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Lactic Asidosis after Metformin Use in a Chronic Hemodialysis Patient

Yıl 2022, Cilt: 2 Sayı: 1, 30 - 32, 29.01.2022

Öz

Metformin is a biguanide and is used especially in metabolic syndrome where insulin resistance is at the forefront and in Type 2 diabetes mellitus, both by suppressing the endogenous glucose production in the liver and increasing the sensitivity of insulin in peripheral tissues such as fat and muscle tissue (1). The most rare but life-threatening side effect of metformin is the development of lactic acidosis. Therefore, the glomerular filtration rate is 30 ml/min. its use is contraindicated in patients with chronic kidney disease (2). Lactic acidosis is the cause of metabolic acidosis with increased anion gap; occurs when the plasma lactate concentration exceeds 4-5 millimol/Liter (mmol/L) (Normal range: 0.5-1.5 mmol/L) (3). Here, we present the development of lactic acidosis due to metformin use in an 84-year-old female patient who has been on chronic hemodialysis treatment for 4 months. The patient applied to the emergency department twice because of confusion. The patient, who was found to have acidosis in the blood gas, regained consciousness after he was taken to hemodialysis and was referred to the nephrology outpatient clinic, considering that she might have dialysis insufficiency. The patient, who learned that she used metformin in his anamnesis, did not recur after the drug was stopped. The use of metformin in advanced age and renal failure may cause fatal complications. Glomerular filtration rate 45 ml/min. metformin should be used with caution in patients with should not be given to those below.

Kaynakça

  • 1. Oral agents for the treatment of type 2 diabetes mellitus: pharmacology, toxicity, and treatment. Harrigan RA, Nathan MS, Beattie P. Ann Emerg Med. 2001;38:68–78.
  • 2. Metformin. A review of its pharmacological properties and therapeutic use in non-insulin-dependent diabetes mellitus. Dunn CJ, Peters DH. Drugs. 1995;49:721–749.
  • 3. The role of metformin in metformin-associated lactic acidosis (MALA): Case series and formulation of a model of pathogenesis. Duong JK, Furlong TJ, Roberts DM, et al. Drug Saf. 2013;36:733–746.
  • 4. Metformin accumulation: lactic acidosis and high plasmatic metformin levels in a retrospective case series of 66 patients on chronic therapy. Vecchio S, Giampreti A, Petrolini VM, et al. Clin Toxicol (Phila) 2014;52:129–135.
  • 5. Lactic acidosis in metformin-treated patients. Prognostic value of arterial lactate levels and plasma metformin concentrations. Lalau JD, Race JM. Drug Saf. 1999;20:377–384.
  • 6. Acetaminophen-induced hepatotoxicity: a comprehensive update. Yoon E, Babar A, Choudhary M, et al. J Clin Transl Hepatol. 2016;4:131–142.
  • 7. Renal gluconeogenesis: its importance in human glucose homeostasis. Gerich JE, Meyer C, Woerle HJ, Stumvoll M. Diabetes Care. 2001;24:382–391.
  • 8. Targeting oxygen-sensing prolyl hydroxylase for metformin-associated lactic acidosis treatment. [Jan;2018 ];Oyaizu-Toramaru T, Suhara T, Hayakawa N, et al. Mol Cell Biol. 2017 37:0–17.
  • 9. Misbin RI. The phantom of lactic acidosis due to metformin in patients with diabetes. Diabetes Care. 2004;27(7):1791–3.
  • 10. Bodmer M, Meier C, Krähenbühl S, Jick SS, Meier CR. Metformin, sulfonylureas, or other antidiabetes drugs and the risk of lactic acidosis or hypoglycemia a nested case-control analysis. Diabetes Care. 2008;31(11):2086–91.
  • 11. US Food and Drug Administration. FDA Drug Safety Communication: FDA revises warnings regarding use of the diabetes medicine metformin in certain patients with reduced kidney function; 2017
Yıl 2022, Cilt: 2 Sayı: 1, 30 - 32, 29.01.2022

Öz

Kaynakça

  • 1. Oral agents for the treatment of type 2 diabetes mellitus: pharmacology, toxicity, and treatment. Harrigan RA, Nathan MS, Beattie P. Ann Emerg Med. 2001;38:68–78.
  • 2. Metformin. A review of its pharmacological properties and therapeutic use in non-insulin-dependent diabetes mellitus. Dunn CJ, Peters DH. Drugs. 1995;49:721–749.
  • 3. The role of metformin in metformin-associated lactic acidosis (MALA): Case series and formulation of a model of pathogenesis. Duong JK, Furlong TJ, Roberts DM, et al. Drug Saf. 2013;36:733–746.
  • 4. Metformin accumulation: lactic acidosis and high plasmatic metformin levels in a retrospective case series of 66 patients on chronic therapy. Vecchio S, Giampreti A, Petrolini VM, et al. Clin Toxicol (Phila) 2014;52:129–135.
  • 5. Lactic acidosis in metformin-treated patients. Prognostic value of arterial lactate levels and plasma metformin concentrations. Lalau JD, Race JM. Drug Saf. 1999;20:377–384.
  • 6. Acetaminophen-induced hepatotoxicity: a comprehensive update. Yoon E, Babar A, Choudhary M, et al. J Clin Transl Hepatol. 2016;4:131–142.
  • 7. Renal gluconeogenesis: its importance in human glucose homeostasis. Gerich JE, Meyer C, Woerle HJ, Stumvoll M. Diabetes Care. 2001;24:382–391.
  • 8. Targeting oxygen-sensing prolyl hydroxylase for metformin-associated lactic acidosis treatment. [Jan;2018 ];Oyaizu-Toramaru T, Suhara T, Hayakawa N, et al. Mol Cell Biol. 2017 37:0–17.
  • 9. Misbin RI. The phantom of lactic acidosis due to metformin in patients with diabetes. Diabetes Care. 2004;27(7):1791–3.
  • 10. Bodmer M, Meier C, Krähenbühl S, Jick SS, Meier CR. Metformin, sulfonylureas, or other antidiabetes drugs and the risk of lactic acidosis or hypoglycemia a nested case-control analysis. Diabetes Care. 2008;31(11):2086–91.
  • 11. US Food and Drug Administration. FDA Drug Safety Communication: FDA revises warnings regarding use of the diabetes medicine metformin in certain patients with reduced kidney function; 2017
Toplam 11 adet kaynakça vardır.

Ayrıntılar

Birincil Dil İngilizce
Konular İç Hastalıkları
Bölüm Case Reports
Yazarlar

Mehmet Biricik 0000-0002-5701-4978

Feyzi Bostan

Yayımlanma Tarihi 29 Ocak 2022
Gönderilme Tarihi 30 Ekim 2021
Yayımlandığı Sayı Yıl 2022 Cilt: 2 Sayı: 1

Kaynak Göster

EndNote Biricik M, Bostan F (01 Ocak 2022) Lactic Asidosis after Metformin Use in a Chronic Hemodialysis Patient. DAHUDER Medical Journal 2 1 30–32.



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