[Changes of lactate levels in diabetic ketoacidosis and in newly diagnosed type 1 diabetes mellitus].

Abstract:

:Introduction: It is known that lactate concentration is increased in diabetic ketoacidosis (DKA), however, the pathophysiology and kinetics of lactate changes are still unclear. Normally, L-lactate is the major form in the human body. According to previous data, also D- and L-lactate might be increased in hyperglycaemic disorders. Aim: We aimed to describe the kinetics and mechanisms of lactate concentration changes in ketoacidosis and newly diagnosed diabetes. Method: We performed a prospective study, including 5-18-year-old children with ketoacidosis (DKA, n = 13) and with newly diagnosed type 1 diabetes without ketoacidosis (T1DM, n = 6). We performed routine blood gas analysis 0-12-24-48 hours after admission, which also measured L-lactate levels. We also determined total venous serum lactate level by gas chromatography-mass spectrometry. Results: Initial plasma lactate concentration was increased in ketoacidosis as compared to the newly diagnosed diabetes group (p<0.05). After 12 h of rehydration, lactate levels were greatly reduced in ketoacidotic patients but after 24-48 h it was repeatedly increased (all p<0.01). In the 0-12 h phase, total serum lactate level was higher than L-lactate level, referring to D-lactate production. Conclusion: We described two L-lactate peaks in ketoacidosis. In the first 12 hours anaerobic glycolysis seems to have major role in hyperlactataemia. We assume that stimulated aerobic glycolysis leads to the second lactate peak. However, D-lactate is not routinely measured, it may contribute to the initial hyperlactataemia in both groups and is comparable to L-lactate production in ketoacidosis. Orv Hetil. 2019; 160(45): 1784-1790. :Absztrakt: Bevezetés: A klinikumban ismert a diabeteses ketoacidosisban (DKA) kialakuló hyperlactataemia, azonban a háttérben álló mechanizmusok és a változások kinetikája tisztázatlan. Az emberi szervezetben fiziológiásan főleg a laktát L-izomere van jelen. Hyperglykaemiás állapotokban azonban fokozott lehet a D- és L-laktát-termelés is, így a szöveti hypoperfusio mellett ez a tényező is szerepet játszhat a laktátváltozásokban. Célkitűzés: Vizsgálatunk célja a ketoacidosisban és a frissen diagnosztizált diabetesben jelentkező laktátváltozások kinetikájának és mechanizmusának feltérképezése volt. Módszer: Ketoacidosis (DKA-csoport, n = 13) és frissen diagnosztizált 1-es típusú diabetes mellitus (T1DM-csoport, n = 6) miatt felvett 5–18 éves gyermekek prospektív vizsgálata történt. A felvételt követően 0–12–24–48 órával vérgázvizsgálatot végeztünk, mely az L-laktát-koncentráció meghatározására is alkalmas. Minden időpontban meghatároztuk az összlaktátot (L + D) is gázkromatográfiás tömegspektrometriával. Eredmények: Felvételkor minden ketoacidoticus betegnél kórosan magas L-laktát-koncentrációt mértünk, ami magasabb volt, mint a T1DM-csoportban (p<0,05). 12 óra elteltével az L-laktát-szint ketoacidosisban csökkent, majd ismét megemelkedett 24 és 48 óra után (p<0,01). A T1DM-csoportban csak a 48 órás érték emelkedett szignifikánsan (p<0,05 versus 12 óra). 0–12 óra között az összlaktát-koncentráció jelentősen meghaladta az L-laktát-szintet, ez a D-laktátot tükröző különbség fokozatosan csökkenve 48 óra után megszűnt. Következtetés: A ketoacidosisban észlelt két laktátcsúcs közül az első 12 órában a hyperlactataemia kialakulásában az anaerob glikolízisnek van szerepe. A második, inzulinkezelés és rendezett folyadékháztartás mellett kialakuló csúcs hátterében fokozott aerob glikolízis állhat. Az L-laktát- és összlaktátszintek közötti kezdeti különbség D-laktát képződésére utal, amely a ketoacidosis kezdeti fázisában az L-laktáttal azonos nagyságrendben termelődik. Orv Hetil. 2019; 160(45): 1784–1790.

journal_name

Orv Hetil

journal_title

Orvosi hetilap

authors

Jenei K,Szatmári I,Szabó E,Mariam A,Luczay A,Zsidegh P,Tóth-Heyn P

doi

10.1556/650.2019.31533

subject

Has Abstract

pub_date

2019-11-01 00:00:00

pages

1784-1790

issue

45

eissn

0030-6002

issn

1788-6120

journal_volume

160

pub_type

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