Objective (s): Sepsis can result in severe organ injury by provoking inflammatory cascades and oxidative stress. Several studies are currently underway to find a drug with anti-inflammatory effects to prevent mortality and morbidity during sepsis. The present study was undertaken to assess the effects of METFORMIN on oxidative stress and antioxidant status in sepsis induced by the Cecal Ligation and Puncture (CLP) method.Materials and Methods: Male Wistar rats were divided into 4 groups (n=10): sham, CLP, and 50 and 100 mg/ kg METFORMIN-treated CLP groups. After 12 hr, blood samples were collected and lung tissue was removed for histopathological study to detect tissue damage and degree of inflammation based on neutrophil infiltration and assay of the oxidative stress biomarkers superoxide dismutase (SOD), total antioxidant capacity (TAC), malondialdehyde (MDA), myeloperoxidase (MPO), glutathione peroxidase (GPx), and plasminogen activator inhibitor‐1 (PAI‐1).Results: The MPO activity and MDA level were decreased in the METFORMIN-treated groups (P<0.05). Moreover, the groups receiving METFORMIN showed lower inflammation scores than the CLP group (P<0.05). No significant differences in SOD, GPx, or PAI in the different groups were observed. The TAC level was reduced in the CLP group compared to the sham group (P<0.05), and interestingly, this value was reduced even further in the METFORMIN-treated groups (P<0.05 compared with the CLP group).Conclusion: It was concluded that METFORMIN protects lung tissue against sepsis-induced oxidative damage, and this protective effect may be more related to its anti-inflammatory and reduced neutrophil accumulation and less to its anti-oxidative properties.

Background: Polycystic ovary syndrome (PCOS) is associated with approximately 75% of women who suffer from infertility due to anovulation. Additionally, around 20-25% of anovulatory women with PCOS do not respond at all to clomiphene citrate and are considered to be “clomiphene-resistant”. Aromatase inhibitors have been suggested as an alternative treatment to clomiphene as the discrepancy between ovulation and pregnancy rates with clomiphene citrate has been attributed to its anti-estrogenic action and estrogen receptor depletion.Objective: The aim of this study is to compare results of METFORMIN-letrozole with METFORMIN-clomiphene citrate in clomiphene resistance PCOS patients undergoing IUI.Materials and Methods: In this single blind randomized trial, ovarian cycles were studied in 100 clomiphene- resistant patients with PCOS. The inclusion criteria were patients who received 150mg clomiphene citrate daily for 3 cycles and failed to become pregnant. The patients were matched for their age, body mass index (BMI), and infertility period. They were randomly allocated to a METFORMIN-letrozole group (n=50) and a METFORMIN-clomiphene citrate group (n=50). Chemical and clinical pregnancies were assessed after IUI. Abortion rates were determined in both groups.Results: Regarding pregnancy rate, there was no significant difference between the two groups. One miscarriage (2%) occurred in the METFORMIN-clomiphene citrate group, whereas none was seen in the METFORMIN-letrozole group.Conclusion: There is no significant difference in pregnancy rate between clomiphene citrate and letrozole groups although it has been 2% in the former and 5% in the latter.

Introduction: METFORMIN-associated lactic acidosis is a rare, yet fatal condition, especially in the presence of risk factors. Therapeutic use of METFORMIN may induce lactic acidosis. Gastrointestinal bleeding, dehydration, acute renal failure, and drugs are major risk factors that increase the mortality risk associated with METFORMIN-associated lactic acidosis. In this regard, this case study aimed to present a patient, who died due to METFORMIN-associated lactic acidosis despite treatment. Method: This case study featured a 45-year-old diabetic patient with METFORMIN use, who presented to the emergency department with the complaint of low back pain. He had acute renal failure, severe lactic acidosis, and shock findings. Discussion: The primary purpose of METFORMIN-associated lactic acidosis treatment is to restore acid-base balance and provide hemodynamic support. Hemodialysis reduces the mortality due to METFORMIN-associated lactic acidosis by decreasing lactate clearance. Supportive therapies should be used. Nevertheless, mortality still occurs in approximately 50% of the cases. Conclusion: METFORMIN overdose or even therapeutic levels of METFORMIN use can cause MALA in the presence of various risk factors. MALA, a rare clinical condition, is associated with mortality rates of up to 50%. The most crucial step in treating MALA is hemodialysis/venous hemofiltration. Given that METFORMIN is a frequently used medication, care should be taken in the follow-up of patients using METFORMIN, considering MALA.

Type 2 diabetes mellitus is a serious health hazard all around the world and accounts for 90% to 95% of all diagnosed diabetes cases. It can be complicated with microvascular and macrovascular side effects such as coronary artery disease, stroke, retinopathy, and nephropathy. Although the majority of these complications have a multifactorial pathophysiology related to hyperglycemia, hypertension, dyslipidemia, and insulin resistance, the pathogenesis of vascular complications seems to be beyond hyperglycemia and glycated proteins. Thus, a drug with additional benefits other than glycemic control might be effective in reducing diabetic complications, especially the cardiovascular ones...