The degeneration of retinal neurons and glial cells has recently been postulated in the pathogenesis of diabetic retinopathy. Optical coherence tomography (OCT) allows to perform qualitative and quantitative measurements of retinal thickness (RT) with identification of individual retinal layers. We compared RT, retinal nerve fiber layer (RNFL) thickness, and ganglion cell layer (GCL) thickness obtained by OCT in type 1 diabetic patients with and without clinically diagnosed retinopathy. The study included 77 consecutive patients with type 1 diabetes (39 men, 38 women; median age, 35 years [interquartile range (IQR), 29-42]; median disease duration, 10 years [IQR, 9-14]) and 31 age- and sex-matched controls. We measured RT in the fovea, parafovea, and perifovea, as well as RNFL and GCL thickness. We divided diabetic patients into 2 subgroups, i.e., those with diabetic retinopathy and without retinopathy. We observed thicker perifoveal retina (P = 0.05), mean RNFL (P = 0.002), inferior RNFL (P <0.0001), and superior and inferior GCL (P = 0.05 and P = 0.04, respectively) in diabetic subjects compared with the control group. We detected retinopathy in 23 diabetic patients (29%). Compared with patients without retinopathy, subjects with retinopathy had thinner parafoveal retina (P = 0.05), mean RNFL (P = 0.002), inferior and nasal RNFL (P = 0.002, P = 0.03), superior (P = 0.05) and inferior GCL (P = 0.006). Significant correlations were found between duration of diabetes and nasal RNFL thickness (r = -0.32, P = 0.004) and parafoveal RT (r = -0.47, P <0.001). The results might suggest the loss of intraretinal neural tissue in type 1 diabetic patients with retinopathy. Neurodegeneration in diabetic retinopathy is closly associated with disease duration.

Aims To assess the prevalence of ZnT8-ab and its correlation to other autoimmune markers and diabetic ketoacidosis occurrence in children and adults with T1DM onset. Methods The study included 367 patients (218 children; 149 adults) at the T1DM onset. Selected diabetes-related autoantibodies such as GAD-ab, IA2-ab, ZnT8-ab were tested before the initiation of insulin therapy. Diabetic ketoacidosis was defined as glucose concentration > 13.9 mmol/l, pH < 7.30, concentration of HCO₃ < 15 mmol/l, presence of ketone bodies in the blood and urine. Results The autoantibodies pattern differs in both study groups. Children were mostly positive for two (37.8%) and three (49.5%) autoantibodies, whereas adults for one (32.2%) and two (30.7%). The most frequently detected autoantibodies in youth were ZnT8-ab (81.1%) and IA2-ab (80.7%), while in adults GAD-ab (74.8%). ZnT8-ab (p < 0.0001) titers were significantly higher in children, but adults had higher titer of GAD-ab (p < 0.0001) and IA2-ab (p < 0.0001). Children developed more frequently diabetic ketoacidosis (28.4 vs. 10.7%, p = 0.0002). ZnT8-ab (p = 0.002) and IA2-ab (p = 0.008) were reported mostly in individuals with ketoacidosis. A correlation between the number of positive antibodies and the severity of ketoacidosis was observed (R_s − 0.129 p = 0.014). ZnT8-ab were associated with a greater risk of ketoacidosis independent of gender, age group and the autoantibodies number [OR = 2.44 (95% CI 1.0–5.94), p = 0.04]. Conclusions Children are at greater risk of ketoacidosis at the diagnosis of diabetes. ZnT8-ab and IA2-ab are commonly detected in children, while adults have frequently higher titer of GAD-ab. ZnT8-ab are associated with more acute diabetes onset.

Changes in sensitivity to insulin occur in the course of a number of endocrine disorders. Most of the hormones through their antagonistic action to insulin lead to increased hepatic glucose output and its decreased utilisation in peripheral tissues. Carbohydrate disorders observed in endocrine diseases result from the phenomenon of insulin resistance, and in some cases also a reduction in insulin secretion is present. Abnormalities of glucose metabolism are observed in acromegaly, but also in growth hormone deficiency, hypercortisolism in the course of Cushing’s syndrome, hyper- or hypothyroidism, primary hyperparathyroidism, aldosteronism, pheochromocytoma, congenital hypertrophy of the adrenal glands, polycystic ovaries syndrome, hypogonadism, or other hormonally active neuroendocrine tumours. They are of a secondary nature in relation to impaired hormonal balance. Hyperglycaemia is therefore often reversible, and the most effective method of treatment of impaired insulin sensitivity is successful therapy of specific endocrinopathies. Insulin sensitisers, also with a good effect, are used. Most experiences to date can be attributed to metformin therapy. Attempts have been made at treatment with other agents that are also effective in reducing insulin resistance as incretins or glitazones. In the presented paper, the authors reviewed endocrine diseases in which there is a clinically significant change in insulin sensitivity. Moreover, methods of therapy of concomitant disturbed glucose metabolism were presented. Changes in sensitivity to insulin occur in the course of a number of endocrine disorders. Most of the hormones through their antagonistic action to insulin lead to increased hepatic glucose output and its decreased utilisation in peripheral tissues. Carbohydrate disorders observed in endocrine diseases result from the phenomenon of insulin resistance, and in some cases also a reduction in insulin secretion is present. Abnormalities of glucose metabolism are observed in acromegaly, but also in growth hormone deficiency, hypercortisolism in the course of Cushing’s syndrome, hyper- or hypothyroidism, primary hyperparathyroidism, aldosteronism, pheochromocytoma, congenital hypertrophy of the adrenal glands, polycystic ovaries syndrome, hypogonadism, or other hormonally active neuroendocrine tumours. They are of a secondary nature in relation to impaired hormonal balance. Hyperglycaemia is therefore often reversible, and the most effective method of treatment of impaired insulin sensitivity is successful therapy of specific endocrinopathies. Insulin sensitisers, also with a good effect, are used. Most experiences to date can be attributed to metformin therapy. Attempts have been made at treatment with other agents that are also effective in reducing insulin resistance as incretins or glitazones. In the presented paper, the authors reviewed endocrine diseases in which there is a clinically significant change in insulin sensitivity. Moreover, methods of therapy of concomitant disturbed glucose metabolism were presented.

Purpose Type 1 diabetes mellitus (T1DM) is a disorder of insulin deficiency but with a wide range of hormones simultaneously disturbed. The study was performed to explore relation of free triiodothyronine (FT3) with metabolic control and occurrence of microangiopathic complications. Methods A total of 266 adult T1DM participants [56% men; 32 (interquartile range, IQR: 25–39) years and disease duration 13 (IQR: 8–19) years] in euthyroid state with negative history for hypothyroidism were included to the study. Participants were screened for thyroid-stimulating hormone (TSH), free thyroxine (FT4) and FT3. Moreover, microangiopathic complications (retinopathy, diabetic kidney disease, peripheral and autonomic neuropathy), markers of metabolic control such as glycated hemoglobin (HbA_1c) were evaluated. Results A total of 114 (42.9%) people had diagnosed at least one microangiopathic complication. In multivariable linear regression higher HbA_1c was statistically significant independent predictor of lower FT3 (β = −0.25; p < 0.0001) after adjustment for sex, T1DM duration, HbA_1c, waist-to-hip ratio (WHR) (R² = 0.15, p < 0.0001). Higher FT3 was simultaneously a predictor of lower prevalence of microangiopathy in multivariate logistic regression analysis (odds ratio, 0.51; 95% confidence interval, 0.27–0.98; p = 0.04) after an adjustment for: age, hypertension, HbA_1c, WHR and total cholesterol (TC). Conclusions FT3 as tissue active hormone plays a clinically important role in T1DM people. The higher FT3 concentration is related to the lower prevalence of microangiopathy and better metabolic control of the disease in adult euthyroid people with T1DM.

Objective: The diagnosis of autoimmune diabetes in non-obese adults is based on the detection of glutamic acid decarboxylase autoantibodies (GADA), islet cell antibodies (ICA) and antibodies to tyrosine phosphatase (IA-2A). Zinc transporter 8 (ZnT8) has been identified as a new autoantigen in patients with type 1 diabetes mellitus. The coincidence of autoimmune thyroiditis (AITD) with diabetes is common; therefore, screening of TSH and thyroid peroxidase antibodies (ATPO) is recommended during the diagnosis of diabetes. In this study, we determined whether the occurrence of islet autoantibodies is associated with a positive titre of ATPO in newly diagnosed adult-onset autoimmune diabetic patients.Design and methods: The study involved 80 non-obese adults aged 44 (interquartile range (IQR): 37–51) years with a BMI of 24.0 (IQR: 22.2–26.0) kg/m²and new-onset diabetes. The markers of autoimmune diabetes (GADA, ICA, IA-2A and ZnT8A), TSH and thyroid peroxidase antibodies (ATPO) were evaluated.Results: In the study population, 70% (n=56) of the subjects were positive for at least one of the four assessed markers of autoimmune diabetes (83.9% GADA, 62.5% ICA, 42.8% IA-2A and 33% ZnT8A) and 37.5% of the subjects were positive for ATPO. The ZnT8A-positive subjects had higher ATPO titres than the ZnT8A-negative subjects (172.7 (IQR: 0.36–410.4) vs 92.4 (IQR: 0–23.7) IU/ml,P=0.001). Based on the assessed islet autoantibodies, the occurrence of positive ZnT8A and GADA was found to be related to a positive titre of ATPO using logistic regression (OR=5.48, 95% CI: 1.65–18.14,P=0.006 and OR=3.42, 95% CI: 1.09–10.71,P=0.03 respectively).Conclusions: In non-obese adults with new-onset diabetes, the presence of GADA and especially ZnT8 autoantibodies increases the risk of AITD.

The aim of the study was to assess carotid intima-media thickness (CIMT) as a subclinical marker of atherosclerosis and arterial stiffness in type 1 diabetic patients in relation to microangiopathy. We included 87 type 1 diabetic patients (44 women, 43 men), median age 34 years (interquartile range [IQR] 29-43), median disease duration 10 years (IQR: 9-14), mean ± standard deviation (SD) glycated haemoglobin (HbA1c) 8.4 ±1.4%. Fifty patients had at least one microangiopathic complication. Intima-media thickness (IMT) of the common carotid artery was measured using high resolution ultrasonography. Arterial stiffness was assessed using digital volume pulse analysis and tonometric measurement of wave reflection and central haemodynamics. Subjects with microangiopathy compared with those without had higher values of CIMT (median [IQR]: 0.53 mm [0.45-0.60 mm] vs 0.47 mm [0.34-0.52 mm], p = 0.002), higher central augmentation index (CAIx) (mean ± SD: 120.2 ±19.4% vs. 110.5 ±17.1%, p = 0.016) and higher peripheral augmentation index (PAIx) (65.7 ±18.1% vs. 57.2 ±14.9%, p = 0.023). In the logistic regression analysis, the duration of diabetes, systolic and diastolic blood pressure, postprandial glycaemia, HbA1c and triglycerides predicted the presence of diabetic microangiopathy independently of age and sex. The CIMT, CAIx and PAIx were associated with the presence of diabetic microangiopathy only in the univariate model. In type 1 diabetic patients with microangiopathic complications, increased carotid IMT and arterial stiffness were observed. The study confirms the role of traditional risk factors for late diabetic complications, such as the duration of the disease and metabolic control in the development of microangiopathy.