[Ultrasonic studies of the newborn brain].
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Biomedical subjects
Publications and source records attributed to M Janas.
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A total of 410 proved cases of neonatal septicaemia from seven Finnish hospitals seen between 1976 and 1980 were reviewed. The annual incidence of neonatal septicaemia was 3 per 1000 births, and overall mortality was 23%. Onset was early in most patients. Symptoms of septicaemia occurred within the first 24 hours of life in 44% and within the first week of life in 90%. In the very early onset disease (within 24 hours) mortality was 30%, compared with 17% in all other cases. Group B streptococcus was the leading cause in very early onset disease (52%) but mortality from infection with this organism was similar to that in other very early onset cases. It is concluded that very early onset neonatal septicaemia, probably of intrauterine origin and caused by group B streptococcus in one half of the cases, constitutes the major form of neonatal septicaemia in Finland and should receive the highest priority in preventive measures.
The excretion of sulfadiazine (Adiazin) (n = 8) and sulfafurazole (n = 8) in urine and the risk of crystallization were compared in children, 3-14 years of age. They suffered from acute urinary tract infection and were treated with conventional dosage regimen of either of the sulfonamides. Sulfadiazine (4 mg/kg twice daily, the initial dose 8 mg/kg) produced active serum drug levels which in relation to antimicrobial activity of sulphonamides corresponded to 25-30% of those obtained with sulfafurazole (50 mg/kg four times a day). In urine the corresponding sulfadiazine levels were 21-61% of those of sulfafurazole. In none of the urine fractions sulfadiazine concentrations exceeded the theoretical drug solubility but sulfafurazole exceeded this risk limit altogether in 4 urine fractions (2 patients). Urine sediment showed, however, sulfonamide crystals in only one urine fraction of the sulfafurazole group. The results suggest that with conventional dosage regimen sulfafurazole produces higher effective serum and urine drug concentrations in children than sulfadiazine but shows a higher risk to crystallize in urine.
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Cell-mediated immunity (CMI) was studied in a group of 48 children with urinary tract infections (UTI) using a whole blood micromethod for lymphocyte stimulation in vitro. The patients were subdivided into pyelonephritis group (27 cases) and lower urinary tract infection (LUTI) group (21 cases) on the basis of fever, erythrocyte sedimentation rate, C-reative protein and renal concentration capacity. At the acute stage of infection the lymphocyte responsiveness to leucoagglutinin (LA) and concanavalin A (Con A) was suppressed in both groups, but the suppression was much greater in those with pyelonephritis. By 6 weeks after infection the lymphocyte responses were normal in most but not all cases. We conclude that an acute pyelonephritis is associated with marked suppression of CMI and that the latter can be used as an additional criterion for establishing the level of infection. Patients with UTI did not generally appear to have any primary defect of CMI but when suppression of CMI was present, it seemed secondary to an ongoing infection.
A follow-up study 7--8 years after kanamycin treatment of 83 newborn infants in the Tampere University Central Hospital is described. The Apgar scores ranged from 1 to 10, about half of the patients being premature. Only in 1 case (1.2%) a slight bilateral high-tone loss was found. This patient's birth had been complicated by ablation of the placenta with subsequent cesarean section and he had neonatal sepsis as well. The cause of this hearing defect is thus not necessarily the use of kanamycin. Because of the extended use of reserve antibiotics, microorganisms resistant to modern antibiotics may necessitate in some vital cases the use of kanamycin. Our results indicate that, if serum concentrations are monitored adequately, the use of kanamycin does not necessarily result in a hearing defect.
Studies were performed on 79 subjects, out of which 32 belonged to the control group and 47 suffered from glomerulonephritis. The number of T and B lymphocytes in peripheral blood was determined using the technique of E, EA and EAC-rosette tests. Also, the lymphocyte blast response to non-specific mitogens (PHA, Con A, PWM) was established in vitro. Patients suffering from acute proliferative glomerulonephritis, as compared to the control group, displayed a statistically significant increase of lymphocytes with the receptor for complement (EAC-rosettes). Their reactivity to all three mitogens did not differ from the values obtained in the control group. In patients suffering from chronic glomerulonephritis (proliferative, membranous-proliferative, membranous), shiftings in the contents of the peripheral blood lymphocytes pools were of opposite directions, i.e., statistically significant in comparison with the control group. Also an increase in the absolute number of T lymphocytes (E-rosettes) was observed. Generally speaking, the values of blast transformations after mitogen stimulations were smaller in patients suffering from chronic than in those suffering from acute glomerulonephritis. In 1/3 of them, the decrease of blast response to one of the three mitogens was detected. The decrease exceeded the lower limit of values of healthy subjects, and most often, it was connected with Con A stimulation.
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