Sneppen S B, Main K M, Juul A, Pedersen L M, Kristensen L O, Skakkebaek N E, Feldt-Rasmussen U
Department of Endocrinology, Rigshospitalet, The National University Hospital, Copenhagen, Denmark.
Clin Endocrinol (Oxf). 2000 Nov;53(5):601-8. doi: 10.1046/j.1365-2265.2000.01141.x.
While increased sweating is a prominent symptom in patients with active acromegaly, reduced sweating is gaining status as part of the growth hormone deficiency (GHD) syndrome.
Sweat secretion rate (SSR), as measured by pilocarpine iontophoresis represents the maximal capacity for stimulated sweat secretion in a localized skin area. SSR was studied in 37 patients with a history of acromegaly, 20 adult patients with GHD before and during long-term GH substitution of GHD adults, and 58 control subjects.
Acromegaly: Patients with acromegaly had significantly higher SSR than healthy controls (Z-score + 1.9 (+/- 1.1) mean (+/- SD) (P < 0.001)). SSR was increased irrespective of current clinical disease activity. Thus, the SSR Z-scores in 16 clinically inactive patients were + 2.1 (+/- 1.2), in 10 slightly or doubtfully active patients + 1.5 (+/- 0.7) and in 11 active patients + 1.8 (+/- 1.3). There was no correlation between SSR and IGF-I. GHD: Twenty adult patients participated in an 18-month randomised, placebo controlled, double blinded study of physiological dose GH substitution, followed by 18 months of open GH treatment. SSR at baseline was reduced in male but not in female GHD patients. Mean SSR (95% confidence interval) for 11 male patients was 89.0 mg/30 minutes (51.9-126.1) as compared to 133.5 mg/30 minutes (59.2-259.9) (P = 0.01) in 24 male controls, and for 11 female patients 48.2 mg/30 minutes (25.9-70.6) as compared to 49.2 mg/30 minutes (12.6-93. 9) in 34 female controls. GH treatment in physiological substitution doses for up to 36 months had no effect on SSR.
We have demonstrated that longstanding GH hypersecretion in patients with acromegaly induces irreversible changes of sweat gland function, with persistently elevated SSR despite treatment and clinical cure. In GHD patients, SSR was reduced in males but not in females, which together with the established gender difference in normal controls emphasises the role of androgen deficiency as a cofactor for reduced sweating in hypopituitary patients. Sweat gland development seems to be more susceptible to lack of hormones in childhood and adolescence than in adulthood, whereas growth hormone excess can modify sweat function later in life.
虽然多汗是活动性肢端肥大症患者的一个突出症状，但少汗正成为生长激素缺乏（GHD）综合征的一部分。
通过毛果芸香碱离子导入法测量的汗液分泌率（SSR）代表局部皮肤区域刺激汗液分泌的最大能力。对37例有肢端肥大症病史的患者、20例成年GHD患者（在长期生长激素替代治疗前及治疗期间）以及58例对照者进行了SSR研究。
肢端肥大症：肢端肥大症患者的SSR显著高于健康对照者（Z值+1.9（±1.1），均值（±标准差）（P<0.001））。无论当前临床疾病活动情况如何，SSR均升高。因此，在16例临床无活动症状的患者中，SSR的Z值为+2.1（±1.2），10例轻度或可疑活动症状的患者中为+1.5（±0.7），11例活动症状患者中为+1.8（±1.3）。SSR与胰岛素样生长因子-I无相关性。GHD：20例成年患者参与了一项为期18个月的随机、安慰剂对照、双盲的生理剂量生长激素替代治疗研究，随后进行了18个月的开放生长激素治疗。男性GHD患者基线时的SSR降低，而女性患者则未降低。11例男性患者的平均SSR（95%置信区间）为89.0mg/30分钟（51.9 - 126.1），24例男性对照者为133.5mg/30分钟（59.2 - 259.9）（P = 0.01）；11例女性患者的平均SSR为48.2mg/30分钟（25.9 - 70.6），34例女性对照者为49.2mg/30分钟（12.6 - 93.9）。长达36个月的生理替代剂量生长激素治疗对SSR无影响。
我们已经证明，肢端肥大症患者长期生长激素分泌过多会导致汗腺功能发生不可逆变化，尽管经过治疗且临床治愈，但SSR仍持续升高。在GHD患者中，男性的SSR降低，女性则未降低，这与正常对照者中已确立的性别差异一起，强调了雄激素缺乏作为垂体功能减退患者少汗的一个辅助因素的作用。与成年期相比，儿童期和青春期的汗腺发育似乎更容易受到激素缺乏的影响，而生长激素过多则可在生命后期改变汗液功能。
