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Biomedical subjects

J Fernandes

Publications and source records attributed to J Fernandes.

At least 127 records · Page 7Linked to original sources
PubMed1980

Diagnostic value of sucrose tolerance test in children evaluated by breath hydrogen measurement.

An oral sucrose tolerance test was performed in a group of 103 children, aged between 3 months and 15 years because of episodic diarrhea and/or abdominal pains. Sucrose malabsorption defined as an abnormal increase in expired hydrogen, was found in only 3 children who suffered from congenital sucrase-isomaltase deficiency. This 1% incidence of sucrose malabsorption was lower than the incidence of lactose malabsorption found in this group (33%). Mean rise in blood glucose during the sucrose test was higher (3.4 +/- 1.4 vs. 2.4 +/- 1.2 mmol/l, p less than 0.0001) and the occurrence of false flat blood glucose curves was lower (3% vs. 12.8%, p less than 0.05) than during the lactose test. These findings are consistent with the higher sucrase activity in the small bowel mucosa compared to lactase. In contrast to the lactose tolerance test, sucrose tolerance test should not be used as a screening procedure for secondary disaccharidase deficiency in children.

Adolescent↗
PubMed1980

Sugar malabsorption in healthy neonates estimated by breath hydrogen.

Carbohydrate malabsorption in 110 healthy, term neonates was studied by estimating expired hydrogen (H2) before and after a feed on day 6 or 7. Carbohydrate malabsorption was assumed to be present if the infant excreted > 20 parts per million (ppm) H2. The frequency of carbohydrate malabsorption in 49 breast-fed infants was 25% (n = 12), in 35 infants fed a 7.5% lactose formula it was 31% (n = 11), in 26 infants fed a formula containing 1% lactose and 7.3% maltodextrin it was 15% (n = 4). These differences in frequency were not significant. Peak H2 concentration of the malabsorbers in each group, indicating the degree of carbohydrate malabsorption, was 64, 52, and 32 ppm respectively. The degree of carbohydrate malabsorption did not differ significantly between the breast-fed and the high lactose formula groups, but both groups differed from the low lactose group. H2 excretion was studied for 5 months in an exclusively breast-fed infant. In the first 2 months high concentrations were found and the infant produced 3-5 stools a day. In the next 3 months however, most H2 estimations were normal and only 1-2 stools a week were passed. With the introduction of solids, daily bowel movements promptly reoccurred. Frequency of carbohydrate malabsorption in newborn infants is fairly high and is primarily related to the lactose intake. The frequency and degree of carbohydrate malabsorption were comparable in breast-fed infants and in infants fed on a high lactose formula; this differs from results previously reported.

Bottle Feeding↗
PubMed1979

Folic acid dependent hypersarcosinaemia.

Hypersarcosinaemia is a rare inborn error of metabolism, caused by a deficiency of the sarcosine dehydrogenase complex with tetrahydrofolate as a formaldehyde acceptor needed for the sarcosine-glycine conversion. Prolonged therapy with folic acid on a hypersarcosinaemic patient resulted in a significant effect on the urinary excretion of sarcosine, leading to the conclusion that the patient has a folic acid dependent hypersarcosinaemia.

Amino Acid Metabolism, Inborn Errors↗
PubMed1979

Nocturnal gastric drip feeding in glucose-6-phosphatase deficient children.

UNLABELLED: Six patients with glucose-6-phosphatase deficiency were treated for 12 hr at night with gastric drip feeding (GDF), containing soy milk plus glucose, dextrimaltose, and starch. An alarm system (thermistor), connected to the gastric tube, was devised in case of displacement of the tube by the child. The effects of GDF were as follows. Base deficit and lacticaciduria decreased, but did not normalize. Serum cholesterol levels tended to normalize, but serum triglycerides remained elevated. The hepatic and extrahepatic components of plasma lipoprotein lipase were measured separately 5 and 40 min after iv heparin injection. Hepatic triglyceride lipase activities which were subnormal to normal increased to the lower normal range. Extrahepatic lipoprotein lipase activities, though increasing after GDF, remained abnormally low. Catch-up growth occurred in all four growth-retarded children. The pronounced liver enlargement of the five patients, not previously treated with GDF, decreased markedly. SPECULATION: Nocturnal GDF in glucose-6-phosphatase deficient children, suppresses the tendency for hypoglycemia and acidosis which are causes for stress, catabolism, and anorexia. By suppressing these factors, GDF promotes anabolism and caloric intake, thus accounting for the catch-up growth seen in the patients with growth retardation.

Child↗
PubMed1978

Zinc content of intravenous solutions.

The zinc, copper, and selenium content of commonly used intravenous solutions, aminoacid solutions, and fresh-frozen plasma was determined by atomic absorption spectrometry and fluorimetry. Very small amounts of copper and variable, but substantial, amounts zinc were present in all solutions tested. Zinc contamination could have come from the rubber stoppers for the glass bottles. Selenium could not be detected in any of the solutions. Fresh-frozen plasma contained high levels of zinc and physiological amounts of copper and selenium.

Copper↗
PubMed1978

Respiratory hydrogen excretion as a parameter for lactose malabsorption in children.

Respiratory hydrogen excretion was measured during tolerance tests with lactose, glucose plus galactose, and skim milk in 52 children, 4 to 15 years of age. Ten children appeared to be lactose-malabsorbers, as reflected by increased respiratory hydrogen excretion after administration of 2 g lactose per kilogram, maximum 50 g. Skim milk, equivalent to 0.5 g lactose per kilogram was administered to all lactose-malabsorbers. Eight children were tolerant and two children were "intolerant" for this physiological amount of lactose when administered as skim milk. Disaccharidase activities of jejunal biopsies were determined in all 10 children with lactose malabsorption. Lactase activity was deficient in nine children and normal in one child. The increase of blood glucose during the lactose tolerance test did reflect lactose malabsorption less accurately than the respiratory hydrogen excretion.

Adolescent↗
PubMed1978

Improved accuracy of lactose tolerance test in children, using expired H2 measurement.

Expired hydrogen and blood glucose were measured during an oral lactose tolerance test in 163 children aged between 9 months and 14 years. Lactose malabsorption, defined as an abnormal increase in expired H2 during a lactose tolerance test, was found in 54 children. Of these, 30 were found to be lactose intolerant as the increased expired H2 was accompanied by clinical symptoms. The other 109 children, in whom there was no rise in expired H2, were assumed to have normal lactose absorption. In children with lactose intolerance the increase in expired H2 tended to occur earlier after lactose ingestion than in children with malabsorption. The mean value of the rise in blood glucose was 2.4 mmol/100 ml) in the lactose-tolerant children and 1.0 mmol/1 (18 mg/100 ml) in the lactose-intolerant ones. Although this difference is significant (p less than 0.001), the rise in blood glucose, in predicting the correct diagnosis, was wrong in 13% of cases in the lactose-tolerant group, and wrong in 37% in the lactose-intolerant group (95% confidence limits 9-19% and 22-53% respectively). It is concluded that a rise in blood glucose, whether or not of more that 1.2 mmol/1 (22mg/100 ml) is of little help in differentiating lactose tolerance from intolerance.

Adolescent↗
PubMed1977

Deep venous thrombosis in patients having aorto-iliac reconstruction.

The 125I-labelled fibrinogen test has been used to assess the incidence of deep venous thrombosis in 88 patients who had undergone elective aorto-iliac reconstruction. Deep venous thrombosis was detected in 18 (20.5 per cent). The results suggest that these patients merit prophylaxis.

Adult↗
PubMed1977

The effect of cholestyramine on serum lipids and platelet aggregation of hypercholesterolemic children (type II A) while on high linoleic acid diet.

25 children with familial hypercholesterolemia (type II A) were treated with cholestyramine or placebo in a cross over study during 2 periods of each 10 weeks. The medication was added to a high linoleic acid diet, which had been started at least 1 year earlier. Serum lipids and platelet aggregation were investigated at the end of the 2 periods. On cholestyramine, serum cholesterol levels decreased significantly, whereas the linoleate and oleate content of cholesterylesters and serum triglycerides did not change systematically. Platelet aggregation time, measured with a filtragometer, did not systematically change either.

Adolescent↗
PubMed1976

Isoenzyme pattern of phosphorylase in white blood cells and fibroblasts from patients with liver phosphorylase deficiency.

Isoenzyme patterns of phosphorylase in white blood cells and cultured fibroblasts of a patient affected with liver-type phosphorylase deficiency were studied. Three bands were observed with electrofocusing of white blood cells and liver from controls. In the white blood cells of the patient only two bands were observed. Patient and control fibroblasts showed two bands, probably identical to the two bands observed in the patient's white blood cells. These results indicate that the liver-type phosphorylase is not expressed in the cultured fibroblasts.

Brain↗
PubMed1976

Urinary lactate excretion in normal children and in children with enzyme defects of carbohydrate metabolism.

Urinary lactate was analyzed in 53 normal children, 7 children with glucose-6-phosphatase-deficient glycogenosis, 1 child with fructose-1,6-diphosphatase deficiency and 1 child with pyruvate dehydrogenase deficiency. Lactate in 24-h urine was expressed as concentration, total excretion, excretion per kg body weight and per 1.73 m2 body surface, and as lactate/creatinine quotient. Of these parameters, the lactate concentration in 24-h urine showed the smallest variation in normal children (0.155 +/- 0.053 mM), whereas in patients with one of the above mentioned enzymopathies 10-300-fold elevations were found. The lactate/creatinine quotient, normal range 0.010 to 0.058 (mM/mM) was also used to correct for unnoticed losses of urine. Both parameters, used in conjunction with blood lactate analysis, are suitable for a first screening of patients with enzymopathies of carbohydrate metabolism, and for the follow-up study of the steady or unsteady state of the patient with an enzyme defect of carbohydrate metabolism.

Body Surface Area↗