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Purpose: Cancer can be a source of significant psychological and physical stress. Prolonged stressful stimuli can influence the stress response, mediated by the hypothalamic–pituitary–adrenal (HPA) axis. However, there is limited literature investigating HPA axis function in patients with cancer. Methods: A systematic literature review of case–control studies was conducted comparing individuals with and without cancer examining the HPA axis function. Databases (MEDLINE, PubMed, Scopus) were searched from inception to May 2023. Results: Seventeen studies met eligibility criteria: nine unstimulated‐cortisol studies and eight reporting the effect of HPA stimulation or suppression. Sixteen studies reported altered levels of HPA function in cancer patients relative to controls, including 13 reporting increased baseline or hyperactive cortisol responses, and four—decreased baseline cortisol or blunted cortisol responses, two of which had patient groups with now known cortisol‐suppressing treatments. HPA dysfunction was observed in patients of both sexes, diverse ages, stages of cancer and cancer treatments. Six papers reported on clinical outcomes with cases experiencing higher levels of fatigue, stress, poor memory, poor well‐being and disturbed sleep. There was significant heterogeneity in methodologies across the studies. Conclusion: HPA dysfunction was common in patients with cancer relative to cancer‐free controls. The majority of studies in cancer reported an increased baseline cortisol and increased response to HPA stimulation. There is a need for well‐powered studies using standardised methodology examining the mechanisms of HPA dysregulation and their health outcomes, to enable the development of appropriate tools for the diagnosis and management of HPA dysfunction in cancer. This systematic review of 17 studies comparing HPA axis function in individuals with cancer as compared to controls suggests that HPA dysregulation is common in people with cancer. There was significant variability in methodologies used to measure HPA dysregulation, which limits the interpretation of findings, and few only studies examined the impact of HPA dysregulation on patient outcomes. There is a need for studies that use a standardised approach to HPA axis measurement and examine patient outcomes to determine its clinical impact. [ABSTRACT FROM AUTHOR]

Objective: To investigate glycemic and psychosocial outcomes with hybrid closed-loop (HCL) versus user-determined insulin dosing with multiple daily injections (MDI) or insulin pump (i.e., standard therapy for most adults with type 1 diabetes).Research Design and Methods: Adults with type 1 diabetes using MDI or insulin pump without continuous glucose monitoring (CGM) were randomized to 26 weeks of HCL (Medtronic 670G) or continuation of current therapy. The primary outcome was masked CGM time in range (TIR; 70-180 mg/dL) during the final 3 weeks.Results: Participants were randomized to HCL (n = 61) or control (n = 59). Baseline mean (SD) age was 44.2 (11.7) years, HbA1c was 7.4% (0.9%) (57 [10] mmol/mol), 53% were women, and 51% used MDI. HCL TIR increased from (baseline) 55% (13%) to (26 weeks) 70% (10%) with the control group unchanged: (baseline) 55% (12%) and (26 weeks) 55% (13%) (difference 15% [95% CI 11, 19]; P < 0.0001). For HCL, HbA1c was lower (median [95% CI] difference -0.4% [-0.6, -0.2]; -4 mmol/mol [-7, -2]; P < 0.0001) and diabetes-specific positive well-being was higher (difference 1.2 [95% CI 0.4, 1.9]; P < 0.0048) without a deterioration in diabetes distress, perceived sleep quality, or cognition. Seventeen (9 device-related) versus 13 serious adverse events occurred in the HCL and control groups, respectively.Conclusions: In adults with type 1 diabetes, 26 weeks of HCL improved TIR, HbA1c, and their sense of satisfaction from managing their diabetes compared with those continuing with user-determined insulin dosing and self-monitoring of blood glucose. For most people living with type 1 diabetes globally, this trial demonstrates that HCL is feasible, acceptable, and advantageous. [ABSTRACT FROM AUTHOR]

Vitamin D deficiency is associated with increased arterial stiffness. However, the mechanisms underlying this association have not been clarified. The aim was to investigate whether changes in autonomic nervous system activity could underlie an association between 25 hydroxy vitamin D and arterial stiffness. A total of 49 subjects (age = 60 ± 8 years, body mass index = 26.7 ± 4.6 kg/m², 25 hydroxy vitamin D = 69 ± 22 nmol/L) underwent measurements of pulse wave velocity (PWV) and augmentation index (AIx), spontaneous baroreflex sensitivity, plasma metanephrines and 25 hydroxy vitamin D. Subjects with 25 hydroxy vitamin D ± 50 nmol/L were restudied after 200,000 International Units 25 hydroxy vitamin D. Plasma metanephrine was positively associated with AIx (p = 0.02) independent of age, sex, smoking and cholesterol and negatively associated with 25 hydroxy vitamin D (p = 0.002) independent of age, sex and season. In contrast, there was no association between baroreflex sensitivity and 25 hydroxy vitamin D (p = 0.54). Treatment with vitamin D increased 25 hydroxy vitamin D from 43 ± 5 to 96 ± 24 nmol/L (p < 0.0001) but there was no significant change in plasma metanephrine (115 ± 25 vs. 99 ± 39 pmol/L, p = 0.12). We conclude that as plasma metanephrine was negatively associated with 25 hydroxy vitamin D and positively with AIx, it could mediate an association between these two variables. This hypothesis should be tested in larger interventional studies. [ABSTRACT FROM AUTHOR]

Summary: We describe and characterise the case of a 26-year-old female undergoing surgery for a right-sided sinonasal alveolar rhabdomyosarcoma who developed profound, transient arginine vasopressin deficiency (AVP-D, formerly central diabetes insipidus (DI)) associated with anaesthesia. In this case report, we characterise the development of AVP-D with serial copeptin and paired urine and serum osmolality measurements. Based on the anaesthetic agent's profile and the literature, we attribute this presentation to propofol exposure. We present a description of the literature on anaesthesia-associated DI as well as poignant learning points., Learning Points: Exposure to anaesthetic agents is a rare cause of self-limited but sudden and profound arginine vasopressin deficiency (AVP-D) or arginine vasopressin resistance (AVP-R). Sevoflurane has been associated with AVP-R and propofol with AVP-D, although the responsible agent may be difficult to identify. Differentiation of AVP-R and AVP-D can be made based on copeptin concentration, where available, or clinical response to desmopressin. Whilst the patient is anaesthetised, intravenous fluid replacement should be targeted to match urine output until the patient is able to drink to thirst. This should be clearly communicated to staff and the patient. Rapid resolution of AVP-R/AVP-D when the causative agent is discontinued has been reported with both propofol and sevoflurane. As such, switching the agent used to maintain anaesthesia may terminate increased urine output in a clinically meaningful timeframe.

Background: Patient-initiated action plans are an important component of COPD self-management (SM) interventions. When integrated into SM interventions, these action plans have proven to be effective in reducing exacerbation severity, hospitalisations, and costs and in improving health status in patients with COPD without severe comorbidities. Because of overlap in symptoms, a self-treatment (ST) approach that focuses solely on traditional symptoms of COPD is inadequate for patients with COPD and comorbidities. The COPE-III SM intervention combines (I) patient-initiated action plans that are tailored to the individual's co-morbid disease(s), and (II) ongoing nurse support. In this paper we provide information regarding the integration of information from two previous COPD SM studies (COPE I and II) in the development of the current COPE-III ST approach., Materials and Methods: COPE-III ST materials include daily symptom diaries and action plans that take patient's common comorbidities [chronic heart failure (CHF), anxiety, depression, ischaemic heart disease (IHD), and diabetes] into account. The comorbid diary and action plans components were developed in collaboration with multiple disease-experts., Results: Previous SM studies have highlighted some essential topics that need to be considered when developing a SM or ST approach: 'when to initiate ST', 'how to optimize materials and safety', and 'how to achieve behavioural change'. In the COPE-III study, ST is initiated after a significant change in symptoms. This is consistent with the COPE-II approach and was implemented because disease symptoms are often present even when patients are stable. We have tried to ensure patient safety by providing an easily accessible case-manager to patients throughout their involvement in the study. Furthermore, a psychologist has ensured the use of behavioural change techniques throughout the intervention., Conclusions: We should continue to learn from our experiences with SM interventions to further optimize future SM and ST interventions. The use of materials that are suitable for different levels of patient literacy and the training of health care providers are other points of improvement.

How protein metabolism is perturbed during chronic glucocorticoid excess is poorly understood. The aims were to investigate the impact of chronic glucocorticoid excess and restoration of eucortisolemia in Cushing's syndrome (CS) on whole body protein metabolism. Eighteen subjects with CS and 18 normal subjects (NS) underwent assessment of body composition using DEXA and whole body protein turnover with a 3-h constant infusion of l-[(13)C]leucine, allowing calculation of rates of leucine appearance (leucine R(a)), leucine oxidation (L(ox)), and leucine incorporation into protein (LIP). Ten subjects with CS were restudied after restoration of eucortisolemia. Percentage FM was greater (43.9 +/- 1.6 vs. 33.8 +/- 2.4%, P = 0.002) and LBM lower (52.7 +/- 1.6 vs. 62.1 +/- 2.3%, P = 0.002) in CS. LBM was significantly correlated (r(2) > 0.44, P < 0.005) to leuceine R(a), L(ox), and LIP in both groups. After correcting for LBM, leucine R(a) (133 +/- 5 vs. 116 +/- 5 micromol/min, P = 0.02) and L(ox) (29 +/- 1 vs. 24 +/- 1 micromol/min, P = 0.01) were greater in CS. FM significantly correlated (r(2) = 0.23, P < 0.05) with leucine R(a) and LIP, but not L(ox) in CS. In multiple regression, LBM was an independent determinant of all three indexes of leucine turnover, FM of leucine R(a), and LIP and CS of L(ox). Following restoration of eucortisolemia, L(ox) was reduced (Delta-7.5 +/- 2.6 micromol/min, P = 0.02) and LIP increased (Delta+15.2 +/- 6.2 micromol/min, P = 0.04). In summary, whole body protein metabolism in CS is influenced by changes in body composition and glucocorticoid excess per se, which increases protein oxidation. Enhanced protein oxidation is a likely explanation for the reduced protein mass in CS. Successful treatment of CS reduces protein oxidation and increases protein synthesis to prevent ongoing protein loss.