rss_2.0Endocrine Regulations FeedSciendo RSS Feed for Endocrine Regulations Regulations 's Cover to nanographene oxide induces gene expression dysregulation in normal human astrocytes<abstract> <title style='display:none'>Abstract</title> <p><bold>Objective.</bold> Nanographene oxide, an oxidation derivative of graphene, is considered to be one of the nanomaterials attractive for biomedical applications, although this nanomaterial is toxic. The increasing exploitation of graphene-based materials necessitates a comprehensive evaluation of the potential impact of these materials on the human health. Moreover, it is necessary to investigate in detail the mechanisms of its toxic effect on living cells particularly at the genome level. The present study aimed to evaluate the impact of low doses of nanographene oxide on the expression of key regulatory genes in normal human astrocytes.</p> <p><bold>Methods.</bold> Normal human astrocytes, line NHA/TS, were exposed to low doses of nanographene oxide (1 and 4 ng/ml) for 24 h. RNA was extracted from the cells and used for cDNA synthesis. The expression levels of NAMPT, TSPAN13, BCAR3, BRCA1, PTGS2, P4HA1, and P4HA2 mRNAs as well as microRNAs were measured by quantitative polymerase chain reaction.</p> <p><bold>Results.</bold> It was found that the low doses of nanographene oxide induced a dysregulation in the expression of the key regulatory genes in normal human astrocytes in dose-dependent (1 and 4 ng/ml) and gene-specific manner. Nanographene oxide also strongly suppressed the expression of <italic>NAMPT</italic>, <italic>BCAR3</italic>, and <italic>TSPAN13</italic> genes and significantly up-regulated <italic>BRCA1</italic>, <italic>PTGS2</italic>, <italic>P4HA1</italic>, and <italic>P4HA2</italic> ones with a more significant effect in P4HA1 and P4HA2 genes. The expression of miR-96-5p and miR-145-5p was also down-regulated in astrocytes treated with nanographene oxide in a dose-dependent manner.</p> <p><bold>Conclusion.</bold> The data obtained demonstrate that the low doses of nanographene oxide disturbed the genome functions by changing the expression levels of key regulatory genes in gene-specific and dose-dependent manner. Moreover, a higher dose of nanographene oxide induced more pronounced changes in expression of genes indicating for both genotoxic and neurotoxic possible effects in the normal human astrocytes.</p> </abstract>ARTICLE2022-07-13T00:00:00.000+00:00Comorbid overweight/obesity and chronic pancreatitis exacerbate the dyslipidemia progression in type 2 diabetic patients<abstract> <title style='display:none'>Abstract</title> <p><bold>Objective.</bold> The aim of present study was to analyze the serum lipid profile parameters in patients with type 2 diabetes mellitus (T2DM) and comorbidities [overweight/obesity and/or chronic pancreatitis (CP)] to determine the contribution of these pathologic factors to lipid metabolism disorders in T2DM.</p> <p><bold>Methods.</bold> The study involved 579 type 2 diabetic (T2D) patients with comorbid overweight/ obesity and/or CP. The serum lipid panel parameters [total cholesterol (TC), triglycerides (TG), and high-density lipoprotein cholesterol (HDL-C)] were determined by commercially available kits on a Cobas 6000 analyzer (Roche Hitachi, Germany). Low-density lipoprotein cholesterol (LDL-C), non-HDL-C, and remnant cholesterol (RC) levels were calculated using formulas. The data were statistically analyzed using STATISTICA 7.0.</p> <p><bold>Results.</bold> It was shown that dyslipidemia in T2D patients is characterized by unidirectional changes regardless the presence/absence of comorbid overweight/obesity or CP. At the same time, the most severe dyslipidemia was detected in T2D patients with a combination of comorbid over-weight/obesity and CP. Both the elevated body mass index (BMI) and CP can aggravate lipid metabolism disorders in T2DM. In our study, however, the BMI increase positively correlated with the number of dyslipidemia patients characterized by exceeding all target lipid levels for diabetic patients. This is in contrast to T2D patients with normal body weight and comorbid CP, in whom only LDL-C and TG exceeded the target lipid levels.</p> <p><bold>Conclusions.</bold> A combination of comorbidities, such as obesity and CP in T2D patients, produced a mutually aggravating course defined particularly by common pathogenic links, insulin resistance, chronic generalized low-intensity inflammation, endothelial dysfunction, and dyslipidemia caused primarily by triglyceridemia.</p> </abstract>ARTICLE2022-07-13T00:00:00.000+00:00ACTH-secreting parotid acinic cell carcinoma unusually reported as a paraneoplastic syndrome<abstract> <title style='display:none'>Abstract</title> <p>Paraneoplastic syndromes, induced by an immunological cross-reaction or hormone/peptide secretion, are an atypical presentation of tumors. Some tumors, such as small cell lung cancer and bronchial carcinoid, can be adrenocorticotropic hormone (ACTH) secreting tumors. Less commonly, parotid acinic cell carcinoma can be ACTH-secreting tumor leading to Cushing’s syndrome. Few literature cases have described ACTH related paraneoplastic syndrome of parotid adenocarcinoma. Because of the rarity of the condition, little is known about the management and prognosis of this phenomenon. In this report, we highlighted the case of a 59-year-old male with a past medical history of parotid adenocarcinoma treated with surgery, chemotherapy, and radiation therapy presented with clinical and biochemical signs of hyperaldosteronism. Abdominal ultra-sound, computed tomography, and magnetic resonance imaging showed hepatic mass. Liver biopsy with immunohistochemistry confirmed the presence of parotid adenocarcinoma secreting ACTH. He is on paclitaxel and carboplatin medication with good clinical response.</p> </abstract>ARTICLE2022-07-13T00:00:00.000+00:00Subacute thyroiditis after SARS-Cov2 vaccination: A review of the cases being described and personal experience<abstract> <title style='display:none'>Abstract</title> <p><bold>Objective.</bold> The present study evaluates the occurrence of subacute thyroiditis in temporal connection with SARS-Cov2 vaccinations described in the literature last year and confirmed by our clinical routine.</p> <p><bold>Methods.</bold> Systematic literature search in Medline for studies reporting diagnosis of subacute thyroiditis in temporal connection with vaccinations against Covid 19.</p> <p><bold>Results.</bold> The literature search yielded 24 relevant references out of which 22 were “case reports” and two “Letters to the Editor” and encompassed 37 patient cases, in total. They had received a SARS-Cov2 vaccination shortly before the diagnosis (median interval to vaccination six days). In none of these cases, infection of the upper respiratory tract had previously been identified as a classic trigger of the disease. Newly occurring hyperthyroidism and increased laboratory signs of inflammation were described in 78% and 74% of cases, respectively. Atypical clinical pictures (asymptomatic, euthyroid, no inflammation marks) have been observed in both the literature and our patients suspected of thyroid cancer referred to surgery.</p> <p><bold>Conclusions.</bold> In times of pandemics and the resulting vaccination, new rapidly occurring sonographic changes in the thyroid gland should be revaluated after 2–3 weeks, or recommended to undergo a fine-needle biopsy, in order to avoid unnecessary surgical interventions.</p> </abstract>ARTICLE2022-07-13T00:00:00.000+00:00Impact of hydrocortisone replacement on bone mineral density and bone turnover markers in patients with primary adrenal insufficiency<abstract> <title style='display:none'>Abstract</title> <p><bold>Objective.</bold> The study was aimed to assess the effect of hydrocortisone (HC) replacement therapy on bone mineral density (BMD) and bone turnover markers in patients with primary adrenal insufficiency (PAI).</p> <p>Methods. A cross-sectional study was conducted in 37 PAI patients treated with HC. BMD and selected bone turnover markers (β-crosslaps and osteocalcin) were measured. A stepwise binary logistic regression model was applied to determine the independent variables associated with low BMD.</p> <p>Results. Osteoporosis was noted in 14.3% and osteopenia in 34.3% of cases. These patients were older (p=0.01) and received higher daily HC dose compared to patients with normal BMD (p=0.01). BMD values in the lumbar spine and the femoral neck were negatively correlated with daily HC dose (r=–0.36, p=0.03 and r=–0.34, p=0.05, respectively). Plasma osteocalcin was negatively correlated with disease duration (r=–0.38, p=0.02) and cumulative HC dose (r=–0.43, p&lt;0.01). In multivariate analysis, a daily HC dose ≥12 mg/m2/day was independently associated with a higher risk of osteopenia/osteoporosis [OR (95% CI), 9.0 (1.1–74.6); p=0.04].</p> <p>Conclusions. Impaired bone mineralization in patients with PAI is correlated with HC dose. A daily HC dose ≥12 mg/m<sup>2</sup>/day was associated with an increased risk of osteopenia and osteoporosis in these patients.</p> </abstract>ARTICLE2022-07-13T00:00:00.000+00:00Effects of aerobic exercise on adiponectin levels potentially mediated by vitamin D in type 2 diabetic patients<abstract> <title style='display:none'>Abstract</title> <p><bold>Objective.</bold> The positive effects of exercise on adiponectin and vitamin D have independently been reported. Recent studies have suggested that vitamin D increases adiponectin synthesis through inhibition of the rennin-angiotensin system in adipose tissue. However, studies evaluating the effects of an aerobic exercise on adiponectin and vitamin D simultaneously investigating the potential mechanism of vitamin D-dependent adiponectin pathways in patients with type 2 diabetes mellitus (T2DM) are still limited. This study was undertaken to examine the effects of aerobic exercise on adiponectin and its association with vitamin D in patients with T2DM.</p> <p><bold>Methods.</bold> Total twenty-two patients with T2DM were randomly divided into intervention and control group. The intervention group underwent a moderate intensity of a walking mode treadmill aerobic exercise for four weeks. The exercise protocol was adapted from modified Bruce test with a periodic speed and inclination increase. In both groups, body mass index (BMI), vitamin D, and adiponectin levels, were measured before and after four weeks of the lasting program.</p> <p><bold>Results.</bold> The mean of the increased adiponectin and vitamin D levels after exercise was significantly higher in the intervened than the control group, but statistically significant difference was only found in the adiponectin effect (p=0.017). There was a significant association found between vitamin D and adiponectin in the intervention group after data adjustments to age and BMI (p=0.005).</p> <p><bold>Conclusion.</bold> Moderate intensity of treadmill exercise with increased speed and inclination periodically increased adiponectin level in patients with T2DM. The increased adiponectin might potentially be mediated by increased vitamin D, but the level of their association impact was dependent on the age and BMI.</p> </abstract>ARTICLE2022-07-13T00:00:00.000+00:00Prediction of the cognitive impairment development in patients with autoimmune thyroiditis and hypothyroidism<abstract> <title style='display:none'>Abstract</title> <p><bold>Objective.</bold> The aim of the present work is to define the risk factors that can affect the presence of a cognitive impairment and analyze the associations of the brain-derived neurotrophic factor (BDNF) gene polymorphism (rs6265), vitamin D receptor (VDR) gene polymorphism (rs2228570), and N-methyl-D-aspartate (NMDA) receptor gene polymorphism (rs4880213) with the cognitive impairment in patients with autoimmune thyroiditis and hypothyroidism in the Western Ukraine population and predict the development of cognitive disorders in these patients.</p> <p><bold>Methods.</bold> The study involved 153 patients with various forms of thyroid pathology (hypothyroidism, autoimmune thyroiditis, elevated serum antibodies anti-thyroglobulin and anti-thyroid peroxidase). Cognitive impairment in the examined patients was evaluated based on the results of the Mini-Mental State Examination (MMSE) test. BDNF, GRIN2B, and 25-OH Vitamin D levels in the serum of the patients and healthy individuals were quantified using highly sensitive commercial enzyme-linked immunosorbent assay kits. Genotyping of the VDR (rs2228570), BDNF (rs6265), and NMDA receptor (rs4880213) gene polymorphism was performed using TaqMan probes and Taq-Man Genotyping Master Mix (4371355) on CFX96™Real-Time PCR Detection System. Polymerase chain reaction (PCR) for TaqMan genotyping was carried out according to the kit instructions.</p> <p><bold>Results.</bold> Strong direct relationship between the “Level GRIN2B” and cognitive impairments (p=0.006) was established after evaluating the complex model based on the values of the regression coefficient. An increase in the likelihood of cognitive impairment by 24.898-fold (p=0.012) was seen after assessing the effect of the CT rs6265 genotype. In addition, direct relationship between the influence of the TT rs6265 genotype and an increase in the likelihood of cognitive impairment by a factor of 21.734 (p=0.024) was also established.</p> <p><bold>Conclusion.</bold> The present data indicate that the BDNF, TSH, fT4, and vitamin D levels prognostically belong to the significant indicators of the cognitive impairment development.</p> </abstract>ARTICLE2022-07-13T00:00:00.000+00:00The relationship between body mass index, blood pressure, and atherosclerosis risk factors in type 1 and 2 diabetic patients from northwestern Algeria<abstract> <title style='display:none'>Abstract</title> <p><bold>Objective.</bold> The present work was framed to study the relationship between body mass index (BMI), blood pressure, and atherosclerosis risk factors on the basis of three lipid ratios in type 1 (T1D) and type 2 diabetic (T2D) patients.</p> <p><bold>Methods.</bold> A prospective, comparative, and cross-sectional study was performed at the level of three health facilities in Sidi-Bel-Abbes city (north-western Algeria). Anthropometric parameters, systolic and diastolic blood pressures, and lipid profiles were assessed in adults T1D and T2D patients over a period of eleven months. Individual atherogenic risk factors were estimated based on lipid ratios in relation to corpulence and hypertension.</p> <p><bold>Results.</bold> From the total 237 adult diabetic patients, 90 T1D and 147 T2D ones were involved in the study. Total cholesterol (TC)/high-density lipoprotein (HDL) and triglycerides (TG)/HDL ratios were significantly higher in normal weight T2D comparing to T1D. The TC/HDL ratio was significantly higher (p=0.046) in obese men. Nevertheless, no significant differences were revealed in low-density lipoprotein (LDL)/HDL ratio between T1D and T2D patients. Higher TC/HDL ratios were observed in T2D patients (males and females) with normal blood pressure (systolic blood pressure, SBP ≤13.5 mmHg and diastolic blood pressure, DBP ≤8 mmHg) comparing to T1D patients. Likewise, the LDL/HDL ratio was significantly higher in T2D men with normal DBP (p=0.044).</p> <p><bold>Conclusion.</bold> The lipid ratios constitute good indices while managing diabetes. It is also recommended to screen T1D and T2D patients for hypertension, dyslipidemia, and obesity and initiate the management at early stages to prevent the related complications, such as atherosclerosis, as a priority.</p> </abstract>ARTICLE2022-07-13T00:00:00.000+00:00Mitochondria and mitochondrial disorders: an overview update<abstract> <title style='display:none'>Abstract</title> <p>Mitochondria, the cell powerhouse, are membrane-bound organelles present in the cytoplasm of almost all the eukaryotic cells. Their main function is to generate energy in the form of adenosine triphosphate (ATP). In addition, mitochondria store calcium for the cell signaling activities, generate heat, harbor pathways of intermediate metabolism and mediate cell growth and death. Primary mitochondrial diseases (MDs) form a clinically as well as genetically heterogeneous group of inherited disorders that result from the mitochondrial energetic metabolism malfunctions. The lifetime risk of the MDs development is estimated at 1:1470 of newborns, which makes them one of the most recurrent groups of inherited disorders with an important burden for society.</p> <p>MDs are progressive with wide range of symptoms of variable severity that can emerge congenitally or anytime during the life. MD can be caused by mutations in the mitochondrial DNA (mtDNA) or nuclear DNA genes. Mutations inducing impairment of mitochondrial function have been found in more than 400 genes. Furthermore, more than 1200 nuclear genes, which could play a role in the MDs’ genetic etiology, are involved in the mitochondrial activities. However, the knowledge regarding the mechanism of the mitochondrial pathogenicity appears to be most essential for the development of effective patient’s treatment suffering from the mitochondrial disease. This is an overview update focused on the mitochondrial biology and the mitochondrial diseases associated genes.</p> </abstract>ARTICLE2022-07-13T00:00:00.000+00:00Proton pump inhibitors therapy and risk of hyperprolactinemia with associated sexual disorders<abstract> <title style='display:none'>Abstract</title> <p>Proton pump inhibitors (PPIs) are the most widely prescribed medications in the world. According to numerous studies, PPIs have been linked to hyperprolactinemia, which can lead to a variety of sexual and reproductive issues. This review summarizes the effects of numerous PPIs on the blood prolactin levels and associated sexual dysfunctions, which have an effect on the patient’s life quality and fertility. The study is taken into account all the available resources till January 31, 2021. Out of total 364, only 27 relevant resources were involved in this review. In certain studies, short-term PPIs use has been shown to have little or no effect on the blood prolactin and other reproductive hormones levels. PPIs have been linked to the development of hyperprolactinemia in several case studies with varying degrees of the blood prolactin levels increase seen in individuals taking PPI alone or in combination with medications, like prokinetics. The relative risk of the sexual consequences development, such as gynecomastia, has been documented using lansoprazole and omeprazole in various cohort studies. On the other hand, other bits of data are insufficient to establish a definite relationship that can turn a possibility into certainty. The majority of the literature data is comprising of double-blind, randomized, crossover studies, case reports, and adverse drug reaction incidents reported to various pharmacovigilance centers. To investigate this link, high-quality studies in patients taking PPIs for a longer time period are needed. We conclude this article with a comprehensive discussion of the hyperprolactinemia clinical implications and the PPIs’ function.</p> </abstract>ARTICLE2022-04-30T00:00:00.000+00:00Characteristics and treatment outcomes of micromegaly – acromegaly with apparently normal basal GH: A retrospective study and literature review<abstract> <title style='display:none'>Abstract</title> <p><bold>Objective.</bold> Micromegaly describes a subgroup of patients with clinically evident acromegaly and elevated insulin-like growth factor I (IGF-I) with apparently normal basal growth hormone (bGH) and often a glucose-suppressed growth hormone (GH) of &lt;1 ng/mL at diagnosis. It is controversial whether this condition is a distinct clinical entity or a classic acromegaly in early stages. The aim of the present article was to characterize the prevalence, clinical and biochemical characteristics, and therapeutic outcomes of micromegaly.</p> <p><bold>Methods.</bold> A retrospective study of patients with an acromegaly followed ≥1 year at a tertiary center from 1995 to 2019. Patients without IGF-I or GH measurements at diagnosis were excluded. At diagnosis, bGH was considered normal if &lt;2 ng/mL.</p> <p><bold>Results.</bold> From 74 patients with acromegaly, 6 (8.1%) had normal bGH levels. There was no difference in the gender distribution, median diagnostic delay, and follow-up time between patients with normal bGH and elevated bGH. Patients with normal bGH were significantly older at time of the first acromegalic manifestation and diagnosis they had significantly lower nadir post-glucose GH and IGF-I levels, and tended to have a higher prevalence of obesity than patients with the elevated bGH. The frequency of acromegalic symptoms, signs, and other comorbidities than obesity was similar between groups. Five patients (83.3%) with normal bGH presented microadenomas. Post-operative remission and outcomes at last visit were comparable between patients with or without normal bGH.</p> <p><bold>Conclusions.</bold> Normal bGH acromegaly is relatively uncommon in our patients. These patients showed differentiating characteristics from the classical acromegaly with elevated bGH. Further studies are needed to extend the knowledge about its clinical behavior, therapeutic outcomes, morbidity, and mortality.</p> </abstract>ARTICLE2022-04-30T00:00:00.000+00:00Endothelium function biomarkers and carotid intima-media thickness changes in relation to NOS3 (rs2070744) and GNB3 (rs5443) genes polymorphism in the essential arterial hypertension<abstract> <title style='display:none'>Abstract</title> <p><bold>Objective.</bold> The aim of the present study was to clarify the endothelial function biomarkers and carotid “intima media” thickness (IMT) changes in relation to <italic>GNB3</italic> (rs5443) and <italic>NOS3</italic> (rs2070744) genes polymorphism in the essential arterial hypertension (EAH).</p> <p>Methods. One-hundred EAH patients (48 – control) participated in the case-control study. Soluble vascular cell adhesion molecule (sVCAM-1), total NO metabolites (NO<sub>2</sub><sup>–</sup>+NO<sub>3</sub><sup>–</sup>), transcriptional activity of <italic>NOS3</italic> gene, endothelium-dependent flow-mediated dilation of the brachial artery (FMD BA), and carotid IMT were studied. <italic>GNB3</italic> (rs5443) and <italic>NOS3</italic> (rs2070744) genotyping was performed by TaqMan probes (CFX96™Real-Time PCR).</p> <p>Results. The connection of <italic>NOS3</italic> (rs2070744) with decreased total NO metabolites (F=71.11; p&lt;0.001), reduced <italic>NOS3</italic> genes transcription activity (F=8.71; p&lt;0.001) and increased sVCAM-1 (F=6.96; p=0.002), especially in the <italic>C</italic>-allele carriers (particularly in <italic>CC</italic>-genotype patients with lower NO – 16.46% and 40.88%; p&lt;0.001), lowered the transcription activity of NOS3 gene – 46.03% 7 times (p&lt;0.001), and become higher sVCAM-1 – 35.48% and 89.48% (p&lt;0.001), respectively. ANOVA did not confirm the association of <italic>GNB3</italic> (rs5443) gene with endothelial function and carotid IMT. Severe EAH was associated with increased carotid IMT – 50.0% (p&lt;0.001) and 57.14% (p=0.007), wider carotid arteries – 17.36% (p=0.012) and 21.79% (p=0.004), and decreased NOS3 genes transcription activity – 34.54% (p=0.003). Atherosclerotic plaques were unilateral – 24.77% (χ<sup>2</sup>=5.35; p=0.021) or bilateral – 27.62% (χ<sup>2</sup>=5.79; p=0.016). IMT---gt---0.9 mm was followed by a higher BP (p&lt;0.001), FMD BA 11.80% decrease with compensatory increase in carotid arteries diameters – 17.38% and 21.99% (p&lt;0.001) and sVCAM-1 by 20.49% (p=0.005).</p> <p><bold>Conclusion.</bold> <italic>NOS3</italic> (rs2070744), but not <italic>GNB3</italic> (rs5443), gene associated with the essential arterial hypertension severity relying upon the endothelial function impairment and <italic>NOS3</italic> genes reduced transcription activity.</p> </abstract>ARTICLE2022-04-30T00:00:00.000+00:00The impact of single walled carbon nanotubes on the expression of microRNA in zebrafish (Danio rerio) embryos<abstract> <title style='display:none'>Abstract</title> <p><bold>Objective.</bold> Single-walled carbon nanotubes (SWCNTs) are able to cross the blood-brain barrier, penetrate through the cell membrane, and accumulate in the cell nucleus, which purposefully allows their use in the health sciences as imaging probes and drug carriers in the cancer therapy. The aim of this study was to investigate the effect of low doses of SWCNTs on the expression of microRNAs associated with the cell proliferation and the brain development in zebrafish (<italic>Danio rerio</italic>) embryos.</p> <p><bold>Methods.</bold> The zebrafish embryos (72 h post fertilization) were exposed to low doses of SWCNTs (2 and 8 ng/ml of medium) for 24 or 72 h. The microRNAs (miR-19, miR-21, miR-96, miR-143, miR-145, miR-182, and miR-206) expression levels were measured by quantitative polymerase chain reaction analysis.</p> <p><bold>Results.</bold> It was found that low doses of SWCNTs elicited dysregulation in the expression of numerous cell proliferation and brain development-related microRNAs (miR-19, miR-21, miR-96, miR-143, miR-145, miR-182, and miR-206) in dose- (2 and 8 ng/ml of medium) as well as malformations in the zebrafish embryos brain development in a time-dependent (24 and 72 h) manner.</p> <p><bold>Conclusion.</bold> Taken together, the present data indicate that the low doses of SWCNTs disturbed the genome functions and reduced the miR-19, miR-21, miR-96, miR-143, miR-145, miR-182, and miR-206 expression levels in dose- and time-dependent manners and interrupted the brain development in the zebrafish embryos indicating for both the genotoxic and the neurotoxic interventions.</p> </abstract>ARTICLE2022-04-30T00:00:00.000+00:00Change in levothyroxine requirements after bariatric surgery in patients with hypothyroidism<abstract> <title style='display:none'>Abstract</title> <p><bold>Objectives.</bold> This study aims to evaluate the need to modify the total and weight-adjusted doses of levothyroxine after bariatric surgery, identify predictors, and assess the influence of the weight loss on the levothyroxine requirements.</p> <p><bold>Methods.</bold> A retrospective study in patients with treated hypothyroidism that underwent bariatric surgery. The modification of the levothyroxine dose and its association with the weight loss and other potential predictors were evaluated at 6, 12, and 24 months post-surgery.</p> <p><bold>Results.</bold> Among the 63 patients included, 82.54% needed an adjustment of levothyroxine dose during the follow-up. The total weekly dose of levothyroxine (µg) decreased post-surgery at 6 months (β= −49.1; 95%CI-93.7 to −4.5; p=0.031) and 12 months (β=−54.9; 95%CI-102 to −7.8; p=0.022), but did not significantly change at 24 months (p=0.114). The weekly weight-adjusted dose (µg/k) increased at 6 months (β=1.37; 95%CI 0.91 to 1.83; p&lt;0.001), 12 months (β=2.05; 95%CI 1.43 to 2.67; p&lt;0.001), and 24 months (β=2.52; 95%CI 1.74 to 3.30; p&lt;0.001). The weight loss showed association with the weight-adjusted dose (OR=1.07; 95%CI 1.02 to 1.12; p=0.004), but not the total dose (p=0.320).</p> <p><bold>Conclusions.</bold> This study shows a significant decrease in the total dose of levothyroxine requirements change after bariatric surgery during the first year of the follow-up and an increase in the weight-adjusted dose over the first two years. No predictors of modification of the total dose of levothyroxine were identified.</p> </abstract>ARTICLE2022-04-30T00:00:00.000+00:00Rheumatoid arthritis: current therapeutics compendium<abstract> <title style='display:none'>Abstract</title> <p>Rheumatoid arthritis is a common chronic inflammatory disease with substantial economic, social, and personal costs. Its pathogenesis is multifactorial and complex. The ultimate goal of rheumatoid arthritis treatment is stopping or slowing down the disease progression. In the past two decades, invention of new medicines, especially biologic agents, revolutionized the management of this disease. These agents have been associated with an improved prognosis and clinical remission, especially in patients who did not respond to traditional disease-modifying anti-rheumatic drugs (DMARDs). Improvement in the understanding of the rheumatoid arthritis pathogenesis leads to the development of novel biologic therapeutic approaches. In the present paper, we summarized the current therapeutics, especially biologic agents, available for the treatment of rheumatoid arthritis.</p> </abstract>ARTICLE2022-04-30T00:00:00.000+00:00Diabetic foot care knowledge and practice in type 2 diabetes and relation to microvascular complications in Alexandria (Egypt)<abstract> <title style='display:none'>Abstract</title> <p><bold>Objectives.</bold> Egypt occupies the 8th rank in the prevalence of diabetes mellitus worldwide. The social and financial burden of diabetes and its complications represents a major health problem in Egypt. Diabetic foot and its consequences (ulcers and amputation) are preventable through good education for both physicians and patients.</p> <p><bold>Methods.</bold> This cross-sectional study was conducted on 100 patients with type 2 diabetes attending diabetes outpatient clinic in Alexandria main university hospital (AMUH). Patients were subjected to history taking, physical examination, and laboratory investigations. Screening for peripheral neuropathy was done using Michigan Neuropathy Screening Instrument (MNSI). A pre-tested questionnaire was used to assess the diabetic foot care knowledge and practice in participants.</p> <p><bold>Results.</bold> Only 25% and 24% of participants had good diabetic foot care knowledge and practice, respectively. There was a highly significant positive correlation between knowledge and practice in studied group (p&lt;0.001). The presence of microvascular complications leads to a significantly higher knowledge, but not practice.</p> <p><bold>Conclusions.</bold> Diabetic foot care knowledge and practice are poor in our community. Foot care knowledge, unlike practice, is increased with the presence of microvascular complications. We should develop effective educational programs for patients and physicians to increase knowledge and practice before the development of complications.</p> </abstract>ARTICLE2022-04-30T00:00:00.000+00:00Bredemolic acid restores glucose utilization and attenuates oxidative stress in palmitic acid-induced insulin-resistant C2C12 cells<abstract> <title style='display:none'>Abstract</title> <p><bold>Objective.</bold> Due to insulin resistance and oxidative stress that are associated with type 2 diabetes mellitus (T2DM), T2DM has become a prevalent metabolic disorder that presents various side effects. However, alternative antidiabetic treatment has commonly been used in treating diabetes mellitus in diabetic patients. In our previous studies, bredemolic acid has been reported as an antidiabetic agent that improves glucose uptake, ameliorates insulin resistance, and oxidative stress in the liver, heart, kidney, and skeletal muscle of prediabetic rats. However, these effects have not been validated <italic>in vitro</italic>. Therefore, this study was aimed to investigate the effects of bredemolic acid on insulin-mediated glucose utilization, lipid peroxidation, and the total antioxidant capacity (TOAC) in palmitic acid-induced insulin-resistant C2C12 skeletal muscle cells <italic>in vitro</italic>.</p> <p><bold>Methods.</bold> Insulin resistance was induced in the skeletal muscle cells after 4 h of exposure to palmitic acid (0.5 mmol/l). Different cell groups were incubated in culture media DMEM supplemented with fetal calf serum (10%), penicillin/streptomycin (1%), and L-glutamine (1%) and then treated with either insulin (4 µg/ml) or bredemolic acid (12.5 mmol/l) or with both. Thereafter, the cells were seeded in 24- or 96-well plates for determination of the cell viability, glucose utilization, glycogen formation, and antioxidant capacity.</p> <p><bold>Results.</bold> The results showed that bredemolic acid significantly improved TOAC and promoted glucose utilization via attenuation of lipid peroxidation and increased glycogen formation in the insulin-resistant cells, respectively.</p> <p><bold>Conclusion.</bold> This study showed that bredemolic acid restored the insulin resistance through improved glucose utilization, glycogen formation, and TOAC in the skeletal muscle cells.</p> </abstract>ARTICLE2022-04-30T00:00:00.000+00:00Assessment of hepatic prostaglandin E level in carbamazepine induced liver injury<abstract> <title style='display:none'>Abstract</title> <p><bold>Objective.</bold> Carbamazepine (CBZ), a widely used antiepileptic drug, is one major cause of the idiosyncratic liver injury along with immune reactions. Conversely, prostaglandin E<sub>2</sub> (PGE2) demonstrates a hepatoprotective effect by regulating immune reactions and promoting liver repair in various types of liver injury. However, the amount of hepatic PGE<sub>2</sub> during CBZ-induced liver injury remains elusive. In this study, we aimed to evaluate the hepatic PGE<sub>2</sub> levels during CBZ-induced liver injury using a mouse model.</p> <p><bold>Methods.</bold> Mice were orally administered with CBZ at a dose of 400 mg/kg for 4 days, and 800 mg/kg on the 5th day.</p> <p><bold>Results.</bold> Plasma alanine transaminase (ALT) level increased in some of mice 24 h after the last CBZ administration. Although median value of hepatic PGE<sub>2</sub> amount in the CBZ-treated mice showed same extent as vehicle-treated control mice, it exhibited significant elevated level in mice with severe liver injury presented by a plasma ALT level &gt;1000 IU/L. According to these results, mice had a plasma ALT level &gt;1000 IU/L were defined as responders and the others as non-responders in this study. Even though, the hepatic PGE<sub>2</sub> levels increased in responders, the hepatic expression and enzyme activity related to PGE<sub>2</sub> production were not upregulated when compared with vehicle-treated control mice. However, the hepatic 15-hydroxyprostaglandin dehydrogenase (15-PGDH) expression and activity decreased significantly in responders when compared with control mice.</p> <p><bold>Conclusions.</bold> These results indicate that elevated hepatic PGE<sub>2</sub> levels can be attributed to the downregulation of 15-PGDH expression under CBZ-induced liver injury.</p> </abstract>ARTICLE2022-02-18T00:00:00.000+00:00Extra-adrenal phaeochromocytoma in a resource poor setting: A case report<abstract> <title style='display:none'>Abstract</title> <p>Phaeochromocytomas are catecholamine-secreting tumors arising in the chromaffin cells of the adrenal medulla. They are a rare cause of secondary hypertension. However, catecholamine secreting tumors may also be found in the extra-adrenal sites, producing similar symptoms as the adrenal phaeochromocytoma. The extra-adrenal phaeochromocytomas, are referred to as paragangliomas (PGLs). About 75% of extra-adrenal phaeochromocytomas are intra-abdominal, mostly located in perinephric, periaortic, and bladder regions. Most phaeochromocytomas secrete excessive amount of epinephrine and norepinephrine, whereas most paragangliomas secrete only norepinephrine. The excessive secretion of these products could lead to paroxysms of symptoms that could be life threatening. Medical management is initially offered, but definitive treatment involves surgical removal of the tumor, which requires promptness on the both the clinician and the patient sides. We present a case of an extra-adrenal phaeochromocytoma in an adult male with revealing imaging of a mass surrounding the bladder. The patient was managed with both alpha- and beta-adrenergic blockers. He declined the surgery and eventually died after appearing in an acute hypertensive crisis.</p> </abstract>ARTICLE2022-02-18T00:00:00.000+00:00Insulin receptor substrate 1 gene variations and lipid profile characteristics in the type 2 diabetic patients with comorbid obesity and chronic pancreatitis<abstract> <title style='display:none'>Abstract</title> <p><bold>Objective.</bold> Type 2 diabetes mellitus (T2DM) is one of diseases that develops in a setting of polymorbid processes or more often promotes their development, forming in this spectrum the phenomenon of comorbidity. The aim of this study was to evaluate changes in the lipid panel data in T2DM patients with comorbid obesity and chronic pancreatitis (CP) taking into account the C/A polymorphism of the insulin receptor substrate 1 (<italic>IRS1</italic>) gene (rs2943640).</p> <p><bold>Methods.</bold> The study involved 34 T2DM patients and 10 healthy individuals. The rs2943640 <italic>IRS1</italic> gene polymorphism was genotyped using the TaqMan real-time polymerase chain reaction (PCR) method. Blood serum lipid panel data were determined with commercially available kits on a Cobas 6000 analyzer.</p> <p><bold>Results.</bold> In patients with only T2DM and T2DM + comorbid obesity, an association between <italic>IRS1</italic> gene polymorphism (rs2943640) and lipid profile abnormalities with maximum changes of the lipid characteristics recorded in C/C genotype carriers was found. Within the C/C genotype of the <italic>IRS1</italic> gene (rs2943640) in type 2 diabetic patients with comorbid obesity and CP, significantly lower high-density lipoprotein cholesterol (HDL-C) levels and significantly higher levels of triglycerides (TG), non-HDL-C and remnant cholesterol (RC) in relation to type 2 diabetic patients with comorbid obesity were found. At the same time, within the C/A genotype of the <italic>IRS1</italic> gene (rs2943640), significant changes of lipid panel data were found in type 2 diabetic patients with comorbid obesity relative to the control group (p&lt;0.001).</p> <p><bold>Conclusions.</bold> Our data indicate that the presence of the C allele of <italic>IRS1</italic> gene (rs2943640) in both homozygous and heterozygous states may indicate increased risk of dyslipidemia in type 2 diabetic patients with comorbidities.</p> </abstract>ARTICLE2022-02-18T00:00:00.000+00:00en-us-1