pattismith
Senior Member
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This topic is made to help us with the drugs we are using.
knowing that some of us have elevated blood lactates each times they need an extra energy, we shouldn't take any drugs that make the lactates go higher (these drugs are toxic to mitochondrias)...
So here a summary of the high blood lactates drug induced
"In health, blood lactate concentration is maintained within the approximate range of 0.5-1.5 mmol/L [6]. This reflects a balance between the rate of lactate release to blood from erythrocytes and other tissue cells and rate of lactate clearance from blood, principally by the liver and kidney.
Exercise represents a physiological process in which this balance is temporarily upset due to the rapid increase in lactate production by muscle cells in temporary oxygen debt. In severe exercise, blood lactate may rise to levels in excess of 20 mmol/L but due to the capacity for rapid lactate disposal, in health this rise is only transitory.
Hyperlactatemia and lactic acidosis
Hyperlactatemia is a pathological state in which resting blood lactate concentration is abnormally high (>1.5 mmol/L). Moderate to severe hyperlactatemia (>3.0 to >5.0 mmol/L) is associated with abnormal accumulation of hydrogen ions (H+) and a resulting tendency to acidosis.
The combination of hyperlactatemia and acidosis is called lactic acidosis and although there is no universal agreement for definition of lactic acidosis, the most widely used is blood lactate >5.0 mmol/L in combination with pH <7.35 [7].
Lactic acidosis is the most common cause of metabolic acidosis [8].
Type A lactic acidosis
Tissue hypoxia
Type B lactic acidosis
If lactic acidosis occurs in the context of apparently adequate tissue oxygenation and normal hemodynamics (i.e. normal blood pressure, no volume depletion, normal blood oxygen and oxygen-carrying capacity)
Type B lactic acidosis is a feature of several individually very rare inherited disorders that are characterized by deficiency of specific enzymes involved in lactate metabolism (either gluconeogenesis or pyruvate oxidation). These include pyruvate carboxylase deficiency [15], glucose-6-phosphate dehydrogenase (G6PD) deficiency, fructose-1,6-diphosphatase deficiency [16] and pyruvate dehydrogenase deficiency, the most common [17]. These conditions are collectively referred to as congenital lactic acidosis.
A long list of drugs and toxins can cause lactic acidosis (Table I), and taken together these represent by far the most common cause of Type B lactic acidosis. Biguanides are a class of blood glucose-lowering drugs used in the treatment of diabetes; metformin, the most widely prescribed, has been linked to lactic acidosis [18]. However, in most cases of metformin-associated lactic acidosis, there is some evidence of liver or renal impairment that predisposes to hyperlactatemia.
Biguanides (e.g. metformin)
Ethanol
Methanol
Antiretroviral drugs
Cyanide
Theophylline
Cocaine
Simvastatin
Salicylates
Paracetamol (acetaminophen)
Lactulose
Propylene glycol Epinephrine, norepinephrine"
(I would add Caffeine and Ephedrine, and I may add Amitryptilline that showed evidences of mitochondrial toxicity)
https://acutecaretesting.org/en/articles/lactate-and-lactic-acidosis
http://www.sciencedirect.com/science/article/pii/S0022395611002688
Management of lactic acidosis:
"If this is the case, we may be able to identify many persons at risk for lactic acidosis early and endeavor to intensively manage "mitochondrial stress," particularly during periods of increased risk. This may involve frequent monitoring of lactate levels or, perhaps, anion gap as well as therapy with agents suggested to "support" mitochondrial function, such as carnitine, riboflavin, thiamine, and ubiquinone (coenzyme Q-10).
and the pyruvate dehydrogenase stimulant dichloracetic acid (DCA).[5]
Use of thiamine (vitamin B1) is appropriate if alcohol-related triggering of lactic acidosis is thought likely. In metformin-related lactic acidosis, insulin is required.[5] Additional agents that have been suggested as adjuncts to the management of NRTI-related lactic acidosis include oral or intravenous riboflavin (vitamin B2),[20,21] carnitine, and ubiquinone.[22] Riboflavin has been associated with possible benefit in some cases, although it is unclear from these reports that recovery had not already begun when riboflavin was introduced."
http://www.medscape.com/viewarticle/441083_7
knowing that some of us have elevated blood lactates each times they need an extra energy, we shouldn't take any drugs that make the lactates go higher (these drugs are toxic to mitochondrias)...
So here a summary of the high blood lactates drug induced
"In health, blood lactate concentration is maintained within the approximate range of 0.5-1.5 mmol/L [6]. This reflects a balance between the rate of lactate release to blood from erythrocytes and other tissue cells and rate of lactate clearance from blood, principally by the liver and kidney.
Exercise represents a physiological process in which this balance is temporarily upset due to the rapid increase in lactate production by muscle cells in temporary oxygen debt. In severe exercise, blood lactate may rise to levels in excess of 20 mmol/L but due to the capacity for rapid lactate disposal, in health this rise is only transitory.
Hyperlactatemia and lactic acidosis
Hyperlactatemia is a pathological state in which resting blood lactate concentration is abnormally high (>1.5 mmol/L). Moderate to severe hyperlactatemia (>3.0 to >5.0 mmol/L) is associated with abnormal accumulation of hydrogen ions (H+) and a resulting tendency to acidosis.
The combination of hyperlactatemia and acidosis is called lactic acidosis and although there is no universal agreement for definition of lactic acidosis, the most widely used is blood lactate >5.0 mmol/L in combination with pH <7.35 [7].
Lactic acidosis is the most common cause of metabolic acidosis [8].
Type A lactic acidosis
Tissue hypoxia
Type B lactic acidosis
If lactic acidosis occurs in the context of apparently adequate tissue oxygenation and normal hemodynamics (i.e. normal blood pressure, no volume depletion, normal blood oxygen and oxygen-carrying capacity)
Type B lactic acidosis is a feature of several individually very rare inherited disorders that are characterized by deficiency of specific enzymes involved in lactate metabolism (either gluconeogenesis or pyruvate oxidation). These include pyruvate carboxylase deficiency [15], glucose-6-phosphate dehydrogenase (G6PD) deficiency, fructose-1,6-diphosphatase deficiency [16] and pyruvate dehydrogenase deficiency, the most common [17]. These conditions are collectively referred to as congenital lactic acidosis.
A long list of drugs and toxins can cause lactic acidosis (Table I), and taken together these represent by far the most common cause of Type B lactic acidosis. Biguanides are a class of blood glucose-lowering drugs used in the treatment of diabetes; metformin, the most widely prescribed, has been linked to lactic acidosis [18]. However, in most cases of metformin-associated lactic acidosis, there is some evidence of liver or renal impairment that predisposes to hyperlactatemia.
Biguanides (e.g. metformin)
Ethanol
Methanol
Antiretroviral drugs
Cyanide
Theophylline
Cocaine
Simvastatin
Salicylates
Paracetamol (acetaminophen)
Lactulose
Propylene glycol Epinephrine, norepinephrine"
(I would add Caffeine and Ephedrine, and I may add Amitryptilline that showed evidences of mitochondrial toxicity)
https://acutecaretesting.org/en/articles/lactate-and-lactic-acidosis
http://www.sciencedirect.com/science/article/pii/S0022395611002688
Management of lactic acidosis:
"If this is the case, we may be able to identify many persons at risk for lactic acidosis early and endeavor to intensively manage "mitochondrial stress," particularly during periods of increased risk. This may involve frequent monitoring of lactate levels or, perhaps, anion gap as well as therapy with agents suggested to "support" mitochondrial function, such as carnitine, riboflavin, thiamine, and ubiquinone (coenzyme Q-10).
and the pyruvate dehydrogenase stimulant dichloracetic acid (DCA).[5]
Use of thiamine (vitamin B1) is appropriate if alcohol-related triggering of lactic acidosis is thought likely. In metformin-related lactic acidosis, insulin is required.[5] Additional agents that have been suggested as adjuncts to the management of NRTI-related lactic acidosis include oral or intravenous riboflavin (vitamin B2),[20,21] carnitine, and ubiquinone.[22] Riboflavin has been associated with possible benefit in some cases, although it is unclear from these reports that recovery had not already begun when riboflavin was introduced."
http://www.medscape.com/viewarticle/441083_7
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