Biology of Disease

cholesterol esterase. Fluorescein, but not fluorescein dilaurate, is absorbed

by the small intestine and transported to the liver where it is converted to

fluorescein glucuronide, which is then excreted in the urine. The latter can

be detected by its characteristic fluorescence. The test is controlled for vari-

ations in intestinal absorption, hepatic conjugation and renal excretion by

repeating the test the next day but using an oral dose of fluorescein. The ratio

of fluorescein excreted after administration of fluorescein dilaurate to that

excreted after administration of free fluorescein is greater than 0.3 in normal

individuals. However, a ratio less than 0.2 is indicative of abnormal pancreatic

function. Ratios between 0.2 and 0.3 are inconclusive. Other investigations

of pancreatic function include the para-aminobenzoic acid (PABA) test in

which the patient is given 0.5 g of the synthetic peptide, benzoyltyrosylami-

nobenzoic acid (BTPABA). This is hydrolyzed to PABA in the small intestine by

pancreatic chymotrypsin (Figure 11.24). Following its absorption, the PABA is

excreted unchanged in the urine. The patient is also given a known amount of

radioactively labeled PABA (^14 C-PABA) to correct for variations in the absorp-

tion, metabolism and excretion of PABA formed from BTPABA. The amount

of PABA found in the urine is a measure of the activity of pancreatic chymo-

trypsin. There is reduced excretion of urinary PABA in individuals with abnor-

mal pancreatic function.

X]VeiZg&&/ DISORDERS OF THE GASTROINTESTINAL TRACT, PANCREAS, LIVER AND GALL BLADDER

'.- W^dad\nd[Y^hZVhZ

C

O

NH C

O

NH

CH 2

CH COOH

H 2 O

OH

C

O

NH C

O

N 2 H

CH 2

CH COOH

OH

OH +

BTPABA

PABA

Figure 11.24The hydrolysis of the synthetic peptide,

benzoyltyrosylaminobenzoic acid (BTPABA) by chymotrypsin activity

to release para-aminobenzoic acid (PABA).

Disorders of the Liver, Gall Bladder and Bile Duct

Jaundice is the yellow discoloration of tissues due to an accumulation of

bilirubin (Figure 11.5). Many disorders of the liver give rise to jaundice,

although clinical jaundice may not be seen until the concentration of bilirubin

in the serum is greater than 50 μmol dm–3. The causes of jaundice can be pre-

hepatic, hepatic or posthepatic.

The causes of prehepatic jaundice include hemolysis, where there is an

increased breakdown of hemoglobin producing large amounts of bilirubin

that overloads the conjugating mechanism. Such bilirubin is mostly uncon-