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PubMed1971

[Lactate acidosis].

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Acid-Base Equilibrium↗
PubMed1966

Lactic acidosis.

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Acidosis↗
PubMed1971

Non-ketotic hyperosmolar coma with insulin resistance in a 12-year-old girl.

Although the frequency of recognition of the syndrome of non-ketotic hyperosmolar coma is increasing in all age groups the mortality rate remains high. This paper reports the occurrence of this syndrome in a 12-year-old girl. The pathogenesis is discussed and a planned approach to the management of circulatory collapse, hypokalemia, hyperglycemia and hyperosmolarity over the initial 24 hours is proposed. The phenomenon of insulin resistance which was observed in this case is a rare complication of this syndrome. Awareness of the occurrence of this syndrome in all age groups, early recognition of its features and a planned approach to management are mandatory to reduce the very high mortality rate.

Acidosis↗
PubMed1993

Metabolic problems in northeastern Thailand: possible role of vanadium.

Common metabolic problems in northeastern Thailand include renal stone disease, distal renal tubular acidosis, hypokalemic periodic paralysis, sudden unexplained nocturnal death and malnutrition-related diabetes mellitus. There is evidence of decreased activity of Na,K-ATPase and H,K-ATPase. A preliminary study was made of the vanadium concentration in the soil and water in northeastern Thailand. The urinary and tissue vanadium concentrations were also determined in the northeastern villagers. The soil was found to have high vanadium content. The vanadium content was also high in the urine, kidneys and lungs of the villagers. It is postulated that these metabolic problems are attributed to the inhibition of Na,K-ATPase and H,K-ATPase activity by vanadium.

Humans↗
PubMed2006

Continuous non-invasive end-tidal CO2 monitoring in pediatric inpatients with diabetic ketoacidosis.

INTRODUCTION: Pediatric inpatients with diabetic ketoacidosis (DKA) are routinely subjected to frequent blood draws in order to closely monitor degree of acidosis and response to therapy. The typical level of acidosis monitoring is less than ideal, however, because of the high cost and invasiveness of frequent blood labs. Previous studies have validated end-tidal carbon dioxide (EtCO2) monitoring in the emergency department (ED) for varying periods of time. We extend these findings to the inpatient portion of the hospitalization during which the majority of blood tests are sent. METHODS: All patients admitted to an intermediate care unit in (InCU) a large children's hospital were fitted with an appropriately sized oral/nasal cannula capable of sensing EtCO2. Laboratory studies were obtained according to hospital clinical practice guidelines. In a retrospective analysis, EtCO2 values were correlated with serum total CO2 (stCO2), venous pH (vpH), venous pCO2 (vpCO2), and calculated bicarbonate from venous blood gas (vHCO3-). RESULTS: A total of 78 consecutive episodes of DKA in 72 patients aged 1-21 yr were monitored for 3-38 h with both capnography and laboratory testing, producing 334 comparisons. Initial values were as follows, reported as median (range): stCO2, 11 (4-22) mmol/L; vpH, 7.281 (6.998-7.441); vpCO2, 28.85 (9.3-43.3) mmHg; and vHCO3-, 14 (3-25) mmol/L. EtCO2 was correlated well with stCO2 (r = 0.84, p < 0.001), vHCO3- (r = 0.84, p < 0.001), and vpCO2 (r = 0.79, p < 0.001). CONCLUSIONS: These data support the findings of previous studies limited to ED populations and suggest that non-invasive EtCO2 monitoring is a valuable and reliable tool to continuously follow acidosis in the setting of the acutely ill pediatric patient with DKA. Continuous EtCO2 monitoring offers the practitioner an early warning system for unexpected changes in acidosis that augments the utility of intermittent blood gas determinations.

Adolescent↗
PubMed1989

Gluconeogenesis and the protection of hepatic intracellular pH during diabetic ketoacidosis in rats.

Studies were made of the mechanism whereby hepatic gluconeogenesis is increased in diabetic ketoacidosis (DKA) despite evidence in vitro of inhibition of gluconeogenesis by systemic acidosis. In perfused livers taken from normal rats, marked inhibition of lactate uptake and glucose output was achieved by simulation of metabolic acidosis in the perfusate. In perfused livers obtained from animals with DKA, lactate uptake and glucose output were greater than in normal perfused liver at all values of perfusate pH, and it was not possible to demonstrate significant inhibition of gluconeogenesis from lactate by perfusate acidosis. Varying severity of acidosis was induced in rats by (a) HCl infusion, (b) NH4Cl ingestion or (c) experimental DKA. Hepatic intracellular pH (pHi) was measured in vivo by 31P-n.m.r. spectroscopy. Whereas at the severer degrees of systemic acidosis marked falls in hepatic pHi were seen in the HCl- and NH4Cl-treated animals, little fall was seen in rats with DKA. The protection of hepatic pHi in rats with DKA was not due to differences in respiratory compensation compared with the other groups. It is suggested that this protection of hepatic pHi in DKA may be responsible for the failure of acidotic inhibition of gluconeogenesis from lactate. Possible reasons for pHi protection in DKA are considered. There is no difference in hepatic energy status as assessed in vivo by ATP/Pi ratios between control, DKA and NH4Cl-treated rats. DKA rats show a striking decrease in hepatic glycerophosphoethanolamine content.

3-Hydroxybutyric Acid↗
PubMed1991

Renal failure in adult onset hypophosphatemic osteomalacia with Fanconi syndrome: a family study and review of the literature.

Follow-up of a previously reported family with dominantly inherited adult onset hypophosphatemic osteomalacia with Fanconi syndrome and diabetes mellitus has shown that both the proposita and her affected sister have developed renal glomerular failure. We describe the evolution of renal failure in this family and discuss the possible mechanisms involved. The development of renal tubular acidosis in this condition further impairs renal function and we suggest that correction of systemic acidosis might improve renal function and prevent further decline in these patients.

Acidosis, Renal Tubular↗