Lactic Acidosis In Patients Research Articles

#746 Lactic acidosis in patients with acute kidney injury treated with renal replacement therapy in intensive care unit

Abstract Background and Aims Lactic acidosis (LA) is the most common cause of metabolic acidosis in hospitalised patients. LA is frequent in intensive care unit (ICU) patients with acute kidney injury (AKI) treated with renal replacement therapy (RRT). The aim of our study was to analyse the impact of LA on mortality. Method We conducted a retrospective observational study in a tertiary care hospital with a 12-bed ICU. During the study period of 4 years before the COVID pandemic, 2939 patients were admitted to the ICU, 503 patients were diagnosed with AKI and 210 of them required RRT. Due to missing data, we retrospectively analysed only 176 patients. LA was defined as a serum lactate concentration above 4 mmol/L on admission to the ICU. Demographic data, comorbidities, laboratory data at ICU admission and 30-day survival after ICU admission were obtained from the medical record. Survival was estimated using the Kaplan-Meier method, and factors associated with 30-day mortality were assessed in a Cox regression. Results The mean age of patients was 63.4±12.9 years, and 68.2% were men. Sixty-five (36.9%) of patients had LA. The prevalence of comorbidities prior to admission and baseline laboratory values are shown in Table 1. All patients were treated with RRT, 137 (77.8%) with continuous RRT and 39 (22.2%) with intermittent hemodialysis. The mean ICU stay was 14.6 ± 12 days, and 114 (64.8%) patients died during the observational period of 30 days. A Kaplan-Meier survival analysis showed that the survival was statistically significantly lower (log-rank; p = 0.027) in the group of patients with LA (Fig. 1). Univariate Cox regression analysis showed that LA was a significant predictor of 30-day survival (HR 1.51; 95% CI 1.038-2.197; p = 0.031). In the multivariate Cox regression analysis, which included age, gender, diabetes, hypertension, LA and C-reactive protein, only age (HR 1.029; 95% CI 1.011-1.046; p = 0.001) and LA (HR 1.515; 95% CI 1.030-2.228; p = 0.035) were independent predictors of mortality. Conclusion LA on ICU admission is an independent, highly prognostic factor for death within 30 days of admission in patients with AKI treated with RRT.

Metformin exposure and the incidence of lactic acidosis in critically ill patients with T2DM: A retrospective cohort study.

The objective of this study was to investigate the correlation between metformin exposure and the incidence of lactic acidosis in critically ill patients. The patients with type 2 diabetes mellitus (T2DM) were included from Medical Information Mart for Intensive Care IV database (MIMIC-IV). The primary outcome was the incidence of lactic acidosis. The secondary outcomes were lactate level and in-hospital mortality. Propensity score matching (PSM) method was adopted to reduce bias of the confounders. The multivariate logistic regression was used to explore the correlation between metformin exposure and the incidence of lactic acidosis. Subgroup analysis and sensitivity analysis were used to test the stability of the conclusion. We included 4939 patients. There were 2070 patients in the metformin group, and 2869 patients in the nonmetformin group. The frequency of lactic acidosis was 5.7% (118/2070) in the metformin group and it was 4.3% (122/2869) in the nonmetformin group. There was a statistically significant difference between the two groups (P < 0.05). The lactate level in the metformin group was higher than in the nonmetformin group (2.78 ± 2.23 vs. 2.45 ± 2.24, P < 0.001). After PSM, the frequency of lactic acidosis (6.3% vs. 3.7%, P < 0.001) and lactate level (2.85 ± 2.38 vs. 2.40 ± 2.14, P < 0.001) were significantly higher in the metformin group compared with the nonmetformin group. In multivariate logistic models, the frequency of lactic acidosis was obviously increased in metformin group, and the adjusted odds ratio (OR) of metformin exposure was 1.852 (95% confidence interval (CI) = 1.298-2.643, P < 0.001). The results were consistent with subgroup analysis except for respiratory failure subgroup. Metformin exposure increased lactate level but did not affect the frequency of lactic acidosis in patients of respiratory failure with hypercapnia. However, the in-hospital mortality between metformin and nonmetformin group had no obvious difference (P = 0.215). In sensitivity analysis, metformin exposure showed similar effect as the original cohort. In critically ill patients with T2DM, metformin exposure elevated the incidence of lactic acidosis except for patients of respiratory failure with hypercapnia, but did not affect the in-hospital mortality.

Prescription trend and lactic acidosis in patients prescribed metformin before and after the revision of package insert for allowing metformin administration to patients with moderately decreased kidney function based on real-world data from MID-NET® in Japan.

This study was conducted to understand the impact of package insert (PI) revision in Japan on 18 June 2019 to allow metformin use for patients with moderately decreased kidney function (30 ≤ estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m2). A new user cohort design was employed to examine the prescription trend and the occurrence of lactic acidosis in patients prescribed metformin before and after PI revision using the Medical Information Database Network (MID-NET®). From 12 May 2016 to 31 March 2020, 5,874 patients (before, n = 4,702; after, n = 1,172) were identified as new metformin users, including 1,145 patients (before, n = 914; after, n = 231) with moderately decreased kidney function. Although no marked changes in metformin prescription were observed before and after PI revision, the daily metformin dose at the first prescription decreased after PI revision. For both before and after PI revision, less than 10 cases of lactic acidosis occurred in all patients prescribed metformin, and no lactic acidosis was observed in patients with moderately decreased kidney function. The results of this study are useful for understanding the safety of metformin use in patients with decreased kidney function and suggest no worse impacts of PI revision in Japan, indicating no further safety concerns on metformin use in patients with moderately decreased kidney function under the situation with careful use and safety monitoring of metformin.

Mean value of Perfusion Index in patients resuscitated from an out-of-hospital cardiac arrest predict the incidence of lactic acidosis on ICU admission

Abstract Funding Acknowledgements Type of funding sources: None. Backround Regional and general hypoperfusion cause hypoxia, resulting in excess production of lactate secondary to reduced mitochondrial oxidation. Peripheral perfusion index (PI) is the fraction of the pulsatile blood flow to the non-pulsatile blood in peripheral tissue obtained by standard pulse-oximetry. Recent literature has highlighted its association with both survival and ECG reliability in patients resuscitated from an out-of-hospital cardiac arrest (OHCA). Purpose We raised the hypothesis that the mean value of PI over 30-minutes monitoring (MPI30) after ROSC in patients resuscitated from an OHCA is associated with the probability of detecting a lactic acidosis (LA) at the first arterial blood gas analysis available after ICU admission. Materials and Methods This was a retrospective study, obtaining data from our cardiac arrest registry. Among 172 post-ROSC patients admitted to the ICU (between 1st January 2017 and May 2021) post-ROSC MPI30 was available in 76 patients: 54 (72%) males; median age 70 years (IQR 59-77). PI was automatically and continuously measured by the manual monitor/defibrillator (Corpuls by GS Elektromedizinische Geräte G. Stemple GmbH, Germany) once the pulse oximeter was placed, then registered in the report. The population was divided in quartiles according to MPI30 values, then the incidence along the quartiles were compared with chi-squared test. The association between MPI30 and LA incidence was investigated both with univariate and multivariate logistic regression. Results LA was documented in 57% of the study population. We found a significant trend toward reduction of incidence of LA along the four quartiles (p=0.0386). Univariate logistic regression showed a statistically significant association between MPI30 and LA on admission [OR 0.62 (95%CI 0.44-0.89), p=0.005] which was confirmed after correction for age and sex [OR 0.63 (95%CI 0.43-0.91), p=0.009]. Conclusions Low perfusion as measured by MPI30 after ROSC predicts a higher incidence of lactic acidosis in patients on admission to the ICU. Our results could help clinicians in identifying patients at risk for metabolic derangements even before a blood gas analysis is obtained.

LBODP038 Metformin-Associated Severe Lactic Acidosis: A Case Study Of The Perfect Storm

Abstract Background Metformin carries a rare risk of lactic acidosis. Medications that can increase the concentration of metformin in the serum can increase the risk of lactic acidosis. Similarly, kidney dysfunction leads to decreased clearance of the drug, hence potentiating its adverse effects. Clinical Case A 62-year-old male with HIV (undetectable viral load) on dolutegravir, atazanavir/cobicistat, rilpivrine, type 2 DM (A1C 7.2%) on metformin and dulaglutide presented with 1 day history of dyspnea. He had a respiratory rate of 28 and heart rate of 131. Blood glucose was 43 mg/dL (nl 74-99 mg/dL). Labs were also notable for lactate 23.6 mmol/L (nl 0.4-2 mmol/L), severe anion gap metabolic acidosis with pH &amp;lt;6.8, bicarbonate 5 mmol/L (nl 21-32 mmol/L). Creatinine was 2.29 mg/dL (nl 0.5-1.3 mg/dL) with a normal baseline kidney function. Beta-hydroxybutyrate was elevated at 0.73 mmol/L (nl 0. 02-0.27 mmol/L). Osmolar gap was 17.3 mOsm, ethanol level was 22 mg/dL (nl &amp;lt;10 mg/dL), ethylene glycol was not detected. Patient reported drinking four beers daily but endorsed binge drinking the previous night with associated emesis. Review of records showed that the patient was started on dulaglutide recently and he endorsed nausea and diarrhea with initiation of the medication. He otherwise had no changes in his metformin dose or antiretroviral regimen. He was admitted to the ICU for further management of his severe lactic acidosis. Patient's antiretroviral regimen, dulaglutide, and metformin were held on admission. Medical toxicology was consulted, and metformin associated lactic acidosis was suspected. He was initiated on dialysis and his lactic acidosis resolved within 24 hours. His antiretroviral regimen was resumed prior to discharge when his creatinine improved to 1.38 mg/dL. Metformin was discontinued and he was discharged on dulaglutide with endocrinology follow up. Conclusion This case demonstrates how multiple factors such as alcohol use, kidney injury, and other medications can increase the, otherwise rare, risk of lactic acidosis in patients taking metformin. The patient had experienced GI losses due to emesis from his increased alcohol intake as well as diarrhea with the initiation of dulaglutide leading to dehydration and acute kidney injury. The latter can give rise to decreased metformin clearance. In addition, dolutegravir increases metformin plasma exposure. Together, the constellation of factors had likely led to increased metformin plasma levels and associated severe lactic acidosis. Patients should be counseled on the use of alcohol while taking metformin. Additionally, drug interactions should be monitored, and dose reductions of metformin should be considered in patients taking dolutegravir. Presentation: No date and time listed

Sufentanil: a risk factor for lactic acidosis in patients after heart valve surgery

BackgroundsHyperlactatemia is a common metabolic disorder after cardiac surgery with cardiopulmonary bypass. Epinephrine use has been identified as a potential cause of increased lactate levels after cardiac surgery. Stress can lead to an increase in catecholamines, mainly epinephrine, in the body. Exogenous epinephrine causes hyperlactatemia, whereas endogenous epinephrine released by stress may have the same effect. Opioids are the most effective anesthetics to suppress the stress response in the body. The authors sought to provide evidence through a retrospective data analysis that helps investigate the relationship between intraoperative opioid dosage and postoperative lactic acidosis after cardiac surgery.MethodsThe clinical data of 215 patients who underwent valvular heart surgery with cardiopulmonary bypass from July 2016 to July 2019 were analyzed retrospectively. Blood lactate levels were measured at 0.1 h, 2 h, 4 h, and 8 h after surgery. Patients with continuous increases in lactate levels and lactate levels exceeding 5 mmol/L at two or more time points were included in the lactic acidosis group, whereas the other patients were included in the control group. First, univariate correlation analysis was used to identify parameters that were significantly different between the two groups, and then multivariate regression analysis was conducted to elucidate the independent risk factors for lactic acidosis. Fifty-one pairs of patients were screened by propensity score matching analysis (PSM). Then, lactic acid levels at four time points in both groups were analyzed by repeated measures ANOVA.Resultshe EF (heart ejection fraction) (OR = 0.94, P = 0.003), aortic occlusion time (OR = 10.17, P < 0.001) and relative infusion rate (OR = 2.23, P = 0.01) of sufentanil was an independent risk factor for lactic acidosis after valvular heart surgery. The patients were further divided into two groups with the mean sufentanil infusion rate as the reference point. The data were filtered with PSM (Propensity Score Matching). Lactic acid values in both groups peaked at 4 h after surgery and then declined. The rate of lactic acid decline was significantly faster in the group with a higher sufentanil dosage than in the lower group. The difference was statistically significant (P < 0.05). There was also a significant difference in lactic acid levels at the four time points (0.1 h, 2 h, 4 h and 8 h after surgery) in both groups (P < 0.001).ConclusionThe inadequate intraoperative infusion rate of sufentanil is an independent risk factor for lactic acidosis after heart valve surgery. The possibility of lactic acidosis caused by this factor after cardiac surgery should be considered, which is helpful for postoperative patient management.

Lactic Acidosis in Patients with Solid Cancer.

Significance: Cancer-associated tissue-specific lactic acidosis stimulates and mediates tumor invasion and metastasis and is druggable. Rarely, malignancy causes systemic lactic acidosis, the role of which is poorly understood. Recent Advances: The understanding of the role of lactate has shifted dramatically since its discovery. Long recognized as only a waste product, lactate has become known as an alternative metabolism substrate and a secreted nutrient that is exchanged between the tumor and the microenvironment. Tissue-specific lactic acidosis is targeted to improve the host body's anticancer defense and serves as a tool that allows the targeting of anticancer compounds. Systemic lactic acidosis is associated with poor survival. In patients with solid cancer, systemic lactic acidosis is associated with an extremely poor prognosis, as revealed by the analysis of 57 published cases in this study. Although it is considered a pathology worth treating, targeting systemic lactic acidosis in patients with solid cancer is usually inefficient. Critical Issues: Research gaps include simple questions, such as the unknown nuclear pH of the cancer cells and its effects on chemotherapy outcomes, pH sensitivity of glycosylation in cancer cells, in vivo mechanisms of response to acidosis in the absence of lactate, and overinterpretation of in vitro results that were obtained by using cells that were not preadapted to acidic environments. Future Directions: Numerous metabolism-targeting anticancer compounds induce lactatemia, lactic acidosis, or other types of acidosis. Their potential to induce acidic environments is largely overlooked, although the acidosis might contribute to a substantial portion of the observed clinical effects. Antioxid. Redox Signal. 37, 1130-1152.

Diabetes, Metformin and the Clinical Course of Covid-19: Outcomes, Mechanisms and Suggestions on the Therapeutic Use of Metformin.

Objectives: Pre-existing or new diabetes confers an adverse prognosis in people with Covid-19. We reviewed the clinical literature on clinical outcomes in metformin-treated subjects presenting with Covid-19. Methods: Structured PubMed search: metformin AND [covid (ti) OR covid-19 (ti) OR covid19 (ti) OR coronavirus (ti) OR SARS-Cov2 (ti)], supplemented with another PubMed search: “diabetes AND [covid OR covid-19 OR covid19 OR coronavirus (i) OR SARS-Cov2 (ti)]” (limited to “Clinical Study”, “Clinical Trial”, “Controlled Clinical Trial”, “Meta-Analysis”, “Observational Study”, “Randomized Controlled Trial”, “Systematic Review”). Results: The effects of metformin on the clinical course of Covid-19 were evaluated in retrospective analyses: most noted improved clinical outcomes amongst type 2 diabetes patients treated with metformin at the time of hospitalisation with Covid-19 infection. These outcomes include reduced admission into intensive care and reduced mortality in subgroups with versus without metformin treatment. Conclusion: The pleiotropic actions of metformin associated with lower background cardiovascular risk may mediate some of these effects, for example reductions of insulin resistance, systemic inflammation and hypercoagulability. Modulation by metformin of the cell-surface ACE2 protein (a key binding target for SARS-CoV 2 spike protein) via the AMP kinase pathway may be involved. While pre-existing metformin treatment offers potentially beneficial effects and can be continued when Covid-19 infection is not severe, reports of increased acidosis and lactic acidosis in patients with more severe Covid-19 disease remind that metformin should be withdrawn in patients with hypoxaemia or acute renal disease. Prospective study of the clinical and metabolic effects of metformin in Covid-19 is warranted.

Phenformin increases early hematopoietic progenitors in the Jak2V617F murine model.

Myeloproliferative neoplasms (MPN) are disorders characterized by an alteration at the hematopoietic stem cell (HSC) level, where the JAK2 mutation is the most common genetic alteration found in classic MPN (polycythemia vera, essential thrombocythemia, and primary myelofibrosis). We and others previously demonstrated that metformin reduced splenomegaly and platelets counts in peripheral blood in JAK2V617F pre-clinical MPN models, which highlighted the antineoplastic potential of biguanides for MPN treatment. Phenformin is a biguanide that has been used to treat diabetes, but was withdrawn due to its potential to cause lactic acidosis in patients. We herein aimed to investigate the effects of phenformin in MPN disease burden and stem cell function in Jak2V617F-knockin MPN mice. In vitro phenformin treatment reduced cell viability and increased apoptosis in SET2 JAK2V67F cells. Long-term treatment with 40mg/kg phenformin in Jak2V617F knockin mice increased the frequency of LSK, myeloid progenitors (MP), and multipotent progenitors (MPP) in the bone marrow. Phenformin treatment did not affect peripheral blood counts, spleen weight, megakaryocyte count, erythroid precursors frequency, or ex vivo clonogenic capacity. Ex vivo treatment of bone marrow cells from Jak2V617F knockin mice with phenformin did not affect hematologic parameters or engraftment in recipient mice. Phenformin increased the percentages of LSK, MP, and MPP populations, but did not reduce disease burden in Jak2V617F-knockin mice. Additional studies are necessary to further understand the effects of phenformin on early hematopoietic progenitors.

Metformin use and cardiovascular outcomes in patients with diabetes and chronic kidney disease: a nationwide cohort study.

BackgroundMetformin has recently been shown not to increase the risk of lactic acidosis in patients with chronic kidney disease (CKD). Thus, the criteria for metformin use in this population has expanded. However, the relationship between metformin use and clinical outcomes in CKD remains controversial.MethodsThis study considered data from 97,713 diabetes patients with an estimated glomerular filtration rate of <60 mL/min/1.73 m2. The primary outcome was major adverse cardiac and cerebrovascular events (MACCE), and the secondary outcomes were all-cause mortality and incident end-stage renal disease (ESRD).ResultsMetformin users had a significantly higher risk of MACCE than non-users (hazard ratio [HR], 1.20; 95% confidence interval [CI], 1.14–1.26; p < 0.001). However, metformin users had a lower risk of all-cause mortality (HR, 0.78; 95% CI, 0.74–0.81; p < 0.001) and ESRD (HR, 0.44; 95% CI, 0.42–0.47; p < 0.001) during follow-up than non-users did. The relationships between metformin use and clinical outcomes remained consistent in propensity score matching analyses and subgroup analyses of patients with adequate adherence to anti-diabetes medication.ConclusionTreatment with metformin was associated with an increased risk of MACCE in patients with diabetes and CKD. However, metformin users had a lower risk of all-cause mortality and ESRD during follow-up than non-users did. Therefore, metformin needs to be carefully used in patients with CKD.

Effects of Metformin on Clinical outcomes in Patients with Type 2 Diabetes and Covid-19

Background: The effects of metformin therapy on the prognosis of patients with coronavirus disease 2019 (COVID-19) are unclear. Objective: To review effects of metformin on clinical outcomes, particularly mortality, in patients with type 2 diabetes and COVID-19. Methods: Review of English literature by PUBMED search until April 20, 2021. Search terms included diabetes, COVID-19, metformin, Retrospective studies, meta-analyses, pertinent reviews, and consensus guidelines are reviewed. Results: All available studies in this area are retrospective. Two population-based studies did not find significant association between metformin use and susceptibility to COVID-19. Most, but not all studies, suggest that metformin use prior to hospital admission might be associated with significant decrease in mortality in patients with type 2 diabetes and COVID-19. Continuing metformin use after hospital admission did not have significant impact on COVID-19 related death but may decrease risk of acute respiratory distress syndrome (ARDS). Meanwhile, in-hospital metformin administration may be associated with approximately 4.6 times increase risk of lactic acidosis in patients with severe symptoms of COVID-19, patients taking ≥2 gm/d of metformin, and patients with estimated glomerular filtration rate (eGFR) less than 60 ml/min/1.73 kg/m2. Conclusions: Although most retrospective studies suggest that metformin administration may be associated with decreased risk of COVID-19 mortality, these data should be confirmed by randomized trials. In patients with type 2 diabetes and COVID-19 admitted to the hospital, metformin use should be avoided in presence of severe symptoms of COVID-19, kidney dysfunction (eGFR &lt; 60 ml/min/1.73m2), and in daily doses of ≥ 2 gm due to increased risk of lactic acidosis.

Effects of Metformin on Clinical outcomes in Patients with Type 2 Diabetes and Covid-19

Background: The effects of metformin therapy on the prognosis of patients with coronavirus disease 2019 (COVID-19) are unclear. Objective: To review effects of metformin on clinical outcomes, particularly mortality, in patients with type 2 diabetes and COVID-19. Methods: Review of English literature by PUBMED search until April 20, 2021. Search terms included diabetes, COVID-19, metformin, Retrospective studies, meta-analyses, pertinent reviews, and consensus guidelines are reviewed. Results: All available studies in this area are retrospective. Two population-based studies did not find significant association between metformin use and susceptibility to COVID-19. Most, but not all studies, suggest that metformin use prior to hospital admission might be associated with significant decrease in mortality in patients with type 2 diabetes and COVID-19. Continuing metformin use after hospital admission did not have significant impact on COVID-19 related death but may decrease risk of acute respiratory distress syndrome (ARDS). Meanwhile, in-hospital metformin administration may be associated with approximately 4.6 times increase risk of lactic acidosis in patients with severe symptoms of COVID-19, patients taking ≥2 gm/d of metformin, and patients with estimated glomerular filtration rate (eGFR) less than 60 ml/min/1.73 kg/m2. Conclusions: Although most retrospective studies suggest that metformin administration may be associated with decreased risk of COVID-19 mortality, these data should be confirmed by randomized trials. In patients with type 2 diabetes and COVID-19 admitted to the hospital, metformin use should be avoided in presence of severe symptoms of COVID-19, kidney dysfunction (eGFR &lt; 60 ml/min/1.73m2), and in daily doses of ≥ 2 gm due to increased risk of lactic acidosis.

Characteristics of lactic acidosis in patients with acute poisoning due to drugs and chemicals

Characteristics of lactic acidosis in patients with acute poisoning due to drugs and chemicals

Characteristics of lactic acidosis in patients with acute poisoning due to drugs and chemicals

Characteristics of lactic acidosis in patients with acute poisoning due to drugs and chemicals

Safety of Metformin in Hospitalized Patients with COVID-19

Background: It is unclear whether metformin should be continued or discontinued in patients with coronavirus disease 2019 (COVID-19) admitted to the hospital. Objective: To review metformin safety, particularly its impact on mortality among hospitalized patients with COVID-19. Methods: Review of English literature by PUBMED search until September 11, 2020. Search terms included diabetes, COVID-19, metformin, Retrospective studies, meta-analyses, pertinent reviews, pre-print articles, and consensus guidelines are reviewed. Results: Retrospective studies suggest that metformin use prior to hospital admission may be associated with decreased mortality in patients with diabetes admitted to the hospital with COVID-19. Continuing metformin use after hospital admission did not have a significant impact on 28-day all-cause mortality. Metformin use after hospitalization of patients with COVID-19 was associated with approximately 4.6 times increase risk of lactic acidosis in patients with severe symptoms of COVID-19, patients taking 2 gm/d of metformin or higher, and patients with estimated glomerular filtration rate (eGFR) less than 60 ml/min/1.73 kg/m2. Metformin use in the hospital was associated with a significant decrease in the risk of heart failure and acute respiratory distress syndrome (ARDS). Conclusions: In patients with diabetes and COVID-19 admitted to the hospital, metformin should not be used in presence of severe symptoms of COVID-19, kidney dysfunction (eGFR &lt; 60 ml/min/1.73 m2), and with daily doses of 2 gm or more due to increased risk of lactic acidosis.

Metformin and the Risk of Lactic Acidosis in Patients with CKD Stage 3

Metformin and the Risk of Lactic Acidosis in Patients with CKD Stage 3

Increasing metformin concentrations and its excretion in both rat and porcine ex vivo normothermic kidney perfusion model

IntroductionMetformin can accumulate and cause lactic acidosis in patients with renal insufficiency. Metformin is known to inhibit mitochondria, while renal secretion of the drug by proximal tubules indirectly requires energy....

The impact of metformin in chronic kidney disease-mineral and bone disorder

Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a disorder of mineral and bone metabolism due to chronic kidney disease (CKD). Bone disease and mortality are more common in patients with CKD. In addition of antidiabetic properties of metformin (MET), it possesses anti-inflammatory, anti-fibrotic properties and increases the markers of osteogenic effects. Therefore, it improves bone quality and decreases the risk of fractures in patients with type 2 diabetes. Metformin can also inhibit arterial calcification, maintain calcium-phosphorus balance, decrease cellular infiltration, fibrosis, and inflammation in kidney. Based on evidence, the prevalence of lactic acidosis due to metformin in patients with type 2 diabetes (T2D) and renal dysfunction is lower compared to other oral antidiabetic agents. Metformin decreases all-cause mortality in patients with diabetic nephropathy. The administration of metformin showed no difference in the prevalence of lactic acidosis in patients with T2D who had normal, mild, moderate, or severe renal dysfunction. Therefore, metformin can be used in patients with significant CKD to inhibit CKD-MBD due to its osteogenic effects.

Hepatic Resection and Transplant in Glycogen Storage Diseases

Patients with glycogen storage diseases pose unique management challenges to clinicians.These challenges are exacerbated wheneverthey undergo surgery as the basic anomaly in their glycogen storage pathways make them susceptible to organic acidosis, which may in turn complicate their preoperative, intraoperative, and postoperative course. Because of the rarity of these diseases, clinicians may not be aware of the specific management concerns. In the case reported here, a 37-year-old patient with glycogen storage disease type 1 underwentleft hepatectomy for hepatic adenomatosis, which was complicated by intraoperative severe lactic acidosis that was successfully treated. After successful hepatectomy, the patient underwent liver transplant without major lactic acidosis or hemodynamic instability. Early recognition and aggressive management of blood sugar and lactic acidosis in patients with glycogen storage diseases can allow for successful outcomes even when complex surgical procedures are required.

家庭用洗剤の服毒により重篤な乳酸アシドーシスを来した1例(A case of severe lactic acidosis due to the intoxication of laundry detergent)

要旨 中毒治療において，毒物により引き起こされるアニオンギャップ開大性代謝性アシドーシスは緊急度の高い病態である。今回，自殺目的に家庭用洗剤を服用し重篤な乳酸アシドーシスを来した症例を経験したので報告する。症例は70代の女性である。自殺目的に家庭用洗剤を約400mL服用後，意識障害を来して前医へ搬送となった。しかしJapan coma scale 3桁の意識障害のため当院へ転送された。血液ガス分析で著明な混合性アシドーシスを認め，気管挿管，人工呼吸管理とした。輸液負荷にてバイタルサインは安定したがbase excess &lt;−10mmol/Lの代謝性アシドーシスが継続し，乳酸値は7.1mmol/Lから10.3mmol/Lまで上昇した。この時点で毒物による外因性の乳酸アシドーシスを疑い血液透析を施行した。施行後に乳酸値は低下しアシドーシスは改善，意識レベルもそれに伴って回復し同日に抜管した。誤嚥性肺炎の治療後，希死念慮に対しての治療目的に精神科に転科となった。今回服用した洗剤の中には安定剤として体内で分解されて乳酸を生じうるプロピレングリコールが使用されており，本症例における乳酸アシドーシスの主因と考えられた。血液透析開始後の速やかな回復は特徴的であった。一部の家庭用洗剤はプロピレングリコールを含有するため，服毒すると本症例のような重篤な乳酸アシドーシスを来すことがあり注意を要する。