Objective. Carbamazepine (CBZ), a widely used antiepileptic drug, is one major cause of the idiosyncratic liver injury along with immune reactions. Conversely, prostaglandin E2 (PGE2) demonstrates a hepatoprotective effect by regulating immune reactions and promoting liver repair in various types of liver injury. However, the amount of hepatic PGE2 during CBZ-induced liver injury remains elusive. In this study, we aimed to evaluate the hepatic PGE2 levels during CBZ-induced liver injury using a mouse model. Methods. Mice were orally administered with CBZ at a dose of 400 mg/kg for 4 days, and 800 mg/kg on the 5th day. Results. Plasma alanine transaminase (ALT) level increased in some of mice 24 h after the last CBZ administration. Although median value of hepatic PGE2 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 >1000 IU/L. According to these results, mice had a plasma ALT level >1000 IU/L were defined as responders and the others as non-responders in this study. Even though, the hepatic PGE2 levels increased in responders, the hepatic expression and enzyme activity related to PGE2 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. Conclusions. These results indicate that elevated hepatic PGE2 levels can be attributed to the downregulation of 15-PGDH expression under CBZ-induced liver injury.
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women associated with cardiovascular disease and obesity. The possible benefits of omega-3 supplementation in this syndrome have been discussed much. This study is aimed to verify, based on the scientific data published, if there are any benefits in the omega-3 supplementation in the treatment of PCOS and to indicate its possible dosages for the treatment of polycystic ovary. The work consists of a systematic review of clinical trials and cohort of the MEDLINE/PubMed database from 2009 to October 2019. All studies that analyzed the omega-3 supplementation in women with PCOS were included. Cross-sectional studies, review articles, systematic reviews, meta-analysis, duplicates, studies in animals or cell culture, studies with omega-3 supplementation via food or associated with other supplementations were not included, except those involving vitamin E. In total, 21 articles were selected. Despite the heterogeneity of the studies selected, indirect benefits were observed mainly regarding the glycemic profile, such as insulin resistance reduction, lipid profile modulation (i.e. decrease in total cholesterol, triglycerides, and elevation of high-density lipoprotein), and the regulation of the androgenic profile. As for the anthropometric profile, the studies were scarce and most of them had no significant meaning. Regarding the antioxidant profile and inflammatory biomarkers, the findings differ among studies, but promising results were observed with different doses over 12 weeks of use, such as C-reactive protein (CRP) reduction. Thus, omega-3 fatty acids promote indirect benefits in the treating of women with PCOS. However, to reveal well-defined standards for dosage and supplementation time, further studies are needed.
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.
Cardiovascular complications are the main cause of mortality and morbidity in the diabetic patients, in whom changes in myocardial structure and function have been described. Numerous molecular mechanisms have been proposed that could contribute to the development of a cardiac damage. In this regard, angiotensin II (Ang II), a proinflammatory peptide that constitutes the main effector of the renin-angiotensin system (RAS) has taken a relevant role. The aim of this review was to analyze the role of Ang II in the different biochemical pathways that could be involved in the development of cardiovascular damage during diabetes. We performed an exhaustive review in the main databases, using the following terms: angiotensin II, cardiovascular damage, renin angiotensin system, inflammation, and diabetes mellitus. Classically, the RAS has been defined as a complex system of enzymes, receptors, and peptides that help control the blood pressure and the fluid homeostasis. However, in recent years, this concept has undergone substantial changes. Although this system has been known for decades, recent discoveries in cellular and molecular biology, as well as cardiovascular physiology, have introduced a better understanding of its function and relationship to the development of the diabetic cardiomyopathy.
Objectives. Markers for glucose control in hemodialysis patients (HDP) are debated. Glycosylated hemoglobin (HbA1c%) relies on the stable red blood cell survival. Albumin turnover is faster than hemoglobin. Glycated albumin (GA%) may be used as an index of short-term glycemic control. The predictive value of GA% versus HbA1c% in monitoring the glucose homeostasis in type-2 diabetic HDP is studied. Methods. Forty type-2 diabetic HDP and 20 healthy non diabetic subjects matched age and sex as a control group were included. Calculation of body mass index and Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) and urea reduction ratio were done. Glycosylated hemoglobin, glycated albumin, fasting blood glucose, insulin, total lipid, kidney and liver functions tests, hepatitis markers, electrolytes, complete blood count, and international normalized ratio were performed. Patients were followed up after 6 months. Results. The study showed that GA% is more sensitive than HbA1c%, but less specific in the follow-up of the glucose homeostasis in type-2 diabetic HDP. Diagnostic accuracy is higher in HbA1c% than in GA%. HOMA-IR is superior regarding the sensitivity and the diagnostic accuracy. Conclusion. The present data show that GA% is more sensitive than HbA1c% and has more diagnostic accuracy in the follow-up of the glucose homeostasis in type-2 diabetic HDP.
Objective. 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 (IRS1) gene (rs2943640). Methods. The study involved 34 T2DM patients and 10 healthy individuals. The rs2943640 IRS1 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. Results. In patients with only T2DM and T2DM + comorbid obesity, an association between IRS1 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 IRS1 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 IRS1 gene (rs2943640), significant changes of lipid panel data were found in type 2 diabetic patients with comorbid obesity relative to the control group (p<0.001). Conclusions. Our data indicate that the presence of the C allele of IRS1 gene (rs2943640) in both homozygous and heterozygous states may indicate increased risk of dyslipidemia in type 2 diabetic patients with comorbidities.