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.

For induction of ruminal acidosis, 10 clinically healthy three years old non pregnant female sheep were selected. Prior to the infusion of sucrose (0 hour), rumen and blood samples were obtained in order to determine baseline rumen and blood pH, respectively. Electrocardiogram (ECG) was also recorded. Acute ruminal acidosis was induced experimentally with sucrose at a dose of 18g kg-1 body weigh through rumen fistula. ECG was recorded and blood and rumen samples collected at 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, and 48 hours after the infusion of sucrose. Results indicated that blood and rumen pH decreased significantly at 15, 18, 21, 24, 30, 36 and 48 hours and at 3, 6, 9, 12, 15, 18, 21, 24, 30, 36 and 48 hours, respectively. acidosis produced a marked increasing in heart rate and a decrease in PR interval at 15 and 18 hour significantly with little apparent effect on the ST and PR segment. The P amplitude increased significantly at 6, 9, 12, 15, 18, 21, 24 and 30 hours. The T amplitude increased significantly at 9, 12, 15, 18, 21, 24, 30 and 36 hours. The RR interval decreased significantly at 6, 9, 12, 15, 18, 21, 24, 30, 36 and 48 hours. In conclusion acute ruminal acidosis caused significant changes in ECG of sheep though there was not any detectable arrhythmia in the ECG in acute ruminal acidosis.

Objective(s): Causality of occurrence of metformin-associated Lactic acidosis (MALA) is a clinical problem. Currently, there is no drug available to prevent MALA. The present study was conducted to evaluate the protective effect of Berberine (BBR) against MALA in induced diabetic rat model. Materials and Methods: A sample of 75 healthy male Wistar rats was randomly selected according to inclusion and exclusion criteria. 75 male Wistar rats were randomly divided into a control and 4 experimental groups. Streptozotocin (STZ) in citrate buffer (pH 4. 5) at a dose of 45 mg/kg was injected for induction of diabetes mellitus and rats achieving fasting blood glucose >250 mg/dl were included. Blood samples were collected 18 hr after the last dose of metformin and berberine. Ethical approval was taken before the study was conducted. Staistix 10. 0 (USA) software was used for data analysis. Results: Berberine decreased MALA. Metformin, metformin + BBR 50 mg/kg bwt, and metformin + BBR 100 mg/kg bwt showed serum lactate as 1. 87± 0. 4 mmol/lL, 1. 62 ± 0. 44 mmol/l and 1. 47± 0. 45 mmol/l, respectively (P=0. 0001). Insulin resistance and liver enzymes were improved in BBR treated rats. Conclusion: The present study reports berberine protects against MALA in streptozocin-induced diabetes mellitus.

Introduction. Metformin-associated Lactic acidosis is rare despite its widespread use. It is often associated with the use of metformin in the presence of chronic kidney disease, but it may also occur in people with normal renal function in the case of acute overdose. Case Report. 20 years old (patient 1) and 37 years old (patient 2) women without any chronic disease took 40 gram (727 mg/ kg) and 60 gram (1200 mg/kg) metformin, respectively; for the suicidal attempt. Deep Lactic acidosis was detected in patients. In patient 1, hemodialysis was performed for 4 hours. After the interruption, deep acidosis evolved again and another dialysis session was performed. In patient 2, hemodialysis was performed for 16 hours without any interruption and she did not need any other dialysis session. Conclusion. Metformin has a large distribution volume. It is not correct to make a final decision as to how long the dialysis will continue when dialysis begins. Dialysis should be continued without interruption until clinical and laboratory targets are achieved.

Patients with mitochondrial encephalopathy, Lactic acidosis and stroke-like episodes (MELAS) present with recurrent and partially reversible neurological deficits. Lesions of MELAS classically cause a signal change in both the grey and white matter, predominantly in the occipital and parietal lobes. These lesions mimic infarction. Here, we reported a case of MELAS with rare neuroimaging finding of hemispheric cortical thickening on T2/FLAIR images with intracortical nodular gadolinium enhancement; then we discussed the clinical and radiological differential diagnoses of it.