Androstenedione (A-dione) and 17-hydroxyprogesterone (17-OHP) levels were measured in matched samples of saliva and of plasma collected from patients with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency (eight patients) and 11-hydroxylase deficiency (one patient). Positive correlations were found between salivary and plasma values of either steroid with correlation coefficients of 0.968 for A-dione and 0.935 for 17-OHP. All five inadequately treated patients with 21-hydroxylase deficiency had greatly elevated plasma and salivary 17-OHP concentrations compared to values in age matched controls. In two of three well controlled patients plasma 17-OHP levels were less than 40 nmol/liter and salivary levels were less than 1.5 nmol/liter, the upper limits which have been formulated as a guideline for monitoring control in treated CAH patients. Patients in good control had A-dione levels in plasma (0.6-2.2 nmol/liter) and saliva (0.04-0.15 nmol/liter) which were both within the normal range for prepubertal children (0.14-2.40 nmol/liter and 0.02-0.25 nmol/liter respectively). Patients in poor control had A-dione levels in plasma of 5.2-25.4 nmol and in saliva of 0.50-2.21 nmol/liter. These values exceeded without exception the normal ranges for their respective ages. Salivary A-dione and 17-OHP determinations are a useful adjunct in the diagnosis and the monitoring of CAH patients since they can be obtained easily and nonstressfully.

Five patients with hyper-immunoglobulin D syndrome (hyper-IgD syndrome) were followed up for 3 to 8 years. In all patients studied, serum IgG3 was high. IgM decreased during the follow-up in all patients. In four of the patients serum IgA was elevated. In four patients the serum IgD kappa/lambda ratio was measured and was found to be raised in all. However, the serum total light-chain ratio and IgG, IgA, and IgM kappa/lambda ratios separately were virtually normal. In two of the patients, clinical symptoms preceded the increase in serum IgD. All patients had a history of severe reactions on immunizations in early childhood. We conclude that in hyper-IgD syndrome, other immunoglobulins may also be affected, in particular, IgA, IgM, and IgG3. The IgD light-chain ratio is also disturbed. We emphasize that clinical symptoms may herald immunological changes. This may be the result of an underlying factor causing both the clinical symptoms and, later, the increasing serum IgD levels.

To study the influence of artificial ventilation rate on neonatal heart rate variability (HRV), ECG and respiratory impedance curves were recorded four times a day in 20 preterm infants (<33 wk) during the first 3 d after birth while the infants were ventilated at a wide range of ventilator rates. The contents of selected frequency bands within the R-R interval power spectrum were calculated for 3-min periods. Respiratory distress syndrome severity was assessed at each measurement. Respiratory sinus arrhythmia (RSA) induced by the ventilator appeared to mimic spontaneous RSA. As in spontaneous respiration, the amount of RSA (power in a frequency band around the respiratory rate) increases as the ventilation rate decreases. This phenomenon is most probably due to entrainment with baroreflex-related fluctuations in the heart rate. Although the artificial ventilation rate influences RSA and thus high-frequency HRV, an increase in respiratory distress syndrome severity results in a decrease in low-frequency HRV. Thus, the attenuation of low-frequency HRV by respiratory distress syndrome is not likely to be due to artificial ventilation. (Pediatr Res 37: 124-130, 1995) Abbreviations aRSA, artificial respiratory sinus arrhythmia aVR, artificial ventilation rate HF, high-frequency HRV, heart rate variability LF, low-frequency RDS, respiratory distress syndrome RSA, respiratory sinus arrhythmia VLF, very LF HRV, i.e. the variation in beat-to-beat R-R interval length, is influenced by maturational (e.g. gestational age), physiologic (e.g. respiration), and clinical factors (1, 2). HRV can be assessed by spectral analysis to study the frequency-specific oscillations in the heart rate signal. In the newborn, the following heart rate oscillations may be present. HF oscillations have a frequency equal to the respiratory rate and are known as RSA. LF oscillations are due to intrinsic oscillations of the baroreceptor reflex loop with a frequency of 0.07 Hz (3). A second kind of LF oscillation may result from periodic fluctuations in respiratory depth or tidal volume (4). The last type of HRV features VLF oscillations with a frequency below 0.04 Hz. These are ascribed to thermoregulation. H F oscillations are mediated by the parasympathetic system. LF and VLF oscillations are mediated by both the sympathetic and parasympathetic systems (5). Thus, studying neonatal HRV can give an insight into the maturation of the autonomic nervous system.In newborns suffering from RDS, HRV appears to be atten- HRV returns to normal (2). Several explanations have been proposed for this reversible effect of RDS on HRV. For instance, it has been ascribed to transient depression of the medulla oblongata by hypercarbia (2). The possible influence of artificial ventilation as such on neonatal HRV has not been taken into account in studies regarding the influence of RDS. For the correct interpretation of HRV in infants with RDS, insight into the effect of artificial ventilation on HRV is needed. This influence cannot be studied by simply comparing...

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The influence of maturation, sleep state and respiration on heart rate variability was studied in 16 spontaneously breathing preterm infants (< 33 weeks). ECG, respiratory impedance curve and movements were recorded four times a day, during the first three days of life. The power content of selected frequency bands of the R-R interval power spectrum, as well as respiratory frequency and breath amplitude oscillation frequency, were calculated for 3-min periods. An increase in low-frequency heart rate variability with gestational age was found. High-frequency variability increased during early postnatal life. Sleep state influenced very low-frequency heart rate variability. The amount of respiratory sinus arrhythmia and breath amplitude sinus arrhythmia was determined mainly by respiratory rate and breath amplitude oscillation frequency, respectively. The influences of gestational and postnatal age on heart rate variability might be due to an increase in sympathetic tone before birth and a change in parasympathetic-sympathetic balance after birth. Respiration has an important influence on heart rate variability, even in very preterm infants.