Abstracts
Bartter Syndrome
Bartter Syndrome
On August 3, 1979, MMWR published a report about infants with a Bartter-like syndrome that was associated with use of one brand of a soy-based formula. This episode prompted the Infant Formula Act of 1980, which was the first in a series of major legislative and regulatory steps taken to insure the safety of infant formulas.
Three cases of a Bartter-like syndrome in infants were reported to CDC from Memphis, Tennessee, on July 26, 1979. The infants were less than 10 months of age and were failing to gain weight. They had poor appetites, and one had a history of constipation. All were hypochloremic and hypokalemic, with varying degrees of alkalosis and microhematuria. The 3 infants were taking the same brand of soy-based formula.
To further investigate this possible association, CDC surveyed a sample of pediatric nephrologists throughout the country for cases of metabolic alkalosis diagnosed since January 1, 1979, in infants with a history of failure to thrive, anorexia, or constipation. Infants known to have pyloric stenosis, cystic fibrosis, or diuretic therapy were excluded.
An additional 15 cases were ascertained through the survey, and another 16 cases were determined from other sources. Cases were scattered throughout the country. The infants ranged in age from 2 to 9 months; none died. There was no unusual sex distribution.
Feeding history was available in 27 of the 31 cases. Of these, 26 were on Neo-Mull-Soy (Syntex, Palo Alto, California), the same formula used by the 3 index cases. Neo-Mull-Soy represents 10%-12% of the soy-based formula market. After diagnosis of the alkalosis, infants who were placed on chloride supplement responded favorably; those who, after treatment for and recovery from the alkalosis, went back on the formula - but without chloride supplementation - had a recurrence.
Bartter syndrome is characterized by hypochloremic, hypokalemic alkalosis; normal blood pressure; and increased serum levels of renin and aldosterone. The onset is usually during the first year of life. The pathogenesis is not known.
Insufficient intake of chloride is a known cause of metabolic alkalosis. The cause of this outbreak is not yet clear, but it is possible that the chloride concentration in this formula falls below the daily requirement for infants, if they are not also receiving chloride from other dietary sources. The current tendencies to delay the addition of solids to infants' diets and to remove sodium chloride from commercial and home-prepared baby foods might be additional contributing factors.
There are no regulations pertaining to the optimal level of chloride in infant formulas. The Committee on Nutrition of the American Academy of Pediatrics recommends a minimum of 11 milliequivalents per liter in infant formula.
The children who had hypochloremic metabolic alkalosis as the result of consuming chloride-deficient formula quickly recovered following treatment with small doses of potassium chloride. This clinical response provided a clue to the physician who reported the first three cases that the formula might be the cause of the metabolic alkalosis.
Committee on Nutrition, American Academy of Pediatrics: Commentary on breast-feeding and infant formulas, including proposed standards for formula. Pediatrics 57:278-285, 1976.
Calcium Loading (Alkalosis)
Calcium Loading
The oral "calcium" (Ca) load test ("overflow model") has been applied to estimate the enteral absorbability of Ca "salts" in humans; provided that the deep "bone" compartments are filled up, excess Ca should be excreted in the urine.
Three Ca salts were tested in rats at increasing oral doses of 0 to 14 mmol/kg body weight: CaCO3 and two other compounds containing "chloride" at a Ca:Cl ratio of 1:2 (CaCl2) and 1:1 (Ca-aspartate-hydrochloride).
The carbonate was poorly absorbed and hence did not significantly affect acid-base "metabolism" nor urine pH. Both chloride-containing salts increased Ca excretion to a significantly higher degree in a dose-dependent manner; in contrast to the organic compound, the CaCl2 induced "metabolic" "acidosis" at 14 mmol/kg body weight.
Thus, acid-base alterations must be considered when evaluating the oral load test.
Studies on volunteers reported in the literature suggest, however, that this effect is not relevant for humans.
Classen-HG et al: Different effects of three high-dose oral calcium salts on acid-base metabolism, plasma "electrolytes" and urine parameters of rats. Methods-Find-Exp-Clin-Pharmacol. 1995 Sep; 17(7): 437-42.
Hypophosphatemia (Alkalosis)
Hypophosphatemia
Severe hypophosphatemia is rare, usually affecting chronic "alcoholics" and patients under total "parenteral" "nutrition". The most important clinical features are rhabdomyolysis and neurological deficits.
Complete recovery occurred after adequate substitution of "phosphate".
Zurkirchen-MA et al: [Reversible neurological complications in chronic "alcohol" abuse with hypophosphatemia]. Schweiz-Med-Wochenschr. 1994 Oct 15; 124(41): 1807-12
Sodium Lactate i.v.
Sodium Lactate i.v.
Hyperglycemia and an increased ventilatory demand secondary to an increased CO2 production are frequent undesirable effects of total parenteral nutrition (TPN) in critically ill patients. This study was performed to assess whether sodium lactate as a metabolic substrate may affect these variables.
Compared with TPN-glucose, TPN-lactate decreased glycemia by 20%, insulinemia by 43%, net carbohydrate oxidation (assessed from indirect calorimetry) by 34%, and plasma glucose oxidation (assessed from 13CO2) by 54%. Respiratory oxygen exchange were increased by 3.7% due to a 20% thermic effect of lactate, but respiratory CO2 exchanges did not change. Pao2 decreased by 11.3 mm Hg, indicating that the increased O2 consumption was not matched by an appropriate increase in spontaneous ventilation. Arterial pH increased from 7.41 +/- 0.04 to 7.46 +/- 0.05.
Sodium lactate as a metabolic substrate limits hyperglycemia but induces metabolic alkalosis and does not spare the ventilatory demand.
Chioléro R et al., Metabolic and respiratory effects of sodium lactate during short i.v. nutrition in critically ill patients. JPEN J Parenter Enteral Nutr, 1996 Jul-Aug, 20:4, 257-63.
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