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At least 595 records · Page 33Linked to original sources
PubMed1991

[Hyperchloremic acidosis in metabolic acidosis with anion gap excess. Comparison with diabetic ketoacidosis].

The occurrence of hyperchloremia during diabetic ketoacidosis (DKA) recovery and the lack of correlation between anion gap excess (delta AG) and bicarbonate deficit (delta TCO2) on admission suggest an hyperchloremic acidosis (HCLA) component. The hypothesis that this phenomenon is not specific of DKA and can occur in other metabolic acidoses with increased anion gap was tested. HCLA component, defined by the ratio delta AG/delta TCO2 less than or equal to 0.80, was evaluated on admission and during therapy in 31 patients with DKA and 53 patients with non diabetic metabolic acidosis (ND-MA). HCLA component prevalence was similar on admission (32 p. 100 for DKA versus 41 p. 100 for ND-MA), but it increased during therapy only in DKA patients (86 p. 100 at 9 h - P less than 0.001). In view of the significant correlation (r = 0.636; P less than 0.001) observed between delta AG/delta TCO2 and creatinine, kidney acid base defense appears clearly in DKA patients: the more severe the volume depletion, the greater the ketone retention and the less prominent the HCLA. This phenomenon seems to be secondary to a large tubular excretion of ketones. In the 53 ND-MA patients no correlation between delta AG/delta TCO2 and creatinine could be found. A transfer of chloride from cells to the extracellular space secondary to intracellular diffusion of lactate ions could explain the HCLA component.

Acid-Base Equilibrium↗
PubMed1982

Anion and osmolal gaps in the diagnosis of methanol and ethylene glycol poisoning.

The diagnostic value of determination of the anion and osmolal gaps was studied in 6 patients poisoned with methanol and in 5 poisoned with ethylene glycol. Increased osmolal gap was present on admission in all patients, whereas increased anion gap was present in all except one. In the methanol-poisoned patients the mean blood values were: pH 7.27, anion gap 24 mmol/l, osmolal gap 81 mosmol/kg H2O, methanol 67 mmol/l, ethanol 11 mmol/l and in the ethylene glycol-poisoned patients: pH 6.93, anion gap 38 mmol/l, osmolal gap 35 mosmol/kg H2O and ethylene glycol 24 mmol/l. In the absence of alcoholic acidosis or diabetic coma the finding of a simultaneous increase in both the anion and osmolal gaps indicates methanol or ethylene glycol poisoning. Thus determinations of the anion and osmolal gaps are mandatory whenever facing metabolic acidosis of unknown etiology.

Acid-Base Equilibrium↗
PubMed1988

Glucose and lactate turnover and gluconeogenesis in chronic metabolic acidosis and alkalosis in normal and diabetic dogs.

The turnover rate of glucose, the irreversible disposal rate of lactate, and the rate of gluconeogenesis from lactate were calculated by tracer methods in four normal and four alloxan-diabetic dogs under control conditions as well as in chronic, stable metabolic acidosis and alkalosis. Acidosis was produced by feeding dogs 0.8-1 g.kg-1.day-1NH4Cl over 1 week, alkalosis was produced by feeding dogs a chloride-free diet and injections of furosemide. Mean plasma pH in the three states were 7.28 +/- 0.013, 7.40 +/- 0.024, and 7.51 +/- 0.015 in normal dogs, and 7.22 +/- 0.025, 7.42 +/- 0.009, and 7.49 +/- 0.002 in the diabetic dogs. Respective mean plasma bicarbonate levels were 14.6 +/- 0.88, 22.0 +/- 0.80, and 32.4 +/- 1.88 mequiv. in normal dogs, and 12.3 +/- 1.30, 22.6 +/- 0.66, and 35.0 +/- 1.14 mequiv. in diabetic animals. In normal dogs shifts in acid-base balance had no effect on the level of plasma glucose or the turnover rate of glucose. In diabetic dogs plasma glucose level was significantly elevated by alkalosis. Plasma lactate was positively correlated with plasma pH (r = 0.69, p less than 0.01) and was in general higher in diabetic than in normal animals. The increment in concentration was due to a decreased clearance of lactate from the plasma. The irreversible disposal rate was not changed by the acid-base status. Whereas a larger fraction of lactate removed from the plasma appeared in glucose in diabetic animals, this fraction was not changed significantly by shifts in the acid-base status.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMedDate not supplied

Effect of fluctuations in albumin on serum fructosamine assay.

Serum fructosamine, albumin and plasma glucose were studied in eight patients during recovery from diabetic ketoacidosis, and in eight patients with "decompensated" diabetes without acidosis. In the ketoacidotic group, serum fructosamine had fallen significantly by a mean of 12% by 8h, and fell further during the remainder of the study. A smaller but significant fall in fructosamine (mean 6.1%) was seen in the decompensated group after only 18 h, with again a further fall thereafter. These changes in serum fructosamine were accompanied by decreases in serum albumin. However, when fructosamine was corrected by calculating a fructosamine/albumin index (FAI) (fructosamine X 100/albumin), the FAI did not change significantly in either group until a small reduction was noted in the ketoacidotic group at 5 days, which might reasonably be expected as an index of intermediate-term glycaemia. Therefore minor fluctuations in albumin levels seen in diabetic patients can affect fructosamine, and correction may be be advisable for the test to be a valid measure of glycosylated serum proteins.

Acidosis↗
PubMed1977

Somatostatin. Its possible role in carbohydrate homeostasis and the treatment of diabetes mellitus.

Somatostatin, a peptide inhibitor of growth hormone release originally isolated from the hypothalamus, is also present in D cells of pancreatic islets. Its ability to inhibit the secretion of insulin and glucagon suggests that it may be a local regulator of pancreatic A- and B-cell function. Studies using synthetic somatostatin have provided evidence that glucagon is a physiologically important hormone that exacerbates the consequences of insulin deficiency in human diabetes mellitus. The ability of somatostatin to diminish both fasting and post-prandial hyperglycemia and to forestall the development of ketoacidosis after withdrawal of insulin in insulin-dependent diabetics suggests a potential therapeutic use of this agent in diabetes. Presently, however, its short half-life and diverse actions preclude such use and have prompted the search for more specific and longer-acting analogs.

Acidosis↗
PubMed1981

Interorgan relationships for glutamine metabolism in normal and acidotic rats.

The interorgan relationships for glutamine were investigated in normal, chronically acidotic, and diabetic ketoacidotic rats. In the normal rat, muscle tissue is the major site that releases glutamine into the circulation, and the nonhepatic splanchnic bed (mainly gut) is the major site of glutamine uptake. The liver of normal, postabsorptive rats takes up glutamine also. The kidneys have no significant affect on circulating glutamine in normal rats. In chronic NH4Cl and HCl acidosis, muscle glutamine release doubles. In addition, the liver decreases glutamine uptake and releases glutamine into the circulation. Muscle and liver supply, respectively, about 55 and 45% of the increased glutamine demand of the kidneys during chronic acidosis. No significant changes could be detected in the nonhepatic splanchnic bed during acidosis. In diabetic ketoacidotic rats, the increased demand for glutamine by the kidneys is almost entirely supplied by muscle. No significant changes occur in liver or nonhepatic splanchnic bed.

Acidosis↗
PubMed1981

Serum potassium concentration in acidemic states.

It has been generally accepted that acidosis results in hyperkalemia because of shifts of potassium from the intracellular to the extracellular compartment. There is ample clinical and experimental evidence, however, to support the conclusion that uncomplicated organic acidemias do not produce hyperkalemia. In acidosis associated with mineral acids (respiratory acidosis, end-stage uremic acidosis, NH4Cl-or CaCl2-induced acidosis), acidemia per se, results in predictable increases in serum potassium concentration. In acidosis associated with nonmineral organic acids (diabetic and alcoholic acidosis, lactic acidosis, methanol and the less common forms of organic acidemias secondary to methylmalonic and isovaleric acids, and ethylene glycol, paraldehyde and salicylate intoxications), serum potassium concentration usually remains within the normal range in uncomplicated cases. A number of factors, however, may be responsible for hyperkalemia in some of these patients other than the acidemia per se. These include dehydration and renal hypoperfusion, preexisting renal disease, hypercatabolism, diabetes mellitus, hypoaldosteronism, the status of potassium balance, and therapy. The mechanism(s) of this differing effect of mineral and organic acidemias on transmembrane movement of potassium remains undefined. The prevalent hypothesis, however, favors the free penetrance of the organic anion into cells without creating a gradient for the hydrogen ions and, thus, obviating the efflux of intracellular potassium. The importance of the presence of hyperkalemia in clinical states of organic acidemias is obvious. A search for the complicating factors reviewed above should be undertaken since organic acidemias per se, should not be expected to be accompanied by elevations of serum potassium concentration. Moreover, the classical teaching that the absence of hyperkalemia during severe acidosis is indicative of severe potassium deficiency, may not be universally valid in patients with uncomplicated organic acidemias.

Acidosis↗