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Abstract Inhaled corticosteroids (ICS) are commonly used for airway disease, but concerns about adrenal insufficiency (AI) have arisen. This retrospective observational study investigated the link between ICS use and AI risk using data from the National Health Insurance Service-National Sample Cohort, analyzing 66,631 patients with COPD (Korean Standard Classification of Diseases [KCD] codes J42-J44) or asthma (KCD codes J45-J46). ICS use, daily dosage, and AI cases (hospitalization or ≥ 2 outpatient visits with KCD code E27) were identified via diagnostic codes. Cox proportional hazard survival analysis and inverse probability of treatment weighting (IPTW) addressed baseline differences between ICS and non-ICS users. In total 66,631 patients, the mean age was 57.3 years, 42.6% were male, and 42.2% had a Charlson comorbidity index (CCI) of 2 or higher. Among the patients, 15.5% used ICS, with a mean daily dose of 404.2 µg/day. The incidence of AI was higher in ICS users (1.69 per 1000) than in non-users (0.54 per 1000). ICS use independently increased AI risk (HR: 3.06, 95% CI: 1.82–5.14, p

Abstract Background Adverse events of secondary adrenal insufficiency caused by anti-PD-1 immune agents are relatively rare in clinical practice, so in this article, we retrospectively analyzed three patients who suffered secondary adrenal cortex dysfunction caused by tislelizumab immunotherapy for Non-Small Cell Lung Cancer (NSCLC)and reviewed the literature. This rare immune-related adverse event was investigated by summarizing the clinical features of the patients. Case presentation We reported three NSCLC patients who suffered secondary adrenal cortex dysfunction induced by tislelizumab immunotherapy at our hospital from July 2021 to October 2023. We analyzed and summarized the clinical characteristic, laboratory examination, pathological staging, etc. We also reviewed related literature of pituitary inflammation and adrenal cortex dysfunction caused by immunotherapy. Results The median age of the three patients was 56 years. All the patients had a history of smoking. After receiving tislelizumab treatment (median cycle: 7), laboratory examination showed a decrease in morning cortisol and adrenocorticotropic hormone (ACTH), both were diagnosed with secondary adrenal insufficiency. Only one patient had symptoms of fatigue, vomiting, and weight loss. One of these patients also had simultaneous subclinical hypothyroidism. All three patients discontinued immunotherapy and received replacement therapy with glucocorticoids. At the last follow-up, none of the three patients restarted immunotherapy, because cortisol did not return to normal. This is similar to that of previous reports. Conclusion Based on previous reports and our three cases, when laboratory tests of NSCLC patients receiving immunotherapy showed a decrease in morning cortisol and ACTH levels, especially when clinical symptoms were obvious, the possibility of immunotherapy-related pituitary inflammation causing secondary adrenal cortex dysfunction should be considered. Prompt monitoring and hormone replacement therapy should be provided to prevent adrenal crises.

BACKGROUND. Cancer is the leading cause of death in the world. Chemotherapy is the most effective and in some cases the only method of treating oncopathology. At the same time, chemotherapy can lead to a number of side effects, among which endocrine disorders are noted. OBJECTIVE. To investigate possible diseases of the endocrine system that develop during chemotherapy. MATERIALS AND METHODS. A review of literary sources. RESULTS AND DISCUSSION. In general, the statistics on the development of endocrine diseases during chemotherapy is limited and requires additional research to obtain a more accurate picture. Nevertheless, based on the data of the studied literature, it can be assumed that some of the patients who received chemotherapy developed the following endocrine disorders: hypothyroidism, Hashimoto’s thyroiditis, adrenal dysfunction (hyper- and hypocorticism), hypergonadotropic hypogonadism, diabetes mellitus. CONCLUSIONS. Endocrine diseases that develop as a result of chemotherapy can significantly worsen the patient’s quality of life, and given the fact that chemotherapy is vital and in some cases the only treatment for oncopathology, doctors should timely monitor carbohydrate metabolism, thyroid function and other markers of endocrine diseases. No less important are preventive measures, including rational nutrition and physical activity, the intensity of exercises and movements for wellbeing.

Bacterial sepsis is a serious threat to the body homeostasis and is often associated with high mortality in non-coronary intensive stations. In order to survive sepsis, rapid activation of the hypothalamus-pituitary-adrenal gland axis and sympathomedullary system is necessary. In many patients with sepsis, the function of those two arms of the stress system is dysregulated with underlying mechanisms remaining unknown. In our previous experimental studies, we have demonstrated that LPS-induced systemic inflammation and CLP-induced peritonitis can result in adrenal gland damage. Histological and transcriptomic analysis revealed a potential involvement of the adrenal microvascular endothelium in this process. However, our knowledge about the function of adrenal microvascular cells during sepsis is scarce. In the present study, we have characterized transcriptomic alterations in isolated mouse adrenal microvascular endothelial cells induced by systemic administration of bacterial LPS. Our results revealed that LPS induced a distinct transcriptomic profile in the adrenal microvascular cells, including multiple genes regulating inflammation, activation of the coagulation cascade and vascular permeability. Activation of those genes may be potentially involved in the damage to the microvascular endothelium and altogether contribute to the sepsis-mediated adrenal dysregulation.

Latent varicella zoster virus (VZV) has been detected in human adrenal glands, raising the possibility of virus-induced adrenal damage and dysfunction during primary infection or reactivation. Rare cases of bilateral adrenal hemorrhage and insufficiency associated with VZV reactivation have been reported. Since there is no animal model for VZV infection of adrenal glands, we obtained adrenal glands from two non-human primates (NHPs) that spontaneously developed varicella from primary simian varicella virus (SVV) infection, the NHP VZV homolog. Histological and immunohistochemical analysis revealed SVV antigen and DNA in the adrenal medulla and cortex of both animals. Adrenal glands were observed to have Cowdry A inclusion bodies, cellular necrosis, multiple areas of hemorrhage, and varying amounts of polymorphonuclear cells. No specific association of SVV antigen with βIII-tubulin-positive nerve fibers was found. Overall, we found that SVV can productively infect NHP adrenal glands, and is associated with inflammation, hemorrhage, and cell death. These findings suggest that further studies are warranted to examine the contribution of VZV infection to human adrenal disease. This study also suggests that VZV infection may present itself as acute adrenal dysfunction with “long-hauler” symptoms of fatigue, weakness, myalgias/arthralgias, and hypotension.

Survival of all living organisms depends on maintenance of a steady state of homeostasis, which process relies on its ability to react and adapt to various physical and emotional threats. The defense against stress is executed by the hypothalamic-pituitary-adrenal axis and the sympathetic-adrenal medullary system. Adrenal gland is a major effector organ of stress system. During stress adrenal gland rapidly respond with increased secretion of glucocorticoids and catecholamines into circulation, which hormones, in turn, affect metabolism, to provide acutely energy, vasculature to increase blood pressure and the immune system to prevent it from extensive activation. Sepsis resulting from microbial infections is a sustained and extreme example of stress situation. In many critical ill patients levels of both corticotropin-releasing hormone and adrenocorticotropin, two major regulators of adrenal hormone production, are suppressed. Levels of glucocorticoids however, remain normal or are elevated in these patients, suggesting a shift from central to local intraadrenal regulation of adrenal stress response. Among many mechanisms potentially involved in this process, reduced glucocorticoid metabolism and local intraadrenal activation of hormone production mediated by adrenocortical and chromaffin cell interactions, the adrenal vascular system and the immune-adrenal crosstalk play a key role. Consequently, any impairment in function of these systems, can ultimately affect adrenal stress response. The purpose of this mini review is to present and discuss recent advances in our understanding of the adrenal gland microenvironment, and its role in regulation of stress-induced hormone secretion.