Passive heat treatment has been suggested to improve glycemic control in individuals with type 2 diabetes mellitus (T2DM). Previous studies have focused predominantly on hot water immersion and traditional sauna bathing, as opposed to the more novel method of infrared-based sauna bathing. Here, the impact of a single infrared sauna session on post-prandial glycemic control was assessed in older individuals with T2DM.

Diabetes mellitus (DM) is one of the fastest growing diseases in terms of incidence worldwide and seriously affects cognitive function. The incidence rate of cognitive dysfunction is up to 13% in diabetes patients aged 65-74 and reaches 24% in those aged >75 years. The mechanisms and treatments of cognitive dysfunction associated with diabetes mellitus are complicated and varied. According to previous studies, hyperglycaemia mainly contributes to cognitive dysfunction through mechanisms involving inflammation, autophagy, the microbial-gut-brain axis, brain-derived neurotrophic factors and insulin resistance. Antidiabetic drugs such as metformin, liraglutide and empagliflozin and other drugs such as fingolimod and melatonin can alleviate cognitive dysfunction caused by diabetes. Self-management, indirect fasting and repetitive transverse magnetic stimulation can also ameliorate cognitive impairment. In this review, we discuss the mechanisms linking diabetes mellitus with cognitive dysfunction and propose a potential treatment for cognitive dysfunction related to diabetes mellitus.

To evaluate the accuracy of thyroid imaging reporting and data system (ACR-TIRADS) and the Bethesda system for reporting cytopathology (TBSRCP) classifications for identifying or ruling out thyroid malignancy in relation to the gold standard (post-surgical pathology).

Ocular motor mononeuropathies affect cranial nerves III, IV and VI and are more frequent in diabetes mellitus, with oculomotor nerve involvement being predominant. The aim of this narrative brief review was to discuss the clinical manifestations, diagnosis and management of ocular motor nerve palsies in subjects with diabetes. Clinical manifestations often include ptosis, diplopia, and periorbital pain. A characteristic of third nerve palsy is pupillary sparing. Differential diagnosis may be challenging due to overlapping symptoms with nerve palsies of other aetiologies. Treatment includes optimised glycaemic control and management of vascular risk factors. Neuroprotective agents, mainly alpha-lipoic acid and botulinum toxin A have been occasionally used, as well. Spontaneous recovery is also seen in many cases.

Hypothyroidism is a common side effect of radiotherapy for nasopharyngeal carcinoma. However, the impact of thyroid hormone replacement therapy on patients with radiation-induced subclinical hypothyroidism has not been extensively explored. This study aimed to analyze the efficacy of thyroid hormone replacement therapy in nasopharyngeal carcinoma patients with subclinical hypothyroidism.

Endogenous hypercortisolism presents with variable phenotypes. Etiological factors accounting for the level of hypercortisolism or varying severity of associated comorbidities are lacking. Recently, the adrenal ATP-binding cassette B1 (ABCB1) gene was identified as a modulator of glucocorticoid secretion.

Despite the high sensitivity of neonatal screening in detecting the classical form of congenital adrenal hyperplasia due to 21-hydroxylase deficiency, one of the unclear issues is identifying asymptomatic children with late onset forms. The aim of this nationwide study was to analyse the association between genotype and screened level of 17-hydroxyprogesterone in patients with the late onset form of 21-hydroxylase deficiency and to quantify false negativity.

Maturity-onset diabetes of the young (MODY) is the most common monogenetic form of diabetes with an autosomal dominant inheritance pattern. MODY is caused by mutations in genes important for the development and function of pancreatic beta cells, resulting in impaired insulin secretion capacity. To date, 14 different types have been described. While glucokinase (GCK)-MODY (formerly MODY-2) generally requires no drug therapy, other forms of MODY, such as hepatocyte nuclear factor-1-alpha (HNF1A)-MODY (formerly MODY-3) and HNF4A (formerly MODY-1), usually respond very well to sulfonylurea therapy. However, these MODY forms are characterised by a progressive course, meaning that insulin therapy is often required as the disease progresses. Both sulfonylurea therapy and insulin therapy are associated with an increased risk of hypoglycaemia and frequent weight gain. Newer blood glucose-lowering therapies, such as SGLT2 inhibitors (SGLT2i), DPP-4 inhibitors (DPP4i) and GLP-1 receptor agonists (GLP-1RA), have a much lower risk of hypoglycaemia and usually have a favourable effect on body weight. This review aims to provide an overview of the treatment of MODY patients with SGLT2i, DPP4i and GLP-1RA on the basis of previously published clinical studies, case series and case reports.

Diabetes mellitus is a leading cause of disability with adverse effects on the quality of life. It also affects occupational health by impacting several work-related parameters. This review discusses the relationship between diabetes and absenteeism, presenteeism, work impairment and unemployment. The association between work and diabetic complications such as neuropathic pain, diabetic foot, psychological issues and hypoglycemia due to treatment is also examined. Evidence points to a relationship between diabetes and absenteeism, reduced work productivity, and, thus, overall work impairment. A stronger negative impact on work performance is mediated by painful diabetic neuropathy and diabetic foot. In addition, psychological distress has been positively correlated with total workdays lost and frequency of absence. Depression in the diabetic population has also been linked with increased absenteeism, presenteeism, and work disability. Moreover, hypoglycaemia induced by antidiabetic medication may affect work attendance and performance. Finally, diabetes has been associated with inequality in the work environment, lower job satisfaction and higher unemployment rates, mainly because of its complications.

In recent years, a growing number of clinical and biological studies have shown that patients with type 2 diabetes mellitus (T2DM) are at increased risk of developing Parkinson's disease (PD). Prolonged exposure to hyperglycemia results in abnormal glucose metabolism, which in turn causes pathological changes similar to PD, leading to selective loss of dopaminergic neurons in the compact part of the substantia nigra. Dihydromyricetin (DHM) is a naturally occurring flavonoid with various biological activities including antioxidant and hepatoprotective properties. In this study, the effect of DHM on high glucose-induced dopaminergic neuronal damage was investigated.

Patients with hepatic type of glycogen storage diseases (GSDs) can manifest endocrine features such as hypoglycemia, dyslipidemia, or osteoporosis. This study aimed to investigate the long-term endocrine consequences in patients with hepatic GSDs.

Obstructive sleep apnoea (OSA) is regarded as a major health condition, progressively affecting an increased number of people around the world. The interplay between OSA and type 2 diabetes mellitus (T2DM) has been extensively studied. However, little is known about the relationship between OSA and type 1 diabetes mellitus (T1DM). This review provides insight into the prevalence of OSA in T1DM and its relationship with diabetic complications. Studies have hitherto yielded contradictory results on the occurrence of OSA in T1DM. Indeed, the risk of OSA in T1DM has ranged from 1 in 10 to more than 1 in 2 T1DM subjects. This high occurrence was confirmed by objective polysomnography as well as widely used subjective questionnaires. Multiple studies revealed the important correlation between OSA and diabetes complications. Both microvascular (nephropathy, neuropathy and retinopathy) and macrovascular complications appear to be associated with OSA occurrence, although some associations were not significant due to inadequate data. In conclusion, T1DM subjects carry a higher risk of undiagnosed OSA. Additional studies are needed to clarify the exact correlation between the two conditions.

The diagnosis of adrenal insufficiency (AI) related to traumatic brain injury (TBI) remains a challenge. We investigated the basal and low-dose adrenocorticotropic hormone (ACTH)-stimulated serum cortisol and salivary cortisol (SaC) levels and the diagnostic utility of SaC levels during 28 days following TBI.

Current guidelines recommend dopamine agonists (DA) as the primary therapeutic approach for prolactinomas; however, emerging evidence suggests that surgical intervention can also yield favorable outcomes.

Since the first description of Nelson syndrome 60 years ago, the way to consider corticotroph pituitary neuroendocrine tumors (PitNETs) after bilateral adrenalectomy has evolved. Today, it is globally acknowledged that only a subset of corticotroph PitNETs is aggressive.After adrenalectomy, corticotroph tumor progression (CTP) occurs in about 30 to 40% of patients during a median follow-up of 10 years. When CTP occurs, various CTP speeds (CTPS) can be observed. Using simple metrics in patients with CTP, CTPS was reported to vary from a few millimeters to up to 40 mm per year. Rapid CTPS/ Nelson's syndrome was associated with more severe Cushing's disease, higher adrenocorticotropic hormone (ACTH) in the year following adrenalectomy, and higher Ki67 on pituitary pathology. Complications such as apoplexy, cavernous syndrome, and visual defects were associated with higher CTPS. During follow-up, early morning ACTH, absolute variations properly reflected CTPS. Finally, CTPS was not higher after than before adrenalectomy, suggesting that cortisol deprivation after adrenalectomy does not impact CTPS in a majority of patients.Taken together, rapid CTPS/ Nelson's syndrome probably reflects the intrinsic aggressiveness of some corticotroph PitNETs. The precise molecular mechanisms related to corticotroph PitNET aggressiveness remain to be deciphered. Regular MRIs combined with intermediate morning ACTH measurements probably provide a reliable way to detect early and manage fast-growing tumors and, therefore, limit the complications.

This narrative mini-review discusses the association between peroneal nerve entrapment (PEN) and diabetes mellitus (DM). Generally, PEN is not a common cause of peripheral neuropathy in DM. Poor glycaemic control and DM duration are powerful risk factors for PEN. Underlying mechanisms involve neurodegeneration and entrapment of the peroneal nerve. Patients tend to present with chronic leg pain, gradual foot drop, steppage gait, or weakness of ankle dorsiflexion. Electrodiagnostic and imaging studies are very useful in diagnosis to determine the level at which entrapment occurs. Treatment varies based on the aetiology and severity of symptoms. It is initially conservative. Surgical nerve decompression management is required when entrapment is refractory to non-operative options.

Spermatozoa are susceptible to oxidative radicals when antioxidant defenses are inadequate. The extent to which oxidative radicals contribute to sperm damage in patients with acromegaly remains unclear. This study aimed to investigate and elucidate this relationship.

Changes in postmenopausal hormone levels are associated with a variety of disorders. This study elucidated the mechanism by which follicle-stimulating hormone (FSH) increases cortisol production involved in development of menopause-related diseases.

To assess the relationship between the left ventricular remodeling parameters of cardiac magnetic resonance and NT-pro-BNP in patients with primary aldosteronism (PA).

This study investigated the onset and the choice of treatment in children with very early onset of type 1 diabetes mellitus (T1D).

Food-dependent Cushing's syndrome (FDCS) is a rare presentation of hypercortisolism from adrenal origin, mostly observed in primary bilateral macronodular adrenal hyperplasia (PBMAH) but also in some cases of unilateral adrenocortical adenoma. FDCS is mediated by the aberrant expression of glucose-dependent insulinotropic peptide (GIP) receptor (GIPR) in adrenocortical cells. GIP, secreted by duodenal K cells after food intake, binds to its ectopic adrenal receptor, and stimulates cortisol synthesis following meals. FDCS was first described more than 35 years ago, and its genetic cause in PBMAH has been recently elucidated: inactivation by germline heterozygous pathogenic variants is constantly associated with a loss-of-heterozygosity of the short arm of chromosome 1, containing the locus. This causes biallelic inactivation of , resulting in the GIPR overexpression in the adrenal cortex. These new insights allow us to propose the genetic screening to all PBMAH patients with signs of FDCS (low fasting cortisol that increases after a mixed meal or oral glucose load) and to all first-degree relatives of variant carriers. Given that is a tumor suppressor gene that has also been associated with monoclonal gammopathy of uncertain significance and multiple myeloma, the investigation of FDCS in the diagnostic management of patients with PBMAH and further genetic testing and screening for malignancies should be encouraged.