脓毒症患儿血清皮质醇、促肾上腺皮质激素水平的测定及其临床意义

目的 动态监测脓毒症、严重脓毒症患儿血清皮质醇、促肾上腺皮质激素( adrenocorticotropic hormone,ACTH)水平的变化,探讨其与临床的关系.方法 以我院2010年9月至2011年1月收治的脓毒症患儿30例为研究对象,分为严重脓毒症组(10例)和脓毒症组(20例).在病程的急性期和恢复期分别检测血清皮质醇及ACTH水平,并与同期住院的10例非脓毒症患儿(对照组)进行对比分析.结果 急性期严重脓毒症组血清皮质醇[( 33.97±6.83) μg/ml]明显高于脓毒症组[(26.30±10.43) μg/ml]和对照组[(19.06±6.91) μg/ml],差异有统计学意义(P＜0.01).急性期严重脓毒症组血清ACTH[ (25.47±9.41) pg/ml]明显高于脓毒症组[(15.52±5.85) pg/ml]和对照组[(9.16±3.02) pg/ml],差异有统计学意义(P＜0.01).结论 脓毒症患儿发病早期机体存在应激反应,血清皮质醇、ACTH浓度明显升高;血清皮质醇、ACTH浓度升高的水平与病情严重程度有关,血清皮质醇、ACTH水平可作为评估患儿严重程度,判断预后的指标.     

呼吸衰竭新生儿肾上腺皮质功能状态分析

目的 研究呼吸衰竭新生儿(新生儿呼吸窘迫综合征、肺炎和重症湿肺)肾上腺皮质功能变化、肾上腺皮质功能不全(AI)的发生率及其与病情的关系.方法 研究对象为人住我院的呼吸衰竭新生儿55例(其中早产儿33例,足月儿22例),分别检测清晨血清基础皮质醇和促肾上腺皮质激素(ACTH)浓度,及小剂量ACTH刺激试验30 min后血清皮质醇峰值.血清皮质醇峰值浓度＜200 μg/L为合并AI.结果 呼吸衰竭早产儿基础皮质醇浓度较足月儿高[(139.2±85.4)μg/L vs(92.1±75.0)μg/L,P=0.040 7],而小剂量ACTH刺激试验前后皮质醇差值及ACTH浓度则较足月儿低[(122.3±56.4)μg/L vs(198.2±77.9)μg/L,P=0.000 1;(5.22±2.40)ng/L vs(8.66±5.41)ng/L.P=0.008 4].呼吸衰竭新生儿合并AJ的发生率为20.0%(11/55),其中早产儿组为21.2%(7/33),足月儿组为18.2%(4/22).需机械通气呼吸衰竭新生儿AI的发生率(29.4%)高于非机械通气新生儿(4.8%).AI新生儿中无死亡病例.结论 呼吸衰竭早产儿肾上腺皮质和垂体功能较足月儿差.呼吸衰竭新生儿合并AJ的发生率较高.需机械通气的呼吸衰竭新生儿AJ的发生率高于机械通气者.未发现AJ与病死率相关.小剂量ACTH刺激试验可较好地评估新生儿肾上腺皮质功能.     

先天性甲状腺功能减低症患儿治疗前后血清ghrelin的动态变化

目的 观察甲状腺素替代治疗对先天性甲状腺功能减低症(CH)患儿血清ghrelin水平的影响.方法 研究对象为2007年10月-2008年3月在徐州医学院附属医院确诊并行治疗随访的CH患儿40例及健康体检儿童30例.分组:未治疗组包括甲状腺功能减低的CH患儿20例;治疗组包括新诊断或随访中经甲状腺素片治疗后甲状腺功能正常至少1个月的CH患儿20例;健康对照组年龄、性别相当的健康儿童30例.采用夹心法酶联免疫吸附试验测定3组儿童血清ghrelin水平,采用化学发光法测定三碘甲状腺原氨酸(T3)、四碘甲状腺原氨酸(T4)、促甲状腺激素刺激激素(TSH)水平,同时计算每个样本的体质量指数(BMI)用于相关分析.结果 1.未治疗组ghrelin水平[(2.35±0.23) μg·L-1]虽高于治疗组[(2.16±0.25) μg·L-1]和健康对照组[(1.96±0.27) μg·L-1],但差异无统计学意义(P=0.102).2.Ghrelin与年龄呈负相关(r=-0.325,P<0.05),但与性别、BMI、T3、T4、TSH无相关关系(Pa>0.05).结论 甲状腺激素对中枢或外周ghrelin的产生和分泌可能无调控作用.在不同生长发育时期,不同水平的ghrelin可能有不同的生理作用.     

促肾上腺皮质激素刺激对脓毒症及脓毒性休克患儿肾上腺功能评估的意义

目的 探讨小剂量(1μg/1.73 m2)促肾上腺皮质激素(ACTH)刺激实验评估儿童脓毒症和脓毒性休克肾上腺功能状态的价值.方法 患儿入院24h内完成基础皮质醇(T0)测定,静脉注射1μg/1.73m2 ACTH,30 min后测定血液皮质醇(T1),根据T0和皮质醇增值(△max=T1-T0)判断肾上腺功能,以△max≤90μg/L为肾上腺功能障碍(AI)指标.结果 62例中,脓毒症53例,脓毒性休克9例,病死率为27.4%(17/62).肾上腺功能障碍(adrenal insufficiency,AI)发生率40.3%(25/62),其中脓毒症和脓毒性休克患儿AI发生率分别是39.6%和44.4%,差异无显著统计学意义(P>0.05).两组脓毒症和脓毒性休克平均T0和T1分别是(318.6±230.4)μg/L、(452.3±230.7)μg/L和(454.7±212.7)μg/L、(579.3±231.9)μg/L,差异无统计学意义(P>0.05).存活组和死亡组患儿T0、T1分别是(320.5±223.9)μg/L、(462.3±212.0)μg/L和(384.3±258.3)μg/L、(500.7±470.6)μg/L,两组AI发生率分别是37.8%和47.1%,差异无统计学意义(P>0.05).T0和T1水平与儿童危重病例评分(PCIS)有关(P<0.05),AI发生率与PCIS、PRISMⅢ和器官功能障碍数目无关(P>0.05).结论 儿童脓毒症和脓毒性休克患儿AI发生率较高.小剂量ACTH刺激实验可以判断严重感染患者肾上腺功能,可为激素治疗提供依据.     

儿童重症疾病时肾上腺的功能

目的　成人危重症及儿童感染性休克时肾上腺功能异常已得到阐述 ,未及时诊断与治疗者预后差。但有关其他儿童重症疾病时肾上腺的功能状态尚无报道。作者前瞻性地研究了危重患儿肾上腺功能异常的发生率。方法　以 13例小儿危重症评分≥ 10分和 (或 )血流动力学不稳定(应用血管活性药和 /或需要 2 0ml/kg液体扩容以保证血压稳定 )的患儿为研究对象。入选第 2天 7∶0 0～ 9∶0 0取血测皮质醇、促肾上腺皮质激素 (为基础值 ) ;静脉注射α 1,2 4 促肾上腺皮质激素 ,1h后再次取血检测上述指标。结果　皮质醇的基础值为 0 1～ 37 4 μg/dl [平均 (12 2± 9 6 ) μg/dl]。肾上腺功能不全的诊断标准为清晨皮质醇 <7μg/dl或注射ACTH后皮质醇 <18μg/dl。 13例中有 4例 (31% )肾上腺功能不全 ,其中皮质醇基础值 <7μg/dl的 3例的ACTH值均处于正常下限。发生与未发生肾上腺功能不全的患儿小儿危重评分 (14 7± 4 11、12 7± 2 6 5 ,P =0 37)与入院诊断无差异。结论　一些危重患儿在严重生理应激反应时不能产生足够的皮质醇 ,但对外源性ACTH反应良好。作者对危重症中下丘脑 垂体 肾上腺轴的作用进行了阐述 ,并认为可根据上述生化指标的异常来判断预后     

呼吸衰竭早产儿肾上腺皮质功能的研究

目的 研究呼吸衰竭早产儿肾上腺皮质功能的变化,肾上腺皮质功能不全的发生率及其与病情和预后的关系.方法 研究对象为住院早产儿43例(研究组33例,对照组10例),分别检测清晨血清基础皮质醇浓度及小剂量促肾上腺皮质激素(ACTH)刺激试验后血清皮质醇峰值.结果 需机械通气的呼吸衰竭早产儿血清基础皮质醇浓度[(114.6 ±76.1)μg/L]和小剂量ACTH刺激试验后血清皮质醇峰值[(232.5±74.6)μg/L]比非机械通气早产儿[(182.1 ±86.8)、(312.1 ±93.8)μg/L]低;呼吸衰竭早产儿合并肾上腺皮质功能不全的发生率较高(21.21%);肾上腺皮质功能不全早产儿中无死亡及慢性肺疾病(CLD)病例.结论 呼吸衰竭早产儿具有较高肾上腺皮质功能不全的发生率;需机械通气的呼吸衰竭早产儿肾上腺皮质的合成分泌功能较差;未发现肾上腺皮质功能不全与病死率和CLD的发生相关     

生长激素运动筛查试验与生长激素激发试验对生长激素缺乏症诊断价值的比较

目的 评价生长激素(GH)运动筛查试验和GH激发试验对儿童生长激素缺乏症的诊断价值.方法 选取200例身材矮小患儿,均符合身材矮小诊断标准,无骨代谢、糖尿病等其他内分泌代谢疾病.对患儿均进行GH运动筛查试验及GH激发试验.GH激发试验包括精氨酸激发试验、左旋多巴激发试验及胰岛素激发试验,本研究中所有患儿在3种GH激发试验中任选2种.2种试验均采用放射免疫法进行检测.结果 身材矮小患儿行GH运动试验和GH激发试验的GH峰值强度分别为(12.78±6.98) μg/L和(14.07±5.89) μg/L,二者GH峰值比较无显著性差异(t=1.87 P>0.05).200例患儿中GH激发试验和运动试验均阳性者29例;运动试验阳性而GH激发试验阴性者5例,运动试验存在2.5%假阳性率.2种试验方法阳性率间比较无统计学差异(χ2=0.47 P>0.05).结论 GH运动筛查试验和GH激发试验得出的结果具有很高的一致性.由于运动试验具有操作简单、安全等优点,应将GH运动筛查试验作为身材矮小患儿的首选筛查试验.     

感染性疾病患儿血浆甘露糖结合凝集素浓度分析

目的 分析常见感染性疾病患儿血浆甘露糖结合凝集素(MBL)的浓度.方法 应用ELISA法检测正常对照组(68例)、正常脐血组(48例)和感染性疾病组(124例)患儿血浆MBL浓度并加以比较.结果 正常脐血组MBL浓度(729.31±259.73)μg/L,明显低于正常对照组(898.34±284.58)μg/L(P=0.001);感染性疾病组支气管肺炎患儿、支气管炎患儿、肠炎患儿MBL浓度(分别为766.45±274.34 μg/L,774.82±273.34 μg/L,526.54±280.83 μg/L)与正常对照组比较均有显著性差异(P值分别为0.032,0.019和0.001).上呼吸道感染患儿MBL浓度(792.89±250.01 μg/L)与正常对照组比较无显著性差异(P=0.125).结论 患儿血浆MBL水平降低可能是儿童在免疫脆弱期易发生呼吸道和消化道感染性疾病的原因之一.     

感染性疾病患儿血浆甘露糖结合凝集素浓度分析

目的 分析常见感染性疾病患儿血浆甘露糖结合凝集素(MBL)的浓度.方法 应用ELISA法检测正常对照组(68例)、正常脐血组(48例)和感染性疾病组(124例)患儿血浆MBL浓度并加以比较.结果 正常脐血组MBL浓度(729.31±259.73)μg/L,明显低于正常对照组(898.34±284.58)μg/L(P=0.001);感染性疾病组支气管肺炎患儿、支气管炎患儿、肠炎患儿MBL浓度(分别为766.45±274.34 μg/L,774.82±273.34 μg/L,526.54±280.83 μg/L)与正常对照组比较均有显著性差异(P值分别为0.032,0.019和0.001).上呼吸道感染患儿MBL浓度(792.89±250.01 μg/L)与正常对照组比较无显著性差异(P=0.125).结论 患儿血浆MBL水平降低可能是儿童在免疫脆弱期易发生呼吸道和消化道感染性疾病的原因之一.     

儿童肥胖代谢综合征血促肾上腺皮质激素及皮质醇变化分析

目的通过观察代谢综合征(MS)患儿血促肾上腺皮质激素(ACTH)、皮质醇(COR)变化及其与MS相关指标的相关性,探讨垂体及肾上腺皮质功能在儿童MS发病机制中的意义。方法选取门诊确诊肥胖儿童263例,根据腰围、血压、血脂及血糖等指标将患儿分为MS组101例及非MS组162例,进行人体参数测量并收集临床基本资料,测定身高、体质量、腰围、血压、血ACTH、COR、空腹血糖(FPG)、空腹胰岛素(FINS)、血脂等指标,计算体质指数(BMI)、胰岛素抵抗指数(HOMA-IR)等,对上述资料进行统计学分析。结果 MS组患儿的体质量、腰围、收缩压、舒张压、血FINS、HOMA-IR、三酰甘油(TG)、ACTH、COR高于非MS组,差异具有统计学意义(P均0.05);MS组患儿血高密度脂蛋白胆固酮(HDL-C)低于非MS组,差异具有统计学意义(P均0.05);MS组患儿血ACTH与腰围、收缩压、舒张压、HOMA-IR和MS组分数(nMSc)呈正相关(P均0.01),血COR与腰围、收缩压、舒张压和nMSc呈正相关(P均0.05),与血HDL-C呈负相关(P0.05)。结论 MS儿童血ACTH及COR增高,血ACTH及COR与腰围、血压、血HDL-C、HOMA-IR和nMSc等相关,下丘脑—垂体—肾上腺皮质功能改变可能是儿童MS的发病机制之一。     

Identification of adrenal insufficiency in pediatric critical illness.

OBJECTIVE: To determine physicians' beliefs and practices regarding adrenal dysfunction in pediatric critical illness. DESIGN: Cross-sectional mail survey. SETTING: Canada. PARTICIPANTS: All members of the Canadian Pediatric Endocrine Group and all physicians identified as practicing pediatric intensive care medicine in any of 16 tertiary care teaching centers in Canada. INTERVENTIONS: Three pediatric intensive care physicians and three pediatric endocrinologists reviewed the questionnaire before administration to ensure clarity. We asked participants to report their views on the following: a) the frequency of adrenal insufficiency in pediatric critical illness; b) diagnosis/definition of adrenal insufficiency in pediatric critical illness; and c) the use of empirical glucocorticoids in fluid/vasopressor-resistant hypotension in pediatric critical illness. MEASUREMENTS AND MAIN RESULTS: Forty-six of 57 (80.7%) endocrinologists responded, with 43 participating (75.4%). Among intensivists, 59 of 70 (84.3%) responded with no refusals. Of intensivists, 81.4% believe that adrenal insufficiency occurs sometimes or often in critically ill pediatric intensive care unit patients, whereas 41.8% of endocrinologists believe adrenal insufficiency occurs never or rarely in these patients. Six definitions of adrenal insufficiency were proposed (varying cortisol level vs. peak/increment of cortisol in response to corticotropin), with no consensus on the definition of adrenal insufficiency from the endocrinologists or intensivists. Half (50.9%) of intensivists said they would sometimes or often empirically treat hypotensive pediatric patients with glucocorticoids, whereas 81.0% of endocrinologists would occasionally or never recommend glucocorticoids on this basis. CONCLUSIONS: There is no consensus among pediatric intensivists or endocrinologists as to how often adrenal insufficiency occurs in pediatric critical illness or how to diagnose this condition. Despite this lack of consensus, however, many pediatric intensivists would empirically treat hypotensive patients who they suspect may have adrenal insufficiency. Prospective studies are required to determine the definition, frequency, and appropriate treatment of adrenal insufficiency in critically ill pediatric patients.     

Adrenal insufficiency in septic shock.

BACKGROUND: Functional adrenal insufficiency has been documented in critically ill adults. OBJECTIVE: To document the incidence of adrenal insufficiency in children with septic shock, and to evaluate its effect on catecholamine requirements, duration of intensive care, and mortality. SETTING: Sixteen-bed paediatric intensive care unit in a university hospital. METHODS: Thirty three children with septic shock were enrolled. Adrenal function was assessed by the maximum cortisol response after synthetic adrenocorticotropin stimulation (short Synacthen test). Insufficiency was defined as a post-Synacthen cortisol increment < 200 nmol/l. RESULTS: Overall mortality was 33%. The incidence of adrenal insufficiency was 52% and children with adrenal insufficiency were significantly older and tended to have higher paediatric risk of mortality scores. They also required higher dose vasopressors for haemodynamic stability. In the survivor group, those with adrenal insufficiency needed a longer period of inotropic support than those with normal function (median, 3 v 2 days), but there was no significant difference in duration of ventilation (median, 4 days for each group) or length of stay (median, 5 v 4 days). Mortality was not significantly greater in children with adrenal insufficiency than in those with adequate adrenal function (6 of 17 v 5 of 16, respectively). CONCLUSION: Adrenal insufficiency is common in children with septic shock. It is associated with an increased vasopressor requirement and duration of shock.     

Duration of adrenal insufficiency during treatment for childhood acute lymphoblastic leukemia

Children with acute lymphoblastic leukemia (ALL) recive high doses of glucocorticosteroid as part of their treatment. This may lead to suppression of the hypothalamic-pituitary-adrenal axis, acute adrenal insufficiency, and ultimately to life-threatening conditions. This study explores the adrenal function in 96 children with ALL treated according to common protocols. After cessation of induction glucocorticosteroid therapy, they received hydrocortisone substitution therapy (10 mg/m/24 h) until an adrenocorticotropic hormone test (250 μg tetracosatide) showed a sufficient adrenal response [plasma (p)-cortisol ≥500 nM]. At the first adrenocorticotropic hormone test, 67% of the patients had adrenal insufficiency. When including these patients in a multivariate model, not adjusting for risk factors, the mean elapsed time between end of induction therapy and adrenal sufficiency was 8.5 months (95% confidence interval: 6.3;10.7). Low 0-minute p-cortisol (P=0.02) and low rise in p-cortisol (P<0.0001) at first test caused a longer time of adrenal insufficiency. In addition, patients with B-cell precursor leukemia reached adrenal sufficiency later than those with T-cell leukemia (P=0.067). As adrenal insufficiency is frequent in children treated for ALL and as they often experience infections and other stressors, the adrenal response should be determined and hydrocortisone substitution therapy should be considered during such episodes in patients with adrenal insufficiency.     

Time course of recovery of adrenal function in children treated for leukemia

OBJECTIVE: Many protocols for treating children with early B-cell lineage acute lymphoblastic leukemia use 28 consecutive days of high-dose glucocorticoids during induction therapy. We prospectively studied the effects of this therapy on adrenal function. STUDY DESIGN: Ten children with early B-cell lineage acute lymphoblastic leukemia were evaluated by cosyntropin (corticotropin (1-24)) stimulation testing before initiation of dexamethasone therapy and every 4 weeks thereafter until adrenal function returned to normal. RESULTS: All 10 patients had normal adrenal function before dexamethasone treatment and insufficient adrenal responses 24 hours after completing therapy. Each child felt ill for 2 to 4 weeks after completing therapy. Although 7 patients recovered normal adrenal function after 4 weeks, 3 patients did not have normal adrenal function until 8 weeks after discontinuing therapy. Statistically significant differences in both basal and corticotropin-stimulated cortisol levels were noted when comparing tests performed at baseline, 24 hours after completing therapy, and 4 weeks after completing therapy. CONCLUSION: High-dose dexamethasone therapy, a standard treatment for early B-cell acute lymphoblastic leukemia, can cause adrenal insufficiency lasting more than 4 weeks after cessation of treatment. This problem might be avoided by tapering doses of glucocorticoids and providing supplemental glucocorticoids during periods of increased stress.     

Adrenal insufficiency after glucocorticoid withdrawal in children with rheumatic diseases

Aim: Glucocorticoids (GCs) are often used for the treatment of rheumatic disorders. However, doses are prescribed, which may suppress the hypothalamic–pituitary–adrenal (HPA) axis. After GC withdrawal, recovery of the HPA axis may be delayed putting the patient at risk for adrenal insufficiency. We assessed adrenal function and factors influencing adrenal responsiveness after termination of GC therapy in paediatric patients with rheumatic diseases. Methods: Nineteen patients aged 2–15 years were followed clinically, and adrenal function was tested by low‐dose adrenocorticotropic hormone test 1 month after GC withdrawal. In case of adrenal insufficiency by test, re‐assessment was performed after 6 and 18 months. Results: No signs or symptoms of adrenal insufficiency occurred in any of the patients during and after GC withdrawal. Biochemical examination revealed adrenal insufficiency in 32% (6/19) at 4 weeks and in 11% (2/19) at 20 months after GC withdrawal. Conclusions: In conclusion, current strategies to withdraw GC from paediatric patients with rheumatic diseases are safe. Routine adrenal function testing after GC therapy and withdrawal may not be needed considering the low risk but high number of patients treated with GCs. Nevertheless, awareness of the potential risk and information of patients and their caregivers are crucial to avoid adrenal crisis.     

Hypothalamic‐pituitary‐adrenal axis suppression in asthmatic children on inhaled corticosteroids: Part 1. Which test should be used?

The effect of inhaled corticosteroids (ICS) on the hypothalamic-pituitary-adrenal axis (HPA) has been regarded as a 'benign physiological response'. A recent survey suggests that adrenal crisis might be more common in asthmatic children on ICS than previously thought. The clinical features of adrenal insufficiency are non-specific and can easily be missed. Accurate biochemical assessment of the axis is therefore mandatory. A review of the literature determined that all basal adrenal function tests, including plasma cortisol profiles, cannot identify which children can respond to stress. There is no evidence to suggests that the degree of the physiological adjustment of the HPA to ICS predicts clinically significant HPA suppression. Only gold standard adrenal function tests can assess the integrity of the whole axis. Of the two available tests, the correctly performed overnight metyrapone test (with ACTH levels) is safe and better by far. The use of cortisol profiles should only be used to demonstrate differences in systemic activity of various ICS and delivery devices. Regulatory bodies should insist on trials that evaluate the HPA with a gold standard adrenal function test before it is declared safe and allowed to be marketed. A re-analysis of studies that have utilized gold standard adrenal function tests only might identify the lowest safe dose and duration of ICS.     

Monitoring growth in asthmatic children treated with high dose inhaled glucocorticoids does not predict adrenal suppression

Aims: To determine whether routine outpatient monitoring of growth predicts adrenal suppression in prepubertal children treated with high dose inhaled glucocorticoid. Methods: Observational study of 35 prepubertal children (aged 4–10 years) treated with at least 1000 µg/day of inhaled budesonide or equivalent potency glucocorticoid for at least six months. Main outcome measures were: changes in HtSDS over 6 and 12 month periods preceding adrenal function testing, and increment and peak cortisol after stimulation by low dose tetracosactrin test. Adrenal suppression was defined as a peak cortisol ⩽500 nmol/l. Results: The areas under the receiver operator characteristic curves for a decrease in HtSDS as a predictor of adrenal insufficiency 6 and 12 months prior to adrenal testing were 0.50 (SE 0.10) and 0.59 (SE 0.10). Prediction values of an HtSDS change of –0.5 for adrenal insufficiency at 12 months prior to testing were: sensitivity 13%, specificity 95%, and positive likelihood ratio of 2.4. Peak cortisol reached correlated poorly with change in HtSDS (ρ = 0.23, p = 0.19 at 6 months; ρ = 0.33, p = 0.06 at 12 months). Conclusions: Monitoring growth does not enable prediction of which children treated with high dose inhaled glucocorticoids are at risk of potentially serious adrenal suppression. Both growth and adrenal function should be monitored in patients on high dose inhaled glucocorticoids. Further research is required to determine the optimal frequency of monitoring adrenal function.     

Adrenal axis function after high-dose steroid therapy for childhood acute lymphoblastic leukemia

Background A 4‐week course of high‐dose glucocorticoids may cause prolonged adrenal suppression even after a 9‐day tapering phase. In this study, adrenal function and signs and symptoms of adrenal insufficiency were prospectively assessed in children with acute lymphoblastic leukemia (ALL) after induction treatment including high‐dose prednisone (PDN) or dexamethasone (DXM). Procedures Sixty‐four children with ALL, treated according to the AIEOP ALL 2000 Study protocol, underwent low dose ACTH (LD‐ACTH) stimulation 24 hr after the last tapered steroid dose. In those with impaired cortisol response, additional LD ACTH tests were performed every 1–2 weeks until cortisol levels normalized. Signs and symptoms of adrenal insufficiency were recorded during the observation period. Results All patients had normal basal cortisol values at diagnosis. Twenty‐four hours after last glucocorticoid dose, morning cortisol was reduced in 40/64 (62.5%) patients. LD‐ACTH testing showed adrenal suppression in 52/64 (81.5%) patients. At the following ACTH test 7–14 days later, morning cortisol values were reduced in 8/52 (15.4%) patients and response to the test was impaired in 12/52 (23%). Adrenal function completely recovered in all patients within 10 weeks. No difference was found between patients treated with PDN or DXM. Almost 35% of children with impaired cortisol values at the first test developed signs or symptoms of adrenal insufficiency. One child developed a severe adrenal crisis during adrenal suppression. Conclusions High‐dose glucocorticoid therapy in ALL children may cause prolonged adrenal suppression and related clinical symptoms. Laboratory monitoring of cortisol levels and steroid coverage during stress episodes may be indicated. Pediatr Blood Cancer 2008;50:537–541. © 2007 Wiley‐Liss, Inc.