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The phenomenon of autoimmunity develops as a result of the triggering factor released by damaged cells. This leads to an infiltration of CD4+ cells involved in stimulating the effector cells cytotoxicity and stimulating the humoral response. One of the most common autoimmune disorders are autoimmune thyroid diseases, including Hashimoto's thyroiditis and Graves's diseases. Helper T lymphocytes, which are divided into Th1, Th2, Tregs, and the relatively new groups Th17, Th22, and Th9, are involved in the pathogenesis of AITD. CD4+ cell subtypes mature and differentiate by specific transcription factors and in a specific interleukin environment. Not only are Th1 and Th2 cells involved in the development of AITD, but also Th17, Th22, and Th9 lymphocytes and their correlation to Tregs lymphocytes. The plasticity of the CD4+ cells is very important, affecting the balance between these cells, as well the factors modulating their phenotypic variability. Patients with AITD have an increased percentage of Th17, Th22, and Th9 cells as well as defective function of Tregs lymphocytes. The balance between Th17 cells (and also other cytotoxic T cells) and Treg cells is also very important. Understanding the role of CD4 cells in the pathogenesis of AITD may be important not only for the development of the knowledge, but also for determining therapeutic targets.

Through pleiotropic effects related to the presence of its receptors in major human organs, vitamin D (VD) plays an important role in systemic homeostasis, especially in the proper functioning of muscles and bones. In light of the published data from both animal and human studies, VD deficiency should be considered a risk factor for obesity-related morbidity, prediabetes, and type 2 diabetes (T2D); in addition, VD supplementation in VD deficiency has a beneficial effect on the effects of treatments aimed at normalization of body weight (including incretin drugs) and the metabolism of carbohydrates in prediabetes and T2D. The objective of this paper is to present the current knowledge and evidence on the relationship between VD deficiency and obesity, prediabetes, and T2D. The paper is intended to be used as a practical guide. The authors propose that serum 25(OH)D concentrations be determined in adults who are obese or overweight (i.e., belonging to the group presenting with a multiple increase in the risk of VD deficiency) or adults who are obese or overweight and have prediabetes or T2D. The baseline VD levels should determine the therapeutic dose and be helpful in assessing the effectiveness of therapy. The available literature lacks precise information regarding the recommended doses of VD in obese people, with 4000 IU being a frequently suggested daily dose. Most papers recommend that body weight be taken into account when determining the dose of VD in the obese; the dose should be higher than in individuals with normal body mass index (BMI). The authors suggest that in the case of low VD levels (< 20.0 ng/mL), quite frequently as low as 12.0–15.0 ng/mL, in an adult obese patient, VD therapy should be started at 20,000 IU two times per week or 50,000 IU once a week with 25(OH)D and calcium levels being checked after one month so that a decision can be made on the further course of therapy. The suggested 25(OH)D concentration target range is > 30–50 ng/mL. In a patient-tailored supplementation model, the dose of VD should depend on body weight and, most importantly, on the baseline VD level. In the absence of the expected effects, the authors suggest that the dose of VD (usually vitamin D3) be increased or the treatment be switched to calcifediol or alfacalcidol, or calcitriol in special cases such as impaired kidney or liver function. It is important to emphasize the need to individualize the management and monitor blood calcium and creatinine levels during chronic VD therapy, including high-dose therapy.

INTRODUCTION: Administration of testosterone or dehydroepiandrosterone to subjects with low levels of these hormones was found to reduce thyroid antibody titres. Male-pattern baldness is accompanied by mildly increased androgen levels. The present study was aimed at investigating whether early-onset androgenetic alopecia determines the impact of exogenous levothyroxine on thyroid autoimmunity and hypothalamic–pituitary–thyroid axis activity in young men with autoimmune hypothyroidism. MATERIAL AND METHODS: The study included 2 thyroid-antibody-matched groups of men with autoimmune hypothyroidism: subjects with early-onset androgenetic alopecia (group 1; n = 24) and subjects with no evidence of hair loss (group 2; n = 24). All patients were treated with exogenous levothyroxine. Circulating titres of thyroid peroxidase and thyroglobulin antibodies, as well as levels of thyrotropin, free thyroxine, free triiodothyronine, prolactin, total testosterone, calculated bioavailable testosterone, dehydroepiandrosterone-sulphate, and oestradiol were measured before levothyroxine treatment and 6 months later. RESULTS: In both study groups, levothyroxine decreased thyroid antibody titres, reduced thyrotropin levels and increased free thyroid hormone levels. However, these effects were less pronounced in the men with early-onset male-pattern baldness than in the control men. The degree of reduction in antibody titres and thyrotropin levels correlated with baseline levels of total and calculated bioavailable testosterone, as well with baseline insulin sensitivity and treatment-induced improvement in insulin sensitivity. Concentrations of the remaining variables remained unchanged throughout the study period. Conclusions:The results of the current study suggest that the benefits of levothyroxine therapy in men with autoimmune hypothyroidism are less pronounced in individuals with early-onset androgenetic alopecia.

INTRODUCTION: Ischaemic stroke (IS) is a disease that is a common cause of death and one of the most common causes of disability in adults. There is a continuous need to conduct stroke pathogenesis studies. A certain role here can be attributed to adipose-derived hormones. The aim of this paper is to assess the blood concentration for selected adipocytokines: omentin-1, irisin, protein-1 related with C1q/TNF (CTRP1), vaspin and nesfatin-1 in IS patients, and an attempt to define their role as risk factors for ischaemic stroke. MATERIAL AND METHODS: The study included 46 patients with ischaemic stroke (27 females, 19 males, average 67.6 years of age). The control group consisted of 32 patients (16 females, 16 males, average 64.1 years of age) who had never had cerebrovascular diseases. RESULTS: The concentration of omentin-1 and CTRP1 in the group of stroke patients was higher than in the control group, whereas the concentrations of nesfatin-1 and irisin was significantly lower than in the control group. The vaspin level was similar in both groups of patients. Statistical analysis using logistic regression allows us to find that CTRP1 can be a significant stroke risk factor. A statistically significant positive correlation was found between the concentration of CTRP1 and NIHSS. However, no correlation between the concentration of other adipocytokines under investigation and the severity of ischaemic stroke was found. CONCLUSIONS: From among the adipocytokines under investigation, higher concentrations of omentin-1 and CTRP1 and lower blood concentrations of nesfatin-1, irisin significantly increase the odds of getting to the group of ischaemic patients. It seems that CTRP1 can be an independent predictive factor of IS.

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INTRODUCTION: Despite considerable progress in knowledge, ischaemic stroke is still a disease that causes serious clinical problems. A role in its pathogenesis can be attributed to i.a. adipose tissue hormones. The aim of this paper is to assess the blood levels of selected adipocytokines in patients during the acute phase of ischaemic stroke as compared to healthy persons, and an attempt to indicate a correlation between their blood concentrations and the level of stroke severity and its outcomes. MATERIAL AND METHODS: The study included 46 patients with fresh ischaemic stroke (27 females, 19 males, average age 67.6 years). All patients had a CT scan of the head, their neurological condition was assessed using a stroke severity scale, and their blood levels of resistin, chemerin, and visfatin were tested. The control group consisted of 32 patients (16 females, 16 males, average age 64.1 years) who had never suffered cerebrovascular diseases. RESULTS: Elevated levels of both resistin and chemerin were found in the group of patients with ischaemic stroke (9.17 ± 2.95 ng/mL vs. 6.55 ± 2.01 ng/mL for resistin and 265.0 ± 59.3 ng/mL vs. 191.0 ± 43.6 ng/mL for chemerin). It was also found that the blood concentration of chemerin was higher in females than in males with stroke. However, no difference was found in visfatin blood concentration between the group with ischaemic stroke and the control group (1.65 ± 1.09 ng/mL vs. 1.5 ± 1.39 ng/mL). CONCLUSIONS: Higher resistin and chemerin blood concentrations significantly increase the risk of ischaemic stroke. The level of stroke severity at the moment of its occurrence and during its course do not depend on the concentrations of adipocytokines under analysis.

INTRODUCTION: The aim of this study was to assess the therapeutic effect and the safety of pre-surgical treatment with long-acting octreotide in patients with acromegaly. MATERIAL AND METHODS: This project was conducted in 25 centres across Poland as a non-interventional, multicentre, observational study in patients with acromegaly, in which long-acting octreotide Sandostatin® LAR®) was administered before surgery. They were 148 patients included into the study: 88 females and 60 males aged 18–86 years (51.3 ± 13.4). RESULTS: Eighty patients completed the study (underwent tumour surgery). The CRF included: baseline visit, four follow-up visits every three months before surgery, and two follow-up visits every three months after surgery. Sandostatin® LAR® was administered every four weeks. The efficacy measures were as follows: change of growth hormone (GH) and insulin-like growth factor 1 (IGF-1) levels, number of patients fulfilling criteria of cure, and change of adenoma (micro- and macroadenomas) size during the treatment. Normalisation of GH and IGF-1 concentrations were obtained in 42.4 and 49.1% of patients at the end of medical therapy, respectively. Normalisation of GH and IGF-1 concentrations were obtained in 77.9 and 83.8% of patients after surgery, respectively. Reduction of microadenoma size was documented in 58.8% of patients, and in 70% of patients with macroadenomas at the end of medical therapy. In 74.0% of patients no pituitary tumour was shown on MRI after surgery. CONCLUSION: We have shown good surgical outcome in patients with acromegaly after pre-treatment with somatostatin analogue, and good tolerance and safety of the therapy, supporting the national recommendation for pre-surgical treatment with long-acting somatostatin analogues in acromegaly patients.

The aim of this study was to evaluate the ferric-reducing ability of serum (FRAS), paraoxonase 1 (PON1), ceruloplasmin serum oxidase activity and hsCRP level in patients with type1 diabetes mellitus without and with diabetic retinopathy. The study was performed in 76 patients with type 1 diabetes mellitus, 35 without diabetic retinopathy (group 1) and 41 with preproliferative and proliferative retinopathy (group 2). Control group consisted of 35 nondiabetic, age-, gender-, body mass-matched healthy volunteers who came to the outpatient clinic for a routine health check-up. We evaluated FRAS using the method described by Benzie and Strain; PON1 by kinetic spectrophotometric assay with paraoxon as substrate and ceruloplasmin using its oxidative activity with 3-phenylenodiamine as substrate. CRP was measured with a high sensitive enzyme immunoassay. PON1 activity was significantly decreased in patients with diabetic retinopathy (227.66 ± 123.57 U/l) when compared with control (312.04 ± 129.77 U/l). FRAS was significantly decreased in group 2 (439.33 ± 79.87 μmol/l) when compared with group 1 (522.79 ± 167.56 μmol/l) and control (529.80 ± 81.99 μmol/l). Ceruloplasmin activity was significantly elevated in group 1 (58.36 ± 22.56 U/g protein) when compared with control (45.22 ± 14.96 U/g protein). We have found significant increase in hsCRP level in group 2 (3.71 ± 2.47 mg/l) when compared with group 1 (1.75 ± 1.01 mg/l) and control (0.57 ± 0.46 mg/l). The PON1/CRP ratio in control group was significantly increased when compared with diabetic patients and was significantly decreased in group 2 compared with group 1. We have not found gender-dependent difference in studied parameters in both control and in study groups. We have found tendency to decrease the serum activity of FRAS and hsCRP in elder patients but the difference was significant only in group 2. FRAS and PON 1 activity is decreased in patients with type 1 diabetes mellitus with presence of diabetic retinopathy which confirms that oxidative stress could play a role in pathogenesis of diabetic retinopathy. Significantly elevated levels of hsCRP in diabetic patients with the presence of diabetic retinopathy compared with patients without diabetic retinopathy providing a link between inflammation and the development of microvascular complication of diabetes. Because of the significant difference in PON1/CRP ratio between patients without and with the presence of diabetic retinopathy, it seems that PON1:CRP ratio may be used as a biochemical marker for progression of retinopathy. The link between the antioxidant concentration, inflammation and the development of diabetes complications needs further longitudinal studies in order to confirm our findings.

This review describes precisely the consequence of TGFbeta1 prevalence in the organism, and its significant influence on physiological andpathophysiological processes. Organ and tissue distinctiveness hinder unambiguous characterisation of the cytokine. However, there areconstant functions of TGFbeta1 inducing no controversy: it participates in foetal development, control of cell growth and differentiation,induces fibrosis and scar formation (the process of ‘wound healing’), causes the suppression of immune response, is involved in angiogenesis,the development of tumours, and inflammatory processes. Thus, TGFbeta1 is a multifunctional cytokine. There are three fundamentaldirections of its activities: I. TGFbeta1 regulates cell proliferation, growth, differentiation and cells movement. II. TGFbeta1 has immunomodulatoryeffects. III. TGFbeta1 has profibrogenic effects. TGFbeta1 action can be local and systemic. This review describes TGFbeta1 in pathology:colitis ulcerosa, Crohn’s disease, coeliac disease, diabetic nephropathy, diabetic retinopathy and diabetic foot, pulmonary hypertension,and Alzheimer’s disease. TGFbeta1 and its receptors are also of interest to endocrinologists. Lack of TGFbeta1-dependent growth control mayresult in oncogenesis: papillary, follicular and anaplastic thyroid cancers, prostate, breast and uterine cervical cancer, oesophagus, gastric,colorectal and liver cancers, NSCLC, and malignant melanoma. Excessive TGFbeta1 activity is an integral part of the fibrotic processes occurringin the response to injury. An increased TGFbeta1 expression has been observed in patients with pulmonary, kidney, and liver fibrosis. Inchronic hepatitis, the prolonged stimulation of hepatic stellate cells being the result of chronic damage to hepatocytes results in the releaseof profibrogenic abundant factors such as TGFbeta1 and leads to the development of liver cirrhosis. The results of experimental proceduresand treatment known as anti-TGFbeta1 strategy acting against the fibrosis in various tissues leads to hope regarding the use of anti-TGFbeta1strategy in clinical practice.(Endokrynol Pol 2013; 64 (5): 384–396)