D-lactic acidosis and ataxia in a man with Crohn disease

Abstract

A 49-year-old man presented to the emergency department with an eight-hour history of unsteady gait, impaired concentration, difficulty speaking and blurry vision, which had developed over the previous seven hours. During the preceding two days, he had been excessively thirsty and drank large amounts of water, cola and a "sports drink." He had eaten a large portion of rice with dinner the evening before presentation. On the day he presented, he had awoken in the morning feeling dizzy. As he was leaving for work, he had experienced difficulty using his keys and turning doorknobs.The patient's medical history included Crohn disease and two major small-bowel resections at 33 and 35 years of age that had left about one metre of small intestine. He had undergone an esophageal bougienage three weeks earlier for a stricture related to Crohn disease. After the bougienage, the patient had regained his ability to consume solids and dramatically increased his caloric intake to regain weight. His diet consisted mainly of fast food, candy bars and soft drinks.The patient reported that he did not smoke, consume substantial amounts of alcohol or have any drug allergies. On a daily basis, he took prednisone 20 mg, loperamide 2-4 mg, vitamin B 12 and multivitamins. Except for the addition of prednisone for the Crohn-related stricture, his regimen of medications had not changed during the past year. He had experienced no changes in his usual Crohn symptoms.On clinical examination, the patient was alert, oriented and not in distress. His vital signs were normal and he had no significant postural changes. Other than mild vertical and horizontal nystagmus, the results of cranial nerve testing were normal. The patient had truncal ataxia and notable dysmetria on finger-nose testing. He had an unsteady, wide-based gait and could not tolerate walking more than five steps. Rapid alternating movements and heel-shin tests were normal. His strength and reflexes, and the results of sensory testing, were normal. The rest of the clinical examination was unremarkable except for midline abdominal surgical scars.Initial laboratory investigations are presented in Table 1 and include a serum carbon dioxide level of 10 mmol/L with an anion gap of 22 mEq/L. Complete blood count, creatinine, coagulation studies, liver enzymes and urinalysis were within normal limits. Arterial blood gas analysis showed a pH of 7.21, partial pressure of carbon dioxide (pCO 2 ) of 23, partial pressure of oxygen (pO 2) of 119 and HCO 3 -of 9. Serum lacCases

d(−) Lactic Acid-Induced Adhesion of Bovine Neutrophils onto Endothelial Cells Is Dependent on Neutrophils Extracellular Traps Formation and CD11b Expression

“…Under physiological conditions in the serum, l (+) lactate predominates in comparison to d (−) lactate owing to anaerobic metabolism of mammalian cells ( 23 ). Nonetheless, d (−) lactate concentrations increase under pathophysiological conditions in humans, such as short bowel syndrome [SBS ( 24 , 25 )], fatigue syndrome ( 26 ), diabetes ( 27 , 28 ), Crohn’s disease ( 29 ), and others. Human patients with d (−) lactic acidosis present with neurological dysfunctions characterized by ataxia, slurred speech, confusion, and weakness ( 23 , 30 , 31 ).…”

Faecal D/L Lactate Ratio Is a Metabolic Signature of Microbiota Imbalance in Patients with Short Bowel Syndrome

“…But, the relationship between neurological disorders, microbiota composition, fermentative activity, metabolism and systemic acidosis has not been yet completely understood [7], [26]. Moreover, a survey of SBS patients is difficult since measurement of serum D-lactate concentration is not routinely available in most hospital laboratories or the results come back after the D-lactic acidosis crisis [27], [28]. Our objective was to understand the functional link between the composition/metabolic activity ratio of the faecal microbiota and the SBS clinical characteristics.…”

Diagnostic dilemma: Rare case of recurrent d-lactic acidosis leading to recurrent acute cardiac failure

“…5e7 Sparing of the colon and loss of the small bowel by resection are prerequisites in considering such a possibility. 7,8 Episodes of D-lactic acidosis are triggered by the use of antibiotics against Gram-negative bacteria, ultimately leading to the natural selection of colonic Gram-positive bacteria. 9 With an intact small bowel, these bacteria are not subject to the influence of the highundigested carbohydrates; however, with a major small intestine resection, these carbohydrates would produce D-lactic acid upon reaching the colon.…”

“…10 In heart failure due to PE, a major strain occurs in the right heart leading to a decrease in preload to the left heart, thus causing circulatory failure. 8 The absence of involvement of the right ventricle and isolated severe left ventricular dysfunction were against the possibility of PE leading to the collapse. This was further ruled out by CT angiogram after the initial hemodynamic stabilization.…”