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During gastric secretion studies m any samples are contam inated w ith duodenogastric reflux, m ade obvious by frank bile staining. This reflux introduces errors in the m easurem ent of acid secretion w hich som e workers have sought to overcome by discarding obviously bile stained samples. There is no doubt how ever that duodenogastric reflux

sometimes lacks bile, and to ignore it is to ignore a phenom enon w hich may be im portant. Du Plessis (1965) em phasised the im portance of duodenogastric reflux, not only as an explanation of the observed hypoacidity and hypotonicity of gastric aspirate in patients w ith gastric ulceration, b u t also in the aetiology of the condition. In attem pting to assess the role of duodenogastric reflux, Hobsley (1974) assum ed that the reflux is isotonic and that the sodium concentration in the reflux is

143m m ol/l. O n the basis of these assum ptions he derived a form ula to quantify the reflux(VR):

VR = { V c o r X [N a + ] - 7 } /1 4 3

Vcor is the volum e of gastric juice corrected for pyloric loss, m ultiplied by the concentration of sodium [Na^] m easured in the aspirate, subtracting 7, w hich is the concentration of sodium in m mol 1'^ in prim ary gastric juice, and dividing it by 143, w hich is the concentration of sodium in m m ol 1'^ in duodenogastric reflux.

Based on the tw o-com ponent hypothesis (H ollander 1932) Hobsley, G ardham and H assan (1969) proposed to use sodium as a m arker for the m easurem ent of duodenogastric reflux. The tw o-com ponent theory postulates that the acid com ponent is of constant concentration b u t of variable volum e and the alkaline com ponent is of constant volum e and w ith a com position approxim ately that of interstitial fluid.

In 1974 Faber, R u ssell, Royston et al recognised and m easured the reflux of duodenal contents into the stom ach, especially during the insulin test after a vagotom y and drainage procedure. They studied 37 patients w ith

duodenal ulcer w ho w ere given brom sulphalein (BSP) or indocyanine (ICG), both these dyes being excreted into the bile. They found that

aspirated juice show ed highly significant positive correlations betw een the concentration of each dye and the concentration of duodenal reflux

calculated from a form ula based on the o u tp u t of sodium ions.

Fiddian-G reen et al (1979) used indocyanine green (ICG) intravenously to label the bile in order to m easure the duodenogastric reflux; they found a

large increase in volum e of aspirated gastric juice and the recovery of sodium follow ing the injection of secretin. The possible explanation of the increase in the aspirated volum e was an increase in the

duodenogastric reflux, suggested by the bile staining and increase in concentration of ICG in the aspirate.

99mTc_iabelled iminodiacetic acid was used to radio-label the bile and the duodenogastric reflux was m easured by external scintillation scan. Q uantification was possible over the region of interest (stomach,

duodenum , liver) b u t an accurate m easurem ent of low interm ittent reflux was not possible (Thomas et al 1984). How ever, sodium as a natural

marker is better than an artificially labelled substance to stu d y the

duodenogastric reflux because it exists at the same concentration in all the possible contam inants, bile, pancreatic juice and succus entericus.

Duodenogastric reflux occurs in healthy controls (Johnson and Eyre-Brook 1984) but the am ount of the refluxate is minimal. H ow ever, it is

considered to be present to a pathological extent in patients w ith duodenal ulcer (Thomas et al 1984). It been suggested that increased duodenogastric reflux leads to antral gastritis, and suppression of antral som atostatin. This results in an increase in the gastrin o u tp u t w hich in tu rn increases the parietal cell sensitivity. The net effect is a hypersecretory state, and an increase in acid delivery into the duodenum . This theory has been

challenged by W olverson et al 1984 and MuUer-Lissner et al 1983, they have suggested that the am ount of duodenogastric reflux is the same in patients w ith duodenal ulcer and in controls. In 1987 Frizis, W hitfield and Hobsley found that duodenogastric reflux w as higher in the gastric ulcer group as com pared to controls, the m ean volum e of duodenogastric reflux was greatest in the patients w ith a prepyloric gastric ulcer. The absolute

values of duodenogastric reflux w ere greater during basal conditions and tended to decrease d u rin g m axim al histam ine stim ulation. A t m axim al stim ulation duodenogastric reflux was significantly low er th an u n d er basal conditions in bo th controls and duodenal ulcer group, it w as higher in patients w ith duodenal ulcer than controls d uring basal conditions, b u t there was no difference d u rin g m axim al histam ine stim ulation (Roxburgh 1989).