(1) Background: Graves’ orbitopathy (GO) is an autoimmune inflammation of the orbital tissues and the most common extra-thyroid symptom of Graves’ disease (GD). Mild cases of GO are often misdiagnosed, which prolongs the diagnostic and therapeutic process, leading to exacerbation of the disease. A severe course of GO may cause permanent vision loss. (2) Methods: The article presents an analysis of GO—its etiopathogenesis, diagnostics, current treatment and potential future therapeutic options based on a review of the currently available literature of the subject. (3) Results: Current treatment of the active GO consists predominantly in intravenous glucocorticoids (GCs) administration in combination with orbital radiotherapy. The growing knowledge on the pathogenesis of the disease has contributed to multiple trials of the use of immunosuppressive drugs and monoclonal antibodies which may be potentially effective in the treatment of GO. Immunosuppressive treatment is not effective in patients in whom a chronic inflammatory process has caused fibrous changes in the orbits. In such cases surgical treatment is performed—including orbital decompression, adipose tissue removal, oculomotor muscle surgery, eyelid alignment and blepharoplasty. (4) Conclusions: Management of GO is difficult and requires interdisciplinary cooperation in endocrinology; ophthalmology, radiation oncology and surgery. The possibilities of undertaking a reliable assessment and comparison of the efficacy and safety of the therapeutic strategies are limited due to the heterogeneity of the available studies conducted mostly on small group of patients, with no comparison with classic systemic steroid therapy. The registration by FDA of Teprotumumab, an IGF1-R antagonist, in January 2020 may be a milestone in future management of active GO. However, many clinical questions require to be investigated first.

Background. Diabetes mellitus (DM) is a non-infectious pandemic of the modern world; it is estimated that in 2045 it will affect 10% of the world’s population. As the prevalence of diabetes increases, the problem of its complications, including diabetic retinopathy (DR), grows. DR is a highly specific neurovascular complication of diabetes that occurs in more than one third of DM patients and accounts for 80% of complete vision loss cases in the diabetic population. We are currently witnessing many groundbreaking studies on new pharmacological and surgical methods of treating diabetes. Aim. The aim of the study is to assess the safety of pharmacological and surgical treatment of DM in patients with DR. Material and methods. An analysis of the data on diabetes treatment methods currently available in the world literature and their impact on the occurrence and progression of DR. Results. A rapid decrease in glycaemia leads to an increased occurrence and progression of DR. Its greatest risk accompanies insulin therapy and sulfonylurea therapy. The lowest risk of DR occurs with the use of SGLT2 inhibitors; the use of DPP-4 inhibitors and GLP-1 analogues is also safe. Patients undergoing pancreatic islet transplants or bariatric surgeries require intensive monitoring of the state of the eye, both in the perioperative and postoperative period. Conclusions. It is of utmost importance to individualize therapy in diabetic patients, in order to gradually achieve treatment goals with the use of safe methods and minimize the risk of development and progression of DR.

Autoimmune thyroid disease (AITD) is more common among diabetes mellitus (DM) patients and may impact its microvascular complications. The present study aimed to assess the relationship between AITD and the prevalence of diabetic kidney disease (DKD) in patients with diabetes mellitus type 1 (DM1). Anthropometric parameters, parameters of metabolic control of DM, thyreometabolic status, and the UACR were assessed. DKD was diagnosed if patients’ UACR level was ≥30 mg/g or eGFR level was <60 mL/min. This study involved 144 patients with DM1 aged 36.2 ± 11.7 years: 49 men and 95 women. Significant differences in creatinine, eGFR, and UACR levels were found in patients with DKD. fT3 concentration was significantly lower among DKD patients. A significantly higher probability of DKD was found in DM1 patients with lower fT3 levels. Patients with DM1 and AITD had significantly lower creatinine levels than the control group. However, the study did not show any significant relationship between AITD and the occurrence of DKD in patients with DM1. Significantly lower fT3 concentrations in DKD patients may be caused by metabolic disorders in the course of DKD and require further cohort studies in a larger population of patients with DM1 and AITD.

Autoimmune thyroid disease (AITD) is the most prevalent autoimmune disease all over the world and the most frequent cause of hypothyroidism in areas of iodine sufficiency. The pathogenesis of AITD is multifactorial and depends on complex interactions between genetic and environmental factors, with epigenetics being the crucial link. Iron deficiency (ID) can reduce the activities of thyroid peroxidase and 5′-deiodinase, inhibit binding of triiodothyronine to its nuclear receptor, and cause slower utilization of T3 from the serum pool. Moreover, ID can disturb the functioning of the immune system, increasing the risk of autoimmune disorders. ID can be responsible for residual symptoms that may persist in patients with AITD, even if their thyrometabolic status has been controlled. The human lifestyle in the 21st century is inevitably associated with exposure to chemical compounds, pathogens, and stress, which implies an increased risk of autoimmune disorders and thyroid dysfunction. To summarize, in our paper we discuss how iron deficiency can impair the functions of the immune system, cause epigenetic changes in human DNA, and potentiate tissue damage by chemicals acting as thyroid disruptors.

“Ferrocrinology” is the term used to describe the study of iron effects on the functioning of adipose tissue, which together with muscle tissue makes the largest endocrine organ in the human body. By impairing exercise capacity, reducing AMP-activated kinase activity, and enhancing insulin resistance, iron deficiency can lead to the development of obesity and type 2 diabetes mellitus. Due to impaired browning of white adipose tissue and reduced mitochondrial iron content in adipocytes, iron deficiency (ID) can cause dysfunction of brown adipose tissue. By reducing ketogenesis, aconitase activity, and total mitochondrial capacity, ID impairs muscle performance. Another important aspect is the effect of ID on the impairment of thermogenesis due to reduced binding of thyroid hormones to their nuclear receptors, with subsequently impaired utilization of norepinephrine in tissues, and impaired synthesis and distribution of cortisol, which all make the body’s reactivity to stress in ID more pronounced. Iron deficiency can lead to the development of the most common endocrinopathy, autoimmune thyroid disease. In this paper, we have discussed the role of iron in the cross-talk between glucocrinology, lipocrinology and myocrinology, with thyroid hormones acting as an active bystander.