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Repeated use of inhaled β2 agonists is common in asthma or COPD exacerbations. It can lead to hyperlactatemia.We report two asthmatic patients who presented in the emergency department for an asthma exacerbation. The first patient developed hyperlactatemia at 3.9 mmol/L and the second patient developed hyperlactatemia at 5.6 mmol/L after terbutaline treatment. Both patients had a favorable outcome after adjusting the aerosol dose to clinical parameters.Lactic acidosis induced by the use of inhaled β2 agonists is not synonymous of clinical deterioration. However, this side effect may be complicated by a tachypnea compensating for metabolic acidosis and should be known to avoid unnecessary therapeutic escalation.

Lactate production results from anaerobic glycolysis. This pathway is recruited physiologically during intense and sustained muscular contractions. Hyperlactatemia may develop when tissue oxygenation is jeopardized such as in shock, its absence having been, however, sometimes reported in sepsis in which interactions between infectious agents and the organism's cells might blunt or disrupt hyperlactatemia development. During the course of acute rotavirus gastroenteritis, a 9-month-old girl developed severe dehydration (capillary-refill time, 5 s) leading to hypovolemic shock without signs of sepsis and with hypotension at 62/21 mmHg Surprisingly, the child failed to develop hyperlactatemia during shock. An etiologic search to understand why hyperlactatemia did not occur revealed that this patient had been receiving propranolol since the age of four months for the treatment of a Cyrano hemangioma. Via its inhibitory action on β-adrenergic receptors, propranolol antagonizes the stimulation of glycolysis by catecholamines, which may be rationally proposed to have contributed to preventing hyperlactatemia during hypovolemic shock in this patient. Mechanisms by which propranolol can mediate this antihyperlactatemia action are further illustrated and discussed.

Malgré le manque d’études sur ce sujet, le cancer est considéré comme une des principales causes d’hyperlactatémie de type B chez le chien. Les cellules malignes ont une production accrue de lactates secondaire à une glycolyse aérobie accrue, via l’effet Warburg. Les mécanismes ne sont pas encore clairement établis mais certains auteurs suggèrent que le cancer pourrait causer une hyperlactatémie via l’effet Warburg. Cette étude a pour objectif de déterminer si les tumeurs malignes peuvent être associées à une hyperlactatémie cliniquement significative (≥2,5 mmol/L) chez le chien. Trente-sept chiens atteints de tumeurs malignes ont été recrutés (22 atteints de tumeurs hématopoïétiques et 15 de tumeurs non hématopoïétiques). Le diagnostic était confirmé par analyse histologique, ou cytologique en cas de lymphome. Les autres causes possibles d’hyperlactatémie étaient écartées puis la mesure des lactates sanguins était réalisée sur sang veineux jugulaire immédiatement analysé avec le LactatePro®. Aucun chien n’était hyperlactatémique. La concentration moyenne en lactates sanguins était de 1,09 mmol/L. La concentration moyenne en lactates sanguins pour les chiens atteints de tumeurs non hématopoïétiques et hématopoïétiques était respectivement de 0,95 mmol/L et de 1,19 mmol/L. Les chiens atteints de lymphome (n=18) avaient une concentration moyenne en lactates sanguins de 1,15 mmol/L. Les tumeurs malignes ne sont pas associées à une hyperlactatémie de type B cliniquement significative chez le chien. L’hyperlactatémie tumorale est donc une complication rare chez le chien. Son diagnostic devrait conduire à une investigation minutieuse des autres causes d’hyperlactatémie., Cancer is considered a cause of type B hyperlactatemia in dogs. However, studies evaluating cancer as a cause of clinically relevant type B hyperlactatemia (≥2.5 mmol/L) are lacking. It is well accepted that cancer cells have a higher lactate production due to increased aerobic glycolysis, known as the Warburg effect. The mechanisms through which aerobic glycolysis occurs are not well elucidated but it has been suggested that neoplasia may cause type B hyperlactatemia via this process. The aim of this study is to determine if canine malignant tumors could be associated with a clinically relevant type B hyperlactatemia (≥ 2.5 mmol/L). Thirty-seven dogs with malignant tumors were included: 22 with hematopoietic and 15 with solid tumors. Histology was used to confirm the diagnosis (cytology was considered appropriate for lymphoma). Confounding factors associated with hyperlactatemia were excluded. Lactate measurements were obtained from a free flow jugular whole blood sample and immediately analyzed using the LactatePro®. All dogs had lactate values less than 2.5 mmol/L. The mean blood lactate concentration was 1.09 mmol/L. The mean blood lactate concentration for solid and hematopoietic tumor was 0.95 mmol/L and 1.19 mmol/L respectively. Dogs with lymphoma (n = 18) had a mean blood lactate concentration of 1.15 mmol/L. Malignant tumors were not considered a cause of clinically relevant type B hyperlactatemia. Therefore, cancer related type B hyperlactatemia in dogs with cancer is uncommon and its diagnosis should prompt careful investigation for causes other than cancer.