Jaundice Subject

Seidel, D., Alaupovic, P., and Furman, R. H., A lipoprotein characterizing obstructive jaundice. I. Method for quantitative separation and identification of lipoproteins in jaundiced subjects. J. Clin, hwest. 48, 1211-1223 (1969). 

The use of the icterus index, as described by Meulengracht, for the assessment of jaundice has fallen into disrepute because of the errors caused by the presence of lipochromes, carotenoids, and other yellow pigments. Josephson (J6) in his survey found that the correlation coefficient between icterus index and serum bilirubin concentration was 0.69 in 360 healthy subjects and 0.84 in 40 jaundiced subjects. In newborn infants however, bilirubin is the only yellow pigment likely to be present and the possibility of determining serum bilirubin concentrations by direct measurement has again been re-examined. Abelson and Boggs (Al) diluted serum from infants with erythroblastosis 1 in 50 and studied the absorption curves. They found that in addition to the bili-... 

Necheles et al. (N4) first reported a genetically determined homozygous GSH-Px deficiency associated with neonatal jaundice and mild hemolysis. Spontaneous recovery from hemolysis was noted 3 months after birth. Thereafter, several cases with GSH-Px deficiency were reported. Newborn infants exhibit significantly lower red blood cell GSH-Px activity and serum selenium concentrations than adult control subjects, and a significantly positive correlation between selenium concentration and GSH-Px activity has been observed. Furthermore, the addition of selenium stimulates, both in vivo and in vitro, the GSH-Px activity. The neonatal red blood cell GSH-Px deficiency may be partially due to insufficient availability of selenium during pregnancy (P9). Therefore, the diagnosis of GSH-Px deficiency in newborn infants must be made carefully. 

In the region with pesticide contamination where subjects contracted viral hepatitis A, the pre-jaundice period was 4.2 days (in the control area, 5.1), the jaundice period lasted 32 days (22.4 in the control area), the liver enlarged more than in the control area and took longer to return to normal size, there was a larger number of patients who also had an enlarged spleen, there was more frequent damage to the nervous and cardiovascular systems (1.5-2 times higher than in the control area), mixed syndrome was observed more often (45% of the time, compared to 12.6% in the control area), and the illness was more frequently serious. 

In humans, mild jaundice lasting several days to 4 weeks has been observed after acute occupational exposure to acrylonitrile vapors at high concentrations (Wilson 1944) however, the concentrations of acrylonitrile to which workers were exposed were not reported. The effects were fully reversible. In factory workers exposed to acrylonitrile for 10 years or more, Sakurai et al. (1978) reported an increase in palpable livers of workers. However, the authors considered these results to be inconclusive because the increase was not statistically significant and subjective judgments were involved. Also, blood chemistry evaluations did not indicate liver damage. 

It is generally accepted that in normal subjects, most, but not necessarily all, of the bilirubin formed results from the breakdown of hemoglobin in the reticuloendothelial system. The bilirubin is then conjugated in the liver and excreted into the bile as a water-soluble pigment. The capacity of the liver to conjugate bilirubin is limited (W6), so that in cases of overproduction (e.g., hemolytic jaundice) free bilirubin will appear in the plasma. A similar result will be obtained if the ability of the liver to conjugate bilirubin is diminished (e.g., in the newborn infant). On the other hand, if the excretion of the bile is for some reason... 

The subjective complaints of the patients are reflected in irritability, moodiness, fatigue, vegetative dysfunctions, epigastric discomfort and abdominal bloating. Such complaints, however, show no correlation with the intensity of hyperbilirubinaemia. It is still not clear whether these ailments can be regarded as concomitant symptoms (= epiphenomena) or as a sequela (= hypochondriac reaction) of jaundice. 

Based on a targeted and exact anamnesis, subjective complaints by the patient and careful physical examination (s. tab. 12.5), it is possible in most cases to make a clear distinction between four different categories of jaundice (1.) haematological, (2.) hepatocellular, (J.) biliary obstructive, and (4.) hereditary, (s. tabs. 12.1,12.2,12.4)... 

In approx. 90% of all patients, acute viral hepatitis A is subclinical, i.e. it frequently goes undetected. The end of the prodromal and the beginning of the clinical phase is indicated by a brown colouration of the urine. Urobili-nogenuria persists for a longer period of time than bili-rubinuria. Mild proteinuria and microhaematuria can develop. Stools are usually acholic. With the occurrence of jaundice (60-70% children, 80-90% adults), most of the subjective symptoms of the prodromal stage subside. 

Fatal liver damage was observed particularly in the UK and tended to occur in elderly subjects. The complication initially presented as jaundice or raised liver enzymes (including alkaline phosphatase). Surprisingly, biochemical and histological liver changes were not consistent with major hepatocellular damage. There were three reports of primary biliary cirrhosis, but a causal relation was not proven (SEDA-12, 84). 

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