Endokrynologia Polska最新文献

The pathophysiology of diabetic gastroparesis (DGP), a common complication in diabetic patients, is not fully known. Its development has been linked to several causes, including hyperglycaemia, vagal nerve dysfunction, aberrant Cajal's interstitial cell network (ICC), lack of nerve nitric oxide synthase (nNOS) expression in the intermuscular plexus, and hormonal alterations in the gastrointestinal tract. Glucose management, diet control, gastric stimulants, anti-emetic medications, Helicobacter pylori eradication, stomach electrical stimulation, and surgery are the main current treatments. These methods, however, could have unfavourable consequences. By examining recent studies and literature reviews, we outline the state of the study on diabetic gastroparesis in this paper.

Introduction: Lymphocytic hypophysitis (LH) is a rare inflammatory disorder of the pituitary or/and hypothalamus with variable disease course: from spontaneous remission to pituitary atrophy. The diagnosis, treatment and follow-up remain challenging. The aim of the study is to present long-term data and an individualized therapeutic approach and propose an algorithm for the follow-up of patients with probable LH.

Material and methods: A retrospective analysis of 18 consecutive adult patients (13 W/5 M, mean age 45.2 years) with LH diagnosed and treated in a tertiary referral center.

Results: The first manifestations were headaches (50.0%), polyuria/polydipsia (33.3%) and symptoms of hypopituitarism (16.7%). Somatotropic, adrenal, gonadal and thyroid axis insufficiencies were found in 44.4%, 33.3%, 33.3%, and 27.8% of patients, respectively. Arginine vasopressin deficiency was diagnosed in 8 patients (44.4%). Some of the dysfunctions were transient. Magnetic resonance imaging (MRI) revealed thickened pituitary stalk in all but 2 cases. In 2 patients an anterior pituitary lesion, most likely inflammatory was described. Four patients were given steroids (severe headaches) with clinical recovery and stable/improved MRI. One woman was operated on due to the progressive mass-related symptoms - histopathological examination confirmed LH. In the remaining 13/18 patients watchful waiting approach allowed to obtain hormonal and radiological stabilization/improvement.

Conclusions: LH is a disease with a complex clinical picture and challenging diagnosis. Treatment requires an individual approach: vigilant observation is the cornerstone of therapy, with steroid/surgical treatment reserved for cases with mass-related symptoms. Further multicenter research might help in better understanding of the LH and creating standards of care in this rare disease.

Introduction: Beyond growth acceleration, growth hormone (GH) therapy improves body composition of GH-deficient (GHD) children due to the interaction of GH with lipid and carbohydrate metabolism, possibly mediated by adipokines secreted by adipose tissue and ghrelin. To promote linear growth, it is essential to have normal phosphate homeostasis. Fibroblast growth factor 23 (FGF23) is a known regulator of serum phosphorus and may be responsible for the increased renal phosphorus reabsorption observed during GH therapy. This study aimed to assess the impact of one-year GH therapy on body composition, adipokines, acylated/unacylated ghrelin (AG/UAG), and FGF23 in GHD children.

Material and methods: A prospective observational study of 42 prepubertal, non-obese GHD children followed up in the first year of GH replacement therapy, investigating changes in adipokine profiles, AG/UAG, FGF23, and body composition. Data before therapy onset were compared with measurements obtained after 6 and 12 months of GH therapy.

Results: All children with a mean age of 9.2 ± 2.6 years grew at an accelerated pace. Total body fat decreased significantly, while the lipid profile improved, and total bone mineral density (BMD) significantly increased over the 12 months of treatment. Leptin and UAG levels decreased significantly, whereas adiponectin and AG values increased. A significant increase in plasma FGF23 and insulin growth factor 1 (IGF1) was accompanied by increased serum phosphate. Changes in FGF23 concentration did not have an impact on BMD. The strong association of FGF23 with IGF1 and height standard deviation (SD) could reveal a role of FGF23 in linear growth. In regression analysis models, GH therapy influences the changes of leptin and adiponectin, but not ghrelin, independently of body composition - lean or fat mass.

Conclusions: GH replacement therapy improves body composition and adipokine profile in GHD children and directly impacts leptin and adiponectin concentrations independently of body composition. Also, GHD children have increased serum phosphate, correlated with upregulation rather than with suppression of FGF23, an unexpected observation given the phosphaturic role of FGF23. Further research is needed to identify the molecular mechanisms by which the GH/IGF1 axis influences adipokines secretion and plasma changes of FGF23.

In recent years, there has been a rapid increase in the prevalence of benign and malignant tumours of the thyroid gland worldwide, positioning it as one of the most prevalent neoplasms within the endocrine system. While the pathogenesis of thyroid tumours is still unclear, an increasing number of studies have found that certain lifestyle and residence environments are associated with their occurrence and development. This article endeavours to elucidate the correlation between lifestyle, residential environment, and the increased prevalence of thyroid cancer in recent years. It specifies the frequency of the lifestyle and outlines the scope of the residential environment. It also endeavours to summarise the main mechanistic pathways of various modifiable risk factors that cause thyroid cancer. Factors that prevent thyroid cancer include smoking and alcohol consumption, quality and regular sleep, consumption of cruciferous vegetables and dairy products, and consistent long-term exercise. Conversely, individuals with specific genetic mutations have an elevated risk of thyroid cancer from prolonged and frequent use of mobile phones. In addition, individuals who work in high-pressure jobs, work night shifts, and live near volcanoes or in environments associated with pesticides have an elevated risk of developing thyroid cancer. The impact of living near a nuclear power plant on thyroid cancer remains inconclusive. Raising awareness of modifiable risk factors for thyroid cancer will help to accurately prevent and control thyroid cancer. It will provide a scientific basis for future research on lifestyles and living environments suitable for people at high risk of thyroid cancer.

Introduction: Papillary thyroid cancer (PTC) is a common malignant tumour in the endocrine system with increasing incidence. LncRNA HCG22 (HCG22) was noticed to be dysregulated in PTC, but its specific function and mechanism remain unknown. The function of HCG22 and its underlying molecular mechanism was investigated to evaluate its potential as a biomarker for PTC.

Material and methods: The expression of HCG22 was detected in PTC cells (TPC-1, SNU790, GLAG-66, and BCPAP) and normal thyroid cells (Nthy-ori) using real time quantative polymerase chain reaction (RT-qPCR). HCG22 and miR-425-5p were regulated by cell transfection. The cell proliferation and metastasis were assessed by CCK8 and Transwell assay.

Results: HCG22 was upregulated in PTC cells, of which the knockdown suppressed the proliferation, migration, and invasion of PTC cells. miR-425-5p was downregulated in PTC cells, which was negatively regulated by HCG22. Silencing miR-425-5p could reverse the inhibitory effect of HCG22 knockdown on the cellular processes of PTC.

Conclusions: HCG22 served as a tumour promoter in PTC cells, which regulated cell proliferation and metastasis via negatively regulating miR-425-5p.

Introduction: Drug therapy for Graves' disease (GD) is the first-line treatment in Europe. The use of a specific regimen for the administration of anti-thyroid drugs (ATDs) is still controversial. The objective was to compare block-and-replace therapy (BRT) with a titration (T) regimen in terms of incidence of overt hypothyroidism and development of Graves' orbitopathy (GO) over 18 months of treatment.

Material and methods: Two databases (PubMed, Cochrane Library) and reference lists were searched. Prospective and retrospective observational cohort studies were included. Data collection and analysis were performed independently by 2 authors.

Results: Two studies with 716 GD patients (40.36% treated with BRT, 59.64% with T regimen) were included. No statistically significant differences were observed between the ATDs regimens used in terms of incidence of overt hypothyroidism during 18 months of treatment [Mantel-Haenszel (M-H) odds ratio (OR): 1.54, 95% confidence interval (CI): 0.75-3.16, p-value = 0.24]. GD patients who followed BRT were less likely to achieve control of thyroid function than patients on T regimen (M-H OR: 0.55, 95% CI: 0.34-0.88, p = 0.01). One study reported fewer thyroid function tests (TFT) during BRT than during the T regimen. The other study included patients without GO at baseline and reported a lower incidence of GO during BRT than in the T regimen (9.1% versus 17.8%), with no statistical difference between the 2 regimens (M-H OR: 0.47, 95% CI: 0.19-1.14, p = 0.10).

Conclusion: BRT may be more useful than the T regimen for patients with complicated GD or for those who required fewer TFTs.

Introduction: Non-alcoholic fatty liver disease (NAFLD) is a global disease estimated to affect one-third of the world's population. NAFLD is the hepatic manifestation of metabolic syndrome. In recent years, formulations have been made using haematological laboratory parameters, and it has been reported to be associated with inflammation and fibrosis in the liver. In this study, we aimed to evaluate the neutrophil to high-density lipoprotein (HDL) cholesterol (HDL-C) ratio (NHR) in patients diagnosed with NAFLD by ultrasonographic imaging for the first time in the literature.

Material and methods: The study was carried out by recruiting men and women between the ages of 18 and 65 years who applied to the check-up outpatient clinic of our hospital. Ultrasonography was used as the diagnostic method for hepatosteatosis in all cases. Venous blood samples were taken from the patients for haematological and biochemical measurements.

Results: The study population consisted of 155 patients, 115 of whom were fatty liver patients and 40 were controls. NHR was determined as 99.6 ± 56.8 in those with grade 1 fatty liver, 114.98 ± 39.2 in those with grade 2, 122.9 ± 51.1 in those with grade 3, and 86.17 ± 35.2 in the control group. In the analysis, NHR was statistically significantly higher in grade 2 and 3 fatty liver patients compared with the control group (p = 0.03 and 0.01, respectively). However, there was no statistical difference between grade 1 fatty liver patients and the control group (p = 0.53).

Conclusions: We found higher NHR in patients with NAFLD. NHR is a cheap and easy to access parameter. An elevated NHR with FIB-4 in patients with NAFLD may be a marker of liver inflammation or fibrosis.

Mitophagy is a specific type of autophagy and a selective form of autophagy on a larger scale. It selectively eliminates damaged, misfolded, and surplus mitochondria, particularly those that are cytotoxic, by using autophagic lysosomes. This process is crucial for maintaining a balance of both the quality and quantity of mitochondria, which is necessary for normal cell function and tissue development. However, in certain abnormal situations, such as nutritional deficiencies and hypoxia, the function of mitophagy becomes impaired. This leads to a failure to clear damaged mitochondria in a timely manner, resulting in the production of a large number of reactive oxygen species. These reactive oxygen species further contribute to an inflammatory response and the release of factors that induce apoptosis. Moreover, abnormal mitophagy can also cause mitochondrial dysfunction, disrupt metabolic reprogramming during stress responses, alter cell fate decisions and differentiation, and consequently impact the development and progression of diseases, including cancer. Therefore, mitophagy plays a crucial role in controlling the quality of cancer cells, making it imperative to study its function and impact. Numerous proteins and molecules are involved in the regulation of mitophagy, with Parkin and PTEN-induced kinase 1 (PINK1) serving as key mediators, and the hypoxia-related proteins hypoxia-inducible factor la (HIF1a) and FUN14 domain-containing 1 (FUNDC1) also playing a role. Additionally, proteins such as chromatin licensing and DNA replication factor 1 (CDT-1), insulin-like growth factor 1 (IGF-1), caveolin 1 (Cav-1), and others contribute to the regulation of mitophagy in various ways. This article aims to explore the dual role of mitophagy in tumourigenesis by examining the factors and proteins associated with mitophagy and their regulatory effects. The objective of this review is to provide a new theoretical foundation and direction for cancer treatment.

Introduction: Coronavirus disease 2019 (COVID-19) is a global pandemic that has affected millions of people worldwide. In this paper, we analyse the relationship between stress hyperglycaemia and disease severity in patients with COVID-19.

Material and methods: A total of 252 patients with COVID-19 were included in this study. The patients were divided into the following groups: COVID-19 with stress hyperglycaemia (SHG), COVID-19 with diabetes (DM), and COVID-19 with normal blood glucose (NG). The stress hyperglycaemia rate (SHR) was calculated using the fasting blood glucose (FBG)/glycated haemoglobin (HbA1c) ratio. To further compare the disease characteristics of different SHRs, we divided the SHR into low SHR and high SHR according to the SHR median. Correlations between the severity of the disease and other factors were analysed after adjusting for sex and age. Multivariate analysis was performed using logistic regression to analyse the risk factors predicting the severity of COVID-19.

Results: Compared with the NG group, the SHG group had higher disease severity (p < 0.001); the SHG group had higher HbA1c, FBG, SHR, blood urea nitrogen (BUN), interleukin 6 (IL-6), and neutrophil levels, while lymphocyte, CD3+ T cell, CD8+ T cell, CD4+ T cell, CD16+CD56 cell, and CD19+ cell counts were lower (p < 0.05). Compared with the NG group, the DM group had higher HbA1c, blood glucose, BUN, lactate dehydrogenase (LDH), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and neutrophils, while CD8+ T cell counts were lower (p < 0.05). Compared with the DM group, the SHG group had higher SHR and lower HbA1c, CD3+ T cell, CD4+ T cell, CD16+CD56 cell, and T cell ratio levels (p < 0.05). Compared to the low SHR group, the high SHR group had patients with more severe COVID-19 (p = 0.004). Also, the high SHR grouphad higher age, HbA1c, FBG, asparate aminotransferaze (AST), BUN, LDH, uric acid (UA), CRP, IL-6, and procalcitonin (PCT), while lymphocyte, CD3+ T cell, CD4+ T cell, CD8+ T cell, and CD19+ cell counts were lower (p < 0.05).Binary logistic regression analysis showed that SHR, gender, and lymphocyte count wererisk factorsfor the severity of COVID-19.

Conclusion: Stress hyperglycaemia, as indicated by a higher SHR, is independently associated with the severity of COVID-19.

Introduction: The high prevalence of obesity and thyroid diseases worldwide justifies di per se their simultaneous coexistence. In recent decades, there has been a parallel and significant rise in obesity and thyroid diseases in industrialised countries, although the underlying mechanisms are complex and not well known.

Material and methods: The authors accomplished a comprehensive literature search of original articles concerning obesity and thyroid status. Original papers exploring the association between these two morbidities in children and adults were included.

Results: A total of 79 articles were included in the present analysis. A total of 12% of obese children (mean age 10.9 ± 1.4 years) showed a thyroid disease, and they were younger than healthy obese children (10.9 ± 1.2 vs. 11.0 ± 0.4 years, p < 0.001). Isolated hyperthyrotropinaemia was the most frequent finding in children (10.1%). Autoimmune thyroid disease was more frequent in puberal age. Thyroid antibodies and subclinical hypothyroidism were more frequent in obese that in non-obese patients (7% vs. 3%, p < 0.001; 10% vs. 6%, p < 0.001). Among obese adults, 62.2% displayed a thyroid disease; those affected were younger (35.3 ± 6.8 vs. 41.0 ± 1.9 years, p < 0.001), heavier [body mass index (BMI): 39.4 ± 6.3 vs. 36.1 ± 2.3 kg/m², p < 0.001], and more frequently female (13% vs. 8%, p < 0.001). The most frequent disease was overt hypothyroidism (29.9%). BMI appears to be correlated with TSH levels in obese adults. Overt hypothyroidism was significantly more frequent in obese patients (7% vs. 3%, p < 0.005), but no difference was found in thyroid antibodies (15% vs. 14%, p = 0.178).

Conclusions: An undeniable relationship between obesity and thyroid impairments exists. Isolated hyperthyrotropinaemia is frequently seen in obese children, often followed by spontaneous resolution. Subclinical hypothyroidism should never be treated in children or adults with the aim of reducing body weight.