributed to damage of the pituitary gland and hypothalamic centres. The development of growth hormone deficiency (GHD) in irradiated acromegaly patients is not well defined. OBJECTIVE: Detailed analysis of spontaneous 24-h GH and prolactin (PRL) secretion in relation to other pituitary functions and serum IGF-I concentrations in an attempt to find criteria for GHD in acromegalic patients with a GH response < 3 microg/l during the insulin tolerance test (ITT). DESIGN: Plasma hormone profiles obtained by 10 min sampling for 24 h in postoperatively irradiated acromegalic patients, compared with patients cured by surgery only and matched healthy controls. SETTING/PARTICIPANTS: University setting. Fifteen subjects in each group. OUTCOME MEASURES: GH and PRL secretory parameters quantified by deconvolution, cluster, cosinor and approximate entropy (ApEn) analyses, IGF-I concentrations. RESULTS: Irradiation attenuated pulsatile secretion of GH and PRL, but total PRL secretion was unchanged. GH and PRL secretory regularity were diminished. Circadian timing remained intact. Pulsatile GH secretion and IGF-I were correlated (R = 0.30, P = 0.04). Criteria of pulsatile GH secretion = 12 microg/l/24 h and ApEn = 0.800 separated 12 of 15 irradiated patients from all others. CONCLUSION: Irradiated acromegaly patients with a subnormal GH response to ITT have very limited spontaneous GH secretion, with specific attenuation of the size of GH bursts and a highly irregular pattern, but with retained diurnal properties. These patients are thus likely GH-deficient and might benefit from GH replacement.     

Diminished prolactin reserve in acromegaly

Prolactin (PRL) secretion has been evaluated in twenty acromegalic patients. All had intact LH, FSH, and cortisol levels and normal thyroid function. Five patients had persistent hyperprolactinemia. The remainder had decreased basal PRL levels with impaired PRL responses to TRH and the dopaminergic antagonist metoclopramide (MET). Despite adequate hypoglycemia and an intact cortisol response, there was no PRL rise following insulin hypoglycemia. The impaired PRL response to TRH was evident in treated and untreated patients and was independent of GH levels. Basal hyperprolactinemia may be related to PRL secretion by the tumor cells or interference with the transport of PIF by the tumor. The decreased PRL reserve noted in the majority of the patients may be related to a decrease in lactotrope cell mass or, alternatively, to enhanced dopaminergic activity.     

Diminished diurnal secretion of corticosterone in aging female but not male rats

Since very little is known about the impact of aging on adrenocortical function in female rats, it was of interest to compare the age changes in the circulating levels of adrenocorticotropin (ACTH) and corticosterone in male and female Sprague-Dawley rats, and correlate these changes with those in plasma prolactin (Prl), which is known to stimulate adrenal steroid secretion. Hormones were measured in young (3-4 months) and old (24-26 months) male rats as well as in young (3-4 months), old (25 months) and senescent (33-35 months) female rats. Sequential plasma samples were obtained from chronically cannulated animals every 30 min from 11:30 a.m. to 4:30 p.m. ACTH was measured in trunk serum--obtained between 11:30 a.m. and 1:30 p.m.--whereas corticosterone and prolactin were measured in plasma using specific RIAs for the corresponding hormones. No age changes were detected in serum ACTH in either sex. The integrated values of plasma corticosterone did not change with age in males but decreased significantly (p less than 0.05) in old and senescent as compared to young females. Plasma corticosterone was higher in young females than in young males but this sex-related difference disappeared with age. Plasma Prl increased significantly with age in both male (p less than 0.05) and female (p less than 0.001) rats but showed no significant correlation with corticosterone levels. The present results suggest that ACTH secretion does not show major age- or sex-related changes. Our corticosterone data are compatible with the idea that gonadal aging has a significant impact on plasma glucocorticoid regulation in female rats but not in males.     

Growth hormone-releasing hormone infusion in patients with active acromegaly

To determine GH-releasing hormone (GHRH)-stimulated GH secretion in patients with active acromegaly, nine patients received a 50-microgram GHRH-(1-44) bolus dose followed by a 2-h infusion with 100 micrograms GHRH/h, after which a second 50-microgram GHRH bolus dose was given. Serum GH, PRL, and immunoreactive GHRH levels were measured from 2 h before to 1 h after the end of the infusion and compared with hormone levels in six normal subjects subjected to the same protocol. In addition, seven of the nine acromegalic patients received 100 micrograms GHRH as an iv bolus dose, followed by a 2-h saline infusion on a different day. After the 100-micrograms GHRH bolus dose, the mean GH level increased from 55.9 +/- 18.0 (+/- SE) to 148.5 +/- 40.0 ng/ml within 15 min. Thereafter, GH levels decreased and were significantly lower at 90 and 120 min compared to the peak level 15 min after GHRH injection. After the 50-micrograms GHRH bolus dose, all acromegalic patients except two also had a clear-cut rise of GH levels, with the mean GH level increasing from 37.5 +/- 13.2 to 108.4 +/- 55.0 ng/ml at 60 min. Thereafter, elevated GH levels were sustained in the acromegalic patients throughout the GHRH infusion. In contrast, normal subjects had a significant decrease in the initially elevated GH levels, despite continuous GHRH infusion. There were no significant differences between PRL secretion and immunoreactive GHRH levels in either group. These findings suggest that patients with active acromegaly not only have elevated basal GH levels, but also have a greater ready releasable GH pool and/or accelerated GH turnover compared to those of normal subjects, which cannot be exhausted by a 2-h GHRH infusion.     

Pituitary resistance to thyroid hormone action with preserved circadian rhythm of thyrotropin in a postmenopausal woman.

We assessed the 24-h behavior of circulating TSH and the dopaminergic control on TSH release in a postmenopausal woman, who had elevated levels of serum thyroid hormones and an inappropriately high concentration of serum TSH, indicating pituitary resistance to thyroid hormone action. The patient was found to have a daily profile of serum TSH similar to that of normal subjects, except for the persistently elevated 24 h levels, suggesting that alterations in thyroid hormone negative feedback control did not affect substantially circadian TSH rhythm. The acute administration of a dopamine antagonist drug (metoclopramide) resulted in a markedly elevated peak of serum TSH, similar both in the morning and in the evening. The chronic administration of a dopamine agonist drug (bromocriptine) reduced basal and TRH-stimulated TSH, restored circadian TSH variations to lower levels, and normalized other thyroid function tests. Although the metoclopramide test results confirmed the existence of an increased dopaminergic inhibitory tone in nonneoplastic inappropriate secretion of TSH, the outcome of bromocriptine treatment indicated that the dopaminergic control over TSH release was not enough in this case of PRTH.     

Baseline and stimulated catecholamine secretion in normotensive patients with active acromegaly: acute effects of continuous octreotide infusion

OBJECTIVE: Alterations in catecholamine plasma levels may contribute to the cardiovascular complications of acromegaly. Since few data are available on the catecholamine secretory dynamics in active acromegaly and no evidence exists on catecholamine variations during GH decrease, we studied acromegalic patients before and during octreotide administration. METHODS: We evaluated the catecholamine responses to upright posture and a cold pressure test (CPT) in 11 acromegalic (A) patients before and during continuous administration of octreotide (500 microgram/24h by s.c. pump) compared with 11 normal (N) subjects. RESULTS: All the acromegalic patients showed left ventricular cardiac hypertrophy. The cardiovascular responses to upright posture were similar between normal subjects and acromegalics both before and during octreotide treatment. The basal levels of norepinephrine (NE) were significantly higher in A patients compared with N subjects (423+/-45 vs 264+/-32pg/ml, P<0. 05) and decreased during therapy (291+/-32pg/ml; P<0.01). The increase in plasma NE during upright posture was significantly lower in A than in N subjects (P<0.01), but was restored to normal during octreotide treatment. CPT increased systolic and diastolic blood pressure, pulse rate and NE plasma levels in N (P<0.05) but not in A subjects both before and during octreotide treatment. CONCLUSIONS: Our data demonstrate the presence of increased basal NE levels in acromegalic patients with a defective sympathetic response to stimuli. Short-term octreotide infusion is able to induce a reduction in the basal levels of NE and a normalization of the catecholamine response to posture.     

Thyroid vascularity is increased in patients with active acromegaly

OBJECTIVE: To determine whether acromegalic patients have increased thyroidal vascularity and blood flow on colour flow Doppler sonography (CFDS). DESIGN: Prospective study of consecutive patients. PATIENTS: Twenty-four acromegalic patients (11 men, 13 women, age 49 +/- 9 years); 38 patients with nontoxic goitre (NTG; 12 men, 26 women, age 50 +/- 7 years); 36 normal subjects (controls; 16 men, 20 women, age 46 +/- 9 years). Among acromegalic patients, 10 had active, untreated disease (Acro-U), seven were in remission after surgery (Acro-R), seven had active disease under treatment with somatostatin analogues (SMSa) (Acro-SA) (Sandostatin LAR, 20 mg, every 28 days). MEASUREMENTS: CFDS pattern and intrathyroidal peak systolic velocity (PSV) were determined by a colour Doppler system with a 7.5-MHz linear transducer. PSV measurements were made at the level of the intrathyroidal arteries (normal values 3.8 +/- 1.0 cm/s). Thyroid volume was calculated by the ellipsoidal model. Assays included measurements of serum GH, IGF-I, free T4, free T3, TSH, antithyroglobulin (anti-Tg) and antithyroperoxidase (anti-TPO) antibodies, TSH-receptor antibodies (TRAb). RESULTS: Serum GH (+/- SD) and IGF-I (+/- SD) levels were: Acro-U: GH 26 +/- 31 microg/l, IGF-I 783 +/- 299 microg/l; Acro-SA: GH 15 +/- 25 microg/l, IGF-I 366 +/- 212 microg/l; Acro-R: GH 1.3 +/- 1.0 microg/l, IGF-I 241 +/- 99 microg/l. To convert values for serum GH to mU/l multiply by 2.6; to convert values for serum IGF-I to nmol/l multiply by 0.13075. All controls had CFDS pattern 0 (absent vascularity or minimal spots); among NTG patients, 36 had pattern 0 and two had pattern I (parenchymal blood flow with patchy uneven distribution). Five patients with acromegaly had pattern 0, 12 had pattern I and seven pattern II (mild increase of colour flow Doppler signal with patchy distribution). Among the five acromegalic patients with pattern 0, three were Acro-R and two were Acro-SA. Among patients with pattern I, six were Acro-U, two were Acro-SA and four were Acro-R. Among patients with pattern II, four were Acro-U and three Acro-SA; two patients of the latter group had elevated serum IGF-I under SMSa treatment. Intrathyroidal PSV was 3.8 +/- 1.0 cm/s in controls, 4.0 +/- 1.1 cm/s in NTG, 7.4 +/- 0.8 cm/s in Acro-U, 4.9 +/- 1.3 cm/s in Acro-SA treatment and 4.5 +/- 1.0 in Acro-R. (Acro-U vs. Acro-SA, P = 0.0003; vs. Acro-R, Controls, or NTG, P < 0.0001). PSV values in Acro-SA were higher than those observed in NTG or controls (P = 0.05, P = 0.01, respectively); PSV values in Acro-R did not differ from those in NTG or controls. Intrathyroidal PSV values were correlated with serum IGF-I (r = 0.73, P < 0.0001) and, although less strongly, GH levels (r = 0.54, P = 0.01). Goitre was present in 19 of 24 patients; diffuse in three and nodular in 16. Thyroid function was normal in all subgroups of acromegalic patients. Anti-Tg, anti-TPO antibodies and TRAb were negative in all subjects. CONCLUSIONS: Patients with active acromegaly have increased intrathyroidal blood flow (colour flow Doppler sonography pattern II, increased peak systolic velocity values); this was not observed in the large majority of patients under treatment with somatostatin analogues and in any patient in remission. Accordingly, colour flow Doppler sonography and peak systolic velocity measurements may be considered an additional useful peripheral parameter for rapid assessment of the activity of acromegaly.