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DeCure for Lactic acidosis

DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for lactic acidosis — screening already-approved drugs against its 10-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.

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The disease map

Disease moduleLactic acidosis maps to a 10-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.

Research record

01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash

Current lead

No approved-drug candidate for lactic acidosis is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.

Molecular view

dihydrolipoamide dehydrogenase (DLD) — DLD is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.

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helix sheet faddrag to rotate · scroll to zoom

RCSB Protein Data Bank · entry 6I4R · 1.439 Å · ligand FLAVIN-ADENINE DINUCLEOTIDE (FAD). Experimental structure, not a prediction.

What the evidence adds up to

Lactic acidosis is defined as a blood lactate concentration of at least 5 mmol/L and an arterial pH of 7.2 or less. Among adult hospitalised patients not having surgery, the reported incidence is about 1%. Approximately 60% to 70% of all patients with lactic acidosis die, and when hypotension is also present mortality approaches 100%. A 1986 editorial argues that present therapy is inadequate and makes the case against sodium bicarbonate, the standard treatment at the time. The editorial cites evidence that bicarbonate may be detrimental in hypoxic lactic acidosis, and notes that in one case bicarbonate administration stimulated lactate production in a patient with a solid neoplasm.

Lactic acidosis is a rare but usually fatal complication of malignancy. A 1988 review of four new cases and all previously reported cases meeting the criteria (pH ≤ 7.35, serum lactate ≥ 5 mEq/L) found that rapid recognition and prompt chemotherapy reversed the acidosis in three of the four patients. However, long-term survival depended on the responsiveness of the underlying tumour, not on the acidosis treatment itself.

A 2013 prospective randomised study of 41 intensive care unit patients with lactic acidosis compared early continuous blood purification (CBP) against standard care. The CBP group had significantly lower lactate levels at 12, 24 and 72 hours (e.g., 4.46±1.57 vs. 10.54±3.48 mmol/L at 24 hours), lower APACHE II scores, shorter ICU stay (6.58±3.45 vs. 11.65±4.94 days), and lower 28-day mortality (23.8% vs. 45.0%). A 2011 review of two cases reiterates that the primary aim of treatment must be reversal of the underlying cause, and that various methods are used but clinicians must be careful.

What is still missing are large, multicentre randomised trials comparing CBP against other supportive measures in defined patient subgroups, and prospective studies that stratify by the underlying cause of lactic acidosis (sepsis, malignancy, ischaemia) rather than treating it as a single entity. The evidence against bicarbonate is decades old but no adequately powered trial has ever settled the question, and the optimal timing and technique for blood purification remain unstandardised.

Evidence

Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.

Annals of Internal Medicine · 1986 · 145 citations

Lactic Acidosis: The Case Against Bicarbonate Therapy

AbstractEditorials1 August 1986Lactic Acidosis: The Case Against Bicarbonate TherapyPETER W. STACPOOLE, Ph.D, M.D.PETER W. STACPOOLE, Ph.D, M.D.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-105-2-276 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptLactic acidosis is perhaps the commonest and most poorly treated acid-base disorder. If a blood lactate concentration of at least 5 meq/L (5 mmol/L) and an arterial pH of 7.2 or less are the criteria, the reported incidence of lactic acidosis among adult hospitalized patients not having surgery is about 1% (1). Approximately 60% to 70% of all patients with lactic acidosis die (1, 2) and, among those in whom hypotension coexists, mortality approaches 100% (3-6).Based on these statistics alone, the conclusion is inescapable that present therapy for lactic acidosis is inadequate. Not as readily apparent, however, is whether any...References1. LUFTDEICHSELSCHMULLINGSTEINEGGSTEIN DGRWM. Definition of clinically relevant lactic acidosis in patients with internal diseases. Am J Clin Path. 1983;80:484-9. CrossrefMedlineGoogle Scholar2. COHENWOODS RH. Clinical and Biochemical Aspects of Lactic Acidosis. Oxford: Blackwell Scientific Publications; 1976. Google Scholar3. PERETZMCGREGORDOSSETOR DMJ. Lactic acidosis: a clinically significant aspect of shock. Can Med Assoc J. 1964;90:673-5. MedlineGoogle Scholar4. BLAIRCOWLEYTAIT ERM. Refractory septic shock in man: role of lactate and pyruvate metabolism and acid-base balance in prognosis. Am Surg. 1965;31:537-40. MedlineGoogle Scholar5. MACLEANMULLIGANMCLEANDUFF LWAJ. Patterns of septic shock in man—a detailed study of 56 patients. Ann Surg. 1967;166:543-62. CrossrefMedlineGoogle Scholar6. OLIVA P. Lactic acidosis. Am J Med. 1970;48:209-25. CrossrefMedlineGoogle Scholar7. FOSTER D. Lactic acidosis. In: PETERSDORF RG, ADAMS RA, BRAUNWALD P, ISSELBACHER KJ, MARTIN JB, WILSON JD, eds. Harrison's Principles of Internal Medicine. 10th ed. New York: McGraw-Hill; 1983:679-82. Google Scholar8. SAPIRWALKER DW. Acid-base disturbances. In: HARVEY AM, JOHNS RJ, MCKUSICK VA, OWENS AH JR, ROSS RS, eds. The Principles and Practice of Medicine. 21st ed. Norwalk, Connecticut: Appleton-Century-Crofts; 1984:70-84. Google Scholar9. ANDREOLI T. Disorders of fluid balance, electrolyte, and acid-base balance. In: WYNGAARDEN JB, SMITH LH JR, eds. Cecil Textbook of Medicine. 17th ed. Philadelphia: W.B. Saunders; 1985:515-44. Google Scholar10. KARAM J. Diabetes mellitus, hypoglycemia, and lipoprotein disorders. In: KRUPP MA, CHATTON MJ, WERDEGAR D, eds. Current Medical Diagnosis and Treatment. Los Altos, California: Lange Medical Publishers; 1985:761-92. Google Scholar11. COGANRECTORSELDIN MLD. Acid-base disorders. In: BRENNER BM, RECTOR FC JR, eds. The Kidney. 2nd ed. Philadelphia: W.B. Saunders; 1981:841-907. Google Scholar12. ALBERTINATTRASS KM. Lactic acidosis. Lancet. 1977;2:25-9. CrossrefMedlineGoogle Scholar13. FELTS P. Ketoacidosis. Med Clin North Am. 1983;67:831-43. CrossrefMedlineGoogle Scholar14. ARIEFFLEACHPARKLAZAROWITZ AWWV. Systemic effects of NaHCO3 in experimental lactic acidosis in dogs. Am J Physiol. 1982;242:F586-91. MedlineGoogle Scholar15. MISBIN R. Phenformin-associated lactic acidosis: pathogenesis and treatment. Ann Intern Med. 1977;87:591-5. LinkGoogle Scholar16. GRAFLEACHARIEFF HWA. Evidence for a detrimental effect of bicarbonate therapy in hypoxic lactic acidosis. Science. 1985;227:754-6. CrossrefMedlineGoogle Scholar17. BISHOPWEISFELDT RM. Sodium bicarbonate administration during cardiac arrest: effect on arterial pH PCO2, and osmality. JAMA. 1976;235:506-9. CrossrefMedlineGoogle Scholar18. MINOTDADDSAUNDERS AKJ. The acidosis of guanidine intoxication. J Clin Invest. 1934;13:917-32. CrossrefMedlineGoogle Scholar19. WATERSHALLSCHWARTZ WJW. Spontaneous lactic acidosis. Am J Med. 1963;35:781-93. CrossrefMedlineGoogle Scholar20. KAY R. Diabetic ketoacidosis—the bicarbonate controversy. J Pediatr. 1975;87:156-9. CrossrefMedlineGoogle Scholar21. LUFTSCHMULLINGEGGSTEIN DRM. Lactic acidosis in biguanide-treated diabetics: a review of 330 cases. Diabetologia. 1978;14:75-87. CrossrefMedlineGoogle Scholar22. SINGERCLARKBARKERCORSLEYELKINTON RJEAJ. The acute effects in man of rapid intravenous infusion of hypertonic sodium bicarbonate solution. Medicine. 1955;34:51-95. CrossrefMedlineGoogle Scholar23. GARELLADANACHAZAN SCJ. Severity of metabolic acidosis as a determinant of bicarbonate requirements. N Engl J Med. 1973;289:121-6. CrossrefMedlineGoogle Scholar24. HAZARDGRIFFIN PJ. Calculation of sodium bicarbonate requirement in metabolic acidosis. Am J Med Sci. 1982;283:18-22. CrossrefMedlineGoogle Scholar25. POSNERPLUM JF. Spinal fluid pH and neurologic symptoms in systemic acidosis. N Engl J Med. 1967;277:605-13. CrossrefMedlineGoogle Scholar26. TIZIANELLODE FERRARIGURRERIACQUARONE AGGN. Effects of metabolic alkalosis, metabolic acidosis and uraemia on whole-body intracellular pH in man. Clin Sci Mol Med. 1977;52:125-35. MedlineGoogle Scholar27. PARKLEACHARIEFF RWA. Determination of liver intracellular pH in vivo and its homeostasis in acute acidosis and alkalosis. 1979; Am J Physiol. 1979;236:F240-5. MedlineGoogle Scholar28. MATTAR J. Cardiac arrest in the critically ill: hyperosmolar states following cardiac arrest. Am J Med. 1974;56:162-8. CrossrefMedlineGoogle Scholar29. LEVERJASPAN EJ. Sodium bicarbonate therapy in severe diabetic ketoacidosis. Am J Med. 1983;75:263-8. CrossrefMedlineGoogle Scholar30. BELLINGHAMDETTERLENFANT AJC. Regulatory mechanisms of hemoglobin oxygen affinity in acidosis and alkalosis. J Clin Invest. 1971;50:700-6. CrossrefMedlineGoogle Scholar31. THOMASLEFRAKIRWINFRITTSCALDWELL HSRHP. The oxyhemoglobin dissociation curve in health and disease: role of 2, 3-disphosphoglycerate. Am J Med. 1974;57:331-48. CrossrefMedlineGoogle Scholar32. BRODERWEIL GM. Excess lactate: an index of reversibility of shock in human patients. Science. 1964;143:1457-9. CrossrefMedlineGoogle Scholar33. YATANIFUJINOKINOSHITAGOTO ATKM. Excess lactate modulates ionic currents and tension components in frog atrial muscle. J Mol Cell Cardiol. 1981;13:147-61. CrossrefMedlineGoogle Scholar34. JURKOWITZSCOTTALTSCHULDMEROLABRIERLEY MKRAG. Ion transport by heart mitochondria: retention and loss of energy coupling in aged heart mitochondria. Arch Biochem Biophys. 1974;165:98-113. CrossrefMedlineGoogle Scholar35. MOCHIZNKIKOBAYASKINEELY SKJ. Effect of P-lactate on glyceraldehyde-3-P dehydrogenase in heart muscle. Recent Adv Stud Cardiac Struct Metab. 1978;12:175-82. Google Scholar36. DAVIES A. Rapid desensitization and uncoupling of human beta-adrenergic receptors in an in vitro model of lactic acidosis. J Clin Endocrinol Metab. 1984;59:398-405. CrossrefMedlineGoogle Scholar37. FINCHGOLLNICKHLASTALAMILLERDILLMANMACKLER CPMLEB. Lactic acidosis as a result of iron deficiency. J Clin Invest. 1979;64:129-37. CrossrefMedlineGoogle Scholar38. FRALEYADLERBRUNSZETT DSFB. Stimulation of lactate production by administration of bicarbonate in a patient with a solid neoplasm and lactic acidosis. N Engl J Med. 1980;303:1100-2. CrossrefMedlineGoogle Scholar39. NAPARSTEKFRIEDLAENDERRUBINGERPOPOVTZER YMDM. Lactic acidosis and peritoneal dialysis. Isr J Med Sci. 1982;18:513-4. MedlineGoogle Scholar40. NASHRUSSO MJ. Neonatal lactic acidosis and renal failure: the role of peritoneal dialysis. J Pediatr. 1977;91:101-5. CrossrefMedlineGoogle Scholar41. VAZIRINESSWELLIKSONBARTONGREEP NRLCN. Bicarbonate-buffered peritoneal dialysis: an effective adjunct in the treatment of lactic acidosis. Am J Med. 1979;67:392-6. CrossrefMedlineGoogle Scholar42. COLOMBITHOLEN AH. Hemodialysis in the treatment of lactic acidosis associated with acute hepatic and renal failure. Postgrad Med J. 1971;47:628-31. CrossrefMedlineGoogle Scholar43. TOBINMOOKERJEE MB. Hemodialysis for phenformin associated lactic acidosis. J Dial. 1978;2:273-85. CrossrefMedlineGoogle Scholar44. STACPOOLEHARMANCURRYBAUMGARTNERMISBIN PESTR. Treatment of lactic acidosis with dichloroacetate. N Engl J Med. 1983;309:390-6. CrossrefMedlineGoogle Scholar45. KITABCHIYOUNGSACKSMORRIS ARHL. Diabetic ketoacidosis: reappraisal of therapeutic approach. Annu Rev Med. 1979;30:339-57. CrossrefMedlineGoogle Scholar46. MARRTRAISMANTRAISMANTYPLINBAN THEBS. Juvenile ketoacidosis: the use of sodium bicarbonate in the treatment of diabetic children. 1981; J Kans Med Soc. 1981;82:282-4. MedlineGoogle Scholar47. HALECRASENATTRASS PJM. Metabolic effects of bicarbonate in the treatment of diabetic ketoacidosis. Br Med J. 1984;289:1035-8. CrossrefMedlineGoogle Scholar48. BISHOPWEISFELDT RM. Sodium bicarbonate administration during cardiac arrest: effect on arterial pH PCO2, and osmolality. JAMA. 1976;235:506-9. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: University of Florida College of Medicine Gainesville, Florida PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byAppropriate Clinical Use of Lactate MeasurementsEffect of a serum lactate monitoring recommendation policy on patients treated with linezolidCritical Care and Fluid TherapyEmergency Department Management of Acute Kidney Injury, Electrolyte Abnormalities, and Renal Replacement Therapy in the Critically IllLactic Acidosis: A Rare Oncological Emergency in Solid Tumors at PresentationAcid-Base BalanceHemodynamic consequences of severe lactic acidosis in shock states: from bench to bedsideConcentration-independent MRI of pH with a dendrimer-based pH-responsive nanoprobeEfficient Extra- and Intracellular Alkalinization Improves Cardiovascular Functions in Severe Lactic Acidosis Induced by Hemorrhagic ShockThe Pathophysiology of Hypoglycemia and Lactic Acidosis in MalariaLactic acidosisMixed Acid–Base DisordersClinical Syndromes of Metabolic AcidosisAcute Kidney InjuryMetabolic Acid-Base DisordersManagement of Emergencies in LeukemiasPhysiologic Foundations of Cardiopulmonary ResuscitationAcid-Base BalanceCoagulopathy by Hypothermia and Acidosis: Mechanisms of Thrombin Generation and Fibrinogen AvailabilityBicarbonate Therapy in Severe Metabolic AcidosisLactic acidosisDiagnosis and Therapy of Metabolic AlkalosisTroubles acidobasiquesClinical Syndromes of Metabolic AcidosisEvaluation of tris-hydroxymethylaminomethane on reversing coagulation abnormalities caused by acidosis in pigs*Use of base in the treatment of acute severe organic acidosis by nephrologists and critical care physicians: results of an online surveySodium bicarbonate improves outcome in prolonged prehospital cardiac arrestMetabolic Acid-Base DisordersCardiac Arrest and Cardiopulmonary ResuscitationPhysiologic Foundations of Cardiopulmonary ResuscitationLife Support and Management of Cardiac ArrestAnions and the anaesthetist 1Use of base in the treatment of severe acidemic statesInitial effect of sodium bicarbonate on intracellular pH depends on the extracellular nonbicarbonate buffering capacityEffect of NaHCO3 on cardiac energy metabolism and contractile function during hypoxemiaSodium Bicarbonate Controversy in Lactic AcidosisBikarbonatDoes bicarbonate therapy improve the management of severe diabetic ketoacidosis?Quels sont les moyens symptomatiques de corriger une acidose métabolique?Alcalinisation plasmatique avec les solutions tamponsHyperventilation, épuration extrarénale et dichloroacétate dans le traitement des acidosesA Review of the Role of Blood Lactate Measurements in the ICUAlkaline buffers for correction of metabolic acidosis during cardiopulmonary resuscitation with focus on Tribonat®—A reviewEvaluation of the Neonate with a Potential Metabolic DefectFluid, Electrolyte, and Acid-Base DisordersTherapy of Lactic AcidosisCorrection of acid-base derangementsManagement of Life-Threatening Acid–Base DisordersInfluence of alkaline buffers on cytoplasmic pH in myocardial cells exposed to hypoxiaTreatment of Severe Respiratory Failure During Status Asthmaticus in Children and Adolescents Using High Flow Oxygen and Sodium BicarbonateInfluence of alkaline buffers on cytoplasmic pH in myocardial cells exposed to metabolic acidosisEffect of sodium bicarbonate on intracellular pH under different buffering conditionsSodium bicarbonate in cardiac arrest: A reappraisalBicarbonate dialysate for continuous renal replacement therapy in intensive care unit patients with acute renal failurePEDIATRIC CARDIOPULMONARY RESUSCITATIONEffect of pH and Lidocaine on β-Adrenergic Receptor BindingHaemodynamic and metabolic effects in diabetic ketoacidosis in rats of treatment with sodium bicarbonate or a mixture of sodium bicarbonate and sodium carbonateACUTE HYPOTENSION RELATED TO SEPSIS IN THE OBSTETRIC PATIENTMechanisms of myocardial depression after bolus injection of sodium bicarbonateTreatment of Critical Status Asthmaticus in ChildrenNatural history and course of acquired lactic acidosis in adultsMONITORING IN THE INTENSIVE CARE UNITFluid, Electrolyte, and Acid-Base DisordersImportance of tonicity of carbicarb on the functional and metabolic responses of the acidotic isolated heartCarbicarb, Sodium Bicarbonate, and Sodium Chloride in Hypoxic Lactic AcidosisBicarbonate Does Not Increase Left Ventricular Contractility During L-Lactic Acidemia in PigsLactic AcidosisNuclear magnetic resonance measurements of intracellular pH: Biomedical implicationsBicarbonate in the treatment of metabolic acidosis: Effects on hepatic intracellular pH, gluconeogenesis, and lactate disposal in ratsThe use of isotonic sodium chloride in the early treatment of cholera diarrhea: the Peruvian experienceResuscitation from Severe Acute HypercapniaEthylene Glycol IntoxicationBicarbonate does not improve left ventricular contractility during resuscitation from hypovolemic shock in pigsEffect of prolonged bicarbonate administration on plasma potassium in terminal renal failureIntensive Care TherapeuticsCardiopulmonary ResuscitationManagement of ShockAcid-Base DisturbancesTherapy of Lactic Acidosis: Alternatives to Sodium BicarbonatePathogenesis of Metabolic Acidosis with HypoxiaLactic Acidosis, Type APrehospital bicarbonate use in cardiac arrest: A 3-year experienceBibliographyAlcaliniser une acidose lactique ?Severe lactic acidosis following theophylline overdoseMetabolic AcidosisRespiratory Acid-base DisturbancesShould Lactic Acidosis Be Corrected?BikarbonatFaut-il alcaliniser les acidoses métaboliques ?Hemodynamic and hepatic pH responses to sodium bicarbonate and carbicarb during systemic acidosisDifferent effects of sodium bicarbonate and an alternate buffer (Carbicarb) in normal volunteersInadequate bicarbonate resuscitation in trauma patients requiring crossclamping of the aortaEffect of alkalinization and fluids on survival in acute, non-hypoxic respiratory acidosisParadoxical effect of bicarbonate on cytoplasmic pHBicarbonate Does Not Improve Hemodynamics in Critically III Patients Who Have Lactic Acidosis A Prospective, Controlled Clinical StudyD. James Cooper, BM, BS, Keith R. Walley, MD, Barry R. Wiggs, MSC, James A. Russell, MDAcid-Base Disorders in End-Stage Renal Disease: Part IThe pharmacology of dichloroacetateMetabolic AcidosisAcidosis In Cardiopulmonary ArrestFace-Mask CPAP and Sodium Bicarbonate Infusion in Acute, Severe Asthma and Metabolic AcidosisMetabolic and hemodynamic consequences of sodium bicarbonate administration in patients with heart diseaseLactic acidosisFluid Therapy in the Critically Ill PatientAcid-Base Homeostasis in Clinical DialysisCardiovascular collapse and death in a 55-year-old woman with cervical cancerDichloroacetate in the Treatment of Lactic AcidosisPETER W. STACPOOLE, M.D., Ph.D., ANTHEA C. LORENZ, R.N., RONALD G. THOMAS, Ph.D., ELOISE M. HARMAN, M.D.Improved hemodynamic function during hypoxia with Carbicarb, a new agent for the management of acidosis.Sodium Bicarbonate in the Perinantal Settting—RevisitedLactate MetabolismLactic Acidosis and Bicarbonate TherapyROBERT C. HOLLANDER, M.D.Bicarbonate Therapy for Organic Acidosis: The Case for Its Continued UseROBERT G. NARINS, M.D., JORDAN J. COHEN, M.D.Lactic Acidosis: An UpdateImprovements of metabolic imbalances after enteral sodium bicarbonate supplementation in infants of very low birth weight (VLBW) (Short communication)Emergencies in Acute Lymphoblastic Leukemia 1 August 1986Volume 105, Issue 2Page: 276-279KeywordsAttentionBicarbonatesBloodHypotensionLactatesLactic acidosisMortalitySurgery Issue Published: 1 August 1986 PDF downloadLoading ...

https://doi.org/10.7326/0003-4819-105-2-276
Cancer · 1981 · 48 citations · open access

Chronic lactic acidosis in a patient with cancer: Therapy and metabolic consequences

AbstractLactic acidosis is a life-threatening disorder in some cases. Treatment should be directed at the primary cause. Sodium bicarbonate should be added if the acidosis is very severe, or if the rate of hydrogen ion production is very rapid and not controlled. In contrast, with moderate degrees of steady state lactic acidosis and poor dietary intake, the risks of therapy with sodium bicarbonate or dichloroacetate may actually outweigh the benefits in a cachectic patient unless a dietary glucose and/or protein load is given.

https://doi.org/10.1002/1097-0142(19810415)47:8<2026::aid-cncr2820470821>3.0.co;2-g
Southern Medical Journal · 1988 · 25 citations

Malignancy-Induced Lactic Acidosis

AbstractLactic acidosis, a rare and usually fatal complication of malignancy, is defined as a clinical condition in which the pH is less than or equal to 7.35 and the serum lactate level greater than or equal to 5 mEq/L. We have described the clinical aspects of four cases of lactic acidosis associated with malignancy, and have reviewed all reported cases of lactic acidosis in malignancy meeting the criteria. Rapid recognition of the condition and prompt institution of chemotherapy led to reversal of lactic acidosis in three of our four patients, but long-term survival is related to the responsiveness of the underlying tumor.

https://doi.org/10.1097/00007611-198804000-00034
PubMed · 2013 · 0 citations

[Treatment of lactic acidosis with early continuous blood purification].

AbstractOBJECTIVE: To observe the therapeutic effect of early continuous blood purification (CBP) on lactic acidosis patients. METHODS: Using prospective randomized study method, 41 patients with lactic acidosis in intensive care unit (ICU) from January 2010 to April 2012 were randomly divided into CBP group (n=21) and control group (n=20). Among them, blood gas analysis, lactic acid, blood biochemistry were prospectively monitored at the time before treatment, 12, 24 and 72 hours after treatment. They were also evaluated with acute physiology and chronic health evaluation II (APACHEII) score, and length of stay in ICU and mortality in 28 days were recorded. RESULTS: Lactic acid level and APACHEII score were gradually decreased after treatment in both groups. Compared with control group, lactic acid at 12, 24 and 72 hours in CBP group was obviously lowered (12 hours: 8.23±3.94 mmol/L vs. 12.47±4.62 mmol/L, 24 hours: 4.46±1.57 mmol/L vs. 10.54±3.48 mmol/L, 72 hours: 2.69±1.03 mmol/L vs. 5.74±1.56 mmol/L, all P<0.01), while the APACHEII score at 12, 24 and 72 hours in CBP group was also significantly lowered (12 hours: 18.23±5.85 vs. 21.64±5.38, 24 hours: 16.49±4.62 vs. 20.61±5.71, 72 hours: 11.54±3.67 vs. 16.02±4.34, all P<0.05). Compared with control group, length of stay in ICU was also significantly shorter in CBP group (6.58±3.45 days vs. 11.65±4.94 days, P<0.05), and 28-day mortality was significantly lower in CBP group (23.8% vs. 45.0%, P<0.05). CONCLUSION: Early correction of lactic acidosis with CBP could reduce the mortality of lactic acidosis.

https://doi.org/10.3760/cma.j.issn.2095-4352.2013.01.012
Turkish Journal of Medical and Surgical Intensive Care · 2011 · 0 citations

Lactic Acidosis: A Short Review of Cases

AbstractLactic acidosis, which is caused by a high anion concentration due to metabolic acidosis, occurs when the plasma lactate concentration exceeds 4 to 5 millimoles/litre (mmol/L) (normal range: 0.5-1.5 mmol/L). Lactate accumulation results from increased metabolism or decreased excretion. Lactic acidosis cases often occurs in intensive care units. In order to carry out effective treatment, the primary aim must be the reversal of the causes underlying the disease. Today, various methods are used to treat lactic acidosis. We have reviewed the occurrence of lactic acidosis in two cases in light of the current literature. Lactic acidosis can have quite serious consequences, and clinicians must be very careful while managing patients with lactic acidosis. (Yogun Bakim Derg 2011; 3: 63-6)

https://doi.org/10.5152/dcbybd.2011.14
International Journal of Occupational Medicine and Environmental Health · 2014 · 0 citations · open access

Lactic acidosis occurrence during exercises in the smoke chamber in a 53-year-old firefighter with no significant medical history

AbstractLactic acidosis is a form of metabolic acidosis with a high anion gap, reduced rate of arterial blood pH under 7.35 mmol/l, and lactic acid concentration over 7 mmol/l. In the literature we can find some descriptions of the cases of lactic acidosis in patients with severe systemic diseases (cancer, acquired immunodeficiency syndrome, sepsis, diabetes with cardiovascular disease and after organ transplantations). We present the case of lactic acidosis in a patient with no chronic disease--a firefighter in whom lactic acidosis has developed during standard exercises in the smoke chamber.

https://doi.org/10.2478/s13382-014-0263-y

Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.

DeCure is a research and publication project, not medical advice and not a treatment. "DeCure for X" describes a research goal, not a claim that a cure exists. Backing a cure is a contribution to fund the research — it is not an investment, and confers no yield, royalty, equity or IP ownership. Papers are published open-access by the DeCure.ai DAO.