Increased Serum Bilirubin Concentrations Research Articles

Modification of galactosamine-induced liver injury in rats by reticuloendothelial system stimulation or depression.

The reticuloendothelial system has been implicated in galactosamine-induced liver injury because of a correlation between phagocytic alterations induced by colloidal carbon or endotoxin, and development of liver necrosis. To evaluate this concept, the influence of galactosamine on liver function and histology was determined in rats in which the reticuloendothelial system was normal, stimulated, or depressed. Methyl palmitate was used as a reticuloendothelial system suppressant, and glucan was used as a reticuloendothelial system activating agent. Administration of galactosamine to control rats resulted in hypoglycemia and increased serum bilirubin concentration, elevated serum glutamic oxalacetic transaminase, lactic dehydrogenase and glutamic pyruvic transaminase activities, and retention of sodium sulfobromophthalein. Histological studies revealed hepatic necrosis, and a polymorphonuclear and lymphocytic cellular infiltrate in galactosamine-treated rats. Pretreatment of rats with methyl palmitate inhibited galactosamine-induced alterations in serum glucose concentration, glutamic oxalacetic transaminase and lactic dehydrogenase activities, and sodium sulfobromophthalein retention. Liver necrosis and inflammatory reactions were also reduced in methyl palmitate-treated galactosamine-injected animals. In contrast, activation of the reticuloendothelial system by glucan increased galactosamine-induced alterations in serum bilirubin, glucose and cholesterol concentrations, glutamic oxalacetic transaminase, glutamic pyruvic transaminase and lactic dehydrogenase activities, and sodium sulfobromophthalein retention. Liver necrosis and inflammation were also increased. These findings suggest that the degree of galactosamine-induced liver injury is directly correlated with macrophage function when specific macrophage-modifying agents are used.

Increased serum concentrations of lactic, pyruvic and uric acid and bilibubin after postoperative xylitol infusion.

Xylitol has been suggested as a more advantageous calory source for intravenous administration than glucose in certain clinical situation, but the general suitability of intravenous xylitol infusion has not been confirmed. Thirty-middle-aged women were infused with 100 g of xylitol as postoperative fluid therapy after gynaecological laparotomy and general anaesthesia. Another 10 women received 50 g of glucose in a similar manner and served as a reference group. Infusion of xylitol both at the rate of 0.25 g/kg/h (1000 ml 10% xylitol in approx. 8 h) and 0.5 g/kg/h (1000 ml 10% xylitol in approx. 4 h) caused a distinct increase in the serum concentrations of lactic acid, pyruvic acid, and uric acid; such an increase was not seen with glucose infusion. The faster infusion of xylitol also distinctly increased serum bilirubin concentrations. Because of the possibility of lactic acidosis and urate deposits in kidneys, infusion of 100 g or more of xylitol at a rate of 0.25 g/kg/h or faster is not safe for postoperative fluid therapy in routine clinical work.

Breast feeding and serum bilirubin values during the first 4 days of life

One hundred ninety-nine breast-fed and bottle-fed infants were studied for the first 4 days of life to determine if breast feeding and hyperbilirubinemia were related, and to see if altering the standard hospital breast-feeding regimen would affect bilirubin levels. Breast feeding did not results in increased serum bilirubin concentrations. Regardless of feeding regimen, breast- and bottle-fed groups had similar mean bilirubin values, and a similar low incidence of hyperbilirubinemia. Incidental findings included an 8 per cent mean weight loss in infants who were breast fed without supplements, compared to a 4 per cent weight loss in all other infants. Hyperbilirubinemia was not related to weight loss.

The short-term prognosis of severe primary infantile malnutrition.

1. Among a series of 343 children with severe primary malnutrition there were 248 for whom, on admission, there were reliable records of age, weight, height, liver size, severity of oedema, skin lesions and angular stomatitis, and concentration of total serum protein, haemoglobin and sodium. For eighty-four of these children the serum bilirubin concentration was also known.2. The correlations of these characteristics of the children on admission, with mortality, and with the rate of recovery were investigated.3. Age, weight, oedema and haemoglobin concentration were not significantly related to mortality or to rate of recovery. A multiple regression analysis showed that an increased serum bilirubin concentration and a decreased serum sodium concentration indicated a bad prognosis, and these two factors contributed almost the whole of the multiple correlation coefficient of 0.63 with respect to mortality and 0.59 with respect to speed of rccovery.4. We conclude that in our series of children death was more closely associated with liver failure or overhydration than with protein depletion, and suggest that the administration of ton much protein or water to an acutely ill malnourished child may precipitate death.5. This analysis shows that the mortality observed in our series cannot be adequately explained by any combination of the characteristics considered above; there must, therefore, be other factors of importance for which we do not have suitable measurements.