Endokrynologia Polska最新文献

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Introduction: Rathke's cleft cyst (RCC) and primary empty sella syndrome (PESS) are usually incidental findings on magnetic resonance imaging (MRI) scans. In most cases, these lesions do not cause mass effect symptoms and do not require surgical intervention. In patients with RCC or PESS, it is important to exclude secondary adrenal insufficiency (SAI), which may be a life-threatening condition.

Material and methods: The incidence of SAI was assessed in patients with RCC or PESS detected by MRI, using the 1 μg Synacthen stimulation test. A total of 38 patients were analysed. Test results were linked to clinical symptoms and the type of cystic lesion.

Results: Assuming that cortisol levels < 14.6 μg/dL in Synacthen test are the criterion of SAI diagnosis, SAI was diagnosed only in 2 patients (5%). Adopting the traditional criterion of cortisol levels < 18 μg/dL, SAI would be diagnosed in 7 patients (18.4 %). Dizziness (Chi2 = 3.89; p = 0.049) and apathy (Chi2 = 3.87; p = 0.049) were significantly more frequent in the PESS group than in the RCC group.

Conclusions: The incidence of SAI in the general patient population with empty sella syndrome and Rathke's cleft cysts is low. The 1 μg Synacthen test seems to be a valuable tool in the diagnosis of SAI among patients with RCC and PESS. Further studies are necessary to determine the sensitivity and specificity of the 1 μg Synacthen test with the standardization of test protocol and considering the cortisol level at the 20-minute timepoint. PESS patients report dizziness and apathy more frequently than RCC patients, which does not result from the disturbance of the hypothalamic-pituitary-adrenal axis, but probably from the different pathogenesis of these cystic lesions.

Introduction: There have been many studies assessing whether abnormal metabolic and hormone levels among women with polycystic ovary syndrome (PCOS) are associated with a greater risk of non-alcoholic fatty liver disease (NAFLD). However, previous studies repported no consistent outcomes. To provide a comprehensive evaluation regarding the role of PCOS in the risk of NAFLD, we updated the published literature and conducted this systemic review and meta-analysis.

Material and methods: Electronic databases (Web of Science and PubMed) were searched for literature up to October 2022. We used STATA 12.0 software to compute odds ratios (ORs) and 95% confidence intervals (CIs), to evaluate the association between PCOS and risk of NAFLD.

Results: The study indicated that PCOS was significantly related to an elevated risk of NAFLD (OR = 2.93, 95% CI 2.38 to 3.62, I2 = 83.7%, p < 0.001). Meta-regression analysis showed that age and body mass index (BMI) were not responsible for heterogeneity across the studies (age: p = 0.096; BMI: p = 0.418). Sensitivity analysis indicated no alteration in the direction of effect when any study was eliminated. Begg's test, Egger's test, Begg's test, and funnel plot indicated a significant risk of publication bias (Egger's test: p = 0.028; Begg's test: p < 0.001).

Conclusion: This meta-analysis reported that PCOS was associated with an elevated risk of NAFLD. Early proper detection of NAFLD for PCOS women is essential. All patients with PCOS should undergo appropriate diagnostics for early detection of fatty liver and fibrosis.

Obesity is currently one of the most serious public health problems which affects up to 30-40% of the population, and its prevalence is higher in men than in women. Complications of obesity include atherosclerosis, cardiovascular diseases, and type 2 diabetes mellitus, but it also has a negative impact on the hormonal system and fertility. The hormonal consequences of excess body fat in men are functional hypogonadism, which not only causes clinical symptoms of testosterone deficiency, but is also a risk factor for obesity (a vicious circle mechanism). Reduced fertility in obese men may be a consequence of functional hypogonadotropic hypogonadism (decreased gonadotropins and testosterone secretion, reduced libido, and erectile dysfunction), but other mechanisms associated with excess adipose tissue, like hyperinsulinaemia, hyperleptinaemia, chronic inflammation, and oxidative stress also play an important role. Therefore, in obese men deterioration of semen parameters (sperm concentration, motility, and morphology) and reduced fertility are observed, also concerning the effectiveness of assisted reproductive techniques. Reducing the mass of adipose tissue causes an increase in testosterone concentrations and has a beneficial effect on semen parameters. Functional hypogonadism in obese men should be diagnosed only after exclusion of organic causes of hypogonadism. Lifestyle changes, including physical exercise and low-caloric diet, and optimization of comorbidities, are still first line of treatment. In some patients, if such treatment is ineffective, pharmacotherapy or bariatric surgery may be considered. Testosterone replacement therapy is contraindicated in obese men with functional hypogonadism, especially in those who desire fertility. Selective oestrogen receptor modulators and aromatase inhibitors improve sperm quality but are not recommended for the treatment of hypogonadism in obese men. GLP-1 analogues appear to be effective and safe in the treatment of low testosterone and infertility in obese men and may be the main method of pharmacotherapy in the future.

Over the past few years, there have been significant advances in our understanding of hypoparathyroidism (HypoPT) in terms of its epidemiology, clinical presentation, etiology, and skeletal and renal complications. Moreover, the available treatment options for HypoPT have changed. This position statement of the Expert Group of the Polish Society of Endocrinology summarizes the current state of knowledge and provides recommendations for optimal management to assist clinicians in the diagnosis, treatment, and monitoring of HypoPT in Poland. The specific aspects of HypoPT management in children, pregnant and lactating women, and patients with chronic kidney disease are also discussed. HypoPT is a rare disorder characterized by hypocalcemia and the lack or deficiency of parathyroid hormone (PTH). Hypoparathyroidism can be associated with complications, including nephrocalcinosis, nephrolithiasis, renal insufficiency, cataract, seizures, cardiac arrhythmia, depression, and an increased risk of infection. Minimizing complications of HypoPT requires careful evaluation and close monitoring of laboratory parameters. Conventional management of HypoPT has focused on maintaining serum calcium levels using oral calcium and active vitamin D. However, this approach is limited because it does not restore normal PTH function, is often associated with inadequate biochemical control, and raises concerns as to long-term side effects. HypoPT is the only classic endocrine insufficiency that is not commonly treated with the substitution of the missing hormone. Recently, recombinant human PTH(1-84) has become available, offering hope that the use of the missing hormone in the treatment of HypoPT will help achieve better control and reduce the risk of complications. However, this treatment is currently unavailable in Poland.

Introduction: Apolipoprotein C3 (APOC3) is known for its important functions in metabolism-related diseases. However, the function and molecular mechanism of APOC3 in polycystic ovarian syndrome (PCOS) have not been reported.

Material and methods: Quantitative polymerase chain reaction and western blot assays were used to detect the expression of APOC3 in KGN cells. Small interference APOC3 (siAPOC3) was applied to reduce APOC3 expression, and the proliferation ability of human granulosa cell line (KGN cells) was measured by cell counting kit-8 and colony formation assays. The protein levels of key genes related to apoptosis were detected by western blot assay. The transcriptional regulator of APOC3 was predicted by the UCSC and PROMO website, and verified by dual luciferase assay. siAPOC3 and pcDNA3.1-specific protein 1 (SP1) vector were co-transfected into KGN cells to detect the function of SP1 and APOC3 in KGN cells.

Results: APOC3 was overexpressed in KGN cells, and siAPOC3 transfection significantly reduced the growth ability of KGN cells and increased the apoptosis ability of KGN cells. SP1 directly bound to the promoter of APOC3 and transcriptional regulated APOC3 expression. Overexpression of SP1 increased the growth ability of KGN cells and decreased the apoptosis ability of KGN cells, which were reversed after siAPOC3 transfection. The increased levels of toll-like receptor 2 (TLR2) and p65 phosphorylation (p-P65) nuclear factor kappa B (NF-κB) caused by SP1 overexpression were inhibited by siAPOC3 transfection. APOC3, transcriptionally regulated by SP1, promoted the growth of KGN cells, and inhibited the apoptosis by regulating TLR2/NF-κB signalling pathway.

Fine needle aspiration biopsy (FNAB) guided by ultrasonography is routinely used to identify thyroid nodules prior to surgery. Although FNAB has great diagnostic accuracy and safety, it is limited by its relatively low diagnostic accuracy in follicular lesions, such as non-diagnostic or atypia of unclear significance (AUS)/follicular lesion of uncertain significance (FLUS). Additional diagnostic tests are required to overcome these challenges in evaluating thyroid nodules. Thyroid nodules can now be diagnosed with spring-activated single- or double-action needles following the introduction of core needle biopsy (CNB). CNB has the ability to address the limitations of FNAB by obtaining a sizeable tissue sample with more details on the histological structure supporting the capsule and fewer non-diagnostic effects brought on by the absence of follicular cells. Compared to repeated FNAB, CNB has been demonstrated to produce fewer ambiguous results, such as non-diagnostic or AUS/FLUS results. The Korean Endocrine Pathology Thyroid CNB Working Group issued its first set of guidelines for "Pathology Reporting of Thyroid Core Needle Biopsy" in 2015. In 2017, the Korean Society of Thyroid Radiology (KSThR) published "Core Needle Biopsy of Thyroid: 2016 Consensus Statement and Recommendations from the Korean Society of Thyroid Radiology". The main objectives of thyroid CNB are to detect individuals with thyroid illness who require surgery and to obtain a significant number of thyroid lesions with low morbidity.

Radioactive iodine therapy (RIT) is an effective, safe, and cheap method in benign and malignant thyroid diseases. There is still an unresolved question of whether RIT treatment also plays a role in the treatment of, for example, breast cancer, lung cancer, or glioblastoma multiforme (GBM). These studies are currently being carried out in rats in combination with genes, but it may be an interesting challenge to assess "pure" RIT alone, thanks to the expression of sodium iodide symporter (NIS), is effective in other organ nodules, both benign and malignant. Cloning of the NIS in 1996 provided an opportunity to use NIS as a powerful theranostic transgene. In addition, NIS is a sensitive reporter gene that can be monitored by high-resolution PET imaging using the radiolabels [¹²⁴I]sodium iodide ([¹²⁴I]NaI) or [18F] tetrafluoroborate ([¹⁸F]TFB). Based on published positron emission tomography (PET) results, [¹²⁴I]sodium iodide and internally synthesized [18F]TFB were compared in an orthotopic animal model of NIS-expressing glioblastoma. The results showed improved image quality using [¹⁸F]TFB. Based on these results, we will be able to extend the NIS gene therapy approach using non-viral gene delivery vehicles to target orthotopic tumour models with low-volume disease such as GBM. Is it possible to treat RIT alone without using the NIS gene in GBM? After all, the NIS symporter was detected not only in the thyroid gland, but also in different tumours. The administration of RIT is completely harmless; the only complication is hypothyroidism. Indeed, recently it has been shown that, for example, in the case of thyroid cancer, the maximum RIT is 37000 MBq (1000 mCi). When beneficial effects of therapy in GBM are not possible (e.g. neurosurgery, modulated electro-hyperthermia, chemotherapy, immunotherapy, cancer vaccines, or oncolytic viruses), could RIT provide a "revolution" using NIS?

Introduction: The most common cause of death in nonalcoholic fatty liver disease (NAFLD) is cardiovascular disease. Choroidal microvascular structure in the eye may be a predictor of systemic vascular disease. We aimed to evaluate the effects of NAFLD on the choroidal microvascular structure using enhanced depth optical coherence tomography (EDI-OCT).

Material and methods: This prospective study was conducted by evaluating a total of 96 patients, 52 with steatosis and 44 without steatosis. After anthropometric measurements and ultrasonography were performed in the Gastroenterology Clinic, venous blood samples were taken for biochemical examinations. Then, all patients underwent an eye examination by an ophthalmologist. Subfoveolar choroidal thickness (SFCT) values of the cases were measured with EDI-OCT. Choroid vascular index (CVI) measurements were obtained by dividing the subfoveal choroidal area in the EDI-OCT images into luminal and stromal areas using the image binarization technique (ImageJ). In statistical analysis, the chi-square test was used to compare categorical data, and the independent t-test and Mann-Whitney U test were used to compare quantitative data.

Results: The mean age of those with fatty liver was 41±15.7 years, and of those without fatty liver it was 46 ± 10.7 years. There was nostatistically significant difference between the groups in terms of age (p = 0.064). Body mass index (BMI), waist circumference (WC), glucose, uric acid, alanine aminotransferase (ALT), gamma glutamyl transpeptidase (GGT), total cholesterol (TC), ferritin, insulin, and Homestatic Model Assesment - Insuline Restistance (HOMA-IR) were statistically significantly higher in the NAFLD group. On the other hand, there was no statistically significant difference between the groups in terms of low-density lipoprotein (LDL)-cholesterol, high-density lipoprotein (HDL)-cholesterol, triglyceride, and aspartate aminotransferase (AST) values. The mean SFCT was measured as 280.26 ± 23.68 microns in the NAFLD group, and 308.96 ± 18.57 microns in the control group. There was no statistically significant difference in SFCT between the groups (p = 0.077). CVI measurements were 0.63 and 0.65, respectively, and they were significantly lower in the group with NAFLD (p = 0.045).

Conclusions: This is the first study in the literature to compare patients with and without ultrasonographic fatty liver in terms of choroidal vascular changes. We found that the choroidal vascular index decreased in NAFLD. This result proves that NAFLD causes changes at the microvascular level and is a multisystemic disease.

The health of post-menopausal women has become of paramount concern due to the aging of the world's population. Concurrently, the prevalence of obesity among postmenopausal women is expected to increase, presenting a significant public health challenge. Although weight gain during menopause is a well-observed phenomenon, its underlying causes and mechanisms remain incompletely understood. This manuscript reviews the literature to explore potential hormonal factors and pathomechanisms contributing to obesity during perimenopause, aiming to identify pathogenic factors that can guide treatment selection. Menopause-induced hormonal changes, including hypoestrogenaemia, hypergonadotropinaemia, relative hyperandrogenaemia, growth hormone deficiency, leptin resistance, and chronic stress affecting the hypothalamic-pituitary-adrenal axis, have been implicated in the onset of obesity in perimenopausal women. These hormonal fluctuations, alongside lowered daily energy expenditure, lead to metabolic alterations that elevate the risk of developing metabolic disorders and cardiovascular diseases. Weight gain in perimenopausal women is associated with higher total and abdominal adipose tissue and lower lean body mass. Addressing this issue requires individualized behavioural management, supported by effective pharmacological therapy, and, when warranted, complemented by bariatric surgery. Modern obesity treatment therapies have demonstrated safety and efficacy in clinical trials, offering the potential to reduce excess body fat, improve metabolic profiles, lower cardiovascular risk, and enhance the quality and longevity of women's lives. In addition to standard obesity therapies, the article examines different treatment strategies based on obesity's pathogenic factors, which may offer promising options for treating obesity with or without complications in perimenopausal women. One such potential approach is menopausal hormone therapy (MHT), which hypothetically targets visceral obesity by reducing visceral adipose tissue accumulation, preserving metabolically active lean body mass, and improving lipid profiles. However, despite these reported benefits, gynaecological and endocrinological societies currently do not recommend the use of MHT for obesity prevention or treatment, necessitating further research for validation. Emerging evidence suggests that visceral obesity could result from hypoestrogenaemia during perimenopause, potentially justifying the use of MHT as a causal treatment. This highlights the importance of advancing research efforts to unravel the intricate hormonal and metabolic changes that occur during perimenopause and their role in obesity development.