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Journal articles on the topic 'HYPERLACTEMIA'

Author: Grafiati

Published: 7 September 2021

Last updated: 3 February 2022

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1

Sharma, Ashima, and Mohammed Ismail Nizami. "Hyperlactemia and the Heart." Indian Journal of Cardiovascular Disease in Women WINCARS 04, no. 02 (2019): 066–67. http://dx.doi.org/10.1055/s-0039-1697077.

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2

McDonald, J. R., M. L. Goodwin, Yi Sun, et al. "Establishing Prolonged Hyperlactemia in Anesthetized Dogs." Medicine & Science in Sports & Exercise 43, Suppl 1 (2011): 848. http://dx.doi.org/10.1249/01.mss.0000402363.15306.ca.

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3

Druml, W., G. Kleinberger, K. Lenz, A. Laggner, and B. Schneeweiss. "Fructose-induced hyperlactemia in hyperosmolar syndromes." Klinische Wochenschrift 64, no. 13 (1986): 615–18. http://dx.doi.org/10.1007/bf01735263.

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4

Bozzuto, Thomas M. "Severe metabolic acidosis secondary to exertional hyperlactemia." American Journal of Emergency Medicine 6, no. 2 (1988): 134–36. http://dx.doi.org/10.1016/0735-6757(88)90051-4.

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5

Samalavičius, Robertas, Irina Misiūrienė, Karolis Urbonas, et al. "Padidėjusi laktatų koncentracija plazmoje kaip prognostinis didesnio mirštamumo ir komplikacijų po miokardo revaskuliarizavimo operacijų rodiklis." Lietuvos chirurgija 5, no. 3 (2007): 0. http://dx.doi.org/10.15388/lietchirur.2007.3.2195.

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Robertas Samalavičius1, Irina Misiūrienė1, Karolis Urbonas1, Ieva Norkienė1, Gintaras Kalinauskas2, Gediminas Norkūnas2, Arūnas Valaika2, Alis Baublys11 Vilniaus universiteto ligoninės Santariškių klinikų Anesteziologijos,intensyvios terapijos ir skausmo gydymo centras, Santariškių g. 2, LT-08661 Vilnius2 Vilniaus universiteto Širdies chirurgijos centras,Santariškių g. 2, LT-08661 VilniusEl paštas: robertas.samalavicius@santa.lt Įvadas / tikslas Šio darbo tikslas buvo nustatyti padidėjusios laktatų koncentracijos miokardo revaskuliarizavimo operacijų metu dažnį ir įvertinti šio rodiklio galimybes prognozuojant pooperacinį mirštamumą ir pooperacinių komplikacijų kilimą. Ligoniai ir metodai Nuo 2003 m. sausio 5 d. iki 2003 m. gruodžio 31 d. mūsų klinikose atlikta 600 vainikinių arterijų apeinamųjų jungčių suformavimo operacijų dirbtinės kraujo apytakos sąlygomis. Šie ligoniai ir sudarė tiriamąją grupę. Laktatų koncentracija plazmoje buvo nustatoma prieš prijungiant dirbtinę kraujo apytaką, prieš atleidžiant aortą, neutralizavus hepariną protaminsulfatu ir ligonio atkėlimo po operacijos į Intensyvios terapijos skyrių metu. Rezultatai Didesnė nei 5 mmol/l laktatų koncentracija plazmoje buvo nustatyta 2,5% ligonių dirbtinės kraujotakos metu, 6,7% – protamino neutralizavimo metu ir 10,8% – atvykimo į Intensyviosios terapijos skyrių metu. Ligonių, kurių laktatų koncentracija kraujyje buvo didesnė nei 5 mmol/l, mirštamumas siekė 19,3% ir 59,6%, taip pat jiems pooperaciniu laikotarpiu pasitaikė komplikacijų, o ligonių, kurių laktatų koncentracija mažesnė, mirštamumas buvo 3,2%, ir tik 10,3% jų pooperaciniu laikotarpiu pasitaikė komplikacijų. Išvados Laktatų koncentracija plazmoje po kardiochirurginių operacijų gana dažnai padidėja. Didesnė nei 5 mmol/l laktatų koncentracija kraujyje buvo daugiau nei 10% pacientų atvykimo į Intensyviosios terapijos skyrių po miokardo revaskuliarizavimo operacijų metu. Padidėjusi laktatų koncentracija poperfuziniu laikotarpiu leidžia nustatyti, kurių ligonių operacinio mirštamumo ir komplikacijų susidarymo rizika gerokai didesnė. Pagrindiniai žodžiai: laktatai, rizikos veiksniai, mirštamumas, pooperacinės komplikacijos Serum lactate level as predictor of mortality and morbidity following coronary artery bypass grafting Robertas Samalavičius1, Irina Misiūrienė1, Karolis Urbonas1, Ieva Norkienė1, Gintaras Kalinauskas2, Gediminas Norkūnas2, Arūnas Valaika2, Alis Baublys11 Vilnius University Hospital „Santariškių klinikos“, Center of Anesthesia,Intensive Care and Pain Management, Santariškių str. 2, LT-08661 Vilnius, Lithuania2 Vilnius University , Heart Surgery Center,Santariškių str. 2, LT-08661 Vilnius, LithuaniaE-mail: robertas.samalavicius@santa.lt Background / objective Risk stratification for predicting mortality and morbidity is widely used in cardiac surgery. However, prediction of individual outcome shortly after cardiac surgery is difficult. Postoperative hyperlactemia has been related to an increased rate of postoperative complications and increased mortality following cardiac surgery. The aim of this study was to evaluate the frequency of intraoperative and postoperative hyperlactemia and to assess the value of serum lactate level in predicting mortality and morbidity following surgery. Patients and methods 600 consecutive CABG from January 5, 2003 to December 30, 2003 at the Vilnius University Hospital Santariskiu Clinics were investigated. Serume lactate levels were measured before cardiopulmonary bypass, before declamping of the aorta, after heparin neutralization and at ICU admission. Morbidity was defined as the presence of one or more of the following categories of complications: cardiac, pulmonary, neurological and renal. Results Lactate level greater than 5 mmol/l was found in 2.5% of patients during cardiopulmonary bypass, in 6.7% of patients shortly after weaning from CPB, and in 10.8% of patients on ICU admission. The mortality rate of patients with hyperlactemia at ICU admission was 19.3% and morbidity 59.6%. The mortality rate of patients without hyperlactemia was 3.2% and morbidity 10.3%. Conclusions Hyperlactemia was quite frequent following cardiac surgery. Increased lactate levels (> 5 mmol/l) were found in more than 10% of patients following CABG surgery on ICU admission. Increased serum lactate levels following coronary artery bypass grafting identifies a group of patients with an increased risk of postoperative mortality and morbidity. Key words: hyperlactemia, outcomes, morbidity, mortality

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6

Watanabe, Izuru, Toshihiko Mayumi, Takuro Arishima, et al. "HYPERLACTEMIA CAN PREDICT THE PROGNOSIS OF LIVER RESECTION." Shock 28, no. 1 (2007): 35–38. http://dx.doi.org/10.1097/shk.0b013e3180310ca9.

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7

Watanabe, I., T. Mayumi, T. Arishima, H. Takahashi, and J. Takezawa. "CAN HYPERLACTEMIA PREDICT THE PROGNOSIS OF LIVER RESECTION?" Shock 25, Supplement 1 (2006): 35. http://dx.doi.org/10.1097/00024382-200606001-00105.

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8

Ioannoni, Eleonora, Giuseppe Grande, Alessandro Olivi, Massimo Antonelli, Anselmo Caricato, and Nicola Montano. "Factors affecting serum lactate in patients with intracranial tumors – A report of our series and review of the literature." Surgical Neurology International 11 (March 6, 2020): 39. http://dx.doi.org/10.25259/sni_552_2019.

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Background: A hyperlactemia may occur in the presence of tissue hypoperfusion, in diseases affecting metabolism and in cases of malignant neoplasm. However, the factors affecting the serum lactate levels in patients submitted to craniotomy for the resection of an intracranial tumor have been investigated only marginally. Here, we assessed the factors possibly affecting the levels of serum lactate in intracranial tumors and carried out a thorough literature review on this topic. Methods: All patients submitted to elective craniotomy from January 2017 to August 2018 for the resection of a glioblastoma (GBM; 101 cases) and a benign meningioma (WHO I; 105 cases) were included in this study. The sex, age, histological diagnosis, body mass index (BMI), and diabetes were assessed as possible factors affecting the level of the preoperative and postoperative serum lactate in these patients. Results: We found that preoperative hyperlactemia (> 2 mmol/l) was more frequent in patients with GBM than in patients with meningioma (P = 0.0003). Moreover, a strong correlation between a preoperative lactemia and postoperative lactemia (P < 0.0001) was observed. On univariate analysis, we found increased preoperative serum lactate levels in GBM patients (P = 0.0022) and in patients with a BMI ≥30 (P = 0.0068). Postoperative serum lactate levels were significantly higher in GBM patients (P = 0.0003). On multivariate logistic regression analysis, a diagnosis of GBM was an independent factor for higher level of preoperative (P = 0.0005) and postoperative (P < 0.0001) serum lactate. Conclusion: The malignant phenotype of GBM is the strongest factor associated with a pre- and postoperative hyperlactemia in patients submitted to craniotomy for the resection of an intracranial tumor.

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9

Pant, Manish Nath, Subash Dawadi, and Ashish Thapa. "A Study on Shock Index in Early Diagnosis of Sepsis in Emergency Department of Tertiary Care Centre of Nepal." Nepal Medical Journal 2, no. 2 (2019): 37–42. http://dx.doi.org/10.37080/nmj.68.

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    Introduction: Sepsis and its consequences, severe sepsis and septic shock is at menace in country like ours where infectious disease are at toll. Early diagnosis and treatment is very important to decrease the morbidity and mortality. Shock index is one of such tool that is very handy in these situations as this is just a mathematical calculation using heart rate(HR) and systolic blood pressure(SBP). The main aim of this study was to find the effectiveness of using SI as an adjunct to blood lactate in diagnosing patients in sepsis. Methods: This was an observational hospital-based study conducted at Emergency Department of TUTH, Maharajgunj on 104 patients, obtained by purposive sampling method, who had presented to the “Red Area”, aged between 18 to 65 years. These patients were screened for severe sepsis using triage vital signs, basic laboratory tests and an initial serum lactate level. Test characteristics were calculated for hyperlactatemia. I considered the following covariates in our analysis: heart rate >90 beats/min; mean arterial pressure <65 mmHg; respiratory rate > 20 breaths/min; ≥2 SIRS including white blood cell count; SI <0.6; SI 0.6 to 1; SI 1 to 1.4and SI ≥ 1.4.  Results: There was a positive correlation between shock index and blood lactate level, r=0.2, n=104, p=0.042. No relationship was found between SI>=1 and hyperlactemia, X2 (.285, N = 104) = 1, p =.594 and relationship was found between SI >=0.7 and hyperlactemia, X2 (4.1, N = 104) = 1, p =.04. sensitivity and specificity for detecting hyperlactemia of SI>=1, SI.=0.7, SIRS was 84% and 20%, 93% and 0%, 79% and 20% respectively. Conclusions: There was weak correlation between the lactate level and shock index with statistically significant correlation between the shock index grouped >=0.7 and hyperlactatemia with high sensitivity and very low specificity.   

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10

Bethke, Richard A., Matthew Gratton, and William A. Watson. "Severe hyperlactemia and metabolic acidosis following cocaine use and exertion." American Journal of Emergency Medicine 8, no. 4 (1990): 369–70. http://dx.doi.org/10.1016/0735-6757(90)90101-5.

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11

Omar, AmrS, Masoodur Rahman, and Said Abuhasna. "Reported survival with severe mixed acidosis and hyperlactemia after toluene poisoning." Saudi Journal of Anaesthesia 5, no. 1 (2011): 73. http://dx.doi.org/10.4103/1658-354x.76474.

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12

Ribeiro, Luiz Fernando Paulino, Cássio Gustavo Santana Gonçalves, Daniele Preto Kater, Manoel Carlos Spiguel Lima, and Claudio Alexandre Gobatto. "Influence of recovery manipulation after hyperlactemia induction on the lactate minimum intensity." European Journal of Applied Physiology 105, no. 2 (2008): 159–65. http://dx.doi.org/10.1007/s00421-008-0885-5.

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13

Brenner, M., G. Bochicchio, K. Bochicchio, S. Zhu, and T. Scalea. "Prevention Of Rebound Hyperlactemia Decreases Morbidity And Mortality In Critically Ill Trauma Patients." Journal of Surgical Research 165, no. 2 (2011): 341. http://dx.doi.org/10.1016/j.jss.2010.11.115.

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14

Zagatto, Alessandro M., Johnny Padulo, Paulo T. G. Müller, Willian E. Miyagi, Elvis S. Malta, and Marcelo Papoti. "Hyperlactemia Induction Modes Affect the Lactate Minimum Power and Physiological Responses in Cycling." Journal of Strength and Conditioning Research 28, no. 10 (2014): 2927–34. http://dx.doi.org/10.1519/jsc.0000000000000490.

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15

Leisman, Daniel E., Jason A. Zemmel D'Amore, Jeanie L. Gribben, et al. "Early sepsis bundle compliance for non-hypotensive patients with intermediate versus severe hyperlactemia." American Journal of Emergency Medicine 35, no. 6 (2017): 811–18. http://dx.doi.org/10.1016/j.ajem.2017.01.029.

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16

Bennett, Jeremy M., Eric S. Wise, Kyle M. Hocking, Colleen M. Brophy, and Susan S. Eagle. "Hyperlactemia Predicts Surgical Mortality in Patients Presenting With Acute Stanford Type-A Aortic Dissection." Journal of Cardiothoracic and Vascular Anesthesia 31, no. 1 (2017): 54–60. http://dx.doi.org/10.1053/j.jvca.2016.03.133.

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17

Leung, L., A. Manini, and D. Wilson. "365: Fatal Toxicity From Nucleoside Reverse Transcriptase Inhibitor Use: Factors Implicated With Symptomatic Hyperlactemia Emergencies." Annals of Emergency Medicine 54, no. 3 (2009): S115. http://dx.doi.org/10.1016/j.annemergmed.2009.06.397.

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18

Ganert, Andrey N., E. V. Kokorev, P. S. Zhbannikov, and A. V. Zabusov. "THE HEMOFILTRATION AT INFUSION THERAPY OF SEVERE ACUTE PANCREATITIS." Medical Journal of the Russian Federation 24, no. 3 (2018): 120–23. http://dx.doi.org/10.18821/0869-2106-2018-24-3-120-123.

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The 64 patients with severe acute pancreatitis at admission in hospital arterial hypertension, low venous saturation of oxygen (ScvO2), hyperlactemia, oligoanuria and hypercreatininemia were observed. This occurrence became an indication for infusion therapy to recover and optimize hemodynamics. After 6 hours of therapy, 30 patients were lacked increasing of diuresis related to infusion load and hypercreatininemia increased and also significantly increased positive fluid balance s compared to other patients. These 30 patients were additionally applied hemofiltration during 66 hours. The infusion therapy was characterized by difficulty of restoration and optimization of hemodynamic, large volumes of infusion mediums та frequent application of sympathomimetics. In patients without hemofiltration a significant increasing of cumulative fluid balance was added. The hemofiltration permitted to normalize diuresis, to prevent surplus cumulation of fluid and to support blood circulation at the optimal level.

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19

Ascione, Raimondo, Andrea Venturini, Elvio Polesel, et al. "Source, Triggers and Clinical Implications of Hyperlactemia in Patients Undergoing Mitral Valve Surgery Using Custodiol Cardioplegia." World Journal of Cardiovascular Surgery 03, no. 05 (2013): 131–38. http://dx.doi.org/10.4236/wjcs.2013.35027.

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20

Al-Hwiesh, Abdullah K., Ibrahiem Saeed Abdul-Rahman, Abdul-Salam Noor, et al. "The Phantom of Metformin-Induced Lactic Acidosis in End-Stage Renal Disease Patients: Time to Reconsider with Peritoneal Dialysis Treatment." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 37, no. 1 (2017): 56–62. http://dx.doi.org/10.3747/pdi.2015.00309.

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ObjectiveMetformin continues to be the safest and most widely used antidiabetic drug. In spite of its well-known benefits; metformin use in end-stage renal disease (ESRD) patients is still restricted. Little has been reported about the effect of peritoneal dialysis (PD) on metformin clearance and the phantom of lactic acidosis deprives ESRD patients from metformin therapeutic advantages. Peritoneal dialysis is probably a safeguard against lactic acidosis, and it is likely that using this drug would be feasible in this group of patients.Material and methodsThe study was conducted on 83 PD patients with type 2 diabetes mellitus. All patients were on automated PD (APD). Metformin was administered in a dose of 500 - 1,000 mg daily. Patients were monitored for glycemic control. Plasma lactic acid and plasma metformin levels were monitored on a scheduled basis. Peritoneal fluid metformin levels were measured. In addition, the relation between plasma metformin and plasma lactate was studied.ResultsMean fasting blood sugar (FBS) was 10.9 ± 0.5 and 7.8 ± 0.7, and mean hemoglobin A1-C (HgA1C) was 8.2 ± 0.8 and 6.4 ± 1.1 at the beginning and end of the study, respectively (p < 0.001). The mean body mass index (BMI) was 29.1 ± 4.1 and 27.3 ± 4.5 at the beginning and at the end of the study, respectively (p < 0.001). The overall mean plasma lactate level across all blood samples was 1.44 ± 0.6. Plasma levels between 2 and 3 mmol/L were found in 11.8% and levels of 3 - 3.6 mmol/L in 2.4% plasma samples. Hyperlactemia (level > 2 and < 5 mmol/L) was not associated with overt acidemia. None of our patients had lactic acidosis (levels > 5 mmol/L). Age ≥ 60 was a predictor for hyperlactemia. No relationship was found between plasma metformin and lactate levels.ConclusionMetformin may be used with caution in a particular group of ESRD patients who are on APD. Metformin allows better diabetic control with significant reduction of BMI. Information on the relationship between metformin and plasma lactate levels is lacking. Peritoneal dialysis appears to be a safeguard against the development of lactic acidosis in this group of patients.

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21

Roef, Mark J., Kees de Meer, Dirk-Jan Reijngoud, et al. "Triacylglycerol infusion does not improve hyperlactemia in resting patients with mitochondrial myopathy due to complex I deficiency." American Journal of Clinical Nutrition 75, no. 2 (2002): 228–36. http://dx.doi.org/10.1093/ajcn/75.2.228.

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22

Wang, Ming-Wei, Pamela Carlo, Mark Fineman, Timothy J. Rink, and Andrew A. Young. "Induction of Acute Hyperglycemia, Hyperlactemia and Hypocalcemia in Fed and Fasted Balb/c Mice by Intravenous Amylin Injection." Endocrine Research 18, no. 4 (1992): 321–32. http://dx.doi.org/10.3109/07435809209111040.

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23

Gribben, J., A. Bianculli, J. Van de Rijn, et al. "64 Three-Hour Bundle Compliance May Confer Greater Mortality Benefit for Sepsis Patients Presenting With Less Severe Hyperlactemia." Annals of Emergency Medicine 68, no. 4 (2016): S28. http://dx.doi.org/10.1016/j.annemergmed.2016.08.075.

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24

Zindovic, Igor, Cecilia Luts, Henrik Bjursten, et al. "Perioperative Hyperlactemia Is a Poor Predictor of Outcome in Patients Undergoing Surgery for Acute Type-A Aortic Dissection." Journal of Cardiothoracic and Vascular Anesthesia 32, no. 6 (2018): 2479–84. http://dx.doi.org/10.1053/j.jvca.2018.03.030.

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25

Turbow, R. M., D. Curran-Everett, W. W. Hay, and M. D. Jones. "Cerebral lactate metabolism in near-term fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 269, no. 4 (1995): R938—R942. http://dx.doi.org/10.1152/ajpregu.1995.269.4.r938.

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The present study was designed to see if lactate can cross the blood-brain barrier of the near-term fetal sheep and replace glucose as an oxidative substrate during normoglycemia and acute insulin-induced hypoglycemia. Cerebral uptake of glucose, oxygen, lactate, and [14C]lactate as well as cerebral production of 14CO2 were measured under three conditions: 1) normoglycemia-normolactemia, 2) acute hypoglycemia-normolactemia, and 3) hypoglycemia-steady-state hyperlactemia. Although uptake of tracer [14C]lactate was consistent, there was no net uptake of unlabeled lactate during either normoglycemia or hypoglycemia. When arterial lactate concentration was raised from 2.2 +/- 0.5 to 3.3 +/- 0.4 (SE) mM by sodium lactate infusion, however, lactate was taken up. Comparison of cerebral [14C]lactate uptake with 14CO2 production indicated that the principal metabolic fate of lactate is oxidation. At increased concentrations, exogenous lactate accounted for approximately 7% of cerebral oxygen consumption. This study demonstrates that lactate crosses the blood-brain barrier of the near-term fetal sheep, is oxidized, and at elevated concentrations can partially replace glucose as an oxidative substrate during acute hypoglycemia.

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26

Migliorini, R. H., M. A. Garofalo, J. E. Roselino, and I. C. Kettelhut. "Rapid activation of gluconeogenesis after intracerebroventricular carbachol." American Journal of Physiology-Endocrinology and Metabolism 257, no. 4 (1989): E486—E490. http://dx.doi.org/10.1152/ajpendo.1989.257.4.e486.

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Intracerebroventricular administration of carbachol (27 nmol in 5 microliters 0.15 M NaCl) produced marked hyperglycemia in 24-h fasted rats, despite the negligible amounts of preformed liver glycosyl residues. To investigate the possibility of a stimulation of gluconeogenesis, conscious unrestrained rats were continuously infused with [14C]bicarbonate (0.51 microliters, 0.18 muCi/min) and label incorporation into circulating glucose determined before and after intraventricular injection. The rate of 14C incorporation into blood glucose of fed rats was not affected by intraventricular injection of 0.15 M NaCl but increased significantly after carbachol administration. In both fed and 24-h fasted rats the hyperglycemia induced by intraventricular carbachol was accompanied by marked increases in plasma lactate. Previous adrenodemedullation prevented both the hyperglycemia and the hyperlactemia. Liver pyruvate kinase activity was reduced in carbachol-treated rats, when the enzyme was assayed with suboptimal concentrations of phosphoenolpyruvate and in the absence of fructose 1,6-biphosphate. Phosphoenolpyruvate carboxykinase activity was not affected. The data suggest that central chemical stimulation with cholinergic agents induces a rapid activation of liver gluconeogenesis, which probably results from an increased sympathetic outflow for epinephrine secretion by the adrenal medulla.

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27

Torti, Marin, Josipa Kuleš, Vesna Matijatko, et al. "Acid-base status in canine babesiosis caused by Babesia canis." Veterinarski arhiv 90, no. 6 (2020): 603–10. http://dx.doi.org/10.24099/vet.arhiv.1230.

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Acid-base disturbances have been reported in severe canine babesiosis caused by Babesia rossi (B. rossi), but they have not been studied in babesiosis caused by B. canis. The objective of this study was to determine the acid-base status, blood gases and electrolyte concentrations in naturally occurring canine babesiosis caused by B. canis, and to compare the results to those in healthy dogs. Two groups of animals were used: group 1 consisted of 10 healthy dogs, and group 2 consisted of 14 dogs naturally infected with B. canis. The following acid-base disturbances occurred in the dogs with naturally occurring babesiosis: half of the dogs had a mixed acid-base disorder, and the other half a simple acid-base disorder. The most common mixed disorder was metabolic acidosis with metabolic alkalosis. It may be said that a variety of acid-base disorders occurs in canine babesiosis. The dogs in the present study had metabolic acidosis due to hyperlactemia and hyperchloremia, metabolic alkalosis due to hypochloremia and hypoalbuminemia, and respiratory alkalosis due to hypoxemia. With the use of the strong-ion difference approach clearer recognition of mixed acid-base disorders and their better understanding is possible.

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Powner, David J., John A. Kellum, and Joseph M. Darby. "Concepts of the Strong Ion Difference Applied to Large Volume Resuscitation." Journal of Intensive Care Medicine 16, no. 4 (2001): 169–76. http://dx.doi.org/10.1177/088506660101600402.

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The occurrence of acidosis following trauma or other clinical conditions that require large volumes of resuscitation fluid may be modified by manipulation of the physical chemistry properties of substances within plasma. These include the strong ion difference, modification of hydrogen ion production through control of alveolar ventilation, and protection/provision of protein and phosphate-based weak acids. An understanding of these principles as an alternative method to analyze/anticipate acid-base abnormalities is important during resuscitation. Loss of protein-based weak acids may often occur after trauma or other conditions requiring large-volume resuscitation. These losses may potentially be replaced with albumin-based colloid solutions. Large quantities of normal saline should be avoided so as to avoid hyperchloremia-induced metabolic acidosis. Ringer's lactate solution is preferred. Alveolar ventilation must be adjusted so as to eliminate further hydrogen ion production caused by hypercarbia. The serum base excess and/or hyperlactemia have only limited value in diagnosing acidosis and guiding resuscitation. Current experimental data and reviews of this topic were obtained from a Medline literature search. In addition, the personal experience and investigations of the authors in critically ill and injured patients were used to formulate recommendations.

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Beaumont, K., C. X. Moore, R. A. Pittner, et al. "Differential antagonism of amylin's metabolic and vascular actions with amylin receptor antagonists." Canadian Journal of Physiology and Pharmacology 73, no. 7 (1995): 1025–29. http://dx.doi.org/10.1139/y95-144.

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High affinity amylin binding sites are present in the rat nucleus accumbens. These sites bind [125I]amylin with an affinity of 27 pM and have high affinity for salmon calcitonin (sCT) and moderately high affinity for calcitonin gene related peptide (CGRP). N-terminally truncated peptides were tested for their ability to compete for [125I]amylin binding to these sites and to antagonize the metabolic and vascular actions of amylin. CGRP(8–37), sCT(8–32), and ac-[Asn30,Tyr32]sCT(8–32) (AC187) inhibited [125I]amylin binding to rat nucleus accumbens. Order of potency at inhibiting amylin binding (AC187 > sCT(8–32) > CGRP(8–37)) differed from the order of potency at inhibiting [125I]CGRP binding to SK-N-MC neuroblastoma cells (CGRP(8–37) > AC187 > sCT(8–32)). AC187 was the most potent antagonist of amylin's effects on isolated rat soleus muscle glycogen metabolism, and it was more effective than either sCT(8–32) or CGRP(8–37) at reducing amylin-stimulated hyperlactemia in rats. In contrast, CGRP(8–37) was the most potent peptide at antagonizing amylin-induced hypotension in rats. Amylin's hypotensive actions appear to be mediated by a weak action at CGRP receptors, while its metabolic actions are mediated by receptors with a distinct antagonist profile. AC187 is a potent antagonist of amylin binding sites in nucleus accumbens and of amylin's metabolic actions.Key words: amylin, calcitonin gene related peptide, diabetes, skeletal muscle, peptide receptors.

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30

Cruz Junior, Ruy J., Alejandra G. Garrido, and Maurício Rocha e. Silva. "Early hemodynamics and metabolic changes after total abdominal evisceration for experimental multivisceral transplantation." Acta Cirurgica Brasileira 24, no. 2 (2009): 156–61. http://dx.doi.org/10.1590/s0102-86502009000200014.

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PURPOSE: Multivisceral transplantation (MVTx) has been accepted as standard therapeutic modality for patients with short-bowel syndrome associated with irreversible liver failure. Even nowadays, experimental models of MVTx grounds high incidence of intraoperative or early recipient mortality. Despite the known deleterious effects of hepatosplanchnic exenteration the impact of this procedure on systemic hemodynamics and metabolism remains to be determined. METHODS: Nine dogs (20.1±0.5 kg) were subjected to an en bloc resection of all abdominal organs including, stomach, duodenum, pancreas, liver, spleen, small bowel, and colon. A woven double velour vascular graft was interposed between the suprahepatic and infrahepatic vena cava. Systemic hemodynamic were evaluated through a Swan-Ganz catheter, ultrasonic flowprobes, and arterial lines. Systemic O2-derived variables, glucose, and lactate metabolism were analyzed throughout the experiment. RESULTS: Complete abdominal exenteration was associated with significant reduction in cardiac output, and mean arterial pressure (57% and 14%, respectively). Two hours after reperfusion a significant reduction in arterial pH and glucose were also observed. Oxygen consumption remained unaltered during the first two hours of the experiment, with a significant increase of lactate levels (1.4±0.3 vs. 7.6±0.4, p<0.05). Three animals died before the 3 hours of reperfusion were completed. Total abdominal exenteration for MVTx in dogs is associated with early major hemodynamics, and metabolic changes. CONCLUSION: The deleterious hemodynamic alterations observed are probably related with the association of severe acidosis, hyperlactemia, hypoglycemia, and reduction of total circulating blood volume. Close hemodynamic and metabolic monitoring should be provided during experimental MVTx in order to promote an increase in successful rates of this complex and challenging procedure.

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Tereshchenko, I. V. "HYPERLACTATEMIA IN TREATMENT OF DIABETES TYPE 2 BY METFORMIN." Tavricheskiy Mediko-Biologicheskiy Vestnik 23, no. 2 (2020): 201–5. http://dx.doi.org/10.37279/2070-8092-2020-23-2-201-205.

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It was previously found that when it is treated type 2 diabetes mellitus (DM2) by metformin, hyperlactemia does not develop or occurs extremely rarely, and due to concomitant pathology. Clinicians usually do not monitor blood lactate levels. Goal: to analyze the frequency of hyperlactatemia in patients with DM2, its possible causes and role in this of metformin, clinical manifestations, ways of elimination and prevention. We observed in the dynamics of 38 patients with DM2 receiving metformin in doses of 1500–3000 mg / day. All patients were tested the level of lactate in the blood. Hyperlactatemia was detected in 6 cases (12.8% of patients), of which two patients (5.3%) showed lactic acidosis: the blood lactate level of them was 4.0 μmol/L and 4.6 μmol/L. A correlation between the level of lactic acid and the dose of metformin has not been established. All observed patients had polymorbidity and compelled polypharmacy. Hypothyroidism was observed in 42.1% of patients; in patients with lactic acidosis hypothyroidism was decompensated, i.e. it was chronic oxygen starvation of tissues. Conclusion: Observations confirmed that treatment of DM2 with metformin is rarely complicated by lactic acidosis and even moderate hyperlactatemia. Complications of diabetes, concomitant pathology and compelled polypharmacy, including metformin, disrupt the metabolism of lactic acid, its elimination, utilization in gluconeogenesis processes; in ≈12.8% of cases, the level of lactate in the blood rises. The risk of lactic acidosis, i.e. death threat occurs in ≈5.3% of patients. Along with the etiological factors of lactic acidosis widely presented in publications in patients with type 2 diabetes mellitus, in ≈42.1% of cases, lactate accumulation is promoted by hypothyroidism, the decompensation of which creates chronic oxygen starvation of tissues. To check periodically the level of lactic acid and monitor the function of the thyroid gland it is necessary in all patients with DM2, even if they are not treated with metformin.

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Tereshchenko, I. V. "HYPERLACTATEMIA IN TREATMENT OF DIABETES TYPE 2 BY METFORMIN." Tavricheskiy Mediko-Biologicheskiy Vestnik 23, no. 2 (2020): 201–5. http://dx.doi.org/10.37279/2070-8092-2020-23-2-201-205.

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Abstract:

It was previously found that when it is treated type 2 diabetes mellitus (DM2) by metformin, hyperlactemia does not develop or occurs extremely rarely, and due to concomitant pathology. Clinicians usually do not monitor blood lactate levels. Goal: to analyze the frequency of hyperlactatemia in patients with DM2, its possible causes and role in this of metformin, clinical manifestations, ways of elimination and prevention. We observed in the dynamics of 38 patients with DM2 receiving metformin in doses of 1500–3000 mg / day. All patients were tested the level of lactate in the blood. Hyperlactatemia was detected in 6 cases (12.8% of patients), of which two patients (5.3%) showed lactic acidosis: the blood lactate level of them was 4.0 μmol/L and 4.6 μmol/L. A correlation between the level of lactic acid and the dose of metformin has not been established. All observed patients had polymorbidity and compelled polypharmacy. Hypothyroidism was observed in 42.1% of patients; in patients with lactic acidosis hypothyroidism was decompensated, i.e. it was chronic oxygen starvation of tissues. Conclusion: Observations confirmed that treatment of DM2 with metformin is rarely complicated by lactic acidosis and even moderate hyperlactatemia. Complications of diabetes, concomitant pathology and compelled polypharmacy, including metformin, disrupt the metabolism of lactic acid, its elimination, utilization in gluconeogenesis processes; in ≈12.8% of cases, the level of lactate in the blood rises. The risk of lactic acidosis, i.e. death threat occurs in ≈5.3% of patients. Along with the etiological factors of lactic acidosis widely presented in publications in patients with type 2 diabetes mellitus, in ≈42.1% of cases, lactate accumulation is promoted by hypothyroidism, the decompensation of which creates chronic oxygen starvation of tissues. To check periodically the level of lactic acid and monitor the function of the thyroid gland it is necessary in all patients with DM2, even if they are not treated with metformin.

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ZARETSKY, DMITRY, and ANDREW A. YOUNG. "The Hyperinsulinemic Isoglycemic Hyperlactemic Clamp." Diabetes 67, Supplement 1 (2018): 1959—P. http://dx.doi.org/10.2337/db18-1959-p.

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Al-Hwiesh, Abdulla Khalaf, Ibrahiem Saeed Abdul-Rahman, Mohammad Ahmad Nasr El-Deen, et al. "Metformin in Peritoneal Dialysis: A Pilot Experience." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 34, no. 4 (2014): 368–75. http://dx.doi.org/10.3747/pdi.2013.00048.

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Objective In a number of patients, the antidiabetic drug metformin has been associated with lactic acidosis. Despite the fact that diabetes mellitus is the most common cause of end-stage renal disease (ESRD) and that peritoneal dialysis (PD) is an expanding modality of treatment, little is known about optimal treatment strategies in the large group of PD patients with diabetes. In patients with ESRD, the use of metformin has been limited because of the perceived risk of lactic acidosis or severe hypoglycemia. However, metformin use is likely to be beneficial, and PD might itself be a safeguard against the alleged complications. Methods Our study involved 35 patients with insulin-dependent type 2 diabetes [median age: 54 years; interquartile range (IQR): 47–59 years] on automated PD (APD) therapy. Patients with additional risk factors for lactic acidosis were excluded. Metformin was introduced at a daily dose in the range 0.5 – 1.0 g. All patients were monitored for glycemic control by blood sugar levels and HbA1c. Plasma lactic acid levels were measured weekly for 4 weeks and then monthly to the end of the study. Plasma and effluent metformin and plasma lactate levels were measured simultaneously. Results In this cohort, the median duration of diabetes was 18 years (IQR: 14 – 21 years), median time on PD was 31 months (IQR: 27 – 36 months), and median HbA1c was 6.8% (IQR: 5.9% – 6.9%). At metformin introduction and at the end of the study, the median anion gap was 11 mmol/L (IQR: 9 – 16 mmol/L) and 12 mmol/L (IQR: 9 – 16 mmol/L; p > 0.05) respectively, median pH was 7.33 (IQR: 7.32 – 7.36) and 7.34 (IQR: 7.32 – 7.36, p > 0.05) respectively, and mean metformin concentration in plasma and peritoneal fluid was 2.57 ± 1.49 mg/L and 2.83 ± 1.7 mg/L respectively. In the group overall, mean lactate was 1.39 ± 0.61 mmol/L, and hyperlactemia (>2 mmol/L to 5 mmol/L) was found in 4 of 525 plasma samples (0.76%), but the patients presented no symptoms. None of the patients registered a plasma lactate level above 5 mmol/L. We observed no correlation between plasma metformin and plasma lactate ( r = 0.27). Conclusions Metformin may be used with caution in APD patients with insulin-dependent type 2 diabetes. Although our study demonstrated the feasibility of metformin use in APD, it was not large enough to demonstrate safety; a large-scale study is needed.

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Young, Andrew A., Timothy J. Rink та Ming-Wei Wang. "Dose response characteristics for the hyperglycemic, hyperlactemic, hypotensive and hypocalcemic actions of amylin and calcitonin gene-related peptide-I (CGRPα) in the fasted, anaesthetized rat". Life Sciences 52, № 21 (1993): 1717–26. http://dx.doi.org/10.1016/0024-3205(93)90480-q.

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"Hyperlactemia in dogs with cancer." Advances in Small Animal Medicine and Surgery 25, no. 7 (2012): 6–7. http://dx.doi.org/10.1016/j.asams.2012.06.007.

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"Hyperlactemia in Patients Undergoing Continuous Arteriovenous Hemofiltration with Dialysis." Critical Care Medicine 18, no. 5 (1990): 582. http://dx.doi.org/10.1097/00003246-199005000-00026.

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