Search

Music therapy is a therapeutic method used in dealing with people suffering from various somatic and mental disorders. The pa¬per discusses the current state of knowledge about the use of music therapy in the management of people suffering from obesity. Attention was paid to the possible positive effect of music therapy on weight control. It also reviews the literature of controlled clinical trials conducted over the past 10 years on the importance of music therapy in the treatment of obesity. These studies show that music therapy can have a positive effect on both weight loss and maintaining an adequate caloric supply of food. The small number of studies, however, does not allow to formulate precise conclusions and unambiguous conclusions. The issue of the ef¬fect of music therapy on the clinical condition of patients suffering from obesity requires further research.

Type two diabetes has become a civilization disease in the recent years, and the accompanying obesity, metabolic syndrome and non-alcoholic fatty liver are often the inseparable components of the clinical presentation in patients with diabetes of this type. The treatment of each of these elements is important for optimal metabolic control of the patients, as well as directly affecting their life expectancy. However, The ideal solution would be to take as few drugs as possible, preferably drugs that have a beneficial effect on several coexisting diseases at the same time. In the recent years, there have been more and more reports about the pleiotropic effect of drugs affecting the incretin axis - GLP-1 analogues. The presented paper provides an overview of the latest knowledge on the effect of GLP-1 receptor agonists on weight reduction and reduction of changes in the course of non-alcoholic fatty liver disease.

Research results indicate the presence of an association between mental disorders, certain antipsychotics, and the risk of developing prediabetes (preDM) and specific type diabetes mellitus (DM). However, there are no precise recommendations for their diagnosis and treatment. The obtained data suggest the necessity to perform diagnostics of carbohydrate disorders at the onset of the first symptoms of psychosis, even before the implementation of antipsychotic drugs, and the oral glucose tolerance test (OGTT) seems to be the optimal tool. There is a lot of controversy regarding the timing of control tests addressing the development of dysglycaemia during the use of antipsychotic drugs. We suggest that it should be carried out during the first 4-8 weeks, and in the absence of disorders it should be repeated once a year or with a change in antipsychotic treatment. The diagnostic regimen should then include the need for OGTT supported by routine determination of the percentage of glycated haemoglobin. If dysglycaemia is diagnosed, the therapeutic management should include non-pharmacological management and hypoglycaemic agents. These recommendations should be individually tailored to each patient and take into account the presence of obesity, which is often found in this group of patients. Weight reduction can be achieved with a properly balanced diet, physical effort, and in justified situations also with drugs effectively reducing body weight. For this reason, drugs are recommended that, if preDM and DM are diagnosed, simultaneously lower glucose levels and reduce body weight. So far, effectiveness in this area has been demonstrated for 2 incretinomimetics: exenatide and liraglutide. Due to the mechanism of preDM/DM development in patients using antipsychotics, the usefulness of other hypoglycaemic drugs with insulin-sensitizing potential - metformin and pioglitazone - has also been suggested. To date, there has been no research on the benefits of other hypoglycaemic drugs in this group of patients.

Oxidative stress is one of the pillars crucial in the development of a non-alcoholic fatty liver disease (NAFLD) and may cause DNA damage. Since the main pathway responsible for the repair of oxidative DNA damage is the base-excision repair (BER) pathway, we examined the relationship between the presence of different genetic variants of BER-associated genes and the risk of NAFLD. The study evaluates seven single nucleotide polymorphisms (SNPs) within five genes, hOGG1, APEX1, NEIL1, LIG3, LIG1, in 150 NAFLD patients and 340 healthy controls. The genotyping was performed using TaqMan probes and the results were presented as odds ratio with its corresponding 95% confidence interval. The following SNPs were assessed in the study: hOGG1 (rs1052133), APEX1 (rs176094 and rs1130409), NEIL1 (rs4462560), LIG3 (rs1052536), LIG3 (rs4796030), and LIG1 (rs20579). Four of the investigated SNPs, i.e., rs176094, rs1130409, rs4462560 and rs4796030, were found to be associated with NAFLD risk. Furthermore, the occurrence of insulin resistance in patients with steatosis depended on various LIG3 genetic variants. The findings imply the impact of genes involved in BER on NAFLD and fatty liver-related insulin sensitivity.

Background: The increasing prevalence of type 2 diabetes mellitus (T2DM) and non-alcoholic fatty liver disease (NAFLD) states a serious problem for public health. The introduction of effective methods of treatment and prevention is crucial to avoid complications of these diseases. Among them, we can specify psychological factors that affect everyday life and determine the patient’s attitude towards therapy, and what follows, their compliance in treatment. The literature indicates these connections in various ways; in our study, we extend this view to include a broader perspective of human personality. Objective: We decided to investigate the associations between personality factors and metabolic parameters in patients with NAFLD and T2DM in order to better understand the patient’s approach to the treatment of a chronic disease, such as those mentioned, and to establish the basis for further research implementing psychological interventions in the treatment of NAFLD and T2DM. Methods: One hundred participants with NAFLD and T2DM underwent blood tests and anthropometric measures. Each of them was asked to complete five questionnaires evaluating their personality properties. Results: We revealed that a rise in body mass index is related to a fall in the emotional intelligence factor of utilizing emotions, and a rise in emotional perception. The decrease in task-oriented coping style and a rise in emotion-oriented coping style are associated with a waist-hip ratio increase. The increase in fasting plasma glucose is predicted by a decrease in task-oriented coping style score. A fall in social diversion coping style score is associated with a high-density lipoprotein increase; in turn, a triglycerides increase is connected with a decline in rhythmicity score. Conclusions: The personality factors are in relationship in the management of NAFLD and T2DM. They affect a patient’s approach to treatment, which is very important, because we know lifestyle and dietary interventions are an important part of the treatment of these diseases. The compliance manifests by lifestyle modifications, taking medications regularly, measuring blood glucose, and inspection visits in outpatients’ clinics are a large part of a diabetic’s life. Future studies introducing psychological intervention to improve, e.g., coping styles or rhythmicity are needed to implement new methods of patient management.

Several studies report elevated blood platelet activation and altered platelet count in COVID-19 patients, but the role of the SARS-CoV-2 spike protein in this process remains intriguing. Additionally, there is no data that anti-SARS-CoV-2 neutralizing antibodies (nAb) may attenuate spike protein activity toward blood platelets. Our results indicate that under in vitro conditions, the spike protein increased the collagen-stimulated aggregation of isolated platelets and induced the binding of vWF to platelets in ristocetin-treated blood. The spike protein also significantly reduced collagen- or ADP-induced aggregation or decreased GPIIbIIIa (fibrinogen receptor) activation in whole blood, depending on the presence of the anti-spike protein nAb. Our findings suggest that studies on platelet activation/reactivity in COVID-19 patients or in donors vaccinated with anti-SARS-CoV-2 and/or previously-infected COVID-19 should be supported by measurements of spike protein and IgG anti-spike protein antibody concentrations in blood.

The onset of schizophrenia symptoms usually occurs in early youth. As a result, the parents of these patients usually become their caregivers. The role of a caregiver for a person with schizophrenia is a considerable mental and physical burden. Therefore, an interesting issue is what motivates these people to take up this challenge. It is probable that, apart from the moral imperative or kinship, the factor determining this decision is the personality structure of the caregiver. The aim of our study was to compare the structure of temperament (according to the model of temperament as formal characteristics of behavior developed by Jan Strelau) in caregivers of young adults (age 18–25 years) with schizophrenia with the structure of temperament of parents of healthy young adults still living in the family home under their care. The study group consisted of 64 people (51 women), who were taking care of young adults (aged 18–25 years) with schizophrenia, while the control group (53 people, 42 women) consisted of parents of healthy adults still living in the family home. Both groups were asked to complete a questionnaire of the authors’ own design on their demographic data as well as The Formal Characteristics of Behavior—Temperament Inventory to assess the temperament traits. The results were given in the number of points obtained on average in each dimension. Both groups did not differ in terms of size and age, with women predominating. Caregivers of young adults with schizophrenia had higher values of briskness (43.22 ± 4.45 vs. 42.90 ± 3.98, p = 0.032), emotional reactivity (46.02 ± 4.39 vs. 41.01 ± 3.12, p = 0.012) and activity level (44.01.89 ± 4.15 vs. 37.59 ± 4.77, p = 0.022) compared to the control group. The remaining dimensions of temperament: perseverance, sensory sensitivity, rhythmicity, and endurance did not differentiate between the two groups. The temperament structure of caregivers of young people with schizophrenia differs from the temperament structure of caregivers of healthy adults. Caregivers of sick people have higher values of briskness, emotional reactivity, and activity level compared to the control group.

Summary Diabetes mellitus (DM) is not a single disease, but a group of diseases that are characterized by chronic hyperglycemia and risk of damage to tissues and organs. The mechanisms of its development are different and due mainly to disorders of insulin secretion or its effects. For this reason, 4 types of DM have been distinguished. One of them is a specific type of DM, determined, inter alia, by the use of certain psychotropic medications. Chronic hyperglycemia often occurs in association with some of these drugs, but in many cases it is categorized erroneously as type 2 (T2DM) or 1 (T1DM). The relationship between DM and psychiatric disorders is bi-directional, involving two mutually independent risk factors for the development of the disease. However, not all patients with a mental illness develop carbohydrate metabolism disorders, which is due to a varied diabetogenic potential and mechanisms of action of psychotropic medications. In clinical practice, questions concerning the frequency of this type of DM, risk factors of its development and hyperglycemic mechanism of psychotropic medications arise. Therefore, the aim of this article is to attempt to answer these questions. From a practical point of view, obtaining such information should allow for the development of appropriate diagnostic and therapeutic procedures.

Background: The aim of the study was to evaluate the relationship between polyphenol or polyunsaturated fatty acids (PUFAs) consumption and the selected metabolic and inflammatory markers in type 2 diabetes (T2DM) patients. Methods: The study enrolled 129 diabetics (49 men, mean age 64.1 ± 9.8 years) with different amounts of polyphenol and PUFAs consumption. Results: A significant effect of polyphenol or PUFAs omega-3 consumption on fasting glucose concentration (FG) or glycated haemoglobin fraction (HbA1c) was reported. A negative association was observed between FG and total polyphenol, flavonoid, flavan-3-ol and stilbene intake. In the group with high flavonoid intake, the FG was significantly lower compared to the group characterised by low flavonoid intake. Polyphenols, except stilbenes, did not modulate HbA1c. Additionally, higher consumption of PUFAs omega-3 significantly decreased HbA1c, and the intake of eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids negatively and significantly correlated with FG and HbA1c. Further analysis confirmed a significant association between EPA + DHA intake and HbA1c, with significant interactions with age and gender or with body mass index and waist-to-hip ratio. The dietary intake of polyphenols or PUFAs was independent of familial diabetes or diabetic diet application. Conclusions: Our study indicates a positive effect of high consumption of flavonoids, omega-3 PUFAs and stilbenes on the markers of carbohydrate metabolism balance and the absence of such an effect on other cardiometabolic markers and inflammatory conditions.

Non-alcoholic fatty liver disease (NAFLD) is a serious health problem due to its high incidence and consequences. In view of the existing controversies, new therapeutic options for NAFLD are still being sought. Therefore, the aim of our review was to evaluate the recently published studies on the treatment of NAFLD patients. We searched for articles in the PubMed database using appropriate terms, including “non-alcoholic fatty liver disease”, “nonalcoholic fatty liver disease”, “NAFLD”, “diet”, “treatment”, “physical activity”, “supplementation”, “surgery”, “overture” and “guidelines”. One hundred forty-eight randomized clinical trials published from January 2020 to November 2022 were used for the final analysis. The results show significant benefits of NAFLD therapy associated with the use of not only the Mediterranean but also other types of diet (including low-calorie ketogenic, high-protein, anti-inflammatory and whole-grain diets), as well as enrichment with selected food products or supplements. Significant benefits in this group of patients are also associated with moderate aerobic physical training. The available therapeutic options indicate, above all, the usefulness of drugs related to weight reduction, as well as the reduction in insulin resistance or lipids level and drugs with anti-inflammatory or antioxidant properties. The usefulness of therapy with dulaglutide and the combination of tofogliflozin with pioglitazone should be emphasized. Based on the results of the latest research, the authors of this article suggest a revision of the therapeutic recommendations for NAFLD patients.

Clinical and epidemiological studies have demonstrated a relationship between alcohol addiction and mood disorders. Alcohol-dependent patients with depression tend to demonstrate clinically more severe manic symptoms, which complicates the process of diagnosis and therapy. However, the predictors indicating the risk of mood disorders in addicted patients remain unclear. The aim of the study was to examine the relationship between personal dispositions, bipolar traits, depth of addiction, quality of sleep, and depressive symptoms in alcohol-dependent men. The study group comprised 70 men (age M = 46.06, SD = 11.29) diagnosed with alcohol addiction. The participants completed a battery of questionnaires: BDI, HCL-32, PSQI, EPQ-R and MAST. The results were tested using Pearson’s correlation quotient and general linear model. The findings indicate that some of the studied patients are likely to have mood disorders of clinically significant severity. High neuroticism and poor sleep quality are independent predictors of depressive symptoms in alcohol-dependent patients. Among the components of sleep quality, problems with falling asleep and waking up at night appear to be most strongly associated with depressive symptoms. The intensity of depressive symptoms may relate to the intensity of certain bipolar features, such as risk-taking activity and irritability. High neuroticism and poor sleep quality are independent predictors of depressive symptoms in the studied group.

Obesity is a growing civilization problem, associated with a number of negative health consequences affecting almost all tissues and organs. Currently, obesity treatment includes lifestyle modifications (including diet and exercise), pharmacologic therapies, and in some clinical situations, bariatric surgery. These treatments seem to be the most effective method supporting the treatment of obesity. However, they are many limitations to the options, both for the practitioners and patients. Often the comorbidities, cost, age of the patient, and even geographic locations may influence the choices. The pharmacotherapy of obesity is a fast-growing market. Currently, we have at our disposal drugs with various mechanisms of action (directly reducing the absorption of calories—orlistat, acting centrally—bupropion with naltrexone, phentermine with topiramate, or multidirectional—liraglutide, dulaglutide, semaglutide). The drugs whose weight-reducing effect is used in the course of the pharmacotherapy of other diseases (e.g., glucose-sodium cotransporter inhibitors, exenatide) are also worth mentioning. The obesity pharmacotherapy is focusing on novel therapeutic agents with improved safety and efficacy profiles. These trends also include an assessment of the usefulness of the weight-reducing properties of the drugs previously used for other diseases. The presented paper is an overview of the studies related to both drugs currently used in the pharmacotherapy of obesity and those undergoing clinical trials, taking into account the individual approach to the patient.

Background: Sleep disturbances are a common problem among patients with Type 2 diabetes mellitus (T2DM). The aim of the study was to identify the phenotype of T2DM patients with poor sleep quality. Methods: An observational, cross-sectional study was conducted between May 2013 and August 2015. One hundred and sixty consecutive patients with T2DM: 74 women and 86 men, with a median age of 69.50 years (59.00, 79.50 years) were enrolled in the study. Sleep quality was evaluated using the Pittsburgh Sleep Quality Index (PSQI) questionnaire. Results: Poor sleep quality was noted in 85 (53%) patients. Sleep disorders were associated with older age, as well as female gender, longer duration of diabetes, lower level of fasting plasma glucose, glycated hemoglobin A1c, estimated glomerular filtration rate, triglycerides, waist-to-hip ratio, and the presence of nephropathy. A multivariate logistic regression revealed that sleep disorders were associated with older age (Odd Ratio (OR) = 1.11, 95% Confidence Interval (CI) 1.07&ndash, 1.15). Fifty-one patients (31.87%) were treated with sleeping pills. We found that older age, female gender, longer duration of diabetes, lower level of fasting plasma glucose, glycated hemoglobin A1c, estimated glomerular filtration rate, triglycerides, and the presence of nephropathy were linked with more frequent usage of hypnotics. A multivariate logistic regression demonstrated that older age (OR = 1.09, 95% CI 1.05&ndash, 1.14) and nephropathy (OR = 2.79, 95% CI 1.24&ndash, 6.28) were associated with a more frequent receiving the hypnotics, whereas male gender (OR = 0.30, 95% CI 0.13&ndash, 0.71) has less frequent hypnotics usage. Conclusion: Although, we assessed a wide range of patients&rsquo, characteristics, age had the most negative impact on the quality of sleep in patients with T2DM. We detected more frequent use of hypnotics in older females, with coexisting nephropathy.

Background: Fibrin formation and structure may be affected by a plethora of factors, including both genetic and posttranslational modifications, such as glycation, nitration or acetylation. Methods: The present study examines the effect of fibrinogen glycation on fibrin polymerization, measured in fibrinogen concentration-standardized plasma of subjects with type 2 diabetes mellitus (T2DM) and in a solution of human fibrinogen exposed to 30 mM glucose for four days. Results: The fibrin polymerization velocity (Vmax) observed in the T2DM plasma (median 0.0056, IQR 0.0049‒0.0061 AU/s) was significantly lower than in non-diabetic plasma (median 0.0063, IQR 0.0058‒0.0071 AU/s) (p &lt, 0.05). Furthermore, significantly lower Vmax was observed for glucose-treated fibrinogen (Vmax 0.046, IQR 0.022‒0.085 AU/s) compared to control protein incubated with a pure vehicle (Vmax 0.053, IQR 0.034‒0.097 AU/s) (p &lt, 0.05). The same tendency was observed in the fibrinogen samples supplemented with 6 mM glucose just before measurements. It is assumed that glucose may affect the ability of fibrinogen to form a stable clot in T2DM subjects, and that this impairment is likely to influences the outcomes of some diagnostic assays. As the example, the impaired clotting ability of glycated fibrinogen may considerably influence the results of the standard Clauss method, routinely used to determine fibrinogen concentration in plasma. The stoichiometric analysis demonstrated that spontaneous glycation at both the sites with high and low glycation potential clearly dominated in T2DM individuals in all fibrinogen chains.

Both the epidemiological data and the everyday medical practice demonstrate the coincidence of various types of diabetes mellitus (DM) in patients with asthma. Specific correlations between the risk of DM in pregnancy, asthma and the consequences of these diseases to the mother and her baby are also explored. The discussion concerning, on the one hand, the impact of asthma-related inflammatory condition on the metabolism of carbohydrates, and, on the other, the presence of chronic hyperglycemia and inflammatory markers observed in patients with asthma, is still ongoing. In the case of asthma and type 1 diabetes mellitus (T1DM), a correlation with the dysfunction of the immune system and the genetic background has been suggested, and in the case of type 2 (T2DM), the vital role of obesity and insulin resistance (IR) to promote excessive proinflammatory immune response. The data indicate that both asthma and DM affect mutually their clinical presentations, including the prognostic values and therapeutic possibilities. The ongoing controversy concerning the effective and safe anti-asthma and hypoglycemizing therapy does not allow for a definitive therapeutic consensus in this group of patients, despite the suggested role of metformin and hyperglycemizing effects of glucocorticoids. Therefore, the objective of the presented paper is a review of the knowledge in the field of DM and asthma coincidence, their probable causal relationships and therapeutic opportunities.

Blood platelets play a crucial role in the early stages of atherosclerosis development. The process is believed to require firm adhesion of platelets to atherosclerosis-prone sites of the artery. However, little evidence exists regarding whether the blood platelets of individuals with pathological conditions associated with atherosclerosis have higher potential for adhesion. This process is to a large extent dependent on receptors present on the platelet membrane. Therefore, the aim of the presented study was to determine whether blood platelets from diabetic patients have higher capacity of adhesion under flow conditions and how diabetes affects one of the crucial platelet receptors involved in the process of adhesion&mdash, GPIIIa. The study compares the ability of platelets from non-diabetic and diabetic humans to interact with fibrinogen and von Willebrand factor, two proteins found in abundance on an inflamed endothelium, under flow conditions. The activation and reactivity of the blood platelets were also characterized by flow cytometry. Platelets from diabetic patients did not demonstrate enhanced adhesion to either studied protein, although they presented increased basal activation and responsiveness towards low concentrations of agonists. Platelets from diabetic patients were characterized by lower expression of GPIIIa, most likely due to an enhanced formation of platelet-derived microparticles PMPs, as supported by the observation of elevated concentration of this integrin and of GPIIIa-positive PMPs in plasma. We conclude that altered functionality of blood platelets in diabetes does not increase their adhesive potential. Increased glycation and decrease in the amount of GPIIIa on platelets may be partially responsible for this effect. Therefore, higher frequency of interactions of platelets with the endothelium, which is observed in animal models of diabetes, is caused by other factors. A primary cause may be a dysfunctional vascular wall.

Elevated admission glycaemia (ABG) in a patient with or without type 2 diabetes (T2DM) is associated with adverse consequences. There is still a lack of accurate data on the adverse effects of ABG on the risk of major cardiovascular events and the development of T2DM in patients hospitalized for unstable angina (UA) or non-ST elevation myocardial infarction (NSTEMI) undergoing percutaneous coronary intervention.The main aim of this study was to evaluate the effect of ABG to the risk of major cardiovascular events and the development of T2DM during one year follow-up in patients with UA and NSTEMI.100 consecutive patients (68% men, mean age 64.2±10.5 years) hospitalized due to non-ST-elevation acute coronary syndrome (NSTE-ACS) were included in observational study. In each patient, medical history was taken and physical examination, standard diagnostics procedures, including venous glucose deterioration and coronarography were performed. Patients were assigned to two groups: UA or NSTEMI and observed during hospitalization and one year after discharge.74 patients were diagnosed with NSTEMI and 26 with UA. 41 patients were treated for T2DM and 28 were diagnosed with impaired fasting glucose (IFG) prior to hospitalization. Both carbohydrate disorders occurred with a similar frequency in the compared groups of patients, and its incidence was comparable in both groups. During observation, T2DM was diagnosed only in 8 patients with IFG. Out of the 8 patients whose ABG was250mg/dl, 7 died during one year, including three during hospitalization, and two during the first month after discharge. These patients were diagnosed with T2DM before hospitalization.Different degrees of impaired glucose homeostasis are present before or develop after occurrence NSTE-ACS. ABG250mg/ dl in this group of patients is associated with the highest risk of death, regardless of the diagnosis of UA or NSTEMI.

Introduction Poor asthma control is probably associated with both biological and psychological factors. Type D pattern of behavior is characterized by negative emotionality and inhibition in social relationships. It was previously found to be associated with cardiovascular diseases. Aim To evaluate the correlation between the degree of asthma control and the severity of the components of type D behavior pattern. Material and methods The research was conducted on a group of 117 subjects with bronchial asthma. The control group consisted of 32 healthy subjects. The degree of bronchial asthma control was determined using the Asthma Control Test. The D pattern of behavior was measured using the DS-14 questionnaire. Results The risk of type D behavior pattern, defined as scoring at least 10 points in both scales (Negative Emotionality and Social Inhibition), was higher in subjects with uncontrolled asthma than in healthy individuals (OR = 5.19; 95% CI: 1.74-15.44), those with partial control of asthma (OR = 6.04; 95% CI: 1.87-19.52) and subjects with good control of asthma (OR = 8.46; 95% CI: 3.09-23.16). The severity of depressiveness correlated positively with the number of infections in the past year. Negative emotionality correlated positively with the number of infections and social inhibition. Conclusions Type D pattern of behavior may be associated with diagnosis and severity of asthma. Due to its link to poor control of asthma symptoms, a high level of negative emotionality among patients with asthma might be of particular interest to the clinicians.

Non-alcoholic fatty liver disease (NAFLD) is one of the most common pathologies of that organ. The development of the disease involves a variety of mechanisms, including insulin resistance, oxidative stress, endoplasmic reticulum stress, endotoxins from the intestinal flora and genetic predispositions. Additionally, clinical data suggest that the presence of NAFLD is associated with excessive activation of the immune system. For practical purposes, attention should be paid to the moment when the subjects predisposed to NAFLD develop inflammatory infiltration and signs of fibrosis in the liver (non-alcoholic steatohepatitis - NASH). Their presence is an important risk factor for hepatic cirrhosis, hepatic failure, and hepatocellular carcinoma, as well as for the occurrence of cardiovascular events. Regardless of the diagnostic methods used, including laboratory tests and imaging, liver biopsy remains the gold standard to identify and differentiate patients with NAFLD and NASH. The search for other, safer, cheaper and more readily available diagnostic tests is still being continued. Attention has been drawn to the usefulness of markers of immune status of the organism, not only for the diagnosis of NASH, but also for the identification of NAFLD patients at risk of disease progression. Despite the effectiveness of medication, no recommendations have been established for pharmacotherapy of NAFLD. Data indicate the primary need for non-pharmacological interventions to reduce body weight. However, there is evidence of the applicability of certain drugs and dietary supplements, which, by their effect on the immune system, inhibit its excessive activity, thus preventing the progression of NAFLD to NASH.

Introduction. In older type 2 diabetes mellitus (T2DM) patients with serious comorbidities, tight glycemic control exceeds the benefits. The aim of the study was to assess glycated hemoglobin A1c (HbA1c) in hospital­ized T2DM patients aged ≥ 80 years and to compare the level of HbA1c in diabetics with and without severe hypoglycemia (SH) at admission. Material and methods. We enrolled 166 consecutive T2DM patients ≥ 80 years of age with a wide spectrum of comorbidities hospitalized between 2009–2013. Results. Patients’ mean age was 83.72 ± 3.19 years and mean diabetes duration was 9.14 ± 5.88 years, body mass index (BMI) was 27.87 ± 4.51 kg/m² and the glomerular filtration rate (GFR) was 58.94 ± 25.87 ml/ /min/1.73 m². Mean HbA1c for the whole group was 7.61 ± 1.87% (59.77 ± 20.48 mmol/mol). Tight glycemic con­trol with HbA1c < 7.0% (53 mmol/mol) was observed in 77 patients (46%). SH was diagnosed in 19 (11%) patients. Subjects with SH had significantly lower mean HbA1c level than those hospitalized for other reason [6.38 ± 1.22 vs. 7.77 ± 1.88% (46.31 ± 13.36 vs. 61.51 ± 20.63 mmol/ /mol), p = 0.002]. A history of myocardial infarction and/ /or stroke was reported almost two-fold more frequently by the diabetics hospitalized for SH than diabetics with­out hypoglycaemia (47 vs. 28%, c² = 3,03, p = 0.082). SH was diagnosed only in patients receiving insulin (n = 10) or sulfonylurea (n = 9). Conclusion. Despite the fact, that harms of intensive hypogylcemic treatment exceed the benefits for older patients with T2DM, half of them reached tight gly­cemic control. Every tenth patient was hospitalized because of SH. Subjects with SH had significantly lower mean HbA1c level than those hospitalized for other reason. Our observations suggest that a substantial proportion of T2DM patients ≥ 80 years may be over­treated. (Clin Diabetol 2018; 7, 2: 102–107)

Background & objectives: Tumour protein p53 (TP53) is a stress sensitive transcription factor responsible for the control of cell survival and death to prevent from tumour formation. In vitro and animal studies have indicated that TP53 also responds to metabolic changes and influences metabolic pathways. This study was undertaken to determine the serum level of TP53 and its correlations with clinical and biochemical parameters in type 2 diabetes mellitus (T2DM) patients in comparison to non-diabetic control individuals. Methods: An observational study was conducted between December 2009 and November 2013 to evaluate TP53 serum level using ELISA. Cases (n=225) were defined as patients who were diagnosed with T2DM. Non-diabetic controls (n=255) were matched by age and sex. Multivariable modelling using logistic regression examined associations between clinical characteristics and TP53 level or T2DM predication was performed. Results: Serum TP53 level was significantly higher in T2DM patients as compared to non-diabetic healthy controls (1.69 vs 2.07 ng/ml, P

Oxidative stress and impaired anti-oxidant defense are regarded as contributory factors for distal symmetric polyneuropathy (DSPN). The purpose of the study was to evaluate the plasma level of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) and the association between polymorphic variants in genes encoding for GPx1, SOD, CAT and the risk of DSPN in T2DM patients.We included 401 individuals: 110 T2DM patients with DSPN, 135 T2DM patients without DSPN, and 156 control subjects with normoglycemia, and without DSPN. We employed RFPL-PCR to genotype polymorphic variants Pro197Leu of Gpx1, +35A/C of SOD1, -262C/T of CAT and ELISA tests to measure plasma level of SOD1, GPx1 and CAT. The odds ratios (ORs) and 95% confidence intervals (CIs) for each genotype and allele were calculated.There was a significant decrease in the level of GPx1 (p0.05), SOD1 (p0.05) in T2DM patients with DSPN compared to healthy subjects. T2DM patients without DSPN showed a statistically lower serum level of GPX1 (p0.05) than healthy subjects. SOD 1 and CAT levels were lower in T2DM patients with DSPN compared to T2DM patients without DSPN (p0.05). The genetic analysis revealed the lack of association between examined polymorphic variants and the risk of DSPN.The examined polymorphic variants are not associated with DSPN in Polish T2DM patients. The obtained results suggest that disturbances in antioxidant defense system may play significant role in the development and progression of DSPN.

Diabetes is a heterogenous group of diseases with chronic hyperglycemia, which is associated with the risk of many complications, including diabetic kidney disease. Micro- and macroangiopathy in hyperglycemic environment leads to organ failure, including end-stage renal disease, requiring dialysis or kidney transplantation. However, diabetes is not the only cause leading to kidney dysfunction in this patient population. A patient with diabetes should be monitored regularly for proteinuria and glomerular filtration rate and depending on advancement of kidney disease or suspicion other than diabetes cause of kidney damage, should also be covered by nephrological care. Appropriately selected hypoglycemic drugs and their doses, in combination with appropriate non-pharmacological treatment, in the patients with different stages of kidney disease, not only reduces the risk of drug-induced side effects but, above all, may slow the progression of kidney damage and reduce the risk of other complications in this group of patients. Recently, there have been many new groups of hypoglycemic agents that can be used in the treatment of patients with kidney disease. The aim of this study is to present the current possibilities of hypoglycemic therapy in patients with different stages of chronic kidney disease. In addition, the relationship between individual groups of hypoglycemic agents and the renal benefits and risk was analyzed.

Background: Metformin is one of the antihyperglycaemic drugs, reducing the risk of major cardiovascular events, including fatal ones. Although it is formally contraindicated in moderate and severe functional stages of heart failure (HF), it is commonly used in patients with concomitant type 2 diabetes mellitus (T2DM). Aim: We sought to evaluate the effect of metformin and T2DM on total mortality and hospitalisation rates in patients with HF. Methods: This retrospective analysis included 1030 adult patients (> 18 years) with HF from the Polish section of the HF Long-Term Registry (enrolled between 2011 and 2014). Patients with T2DM (n = 350) were identified and divided into two groups: those receiving metformin and those not. Both groups were subjected to one-year follow-up. Results: Mean patient age was 65.3 ± 13.5 years, with the predominance of male sex (n = 726) and obesity (mean body mass index 30.3 ± 5.5 kg/m2) and mean left ventricular ejection fraction was 34.3% ± 14.1%. Among patients with T2DM (n = 350) only 135 (38.6%) were treated with metformin. During one-year follow-up, 128 patients with HF died, of whom 53 had T2DM (15.1% vs. 10.9%, hazard ratio [HR] 0.89, 95% confidence interval [CI] 0.87–0.91, p = 0.045). Metformin was associated with a lower mortality rate compared to other antihyperglycaemic agents (9.6% vs. 18.6%, HR 0.85; 95% CI 0.81–0.89, p = 0.023). There were no significant differences in the hospitalisation rate, including that due to HF decompensation, among patients treated with metformin and the remainder (53.5% vs. 40.0%, respectively HR 0.93, 95% CI 0.82–1.04, p = 0.433). Conclusions: Metformin treatment in patients with different degrees of HF and T2DM is associated with a reduction in mortality and does not affect the hospitalisation rate.

Metabolic syndrome is a very serious health issue, not only from internal medicine's point of view. Patients suffering from overweight, arterial hypertension, lipids and carbohydrates metabolism disorders are also in the circle of interest of other areas of medicine, including psychiatry. Currently, one of key problems of pharmacotherapy is a comorbidity of metabolic syndrome and mental disorder. Depression is more common than schizophrenia. Despite the fact that in everyday clinical practice there are more patients with depression than schizophrenia, there is a bigger interest among scientists for metabolic syndrome after antipsychotic drugs than as an effect of use of antidepressant agents.The aim of an analysis was to review literature committed to influence of depression pharmacotherapy on development of metabolic syndrome. 169 results were provided, including 18 original publications. Final analysis consists of 9 that investigate correlation between antidepressive medicines use and metabolic syndrome development (but not its each individual component).In general, antidepressant pharmacotherapy is associated not only with increased risk of metabolic syndrome occurrence but also their worsening. However, it needs to be emphasized that there is a difference between antidepressants groups - tricyclic antidepressive medicines are the most commonly associated with risk of developing metabolic disorders, but also SNRIs and SSRIs are mentioned as significant contributors. Mechanisms of aforementioned changes are still unclear. However, their influence on histamine and serotonin pathways, which take part in regulation of i.e. food intake, is suggested. The search for mechanisms that are precisely responsible for metabolic changes continues, in hope of finding a way to avoid adverse effects of antidepressant medicines use.

It is suggested that nonalcoholic fatty liver disease (NAFLD) correlates with cardiometabolic risk factors in patients with newly diagnosed type 2 diabetes. The aim of this study was to evaluate the prevalence of ultrasound features of NAFLD in patients with newly diagnosed type 2 diabetes and their relationship with cardiometabolic risk factors. The study included 100 consecutive patients (mean age, 55.64 ±13.42 years) with newly diagnosed type 2 diabetes, without other causes of hepatosteatosis. In each patient, medical history was taken, physical and abdominal ultrasound examinations were performed, and anthropometric and biochemical parameters were measured. Based on the results of an ultrasound examination, patients were assigned to 2 groups: with (n = 71) and without (n = 29) NAFLD. NAFLD was present in more than 70% of the patients with diabetes. In patients with NAFLD, significantly higher mean values of body weight, waist and hip circumferences, body mass index, liver enzyme activity, serum C‑reactive protein, total cholesterol, and triglycerides and significantly lower levels of high‑density lipoprotein (HDL) cholesterol were observed. There were no significant differences in the parameters of glycemic control between the groups. A correlation was observed between ultrasound features of NAFLD and some cardiovascular risk factors. Increased waist circumference and serum γ‑glutamyltransferase level and decreased HDL‑cholesterol levels were shown to be independent risk factors of NAFLD. Liver ultrasound should be performed in every patient with newly diagnosed type 2 diabetes. Our findings indicate a relationship between NAFLD and multiple cardiometabolic risk factors. The measurement of selected biochemical and anthropometric parameters may be used to assess the risk of NAFLD in this patient group.

Purpose Metformin is the most commonly prescribed anti-diabetic medication. However, it is often used despite the presence of contraindications and in unlicensed indications. The main aim of this study was to evaluate the frequency of metformin use before hospitalization in spite of contraindications in patients with type 2 diabetes mellitus (T2DM) and to evaluate the prevalence of metformin - associated side effects. Material/Methods 558 hospitalized patients (mean age = 66.65±12.73 years) with poorly controlled T2DM were enrolled. Detailed medical history including the duration of T2DM, duration of hypoglycemic agents usage prior to hospitalization and possible metformin-associated side effects was recorded. Patients were subjected to a thorough physical examination and indispensable biochemical and diagnostic research panel was performed to establish the degree of heart failure, sufficiency of the respiratory system and kidney function. Results 335 out of 558 patients were treated before hospitalization with metformin alone or in combination with other hypoglycemic agents, mostly sulfonylureas. Contraindications to metformin were found in 275 patients and despite this 120 of them were using this medication in an average dose of 1793.91±701.61 mg. However, none of them reported any serious adverse effects and no significant pH changes were observed. Only three patients reported moderate dyspepsia. Conclusions The results of this study indicate a relatively good tolerability of metformin by patients with the traditional contraindications to this drug. These findings support other authors’ suggestion that indications and contraindications to metformin should be re-evaluated.

Introduction. Norwegian (crusted, hyperkeratotic) scabies is a relatively rare form of the disease, but it is highly contagious and easily transmitted. Although skin lesions are typical for that form of the disease, they differ substantially from those observed in typical infection with Sarcoptes scabiei. Objective. To present the difficulties in the diagnosis of Norwegian scabies. Case report. We describe a case of an elderly patient, a resident of a nursing home, with Norwegian scabies in whom itching and skin lesions were initially misdiagnosed as a dermatologic complication of type 2 diabetes mellitus. Additionally, in the nursing home, the results of the implemented therapy were not checked appropriately, which resulted in an outbreak of scabies in the institution as well as infection of several family members. Conclusions . Considering the fact that pharmacological treatment of Norwegian scabies does not differ from other forms of this disease, it seems that early diagnosis and appropriate treatment planning are crucial to prevent transmission of the infection.

Distal symmetric polyneuropathy (DSPN) is common complication of type 2 diabetes (T2DM). In this work we investigated the role of oxidative damage in connection with particular polymorphisms of DNA repair genes and their repair capacity.Materials constitute the peripheral blood of patients with T2DM with and without DSPN and control subjects without disturbance of the carbohydrate fraction. The study of gene polymorphisms which products take part in base excision repair (BER) pathway: 726 Val/Ala adenosine diphosphate ribosyl transferase (ADPRT), 324 His/Glu MutYhomolog (MUTYH) and 148 Asp/Glu human apurinic/apyrimidinic endonuclease (APE) was carried out using restriction fragment length polymorphism polymerase chain reaction (PCR-RFLP) method. The study of DNA damage induced by hydrogen peroxide and the efficiency of their repair was carried out using comet assay.None of the 3 polymorphisms were associated with the risk of DSPN. However, in group of patients together with T2DM and T2DM/DSPN 726 Ala ADPRT allele was significantly susceptible to increased risk of T2DM (OR=1.59; 95% CI: 1.08-2.36). Investigation of DNA damage and repair revealed that T2DM patients have decreased ability to DNA repair. This capacity even drops down in the group of T2DM/DSPN patients compared to subjects with diabetes alone. ADPRT and APE polymorphisms were significantly associated with higher DNA damages (P0.05) in heterozygous and mutant homozygous in correlation to homozygous wild type, but for MUTYH polymorphism relation was not confirmed.Pathogenesis of T2DM and development of DSPN may be related to oxidative stress connected with BER gene polymorphisms.

Oxidative stress is considered to be the cause for onset and the progression of type 2 diabetes mellitus (T2DM) and complications including neuropathy. It is a deleterious process that can be an important mediator of damage to cell structures: protein, lipids and DNA. Data suggest that in patients with diabetes and diabetic neuropathy DNA repair is impaired, which prevents effective removal of lesions. Objective: The aim of our study was to evaluate the association of the hOGG1 (326 Ser/Cys) and XRCC1 (194 Arg/Trp, 399 Arg/Gln) gene polymorphisms whose protein is involved in the BER pathway with DNA repair efficiency in patients with diabetes type 2 and diabetic neuropathy compared to the healthy subjects. Genotypes were determined by PCR-RFLP analysis in 385 subjects, including 117 with type 2 diabetes, 56 with diabetic neuropathy and 212 with normal glucose metabolism. The polymorphisms studied include codon 326 of hOGG1 and 194, 399 of XRCC1 in the base excision repair (BER) genes. Comet assay was carried out using peripheral blood lymphocytes from the patients and controls. This test enabled the evaluation of DNA damage in cells exposed to hydrogen peroxide alone and in the combination with the endonuclease III (Nth). The results of the analysis of polymorphism were statistically examination by calculating the odds ratio (OR) and their 95% confidence intervals (95% CI) using the ¤ç2-tests. Our data indicate that patients with diabetes mellitus type 2 (including those with neuropathy) had higher frequencies of the XRCC1 399Arg/Gln polymorphism in homozygote (GG) (OR: 1.85 [95% CI: 1.07-3.22], P=0.3) and also increased frequency of 399Gln (G) allele (OR: 1.38 [95% CI: 1.03-1.83], P=0.3). No relation to other polymorphisms with increased risk of diabetes or diabetic neuropathy. In T2DM patients complicated by neuropathy, there was less efficient repair of oxidative DNA damage induced by hydrogen peroxide in both the presence and absence of the Nth enzyme. The results of our study suggest that the XRCC1 399 Arg/Gln polymorphism is a significant risk factor of T2DM in Polish population. Obtained data suggest a decreased efficiency of DNA repair in cells from patients with diabetes and neuropathy may be associated with oxidative stress. Additionally, patients with neuropathy are characterized by even greater sensitivity to oxidative damage than patients with diabetes, which suggests participation of free radicals in the pathogenesis of neuropathy., {"references":["Brownlee M, Cerami A. The Biochemistry of the Complications of\nDiabetes Mellitus. Annu Rev Biochem 1981; 50:385-432","Edwards JL, Vincent AM, Cheng HT, Feldman EL. Diabetic\nneuropathy: Mechanisms to management. Pharmacol Ther 2008; 120:1-\n34","Evans JL, Goldfine ID, Maddux BA, Grodsky GM. Oxidative stress and\nstress-activated signaling pathways: a unifying hypothesis of type 2\ndiabetes. Endocr Rev 2002; 23:599-622","Brownlee M. Biochemistry and molecular cell biology of diabetic\ncomplications. Nature 2001; 414:813−820","Cooke MS, Evans MD, Dizdaroglu M, Lunec J. Oxidative DNA\ndamage: mechanisms, mutation, and disease. FASEB J 2003; 17:1195-\n214","Memisoglu A, Samson L. Base excision repair in yeast and mammals.\nMutat Res 2000; 451:39-51","Klungland A, Bjelland S. Oxidative damage to purines in DNA: role of\nmammalian Ogg1. DNA Repair (Amst) 2007; 6:481-8","Caldecott KW. XRCC1 and DNA strand break repair. DNA Repair\n(Amst) 2003; 2:955-69","Cadet J, Bourdat AG, D'Ham C, Duarte V, Gasparutto D, Romieu A,\nRavanat JL. Oxidative base damage to DNA: specificity of base excision\nrepair enzymes. Mutat Res 2000; 462:121-8\n[10] World Health Organization Study Group. Definition, diagnosis and\nclassification of diabetes mellitus and its complications. Part 1:\nDiagnosis and classification of diabetes mellitus. Tech Rep Ser\nWHO/NCD/NCS/99, 2nd ed. World Health Organization, Geneva, 1999\n[11] Singh NP, McCoy MT, Tice RR, Schneider EL. A simple technique for\nquantitation of low levels of DNA damage in individual cells. Exp Cell\nRes 1988; 175:184-91\n[12] Klaude M, Eriksson S, Nygren J, Ahnström G. The comet assay:\nmechanisms and technical considerations. Mutat Res 1996; 363:89-96\n[13] King, H., Aubert, R.E., Herman, W.H. Global burden of diabetes, 1995-\n2025: prevalence, numerical estimates, and projections. Diabetes Care\n1998; 21:1414-31\n[14] Sheetz MJ, King GL. Molecular understanding of hyperglycemia-s\nadverse effects for diabetic complications. JAMA 2002; 288:2579-88\n[15] Dyck, PJ, Kratz KM, Karnes JL, et al. The prevalence by staged severity\nof various types of diabetic neuropathy, retinopathy, and nephropathy in\na population-based cohort: The Rochester Diabetic Neuropathy Study.\nNeurology 1993; 43:817-24\n[16] Rolo AP, Palmeira CM. Diabetes and mitochondrial function: role of\nhyperglycemia and oxidative stress. Toxicol Appl Pharmacol 2006;\n212:167-78\n[17] Sakurai T, Tsuchiya S. Superoxide production from nonenzymatically\nglycated protein. FEBS Lett 1988; 236:406-10\n[18] Wolff SP, Dean RT. Glucose autoxidation and protein modification. The\npotential role of 'autoxidative glycosylation' in diabetes. Biochem J\n1987; 245:243-50\n[19] Wojtczak L, Schönfeld P. Effect of fatty acids on energy coupling\nprocesses in mitochondria. Biochim Biophys Acta 1993; 1183:41-57\n[20] Rao MS, Reddy JK. Peroxisomal beta-oxidation and steatohepatitis.\nSemin Liver Dis 2001; 21:43-55\n[21] Galvez AS, Ulloa JA, Chiong M, Criollo A, Eisner V, Barros LF,\nLavandero S. Aldose reductase induced by hyperosmotic stress mediates\ncardiomyocyte apoptosis: differential effects of sorbitol and mannitol. J\nBiol Chem 2003; 278:384-94\n[22] Obrosova IG. Increased sorbitol pathway activity generates oxidative\nstress in tissue sites for diabetic complications. Antioxid Redox Signal\n2005; 7:1543-52\n[23] James LR, Tang D, Ingram A, Ly H, Thai K, Cai L, Scholey JW. Flux\nthrough the hexosamine pathway is a determinant of nuclear factor\nkappaB- dependent promoter activation. Diabetes 2002; 51:1146-56\n[24] McClain DA, Crook ED. Hexosamines and insulin resistance. Diabetes\n1996; 45:1003-9\n[25] Evans JL, Goldfine ID, Maddux BA, Grodsky GM. Oxidative stress and\nstress-activated signaling pathways: a unifying hypothesis of type 2\ndiabetes. Endocr Rev 2002; 23:599-622\n[26] Koya D, King GL. Protein kinase C activation and the development of\ndiabetic complications. Diabetes 1998; 47:859-66\n[27] Ishii H, Jirousek MR, Koya D, Takagi C, Xia P, Clermont A, Bursell\nSE, Kern TS, Ballas LM, Heath WF, Stramm LE, Feener EP, King GL.\nAmelioration of vascular dysfunctions in diabetic rats by an oral PKC\nbeta inhibitor. Science 1996 3; 272:728-31\n[28] Bierhaus A, Hofmann MA, Ziegler R, Nawroth PP. AGEs and their\ninteraction with AGE-receptors in vascular disease and diabetes\nmellitus. I. The AGE concept. Cardiovasc Res 1998; 37:586-600\n[29] Goode EL, Ulrich CM, Potter JD. Polymorphisms in DNA repair genes\nand associations with cancer risk. Cancer Epidemiol Biomarkers Prev\n2002; 11:1513-30\n[30] Garcia-Closas M, Malats N, Real FX, Welch R, Kogevinas M,\nChatterjee N, Pfeiffer R, Silverman D, Dosemeci M, Tardon A, Serra C,\nCarrato A, Garcia-Closas R, Castano-Vinyals G, Chanock S, Yeager M,\nRothman N. Genetic variation in the nucleotide excision repair pathway\nand bladder cancer risk. Cancer Epidemiol Biomarkers Prev 2006; 15:\n536-42\n[31] Zhang Y, Newcomb PA, Egan KM, Titus-Ernstoff L, Chanock S, Welch\nR, Brinton LA, Lissowska J, Bardin-Mikolajczak A, Peplonska B,\nSzeszenia- Dabrowska N, Zatonski W, Garcia-Closas M. Genetic\npolymorphisms in base-excision repair pathway genes and risk of breast\ncancer. Cancer Epidemiol Biomarkers Prev 2006; 15:353-58\n[32] Wei YH, Lee HC. Oxidative stress, mitochondrial DNA mutation, and\nimpairment of antioxidant enzymes in aging. Exp Biol Med 2002; 227:\n671-82\n[33] Sun C, Liu X, Zhang H, Guo W, Cai Z, Chen H, Zhang K, Zhu D, Wang\nY. Functional polymorphism of hOGG1 gene is associated with type 2\ndiabetes mellitus in Chinese population. Mol Cell Endocrinol 2010;\n325:128-34\n[34] Kasznicki J, Krupa R, B┼éasiak J, Drzewoski J. Association between\npolymorphisms of the DNA repair genes XRCC1 and hOGG1 and type\n2 diabetes mellitus in the Polish population. Pol Arch Med Wewn 2009;\n119:122-8\n[35] Czyzyk A, Szczepanik Z. Diabetes mellitus and cancer. Eur J Intern\nMed 2000; 11:245-52\n[36] Pitozzi V, Giovannelli L, Bardini G, Rotella CM, Dolara, P. Oxidative\nDNA damage in peripheral blood cells in type 2 diabetes mellitus:\nHigher vulnerability of polymorphonuclear leukocytes. Mutat Res 2003;\n529:129-33\n[37] Speit G, Schutz P, Bonzheim I, Trenz K, Hoffmann H. Sensitivity of the\nFPG protein towards alkylation damage in the comet assay. Toxicol Lett\n2004; 146:151-58\n[38] Jain N, Naseem I, Ahmad J. Evaluation of DNA damage and metabolic\nsyndrome parameters in diabetic rabbits supplemented with antioxidants.\nFundam Clin Pharmacol 2009; 23:197-205"]}

Experimental evidences suggest that hyperglycaemia-induced overproduction of reactive oxygen species and subsequent damage to proteins, lipids and DNA may play a key role in the development of distal symmetric polyneuropathy (DSPN)—the most common complication of diabetes mellitus. The study population consisted of 51 individuals aged 52–82 years classified into 3 groups: 16 patients diagnosed with type 2 diabetes mellitus (T2DM) with DSPN, 16 T2DM patients without DSPN and 19 control subjects without diabetes and neuropathy. The study was conducted to determine the activity of antioxidant enzymes: catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX) and total antioxidant status (TAS) in the examined groups. An alkaline comet assay was used to determine the extent of DNA damage of oxidized purines as glicosylo-formamidoglicosylase (Fpg) sites, and oxidized pyrimidines as endonuclease III (Nth) sites. A significant decrease of SOD (P 0.05), and TAS status (P > 0.05) were seen in T2DM patients with neuropathy compared to T2DM patients as well as controls. T2DM patients with or without neuropathy revealed significantly lower (P

Diabetes mellitus is a major risk factor for coronary heart disease (CHD). Matrix metalloproteinases (MMPs) can play a pivotal role in the remodelling of extracellular matrix associated with the development of atherosclerosis. Therefore, the aim of the study was to compare the distribution of genotypes and frequency of alleles of two polymorphisms of the MMP-1 gene promoter, an A/G substitution and a 1G/2G insertion, in correlation with antigen levels of matrix metalloproteinase-1 (MMP-1) in type 2 diabetic patients with or without CHD as well as individuals with normal glucose level without CHD.Genotypes of 115 patients with type 2 diabetes mellitus (T2DM) and a subpopulation of 66 patients with coexisting CHD as well as 120 non-diabetic control subjects were determined by PCR-based restriction fragment length polymorphism (PCR-RFLP).We demonstrated that antigen levels of MMP-1 in the serum of diabetic patients were significantly higher than those of individuals with normal glucose metabolism (p0.05). Elevated levels of MMP-1 positively correlated with CHD occurrence in T2DM patients (p0.01). The distribution of genotypes revealed higher frequency of the 2G/2G polymorphism variant in diabetic patients with CHD [OR 5.76, 95% CI (1.24; 26.87)], thus suggesting its strong association with high level of MMP-1. In T2DM patients with coexisting CHD, a higher frequency of the 2G allele of 1G/2G [OR 1.74, CI 95% (1.01; 2.99)] and the G allele of A/G polymorphism [OR 2.15, 95% CI (1.22; 3.80)] was also found.Our results suggest that type 2 diabetes mellitus is linked with elevated blood level of MMP-1, and polymorphisms of the promoter region of its gene might be associated with CHD.

Amiodarone is an antiarrhythmic drug frequently used in everyday clinical practice. Its mechanism of action involves the interaction with many receptors, including those in the cardiac conduction system. Amiodarone usefulness is protect in the treatment of a variety of tachyarrhythmias, both benign and life-threatening. In contrast to other antiarrhythmic drugs, amiodarone is characterized by high therapeutic efficacy, both in patients with normal and impaired left ventricular systolic function. A significant limitation of its is associated with side effects including thyroid gland dysfunction. Disturbances of this organ associated with amiodarone are an important diagnostic and therapeutic problem. They may contribute to the occurrence of both Amiodarone- Induced Thyrotoxicosis (AIT) and Amiodarone-Induced Hypothyroidism (AIH). The risk of such complications should be considered for each patient individually, taking into account thyroid function at the beginning of pharmacotherapy. Appropriate procedure, both before and after treatment allows a rapid diagnosis and treatment of thyroid disturbances. It seems that the best parameter used to assess the hormonal imbalance during amiodarone therapy is the concentration of the free triiodothyronine (fT3). The evaluation of thyroid function should be performed before starting pharmacotherapy, and then repeated every six months. In the case of a thyroid dysfunction, assessment must be performed immediately according to standard diagnostic and therapeutic regimens. Despite abnormal thyroid function, high efficiency of amiodarone and relatively small risk of thyroid damage allows continuation therapy. Amiodarone therapy requires a care from both cardiologist and endocrinologist. The aim of this paper is to present the state of art of evaluation of the thyroid function and procedures implemented in care of thyroid dysfunction before and during treatment with amiodarone.