Lactic Acidosis Related to Pharmacotherapy and Human Diseases

Christian Zanza, Valentina Facelli, Tastiana Romenskaya, Maria Bottinelli, Giorgia Caputo, Andrea Piccioni, Francesco Franceschi, Angela Saviano, Veronica Ojetti, Gabriele Savioli, Yaroslava Longhitano, Christian Zanza, Valentina Facelli, Tastiana Romenskaya, Maria Bottinelli, Giorgia Caputo, Andrea Piccioni, Francesco Franceschi, Angela Saviano, Veronica Ojetti, Gabriele Savioli, Yaroslava Longhitano

Abstract

Lactic acidosis represents one of the most common conditions that can compromise the health of intensive care unit (ICU) patients, increasing the mortality of patients with high levels of Lactate who do not receive a proper treatment within the first 6 h of hospitalization. There are two enantiomers of lactic acid: L-lactic acid (when the concentration increases, it can lead to a state of severe acidemia risking cardiovascular collapse, causing an increase in mortality in ICU patients) and D lactic acid (produced in the human organism by microbiota and its production increases during some pathological status). Generally, increased levels of serum lactic acid could be due to numerous factors, including hypoxia (caused for example by septic/cardiogenic/hypovolemic or obstructive shock), specific pathologies (e.g., liver disease), use of some drugs (e.g., metformin), presence of toxins, and trauma. Since the underlying cause could be fatal for the ICU patient, it is important to understand the root of this clinical status with a view to correct it and prevent the risk of a poor clinical outcome. Prevention and early treatment are the keys to control the negative clinical consequences. The aim of this review is to revise the scientific literature for further confirmation about the importance of early identification of acidotic statuses and to underline how an early diagnosis can prevent the worst clinical outcome, especially for ICU patients who are more fragile compared to the general population.

Keywords: acid-base and liver pathology; acid-base equilibrium; d-lactic acid metabolite; disease; drugs; hyperlactatemia; illness; l-lactic acidosis; l-lactic acidosis and disease; l-lactic acidosis and medications; lactic acidosis; medications.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Flowchart.
Figure 2
Figure 2
Lactate biochemical pathway. Legend: PGAL: 3-phosphoglyceraldehyde; ADP: Adenosine diphosphate; ATP: Adenosine triphosphate; NAD+: Nicotinamide adenine dinucleotide (oxidized form); NADH: Nicotinamide adenine dinucleotide (reduced form); CO2: carbon dioxide.

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