LACTATE-ACIDOSIS (synonym: lactacidemia, lactic acidosis) — one of forms of disturbance of exchange of acids and the bases which is characterized by accumulation in blood of lactic acid. L. - and. maybe independent disease (so-called hereditary L. - and.).
The etiology and a pathogeny
is the Reason of the strengthened formation of a lactate in tissues of the healthy person the shift of balance between glycolysis (see) and oxidizing metabolism, leading To development acidosis (see). Any disturbance in transport of various substances, in particular nucleotides, through a mitochondrial membrane, disturbance in a cycle Tricarboxylic to - t can be the cause of strengthening of glycolysis with excessive products of a lactate (see. Tricarboxylic acids cycle ), in an electron transport chain, phosphorylations of ADF in ATP.
L. - and. most often arises owing to a peripheral vascular collapse with reduction of perfusion of bodies oxygenic blood. The strengthened glycolysis with a hyper lactacidemia can be observed also at healthy people at heavy physical. to loading, however pH of blood and the maintenance of a lactate in blood are quickly recovered after cancellation of loading.
At a decompensation of a diabetes mellitus increase in maintenance of a lactate in blood results from blocking of a catabolism pyroracemic to - you (pyruvate) and increase in a ratio of NAD-N/NAD (the similar mechanism of development of a hyper lactacidemia is observed at a single dose of high doses of streptocides). The greatest danger to emergence of L. - and. at patients with a diabetes mellitus it is noted at treatment of a feniletilbiguanidama (Phenforminum, Dibotinum) and to a lesser extent at purpose of other guanyl guanidines (Metforminum, glyukofazh, Buforminum, Adebitum). Cases of emergence of L are described. - and. at treatment of a diabetes mellitus only a diet.
Development of L. - and. perhaps at patients with the metastasizing tumors, the Crimea intravenous injections of a streptozototsin became.
Rather high extent of glycolysis at maligniziruyushchy tumors is known long ago. Observed at this L. - and. it is caused, apparently, by the fact that the recovered equivalents generating during glycolysis are insufficiently transported in a mitochondrion; because of the broken ratio of NAD-N/NAD in cytoplasm pyruvate turns into a lactate more, but not into water p carbonic acid.
L. - and. at a glycogenosis of the I type (a disease to Awnless wheat) is an example of damage, a cut can appear owing to ekstramitokhondrialny defect. Assume that this defect consists in disturbance of a normal course of oxidizing decarboxylation of pyruvate. At a glycogenosis of the V type (Mac-Ardla's disease) the hyper lactacidemia arises because of deficit of muscular phosphorylase.
Deficit of polyneuramin 1 , thiamine pyrophosphate, magnesium can also promote emergence of L. - and. owing to unfavorable conditions for oxidizing transformation of pyruvate. Strengthening of a lactate in blood is observed at defeats of a parenchyma of a liver (late stages of hepatitis, cirrhosis), and also at use of sodium lactate with the medical purpose.
A clinical picture
the explicit and erased forms L Are observed. - and. (a hyper lactacidemia without wedge, manifestations), passing into a giperlaktatsidemichesky coma at accession of acute infectious or inflammatory diseases, various intoxications, an alcohol abuse.
Dispeptic frustration (anorexia, nausea, vomiting), increase of breath, apathy, drowsiness or excitement with sleeplessness, pains behind a breast, a muscular adynamy or muscular weakness at physical can be harbingers of a coma. to loading.
Most often the giperlaktatsidemichesky coma develops suddenly. Within several hours the symptom complex develops: drowsiness (excitement is rare), nonsense, a loss of consciousness, symptoms of dehydration, decrease in body temperature, breath like Kussmaul, decrease in the ABP, a collapse with an oligouriya or an anury. At some patients sharp pains behind a breast as a myocardial infarction, a hemorrhagic necrosis of finger-tips of hands and legs, and also ears are noted.
Changes of blood are characteristic biochemical: a heavy decompensated metabolic acidosis (pH of blood decreases to 7,0 — 6,8, standard bicarbonate to 2 — 5 mekv/l); concentration of a lactate in blood serum exceeds 16 mg of % (norm of 9 — 16 mg of %).
Treatment includes correction of a metabolic acidosis (intravenous drop administration of 2,5 — 4% of solution of hydrosodium carbonate under control of pH, at its inefficiency — a hemodialysis), carrying out an oxygenotherapy, artificial respiration, intravenous administration methylene blue (2 — 5 mg on 1 kg of weight of the patient), cocarboxylase and B1 vitamin, hemotransfusion, plasmas, purpose of corticosteroids, introduction of small doses of insulin under control of a sugar content in blood.
Forecast depends on a basic disease, at a giperlaktatsidemichesky coma — adverse.
Prevention consists in careful overseeing by a condition of patients with a diabetes mellitus, especially for patients with associated diseases of kidneys, a liver, cardiovascular system, at accession inf. diseases, and also for patients, it is long accepting guanyl guanidines.
The hereditary lactacidemia
Is described so-called hereditary L. - and., shown at early children's age heavy acidosis with the expressed respiratory disturbances (see. Breath, pathology ). In literature there is no unity of opinion on whether it is manifestation true enzymopathies or its essence comes down to genetically caused delay of maturing of fermental systems.
From the first days of life at children disorder of breath — a polypnea, dispnoe, an astmopodobny state is observed. Tendency to acute respiratory diseases is noted; bronchial pneumonia at them proceed inertly. Attacks dispnoe can be combined with dehydration and a coma. The spasms which are usually not connected with respiratory frustration are often observed - At patients the delay of psychomotor development, a hypomyotonia is noted.
The forecast depends on weight of acidosis, a condition of compensatory mechanisms and on timeliness of recognition of a disease. Usually with age there occurs improvement or total disappearance of crises, however also lethal outcomes are described.
Bibliography: Limanskaya G. F. and Shepherd A. K. Lactic acidosis at a diabetes mellitus, Probl, endocrinins., t. 19, No. 4, page 106, 1973, bibliogr.; With z at z at k A. and. lake of The effect of short-term administration of antidiabetic biguanide derivatives on the blood lactate levels in healthy subjects, Diabetologia, Bd 14, S. 89, 1978, Bibliogr.; Gordon E. E. Etiology of lactic acidosis, Amer. J. med. Sci., v. 265, p. 463, 1973; IT u with k a b e e W. E. Lactic acidosis, Amer. J. Cardiol., v. 12, p. 663, 1963; L u f t D., S with h m u 1 - 1 i n g R. M. a. E g g s t e i n M. Lactic acidosis in biguanide-treated diabetics, Diabetologia, Bd 14, S. 75, 1978, Bibliogr.
L. F. Marchenko.