Lactic acidosis

Oliva, Philip B.

doi:10.1016/0002-9343(70)90117-8

Cited by 221 publications

(71 citation statements)

References 203 publications

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“…arterial pH<7.3) due to an increase in the blood con centration of lactic acid (i.e.>2.0mEq/liter). However, Oliva (6) reported that the concentration of lactic acid of arterial blood increased to 8.0-22mEq/liter (13-to 36-fold higher than normal) during exercise. Oliva (6) also reported that the concentration of lactic acid of arterial blood was increased 3.2-to 56.6-fold in cardiovascular failure, 4.9-to 6.5-fold in acute hypoxemia, more than 3.1-fold in severe anemia, 20-to 40-fold in leukemia, and 17-to 50-fold in diabetes mellitus.…”

Section: Discussionmentioning

confidence: 98%

Effect and fate of orally administered lactic acid in rats.

Morotomi

Sakai

Yazawa

et al. 1981

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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Section: Discussionmentioning

confidence: 98%

Effect and fate of orally administered lactic acid in rats.

Morotomi

Sakai

Yazawa

et al. 1981

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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“…In lactic acidosis, a remarkable increase (more than 10 times) of plasma amino acid levels is noted, especially alanine, a-aminobutyric acid and proline (Oliva 1970). Consequently, hyperaminoacidemia due to hypoglucagonemia in patients with CP is supposed to differ from lactic acidosis.…”

Section: Discussionmentioning

confidence: 99%

Increased Plasma Gluconeogenic and System A Amino Acids in Patients with Pancreatic Diabetes due to Chronic Pancreatitis in Comparison with Primary Diabetes.

Nakamura

Takebe

Kudoh

et al. 1994

Tohoku J. Exp. Med.

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We examined the plasma amino acid profiles of 17 patients with pancreatic diabetes in comparison with those of 14 healthy subjects and 16 patients with primary diabetes of similarly poor glycemic control. We also measured fasting plasma glucagon and free insulin levels in patients with pancreatic diabetes and in those with primary diabetes. The fasting plasma amino acid level was highest in patients with pancreatic diabetes. Furthermore, the plasma glucagon level in patients with pancreatic diabetes was significantly low, and negative correlations were found between glucagon and glucagon-related System A and gluconeogenic amino acids. On the other hand, the levels of branched-chain amino acids (BCAA) and System L amino acids, which are subjected to change in the state of diabetes mellitus, increased in patients with pancreatic diabetes. From the above results, we determined that the amino acid profile in patients with pancreatic diabetes resembled that in patients with total pancreatectomy. It is our opinion that the increases of amino acid levels (gluconeogenic and System A amino acids) in patients with pancreatic diabetes is not dependent on maldigestion/malabsorption under treatment, but is mainly dependent on glucagon deficiency. gluconeogenic and system A amino acids; pancreatic diabetes; hypoglucagonemia With regard to the relationship between amino acid metabolism and chronic pancreatitis, the following three points can be considered; 1) Abnormalities of amino acids as a cause of hereditary familial pancreatitis among chronic pancreatitis sufferers (Gross et al. 1957), 2) possible change in plasma amino acid profile due to malnutrition caused by maldigestion resulting from chronic pancreatitis and 3) abnormal amino acid metabolism due to secondary diabetes

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“…The anion gap was 40 mEq/1 in case 2; the existence of ketones probably constituted a part of this anion gap. The serum lactate, measured by the enzymatic method, was elevated in repeated measurements, reaching a maximum of 6.5 mEq/1 in ease 1 and 17 mEq/1 in case 2 [9].…”

Section: I Etiologymentioning

confidence: 91%

The treatment of lactic acidosis in the diabetic patient by peritoneal dialysis using sodium acetate. A report of two cases

Hayat

1974

Diabetologia

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Lactic acidosis

Cited by 221 publications

References 203 publications

Effect and fate of orally administered lactic acid in rats.

Effect and fate of orally administered lactic acid in rats.

Increased Plasma Gluconeogenic and System A Amino Acids in Patients with Pancreatic Diabetes due to Chronic Pancreatitis in Comparison with Primary Diabetes.

The treatment of lactic acidosis in the diabetic patient by peritoneal dialysis using sodium acetate. A report of two cases

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