Maternal sensitivity and infant autonomic and endocrine stress responses

Background

Early environmental exposures may help shape the development of the autonomic nervous system (ANS) and hypothalamic–pituitary–adrenal (HPA) axis, influencing vulnerability for health problems across the lifespan. Little is known about the role of maternal sensitivity in influencing the development of the ANS in early life.

Aims

To examine associations among maternal sensitivity and infant behavioral distress and ANS and HPA axis reactivity to the Repeated Still-Face Paradigm (SFP-R), a dyadic stress task.

Study design

Observational repeated measures study.

Subjects

Thirty-five urban, sociodemographically diverse mothers and their 6-month-old infants.

Outcome measures

Changes in infant affective distress, heart rate, respiratory sinus arrhythmia (RSA), and T-wave amplitude (TWA) across episodes of the SFP-R were assessed. A measure of cortisol output (area under the curve) in the hour following cessation of the SFP-R was also obtained.

Results

Greater maternal insensitivity was associated with greater infant sympathetic activation (TWA) during periods of stress and tended to be associated with greater cortisol output following the SFP-R. There was also evidence for greater affective distress and less parasympathetic activation (RSA) during the SFP-R among infants of predominantly insensitive mothers.

Conclusions

Caregiving quality in early life may influence the responsiveness of the sympathetic and parasympathetic branches of the ANS as well as the HPA axis. Consideration of the ANS and HPA axis systems together provides a fuller representation of adaptive versus maladaptive stress responses. The findings highlight the importance of supporting high quality caregiving in the early years of life, which is likely to promote later health.     

Adrenal exhaustion in septic patients with vasopressor dependency

Purpose

The use of low-dose corticosteroids for patients with septic shock who remain vasopressor dependent after adequate fluid resuscitation is recommended, but there is lack of agreement on how to diagnose relative adrenal insufficiency (RAI) and when to start steroid supplementation among these patients. This case series reports changes in cortisol concentrations during the course of vasopressor-dependent septic shock.

Methods

Observational study was performed at a university hospital medical intensive care unit. Consecutive adult patients with vasopressor-dependent septic shock admitted to the medical intensive care unit were studied. Clinical data, cortisol concentrations, and dose of vasopressor agents at different times during the course of septic shock were recorded and reported as mean ± SD.

Results

Thirteen patients were included. Mean age was 59 ± 15 years. Mean basal nonstimulated cortisol level was 41.7 ± 30.9 μg/dL (within 24 hours of intensive care unit admission in all but 2 patients). Steroids were initiated in 8 patients and then discontinued after cortisol values were obtained and RAI was ruled out. Because of inability to discontinue vasopressor support, cortisol testing was repeated after 6.2 ± 4.8 days of initial assessment. Repeated concentrations were 10.0 ± 6.3 μg/dL (P < .001). Steroids were then reinitiated, and resolution of vasopressor dependence was achieved 1.5 ± 1.4 days later.

Conclusions

Adrenal function in the critically ill is a dynamic process, and an appropriate initial adrenal response does not preclude later development of RAI.     

腹腔镜在治疗肾及肾上腺囊肿中的临床应用

目的 :探讨应用腹腔镜治疗肾及肾上腺囊肿的有效性。方法 :选择 12例直径 >5cm的肾囊肿 ,3例直径 >4 8cm的肾上腺囊肿 ,应用腹腔镜经腹腔途径切除治疗。结果 :15例肾及肾上腺囊肿均一次切除 ,手术时间肾囊肿组平均 70min ,肾上腺囊肿组平均 90min。术后平均住院 5 2d ,均治愈出院 ,平均随访 12 4个月 ,均无复发。结论 :腹腔镜治疗肾及肾上腺囊肿 ,损伤小、恢复快、疗效好 ,治疗彻底 ,临床可广泛应用     

A randomized and controlled study comparing immunoadsorption and plasma exchange in myasthenic crisis

Myasthenic crisis is the most serious life-threatening event in Myasthenia gravis patients, affecting up to 27% within the first two years after onset of disease. Extracorporeal removal of circulating autoantibodies against the nicotinic acetylcholine receptor (AChRAb) by methods of therapeutic apheresis, e.g. plasma exchange (PE) and immunoadsorption (IA) had been demonstrated as effective treatment especially in acute situations of myasthenic crisis. However, controlled data comparing clinical safety and efficacy of both methods in a clinical study were not available. Here the results of a prospective randomized controlled clinical trial are presented, investigating 19 patients with myasthenic crisis, who were randomized to receive either PE (n = 10) or IA (n = 9) in addition to combined drug treatment. Patients received 3 to 5 (mean 3.5 for PE, and 3.4 for IA) treatments over a period of 7 days with a predefined treatment volume of 1.5 l plasma (i.e., 20-25 ml/kg plasma representing 0.5-0.6 patients' plasma volumes). Clinical courses were monitored using disease specific clinical scores. After initiation of IA or PE the mean value of Myasthenia scores decreased equally until Day 14 of the post-treatment phase. Patients from both treatment groups improved to a stable clinical status of Oosterhuis Classes 1 and 2. Substantial reduction of AChRAb was documented after each session of PE or IA. In the treatment period 16 adverse effects (seven serious adverse events, SAE) in the PE and 10 (1 SAE) in the IA group were observed. In conclusion, IA proved to be equally effective compared with PE treatment in patients with myasthenic crisis. Three to five treatment sessions using low plasma volume dosage of 20-25 ml/kg were adequate to improve clinically relevant symptoms significantly in most patients.     

单孔腹腔镜技术在肾上腺肿瘤切除术中的应用

目的探讨单孔腹腔镜(LESS)在肾上腺肿瘤切除术的优势与可行性。方法比较25例单孔腹腔镜组与50例传统腹腔镜组在肾上腺肿瘤切除术患者的术后切口长度、皮下气肿的发生率、视觉模拟疼痛评分(VAPS)、手术时间及术中出血量等方面有无差异。结果所有手术均获成功,在肾上腺肿瘤切除术中,单孔腹腔镜组在术后切口长度、皮下气肿发生率及VAPS等方面与传统腹腔镜组相比有统计学意义(P<0.05),其他指标差异均无显著性(P>0.05)。结论 LESS在肾上腺肿瘤切除术的临床应用上是可行的,而且其在刀口的美观上、减少术后皮下气肿和缓解疼痛等方面效果明显优越于传统腹腔镜手术。     

Cortisol-dependent stress effects on cell distribution in healthy individuals and individuals suffering from chronic adrenal insufficiency

Chronic adrenal insufficiency (CAI) is characterized by a lack of glucocorticoid and mineralocorticoid production due to destroyed adrenal cortex cells. However, elevated cortisol secretion is thought to be a central part in a well-orchestrated immune response to stress. This raises the question to what extent lack of cortisol in CAI affects stress-related changes in immune processes.To address this question, 28 CAI patients (20 females) and 18 healthy individuals (11 females) (age: 44.3 ± 8.4 years) were exposed to a psychosocial stress test (Trier Social Stress Test: TSST). Half the patients received a 0.03 mg/kg body weight injection of hydrocortisone (HC) post-TSST to mimic a healthy cortisol stress response. Catecholamines and immune cell composition were assessed in peripheral blood and free cortisol measured in saliva collected before and repeatedly after TSST.CAI patients showed norepinephrine (NE) stress responses similar to healthy participants, however, epinephrine (E) as well as cortisol levels were significantly lower. HC treatment post-TSST resulted in cortisol increases comparable to those observed in healthy participants (interaction effects – NE: F = 1.05, p = .41; E: F = 2.56, p = .045; cortisol: F = 13.28, p < .001). Healthy individuals showed the expected pattern of stress-related early lymphocyte increase with subsequent decrease below baseline. The opposite pattern was observed in granulocytes. While exhibiting a similar initial increase, lymphocytes kept increasing over the following 2 h in untreated patients. HC treatment buffered this effect (interaction effects – lymphocyte%: F = 7.31, p < .001; granulocyte%: F = 7.71, p < .001).Using CAI in humans as a model confirms cortisol’s central involvement in post-stress lymphocyte migration from blood into immune-relevant body compartments. As such, future studies should investigate whether psychosocial stress exposure may put CAI patients at an increased health risk due to attenuated immune responses to pathogens.     

Big Events in Greece and HIV Infection Among People Who Inject Drugs

Big Events are processes like macroeconomic transitions that have lowered social well-being in various settings in the past. Greece has been hit by the global crisis and experienced an HIV outbreak among people who inject drugs. Since the crisis began (2008), Greece has seen population displacement, inter-communal violence, cuts in governmental expenditures, and social movements. These may have affected normative regulation, networks, and behaviors. However, most pathways to risk remain unknown or unmeasured. We use what is known and unknown about the Greek HIV outbreak to suggest modifications in Big Events models and the need for additional research.     

Mechanism of adrenocortical toxicity induced by quinocetone and its bidesoxy-quinocetone metabolite in porcine adrenocortical cells in vitro

Quinocetone (QCT) is a new feeding antibacterial agent in the QdNOs family. The mechanism of its adrenal toxicity is far from clear. This study was conducted to estimate the adrenal cell damage induced by QCT and its bidesoxy-quinocetone (B-QCT) metabolite and to further investigate their mechanisms. Following doses of QCT increasing from 5 to 50 μM, cell apoptosis and necrosis, mitochondrial dysfunction and redox imbalance were observed in porcine adrenocortical cells. The mRNA levels of the six components of intermediary enzymes and the adrenal renin-angiotensin-aldosterone system (RAAS) displayed a dysregulation induced by QCT, indicating that QCT might influence aldosterone secretion not only through the upstream of the production but also through the downstream of the adrenal RAAS pathway. In contrast, B-QCT had few toxic effects on the cell apoptosis, mitochondrial dysfunction and redox imbalance. Moreover, LCMS-IT-TOF analysis showed that no desoxy metabolites of QCT were found in either cell lysate or supernatant samples. In conclusion, we reported on the cytotoxicity in porcine adrenocortical cells exposed to QCT via oxidative stress, which raised awareness that its toxic effects resulted from N→O groups, and its toxic mechanism might involve the interference of the steroid hormone biosynthesis pathway.