Relationship between gastro-oesophageal reflux and gastric activity in newborns assessed by combined intraluminal impedance, pH metry and epigastric impedance.

The pathogenesis of gastro-oesophageal reflux disease (GORD) is complex and multifactorial. A motility disorder resulting from immaturity of the gastro-oesophageal tract may be involved. We have combined multichannel intraluminal impedance (MII) and pH monitoring with epigastric impedance (EGI) to evaluate the activity of this tract in neonates with suspected GORD. Multichannel intraluminal impedance, pH and EGI were followed for 3 h in 30 newborns displaying apparent life-threatening events and signs of GORD. Simultaneous application of MII and pH monitoring identifies reflux episodes and illustrates their duration, height and pH. Episodes detected by MII were placed on the EGI curve and the contemporaneous gastric filling state and emptying velocity were calculated. During the total measuring time, 248 reflux episodes were revealed. An inverse correlation was evident for reflux frequency and gastric emptying velocity (r2 = 0.94; P < 0.001), and between acid refluxes and the gastric filling state (r2 = 0.95; P < 0.001), whereas a positive correlation was found between the reflux level and the gastric filling state (r2 = 0.52; P < 0.05). Simultaneous MII, pH and EGI monitoring provided new information on the relationship between refluxes and gastric activity. Data suggest that gastric emptying patterns influence the frequency, level and pH of reflux episodes.

Influence of thyroid in nervous system growth.

Nervous system growth and differentiation are closely correlated with the presence of iodine and thyroid hormones in initial development stages. In the human species, encephalon maturation during the first quarter of pregnancy is affected according to recent studies by the transplacenta passage of maternal thyroid hormones while it depends on initial iodiothyronin secretion by the foetal gland after the 12th week of pregnancy. Thyroid hormone deficiency during nervous system development causes altered noble nervous cells, such as the pyramidal cortical and Purkinje cells, during glial cell proliferation and differentiation alike. Neurons present cell hypoplasia with reduced axon count, dendritic branching, synaptic spikes and interneuron connections. Oligodendrocytes decrease in number and average myelin content consequently drops. Biochemical studies on hypothyroid rats have demonstrated alterations to neuron intraplasmatic microtubule content and organisation, changed mitochondria number and arrangement and anomalies in T3 nuclear and citoplasmatic receptor maturation. Alterations to microtubules are probably responsible for involvement of the axon-dendrite system, and are the consequence of deficient thyroid hormone action on the mitochondria, the mitochondria enzymes and proteins associated with microtubules. Nuclear and citoplasmatic receptors have been identified and gene clonation studies have shown two families of nuclear receptors that include several sub-groups in their turn. A complex scheme of temporal and spatial expression of these receptors exists, so they probably contribute with one complementary function, although their physiological role differs. The action of thyroid hormones occurs by changing cell protein levels because of their regulation at the transcriptional or post-transcriptional level. Genes submitted to thyroid hormone control are either expressed by oligodendrytes, which are myelin protein coders or glial differentiation mediators, or are nervous cell specific, genes coding neurotropins or proteins involved in synaptic excitation. The use of new PMRS and MRI non-invasive techniques has enabled identification of metabolic and biochemical markers for alterations in the encephalon of untreated hypothyroid children. Even an excess of thyroid hormones during early nervous system development can cause permanent effects. Hyperthyroidism in fact initially induces accelerated maturation process including cell migration and differentiation, extension of dendritic processes and synaptogenesis but a later excess of thyroid hormones causes reduction of the total number of dendritic spikes, due to early interruption of neuron proliferation. Experimental studies and clinical research have clarified not only the correlation between nervous system maturation and thyroid function during early development stages and the certain finding from this research is that both excess and deficient thyroid hormones can cause permanent anatomo-functional alterations to the nervous system.