Endokrynologia Polska最新文献

Autoimmune thyroiditis (AIT) is due to an autoimmune process that destroys thyrocytes, leading to hormonal disorders. AIT is more common in women, and the aetiology is multifactorial. The destruction of thyroid cells may release free thyroid hormones into the bloodstream, causing hyperthyroid symptoms. With further destruction of thyroid cells, patients develop euthyroidism and eventually chronic hypothyroidism. The diagnosis of AIT is based on clinical symptoms, positive anti-thyroid antibodies, ultrasound, and histological features. The main goal of treatment is correcting hormonal disorders and achieving euthyroidism. Treatment of AIT involves replacing thyroid hormone deficiency with the use of synthetic hormones. Prophylactic levothyroxine (L-T4) treatment of euthyroid patients with AIT may reduce both serological and cellular markers of autoimmunisation. Attention should be paid to the starting dose of L-T4, potential drug interactions, and drug formulation. A follow-up should be planned to determine the optimal dose. The authors highlighted that a healthy lifestyle and supplementing selected vitamins and microelements appropriately are essential. In selected clinical conditions, thyroidectomy should be considered. There are also alternative therapeutic strategies, such as herbal medicine and acupuncture, but their effectiveness has yet to be conclusively confirmed in research studies. Monitoring the thyroid gland enlargement and the possibility of developing nodular goitre is integral to patient care over AIT patients. In conclusion, treating AIT is complex, involving thyroid hormone replacement therapy, taking care of a healthy diet and lifestyle, and proper supplementation. It requires an individual approach. Regular follow-up is necessary to control the disease and minimise its effects.

Introduction: The aim of the study was to present data on risk factors for fractures in various parts of the skeleton in a cohort of postmenopausal women during a 10-year prospective observation period. It can be hypothesised that fracture risk factors should be different for spine, hip, and peripheral fractures.

Material and methods: 640 postmenopausal women at mean baseline age was 65.0 ± 6.9 years were enrolled into the study. The cohort was randomly selected from the population of the entire Racibórz district. Data on the incidence of fractures and falls were updated annually during the 10-year follow-up period. Information on clinical risk factors for fractures was collected at baseline.

Results: During the observation period, 190 low-traumatic fractures were recorded in 129 patients. The following number of fractures was observed: hip 15, spine 30, non-hip fractures other than spine 145 (including 81 forearm fractures). The effect of falls was insignificant in the case of spine fractures (chi-square test: 3.64; p = 0.06). For all other skeletal sites, the incidence of fractures was significantly increased by falls, with the greatest effect observed for forearm fractures and non-spine and non-hip fractures (chi-square test for hip, forearm, and all non-spine, non-hip fractures was 6.43, p < 0.05; 42.7, p < 0.0001 and 66.7, p < 0.0001, respectively). To determine the factors having a significant impact on the incidence of fractures during the observation period, logistic regression was used separately in subgroups. The following risk factors were taken into account: age, height, body weight, bone mineral density (BMD) at the femoral neck as expressed by T-score, rheumatoid arthritis, steroid use, falls reported at baseline, and the total number of risk factors. Spine fractures depended only on T-score, odds ratio (OR) = 0.42 (0.23-0.76); hip fractures depended only on age, OR = 1.15 (1.07-1.24); forearm fractures depended only on age T-score, OR = 0.69 (0.51-0.92); and non-hip, non-spine on fall rate, OR = 1.86 (1.20-2.87).

Conclusions: Fractures at various skeletal sites recorded in long-term follow-up in postmenopausal women were dependent on various risk factors. Multivariate analysis identified a single, dominant risk factor for each fracture location analysed.

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Type 2 diabetes mellitus (T2DM) represents a chronic metabolic disorder, constituting over 90% of all diabetes cases. Its primary characteristics include insulin deficiency and insulin resistance. The aetiology of T2DM is complex, which is attributed to a convergence of genetic and environmental factors. Moreover, it can engender various complications such as diabetes retinopathy, diabetes nephropathy, and diabetes neuropathy. T2DM cannot be cured fundamentally, it can only delay the development of the disease by controlling the blood sugar level. If the blood sugar is at a high level for a long time, it will aggravate the disease progress, and even lead to death in serious cases. Therefore, understanding the pathogenesis of diabetes, early detection, and intervention are the main means of treatment. S-nitrosylation (SNO), a post-translational modification of proteins based on redox, possesses the capacity to regulate a variety of physiological and pathological processes, and it is also involved in the occurrence and development of T2DM. However, the relationship between the dysregulation of SNO homeostasis and the occurrence of diabetes is not fully understood. This article reviews the correlation between SNO and T2DM, elucidating the mechanism by which SNO contributes to T2DM, encompassing diminishing insulin secretion, inducing insulin resistance, and affecting glucokinase activity. Understanding the correlation between SNO and T2DM provides a new research direction for the pathogenesis and treatment targets of diabetes.

Mental anorexia nervosa is a rare, potentially severe, chronic, and recurrent mental disorder that occurs more often in women than in men, especially during the childbearing years. The disorder is associated with an increased risk of mortality, mainly related to the physical consequences of severe malnutrition and suicide. Malnutrition of the body can cause serious hormonal and somatic problems. Despite significant hormonal disturbances that reduce fertility, a woman with anorexia can become pregnant. A new phenomenon now seen with increasing frequency is pregorexia, an eating disorder associated with pregnancy. It involves the use of dietary restrictions to avoid excessive weight gain during pregnancy. Pregnancy changes the hormonal economy mainly due to the development of the placenta, which secretes many hormones, not just sex hormones. Mental anorexia poses a significant risk to both mother and child if not diagnosed and treated properly. Treatment of anorexia involves simultaneous somatic and psychological treatment. During pregnancy, additional care should be taken to create an optimal environment for the developing foetus. Unfortunately, there is still a lack of research providing guidance in this area. Available studies are mainly case reports or reports focusing on specific clinical situations. It is worth noting that no study to date has attempted a comprehensive assessment of endocrine disruption in pregnant women with anorexia. Recognising the existing knowledge gap on endocrine disorders in pregnant women with anorexia nervosa, a systematic review of the literature was conducted.

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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.

Proton pump inhibitors (PPIs) are one of the most frequently used medications worldwide. The side effects of this class of drugs have been widely studied. However, their impact on the electrolyte balance is frequently forgotten. Long-term PPI administration can lead to profound electrolyte disturbances, namely hypomagnesaemia as well as, secondary to very low magnesium levels, hypocalcaemia and hypokalaemia. In this paper we comprehensively review the complexity of the mechanisms contributing to electrolyte imbalance following PPI (proton pump inhibitors) by changing the pH in the intestinal lumen, interfering with the active cellular transport of magnesium regulated by the transient receptor potential melastatin cation channels TRPM6 and TRPM7. The accompanying hypomagnesaemia causes unblocking of the renal outer medullary potassium channel (ROMK), which results in increased potassium loss in the ascending limb of the loop of Henle. Hypokalaemia caused by hypomagnesaemia is resistant to potassium supplementation because the loss of this element in urine increases with the supply of potassium. Additionally, within the calcium-sensitive receptor (CASR), dissociation of magnesium from the alpha subunit of G protein caused by hypomagnesaemia increases its activity, leading to inhibition of PTH secretion and hypocalcaemia resistant to calcium supplementation. All this means that in some patients, chronic use of proton pump inhibitors by affecting the absorption of magnesium, may lead to life-threatening electrolyte disorders.

Hypothyroidism is one of the most common endocrinopathies worldwide, the treatment of which is based on replacement therapy with levothyroxine. However, this seemingly simple treatment method is fraught with many difficulties and frequent dissatisfaction among patients. In fact, differences in response to levothyroxine probably depend on a complex interaction between individual, environmental, genetic, and epigenetic factors that are still not sufficiently understood. Immunological disturbances, underlying Hashimoto's disease, the most common cause of hypothyroidism, probably play a significant role in these relationships. Indeed, a growing number of studies indicate that autoimmunity through activation of low-grade inflammation can lead to impaired absorption, transport, metabolism, and action of thyroid hormones. This review provides an up-to-date overview of the causes responsible for both the difficulty in achieving target thyrotropin levels and persistence of nonspecific symptoms despite adequate hormone replacement from an immunoendocrine perspective. Understanding these mechanisms points to a new direction in the approach to hypothyroidism, indicating the need for new personalized treatment strategies.

Introduction: The acid-labile subunit (ALS) is a protein best known for its function in stabilising the insulin like growth factor-1/2-insulin-like growth factor-1 binding protein 3/5 (IGF-1/2-IGFBP3/5) binary complex by creating the ternary complex and in consequence regulating the biological activity of IGF-1. The aim of the study was to assess ALS concentrations in a chosen population of children with short stature taking into account their clinical diagnosis.

Material and methods: A total of 109 prepubertal children were involved in the study - 85 children in the study group and 24 in controls. In all the children IGF-1, IGFBP3, and ALS were measured. The study group was divided according to diagnosis into groups: growth hormone deficiency (GHD), constitutional delay of growth and puberty (CDGP), idiopathic short stature (ISS), and familial short stature (FSS).

Results: In the control group the ALS concentration ranged from 4.81 to 13.66 μg/mL. In the whole study group the ALS concentration ranged from 2.73 to 15.81 μg/mL. The difference between both groups was statistically significant (p < 0.0001, R = 0.39). A strong, statistically significant correlation between ALS levels and age was observed, but only in the study group (p < 0.0001, r = 0.59). The ALS standard deviation score (SDS) was not significantly different between the control and CDGP children (p = 0.0644). The ALS concentration was significantly lower in children with short stature. There was, however, no difference between the subgroups of the study group.

Conclusion: There was no significant difference in ALS SDS between the control group and children with constitutional delay of growth and development. The usefulness of ALS in routine short stature diagnostics is uncertain, but it might play a role in the diagnosis of children with ISS and CDGP in the future.