{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,9]],"date-time":"2025-10-09T00:40:08Z","timestamp":1759970408866,"version":"build-2065373602"},"reference-count":49,"publisher":"MDPI AG","issue":"1","license":[{"start":{"date-parts":[[2025,1,17]],"date-time":"2025-01-17T00:00:00Z","timestamp":1737072000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Reports"],"abstract":"<jats:p>Background and Clinical Significance: When lactate production surpasses the body\u2019s clearance capacity, hyperlactatemia (lactate \u2265 2 mmol\/L) or lactic acidosis (lactate \u2265 4 mmol\/L) can develop. Lactic acidosis is classified into type A, which arises from regional or global tissue hypoperfusion, and type B, resulting from metabolic disturbances without tissue hypoxia. Type A lactic acidosis, often associated with conditions like sepsis or shock, is a critical marker of life-threatening conditions, whereas type B lactic acidosis is less frequently recognized in clinical practice. Case Presentation: A 95-year-old man presents with an asthma exacerbation and is treated with an albuterol inhaler. However, he is found to have persistently high lactate levels. Further investigation reveals a congenital intrahepatic portosystemic shunt on imaging. This, in conjunction with the ongoing use of beta-adrenergic receptor agonists, contributes to the development of type B lactic acidosis. Conclusions: The impact of lactic acidosis depends on its severity and clinical context. While beta agonists are a recognized cause of type B lactic acidosis, a potential role for structural liver abnormalities in reduced lactate clearance must be examined further.<\/jats:p>","DOI":"10.3390\/reports8010008","type":"journal-article","created":{"date-parts":[[2025,1,21]],"date-time":"2025-01-21T06:53:32Z","timestamp":1737442412000},"page":"8","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Persistent Lactate Elevation in a Patient with Asthma Exacerbation and a Congenital Portosystemic Shunt: A Case Report and Literature Review"],"prefix":"10.3390","volume":"8","author":[{"given":"Wing Fai","family":"Li","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Jacobi Medical Center, Bronx, NY 10461, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bailey","family":"Fink","sequence":"additional","affiliation":[{"name":"Albert Einstein School of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rehnuma","family":"Khan","sequence":"additional","affiliation":[{"name":"Albert Einstein School of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xinmiao","family":"Luo","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Jacobi Medical Center, Bronx, NY 10461, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-4406-8820","authenticated-orcid":false,"given":"Muhammad","family":"Fahimuddin","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Jacobi Medical Center, Bronx, NY 10461, USA"},{"name":"Albert Einstein School of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2025,1,17]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"R22","DOI":"10.1186\/cc3987","article-title":"Lactate versus Non-Lactate Metabolic Acidosis: A Retrospective Outcome Evaluation of Critically Ill Patients","volume":"10","author":"Gunnerson","year":"2006","journal-title":"Crit. 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