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This article was published in the following journal.
Name: BMJ (Clinical research ed.)
Blix et al. found in a recent meta-analysis (MA) that intrapartum fetal surveillance with ECG ST analysis (STAN) results in a significant 36% decrease in metabolic acidosis at birth compared to cardi...
Treatment of metabolic acidosis using sodium bicarbonate solutions is safe when blood gas analysis is available. The evidence that solutions containing metabolisable buffers can be used as an alternat...
Ischemia/reperfusion (I/R) injury and metabolic acidosis (MA) are two critical conditions that may simultaneously occur in clinical practice. The result of this combination can be harmful to the kidne...
To determine the severity, duration, and contributing factors for metabolic acidosis after deep hypothermic circulatory arrest (DHCA).
The purpose of the present study is to compare the adjunct treatment of metabolic or mixed severe acidosis in the critically ill using Sodium Bicarbonate as a buffer to increase the plasma...
Metabolic acidosis is a common complication that patients experience in the early postoperative period following cardiac surgery. Increasingly, the composition and volume of intravenous fl...
Metformin is the first line drug of choice for the treatment of type II diabetes. Lactic acidosis can develop as a side effect, especially when renal failure leads to drug accumulation. La...
This is a double-blind, placebo-controlled, parallel-design, 4-arm, fixed dose study. The study will enroll up to 100 adult male and female subjects with Stage 3 or 4 chronic kidney diseas...
This is a study to determine the safety of dichloroacetate (DCA) with a low-tyrosine diet given with or without nitisinone (NTBC) in children with chronic lactic acidosis (CLA).
A group of genetic disorders of the KIDNEY TUBULES characterized by the accumulation of metabolically produced acids with elevated plasma chloride, hyperchloremic metabolic ACIDOSIS. Defective renal acidification of URINE (proximal tubules) or low renal acid excretion (distal tubules) can lead to complications such as HYPOKALEMIA, hypercalcinuria with NEPHROLITHIASIS and NEPHROCALCINOSIS, and RICKETS.
Acidosis caused by accumulation of lactic acid more rapidly than it can be metabolized. It may occur spontaneously or in association with diseases such as diabetes mellitus, leukemia, or liver failure.
A congenital or acquired condition of insufficient production of ALDOSTERONE by the ADRENAL CORTEX leading to diminished aldosterone-mediated synthesis of Na(+)-K(+)-EXCHANGING ATPASE in renal tubular cells. Clinical symptoms include HYPERKALEMIA, sodium-wasting, HYPOTENSION, and sometimes metabolic ACIDOSIS.
An inherited metabolic disorder caused by deficient enzyme activity in the PYRUVATE DEHYDROGENASE COMPLEX, resulting in deficiency of acetyl CoA and reduced synthesis of acetylcholine. Two clinical forms are recognized: neonatal and juvenile. The neonatal form is a relatively common cause of lactic acidosis in the first weeks of life and may also feature an erythematous rash. The juvenile form presents with lactic acidosis, alopecia, intermittent ATAXIA; SEIZURES; and an erythematous rash. (From J Inherit Metab Dis 1996;19(4):452-62) Autosomal recessive and X-linked forms are caused by mutations in the genes for the three different enzyme components of this multisubunit pyruvate dehydrogenase complex. One of the mutations at Xp22.2-p22.1 in the gene for the E1 alpha component of the complex leads to LEIGH DISEASE.
Disorders affecting amino acid metabolism. The majority of these disorders are inherited and present in the neonatal period with metabolic disturbances (e.g., ACIDOSIS) and neurologic manifestations. They are present at birth, although they may not become symptomatic until later in life.