Acta paediatrica Scandinavica最新文献

Human leukocyte interferon at doses from 2 million units every two days to 3 million units daily was given to a 2-year-old boy for the treatment of recurrent juvenile laryngeal papilloma. After 7 months of treatment the child developed spastic diplegia, which persisted despite the discontinuation of interferon therapy. The clinical picture was consistent with an upper motor neuron lesion; no evidence of peripheral neuropathy was found.

The aim of the present investigation was to study volume, pH and the levels of gastrin- and somatostatin-like immunoreactivity in gastric aspirates obtained immediately after birth from 25 healthy infants. In addition, the same parameters were measured in amniotic fluid collected from 11 of the mothers. The median volume of the gastric contents was 4 ml (range 0-11) and median pH was 6.96 (range 2.77-9.58). Gastrin and somatostatin median concentrations were 8 pM (range 0-52) and 67 pM (range 15- greater than 1,000), respectively. The corresponding levels in amniotic fluid were 8.2 +/- 3.6 pM and 28.4 +/- 5.3 pM, median pH was 9.22 (range 8.05-9.58). There was a significant correlation between volume and pH of gastric contents. The pH of the gastric aspirate was inversely correlated with the somatostatin levels. No correlation could be demonstrated as regards levels in amniotic fluid and gastric content. Gastric content and amniotic fluid were not correlated regarding pH, gastrin and somatostatin. It is suggested that the foetus drinks about 10 ml portions of amniotic fluid which are gradually emptied from the stomach and that these drinking episodes are associated with gastric exocrine and endocrine secretion normally seen following feeding after birth.

Hypoglycaemia (blood glucose 1.3-2.5 mmol/l) was induced in twenty-eight diabetic children by reduction of their morning meal. Fatigue and pallor were the most common signs of hypoglycaemia. Compared to findings during normoglycaemia, plasma concentrations of adrenalin, noradrenalin and cortisol were significantly higher at glucose nadir. Plasma glucagon concentration at glucose nadir was correlated to the fasting C-peptide concentration and inversely to the duration of diabetes. Children who lacked C-peptide also lacked glucagon response to hypoglycaemia. The parents' opinion of the need to give carbohydrates corresponded to the blood glucose level. The presence of adrenergic signs correlated to the plasma adrenalin and the neuroglucopenic signs to blood glucose. The lowest glucose level correlated inversely to the concentration of free insulin. When facilities for glucose infusion are lacking, a rational step in treating the unconscious hypoglycaemic child seems to be the injection of glucagon, considering the blunted or absent glucagon secretion.

The occurrence of circulating class II antigen-expressing T lymphocytes was examined in 25 children with insulin-dependent diabetes mellitus using an indirect double immunofluorescence assay on prefixed cell samples. In order to exclude sensitization to heterologous insulin as a possible factor affecting the results, the patients were investigated at the day of clinical onset, before receiving insulin. An increased percentage of T cells (CD3+ cells) expressing class II antigens was seen in 19 out of 25 patients and class II expression was observed on cells within both the CD4+ and CD8+ T cell subsets. No correlation was found between the levels of class II expressing T cells and the individual degree of metabolic derangement or indicators of recent infection. Re-testing of 16 patients after one year on insulin treatment revealed a significant decrease of class II expressing T cell levels. Our data suggest that the increased levels of class II expressing T cells seen in IDDM of recent onset directly reflects immune reactions that are related to the disease process.

Hypoglycaemia (blood glucose 1.3-2.5 mmol/l) was induced in thirty diabetic children by reduction of their morning meal. Glucagon, 10 or 20 micrograms/kg was then given by intramuscular or subcutaneous injection. Ten min later, all signs of hypoglycaemia had disappeared and blood glucose concentrations increased by 0.7-3.3 mmol/l. Glucagon plasma concentrations at glucose nadir were low, 23 +/- 8 pmol/l, rose to 300 +/- 42 ten min after the injection and reached peak values after another ten min. Later, a slow decrease was noted. No significant difference of blood glucose or plasma glucagon concentrations were found after subcutaneous or intramuscular injections of 20 micrograms/kg. After 10 micrograms/kg, slightly lower increase of blood glucose was seen, but the clinical effect was equally good. Nausea occurred in four children given 20 micrograms/kg. The rise of blood glucose did not correlate to the peak glucagon concentration obtained after the injection but showed significant correlations to the lowest glucose concentration and, inversely, to the concentration of free insulin in blood at glucose nadir. It is concluded that glucagon injections are effective in hypoglycaemia in insulin-treated diabetic children and that the injection of 10-20 micrograms/kg gives long-standing supraphysiological concentrations which make repeated injections unnecessary.