Chapter 3

Pancreatic Function and Gastrointestinal Function

The gastrointestinal (GI) system is composed of the mouth, esophagus, stomach,
small intestine, and large intestine.

Digestion is the process by which all complex molecules are degraded to simple
constituents for absorption and use in the body.

The pancreas is a large gland that is involved in the digestive process but located
outside of the GI system.

It is composed of both endocrine and exocrine tissues.

The liver is the other major external gland that is involved in the digestive process.

The endocrine functions of the pancreas include production of insulin and glucagon;
both hormones are involved in carbohydrate metabolism.
2
Exocrine function involves the production of many enzymes used in the digestion.

PHYSIOLOGY OF PANCREATIC FUNCTION

The pancreas is weighing about 70 to 105 g.

It is located behind the peritoneal cavity across the upper abdomen at about the level
of the first and second lumbar vertebrae, about 1 to 2 in. above the umbilicus.

It is located in the curve made by the duodenum.

The pancreas is composed of endocrine tissue and exocrine tissue.

3
The endocrine (hormone releasing) component is the smaller of the two and consists
of the islets of Langerhans, which are well-delineated, spherical or ovoid clusters
composed of at least four different cell types.

The islet cells secrete at least four hormones into the blood: insulin, glucagon,
gastrin, and somatostatin.

The larger, exocrine pancreatic (enzyme-secreting) component secretes about 1.5 to

2 L/d of fluid, which is rich in digestive enzymes, into ducts that ultimately empty into
the duodenum.

This digestive fluid is produced by pancreatic acinar cells, which line the pancreas
and are connected by small ducts.

These small ducts empty into progressively larger ducts, eventually forming one
major pancreatic duct and a smaller accessory duct.
4
The major pancreatic duct and the common bile duct open into the duodenum at the
major duodenal papilla.

Normal, protein-rich, pancreatic fluid is clear, colorless, and watery, with an alkaline pH
that can reach up to 8.3.

This alkalinity is caused by sodium bicarbonate present in pancreatic fluid, which is

used to neutralize the hydrochloric acid in gastric fluid from the stomach as it enters
the duodenum.

Pancreatic fluid has about the same concentrations of potassium and sodium as serum.

5
The digestive enzymes are capable of digesting the three major classes of food
substances (proteins, carbohydrates, and fats) and include
(1) the proteolytic enzymes trypsin, chymotrypsin, elastase, collagenase, leucine
aminopeptidase, and some carboxypeptidases;
(2) lipid-digesting enzymes, primarily lipase and lecithinase;
(3) carbohydrate-splitting pancreatic amylase; and
(4) several nucleases (ribonuclease), which separate the nitrogen-containing bases
from their sugar phosphate strands.

Pancreatic activity is under both nervous and endocrine control.

The vagus nerve can cause a small amount of pancreatic fluid secretion when food is
smelled or seen, and these secretions may increase as the bolus of food reaches the
stomach.

Most of the pancreatic action, however, is under the hormonal control of secretin and
cholecystokinin (CCK). 6
Secretin is responsible for the production of bicarbonate-rich and, therefore, alkaline
pancreatic fluid, which protects the lining of the intestine from damage.

Secretin is synthesized in response to the acidic contents of the stomach reaching the
duodenum.

It can also affect gastrin activity in the stomach.

This pancreatic fluid contains few digestive enzymes.

CCK, in the presence of fats or amino acids in the duodenum, is produced by the cells
of the intestinal mucosa and is responsible for release of enzymes from the acinar cells
by the pancreas into the pancreatic fluid.

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 DISEASES OF THE PANCREAS
Other than trauma, only three diseases cause more than 95% of the medical attention
devoted to the pancreas.

If they affect the endocrine function of the pancreas, these diseases can result in
altered digestion and nutrient metabolism.

1. Cystic fibrosis (fibrocystic disease of the pancreas/mucoviscidosis) is an inherited

autosomal recessive disorder characterized by dysfunction of mucous and exocrine
glands throughout the body.

It has various manifestations such as intestinal obstruction of the newborn, excessive

pulmonary infections in childhood, or pancreatogenous malabsorption in adults.

8
The disease causes the small and large ducts and the acini to dilate and convert into
small cysts filled with mucus, eventually resulting in the prevention of pancreatic
secretions reaching the duodenum or, depending on the age of the patient, a plug that
blocks the lumen of the bowel, leading to obstruction.

As the disease progresses, there is increased destruction and fibrous scarring of the
pancreas and a corresponding decrease in function.

Cystic fibrosis has a high degree of penetrance.

The cystic fibrosis gene known as CFTR occurs on chromosome 7.

Genetic screening is now widely carried out.

2. Pancreatic carcinoma is the fourth most frequent form of fatal cancer and
causes about 38,000 deaths each year in the United States
9
The 5-year survival rate is about 6%, and most patients die within 1 year of
diagnosis.

Because the pancreas has a rich supply of nerves, pain is a prominent.

Signs of these tumors are jaundice, weight loss, anorexia, and nausea.

Jaundice is associated with signs of posthepatic hyperbilirubinemia and low levels of

fecal bilirubin, resulting in clay-colored stools.

However, findings are not specific for pancreatic tumors, and other causes of
obstruction must be ruled out.

Islet cell tumors of the pancreas affect the endocrine capability of the pancreas.

If the tumor occurs in beta cells, hyperinsulinism is often seen, resulting in low blood
glucose levels, sometimes followed by hypoglycemic shock. 10
Pancreatic cell tumors, which overproduce gastrin, are called gastrinomas; they cause
Zollinger-Ellison syndrome and can be duodenal in origin.

These tumors are associated with watery diarrhea, recurring peptic ulcer, and
significant gastric hypersecretion and hyperacidity.

Pancreatic cell glucagon secreting tumors are rare; the hypersecretion of glucagon is
associated with diabetes mellitus.

3. Pancreatitis, or inflammation of the pancreas, is caused by autodigestion of the

pancreas as a result of reflux of bile or duodenal contents into the pancreatic duct.

Pathologic changes can include edema, with large amounts of fluid accumulating in the
retroperitoneal space and an associated decrease in blood volume; cellular infiltration,
leading to necrosis of the acinar cells.

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Pancreatitis is classified as acute (no permanent damage to the pancreas), chronic
(irreversible injury), or relapsing/recurrent, which can also be acute or chronic.

Painful episodes usually reaching a maximum within minutes or hours, lasting for
several days or weeks.

Acute pancreatitis is often associated with alcohol abuse or biliary tract diseases such
as gallstones, but patients with hyperlipoproteinemia and those with hyperpara-
thyroidism are also at a significantly increased risk for this disease.

Other etiologic factors associated with acute pancreatitis include mumps, obstruction
caused by biliary tract disease, gallstones, pancreatic tumors, pregnancy, postrenal
transplantation, and hypersensitivity.

Symptoms of acute pancreatitis include severe abdominal pain that is generalized or in

the upper quadrants.
12
The etiology of chronic pancreatitis is similar to that of acute pancreatitis, but chronic
excessive alcohol consumption appears to be the most common predisposing factor

Laboratory findings include high amylase, lipase, triglycerides, and hypercalcemia,

which is often associated with underlying hyperparathyroidism.

Hypocalcemia may be attributed to the sudden removal of large amounts of calcium

from the extracellular fluid because of impaired mobilization or as a result of calcium
fixation by fatty acids liberated by increased lipase action on triglycerides.

Hypoproteinemia is due to the loss of plasma into the retroperitoneal space.

A shift of arterial blood flow from the inflamed pancreatic cells to less affected or
normal cells causes oxygen deprivation and tissue hypoxia in the area of damage.

13
All three conditions can result in severely diminished pancreatic exocrine function,
which can significantly compromise digestion and absorption of ingested nutrients.

This is the essence of the general malabsorption syndrome, which embodies

abdominal bloating and discomfort; the frequent passage of bulky, malodorous feces;
and weight loss.

Failure to digest or absorb fats, known as steatorrhea, renders a greasy appearance

to feces (more than 5 g of fecal fat per 24 hours).

The malabsorption syndrome involves abnormal digestion or absorption of proteins,

polysaccharides, carbohydrates, and lipids.

Severely deranged absorption and metabolism of electrolytes, water, vitamins

(particularly fat-soluble vitamins A, D, E, and K), and minerals can also occur.
14
Malabsorption can involve a single substance, such as vitamin B12, which results in a
megaloblastic anemia (pernicious anemia), or lactose caused by a lactase deficiency.

In addition to pancreatic exocrine deficiency, the malabsorption syndrome can be

caused by biliary obstruction, which deprives the small intestine of the emulsifying
effect of bile, and various diseases of the small intestine, which inhibit absorption of
digested products.

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 TESTS OF PANCREATIC FUNCTION
Pancreatic function may be suspect when there is increase in amylase and lipase.

Other laboratory tests of pancreatic function include:

- those used for detection of malabsorption (e.g., examination of stool for excess fat,
D-xylose test, and fecal fat analysis),
- tests measuring other exocrine function (e.g., secretin, CCK, fecal fat, trypsin, and
chymotrypsin),
- tests assessing changes associated with extrahepatic obstruction (e.g., bilirubin)
- endocrine-related tests (e.g., gastrin, insulin, and glucose) that reflect changes in
the endocrine cells of the pancreas.

Direct evaluation of pancreatic fluid may include measurement of the total volume
and the amount or concentration of bicarbonate and enzymes, which requires
pancreatic stimulation.

16
Stimulation may be accomplished using a predescribed meal or administration of
secretin, which allows for volume and bicarbonate evaluation, or secretin stimulation
followed by CCK stimulation, which adds enzymes to the pancreatic fluid evaluation.

The advantage of these tests, is that the chemical and cytologic examinations are
performed on actual pancreatic secretions.

Because of advances in imaging techniques, these stimulation tests are used less
often.

The sweat test, used for screening cystic fibrosis, is not specific for assessing
pancreatic involvement but, when used along with the clinical picture at the time of
testing, can provide important diagnostic information.

17
Secretin/CCK Test
The secretin/CCK test reflects the exocrine secretory capacity of the pancreas.

The test involves intubation of the duodenum without contamination by gastric fluid,
which would neutralize any bicarbonate.

The test is performed after a 6-hour or overnight fast.

Pancreatic secretion is stimulated by intravenously administered secretin in a dose

varying from 2 to 3 U/kg of body weight, followed by CCK administration.

No single protocol has been uniformly established for the test.

Pancreatic secretions are collected variously for 30, 60, or 80 minutes after
administration of the stimulants.
18
The pH, secretory rate, enzyme activities (e.g., trypsin, amylase, or lipase), and
amount of bicarbonate are determined.

The average amount of bicarbonate excreted per hour is about 15 mmol/L for men
and 12 mmol/L for women, with an average flow of 2 mL/kg.

Concentration of enzymes must be taken in view of total volume output.

Decreased pancreatic flow is associated with pancreatic obstruction and increase in

enzyme concentrations.

Low concentrations of bicarbonate and enzymes are associated with cystic fibrosis,
chronic pancreatitis, pancreatic cysts, and edema of the pancreas.

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Fecal Fat Analysis
Fecal lipids are derived from four sources: unabsorbed ingested lipids, lipids excreted
into the intestine (predominantly in the bile), cells shed into the intestine, and
metabolism of intestinal bacteria.

Patients on a lipid-free diet still excrete 1 to 4 g of lipid in the feces in a 24-hour.

Even with a lipid-rich diet, the fecal fat does not normally exceed about 7 g in a
24hrs.

Normal fecal lipid is composed of about 60% fatty acids; 30% sterols, higher alcohols,
and carotenoids; 10% triglycerides; and small amounts of cholesterol and
phospholipids.

Although significantly increased fecal fat can be caused by biliary obstruction, severe
steatorrhea is usually associated with exocrine pancreatic insufficiency or disease of
the small intestine. 20
Quantitative Fecal Fat Analysis

The definitive test for steatorrhea is the quantitative fecal fat determination, usually
on a 72-hour stool collection, although the collection may be increased to up to 5
days.

The reference range for fecal lipids in adults is 1 to 7 g per 24 hours.

Sweat Electrolyte Determinations

Measurement of the sodium and chloride concentration in sweat is the most useful
test for the diagnosis of cystic fibrosis.

Significantly elevated concentrations of both ions occur in more than 99% of affected
patients.
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The 2- fold increases in sweat sodium and chloride are diagnostic of cystic fibrosis in
children.

Even in adults, no other condition causes increases in sweat chloride and sodium
above 80 mmol/L.

Sweat potassium is also increased, but less significantly so, and is not generally relied
on for diagnosis.

Sweat electrolyte determinations do not distinguish heterozygote carriers of cystic

fibrosis from normal homozygotes.

Induction of sweat included applying plastic bags or wrapping the patient in blankets,
which was fraught with serious risks of dehydration, electrolyte disturbances, and
hyperpyrexia.

22
It is widely accepted that sweat chloride concentrations greater than 60 mmol/L are
diagnostic of cystic fibrosis in children.

Sweat sodium and chloride concentrations in female patients undergo fluctuation with
the menstrual cycle and reach a peak 5 to 10 days before the onset of menstruation
but do not overlap with the ranges associated with cystic fibrosis.

Serum Enzymes
Amylase is the enzyme most commonly relied on for detecting pancreatic disease.

It is not, however, a function test.

Amylase is particularly useful in the diagnosis of acute pancreatitis, in which significant

increases in serum concentrations occur in about 75% of patients.
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Typically, amylase in serum increases within a few hours of the onset of the disease,
reaches a peak in about 24 hours, and because of its clearance by the kidneys
returns to normal within 3 to 5 days, often making urine amylase a more sensitive
indicator of acute pancreatitis.

The magnitude of the enzyme elevation cannot be correlated with the severity of the
disease.

Determination of the renal clearance of amylase is useful in detecting minor or

intermittent increases in the serum concentration of this enzyme.

To correct for diminished glomerular function, the most useful expression is the ratio
of amylase clearance to creatinine clearance, as follows:

where UA is urine amylase, SA is

(Eq. 1) serum amylase, SC is serum
creatinine, and UC is urine creatinine.
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Normal values are less than 3.1%.

Values, averaging about 8% or 9%, occur in acute pancreatitis but may also occur in
burns, sepsis, and diabetic ketoacidosis.

Lipase increases in serum about as soon as amylase in acute pancreatitis and that
increased levels persist somewhat longer than those of amylase.

Consequently, some physicians consider lipase more sensitive than amylase as an

indicator of acute pancreatitis or other causes of pancreatic necrosis.

Both amylase and lipase may be significantly increased in serum in many other
conditions (e.g., opiate administration, pancreatic carcinoma, intestinal infarction,
obstruction, and pancreatic trauma).

Amylase levels are also frequently increased in mumps, cholecystitis, hepatitis,

cirrhosis, ruptured ectopic pregnancy, and macroamylasemia, which is a benign
condition in which amylase binds to an immunoglobulin molecule, causing chronic 25
elevation of serum amylase values but normal urine amylase levels.

Lipase levels are often significantly increased in bone fractures and in association with
fat embolism.

FECAL ELASTASE
Elastase-1 is a chymotrypsin-like enzyme secreted by the pancreas.

The measurement of this enzyme in stool has been proposed as a sensitive test of
pancreatic function.

Fecal elastase is performed on random stool samples and has the advantage of
being noninvasive.

It has been shown to be useful in the diagnosis of cystic fibrosis in children.

26
The reference range for fecal elastase for normal greater than 200 μg/g, moderate
pancreatic insufficiency is between 100 and 200 μg/g and severe pancreatic
insufficiency is less than 100 μg/g.

27
 PHYSIOLOGY AND BIOCHEMISTRY OF GASTRIC SECRETION

Gastric secretion occurs in response to various stimuli:

- Neurogenic impulses by means of the vagal nerves (e.g., responses to the sight,
smell, or anticipation of food)

- Distention of the stomach with food or fluid

- Contact of protein breakdown products, termed secretagogues, with the gastric

mucosa

- The hormone gastrin is the most potent stimulus to gastric secretion; it is secreted
by G cells in the gastric mucosa and the duodenum in response to vagal stimulation
and contact with secretagogues.
28
Inhibitory influences:
- include high gastric acidity, which decreases the release of gastrin.

- Gastric inhibitory polypeptide is secreted by K cells in the duodenum and jejunum in

response to food products such as fats, glucose, and amino acids.

- Vasoactive intestinal polypeptide, produced by H cells in the intestinal mucosa,

directly inhibits gastric secretion, gastrin release, and gastric motility.

Gastric fluid has a high content of hydrochloric acid, pepsin, and mucus.

Hydrochloric acid is secreted against a hydrogen ion gradient as great as 1 million

times the concentration in plasma (i.e., gastric fluid can reach a pH of 1.2 to 1.3
under conditions of augmented or maximal stimulation).

Pepsin is a weak proteolytic enzymes, with pH optima from about 1.6 to 3.6, that
catalyze all native proteins except mucus.. 29
The most important component of gastric secretion is intrinsic factor, which greatly
facilitates the absorption of vitamin B12 in the ileum

CLINICAL ASPECTS OF GASTRIC ANALYSIS

Gastric analysis is used mainly to detect hypersecretion characteristics of the Zollinger-
Ellison syndrome.

This syndrome involves a gastrin-secreting neoplasm, usually located in the pancreatic

islets, and exceptionally high plasma gastrin concentrations.

Basal 1-hour secretion usually exceeds 10 mmol, and the ratio of basal 1-hour to
maximal secretion usually exceeds 60% (i.e., the stomach is not really in the basal
state but rather is pathologically stimulated by the high plasma gastrin level).

30
Gastric analysis is also used to evaluate pernicious anemia in adults.

Gastric atrophy is present in this condition, and the stomach fails to secrete intrinsic
factor, which binds to vitamin B12 to prevent its degradation by gastric acid.

The pH of gastric fluid in this condition typically does not fall below 6, even with
maximum stimulation.

Histamine acid phosphate was used as a stimulus to gastric secretion.

Histamine has now been replaced by pentagastrin, which is a synthetic pentapeptide

composed of the four C-terminal amino acids of gastrin linked to a substituted alanine
derivative.

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Normal gastric fluid is translucent, pale gray, and slightly viscous.

Residual volume should not exceed 75 mL.

Residual specimens occasionally contain flecks of blood or are green, brown, or yellow
from reflux of bile during the intubation procedure.

The presence of food particles is abnormal and indicates obstruction.

TESTS OF GASTRIC FUNCTION

Measuring Gastric Acid in Basal and Maximal Secretory Tests

After an overnight fast, gastric analysis is usually performed as a 1-hour basal test,
followed by a 1-hour stimulated test subsequent to pentagastrin administration (6
μg/kg subcutaneously).
32
Test results reveal wide overlap among healthy subjects and diseased patients, except
for anacidity (e.g., in pernicious anemia) and the extreme hypersecretion found in
Zollinger-Ellison syndrome.

Measuring Gastric Acid

In stimulated secretion specimens, the ability of the stomach to secrete against a
hydrogen ion gradient is determined by measuring the pH.

The total acid output in a timed interval is determined.

After intubation, the residual secretion is aspirated and retained.

Secretion for the subsequent 10 to 30 minutes is discarded to allow for adjustment of

the patient to the intubation procedure.

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Specimens are ordinarily obtained as 15-minute collections for a period of 1 hour.

The gastrin response to intravenous secretin stimulation may be used to investigate

patients with mildly elevated serum gastrin levels.

In this test, pure porcine secretin is injected intravenously, and gastrin levels are
collected at 5- minute intervals for the next 30 minutes.

In patients with Zollinger-Ellison syndrome, the gastrin level increases at least 100
pg/mL over the basal level.

Patients with ordinary peptic ulceration, achlorhydria, or other conditions show a

slight decrease in gastrin concentration

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Plasma Gastrin

Measurement of plasma gastrin levels is invaluable in diagnosing Zollinger Ellison

syndrome, in which fasting levels typically exceed 1,000 pg/mL and can reach 400,000
pg/mL, compared with the normal range of 50 to 150 pg/mL.

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 INTESTINAL PHYSIOLOGY
Each day, the duodenum receives about 7 to 10 L of ingested water and food and
secretion from the salivary glands, stomach, pancreas, and biliary tract.

The materials then enter the jejunum and ileum, where another 1 to 1.5 L of
secretion is added.

Ultimately, however, only about 1.5 L of fluid material reaches the cecum, which is the
first portion of the colon or large intestines.

This considerable absorptive capability is possible because the small intestine (about
20 ft long) has numerous folds called villi, and microscopic projections on the mucosal
cells called microvilli, all of which greatly increase the secretory and absorptive surface
to an estimated 200 m2.

36
The large intestine (about 5 ft
long) has two major functions:
1) water resorption, in which the
1.5 L of fluid received by the
cecum is reduced to about 100
to 300 mL of feces, and
2) storage of feces before
defecation.

Figure 3. The abdominal structures of

the alimentary tract 37
 CLINICOPATHOLOGIC ASPECTS OF INTESTINAL FUNCTION

Testing of intestinal function focuses almost entirely on the evaluation of absorption

and its derangements in various disease states.

The intestinal diseases include celiac sprue, Crohn's disease, intestinal lymphoma,
giardiasis and others.

In addition to the malabsorption syndrome, which causes impaired absorption of fats,

proteins, carbohydrates, and other substances, specific malabsorption states also
occur (e.g., acquired deficiency of lactase, which prevents absorption of lactose, and
Hartnup syndrome, a genetic disorder that involves deficient intestinal transport of
phenylalanine and leucine).

38
 TESTS OF INTESTINAL FUNCTION

Lactose Tolerance Test

Lactase (which cleaves lactose into glucose and galactose) and sucrase (which
cleaves sucrose into glucose and fructose), are produced by the mucosal cells of the
small intestine.

Congenital deficiencies of these enzymes are rare, but acquired deficiencies of lactase
are commonly found in adults.

Affected patients experience abdominal discomfort, cramps, and diarrhea after

ingesting milk or milk products.

Lactose tolerance testing was used to establish this diagnosis, but the test is
subject to many false-positive and false-negative results. This test has largely
been replaced by hydrogen breath testing.
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D-Xylose Absorption Test
D-Xylose is a pentose sugar that is ordinarily not present in the blood.

Pentose sugars are absorbed unaltered in the proximal small intestine and do not
require the intervention of pancreatic lytic enzymes.

Therefore, the ability to absorb D-xylose is of value in differentiating malabsorption of

intestinal etiology from that of exocrine pancreatic insufficiency.

Because only about one-half of orally administered D-xylose is metabolized or lost by

action of intestinal bacteria, significant amounts are excreted unchanged in the urine.

Some protocols have used the measurement of only the D-xylose excreted in the
urine during the 5 hours following ingestion of a 25-g dose by a fasting adult (0.5
g/kg in a child).
40
Blood levels measured one or more times after ingestion of D-xylose (e.g., at 30
minutes, 1 hour, or 2 hours) improve the diagnostic reliability of the test.

Some protocols use smaller doses of D-xylose to avoid abdominal cramps, intestinal
hypermotility, and osmotic diarrhea that frequently accompany the 25-g dose.

D-Xylose Test
After ingestion of a specified solution of D-xylose, blood specimens are obtained
and urine is collected for a 5-hour period to determine the extent of D-xylose
absorption.

After an overnight fast, the patient voids and drinks a D-xylose solution: 25 g of D-
xylose in 250 mL of water for adults and 0.5 g/kg for children, or other dose as
established.

The patient drinks an equivalent amount of water during the next hour.
41
No additional food or fluids are to be taken until the test is completed.

Urine is collected for 5 hours after the D-xylose ingestion.

A blood specimen is collected in potassium oxalate at 2 hours (commonly, 1 hour is

chosen for children).

Normal blood concentrations of D-xylose in association with decreased urine excretion

suggest impairment of renal function or incomplete urine collection.

Aspirin therapy diminishes renal excretion of D-xylose, whereas indomethacin

decreases intestinal absorption.

After ingestion of a 25-g dose of D-xylose, healthy adults should excrete at least 4 g in
the 5-hour period.

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For infants and children, the excretion following a dose of 0.5 g/kg for various ages
expressed as percentages of ingested dose are shown in Table 1.

Table D-Xylose Results for Pediatric Patients .

A blood concentration of less than 25 mg/dL at 2 hours should be considered

abnormal after the 25-g dose.

With the 0.5 g/kg dose, infants younger than 6 months should have a blood
concentration of at least 15 mg/dL at 1 hour, infants older than 6 months and children
should achieve levels of at least 30 mg/dL. 43
Serum Carotenoids
Carotenoids are pigments that are widely distributed in animal tissue; they are
synthesized by many plants.

The major carotenoids in human serum are lycopene, xanthophyll, and beta carotene,
the chief precursor of vitamin A in humans.

Carotenoids are absorbed in the small intestine in association with lipids.

Malabsorption of lipids results in a serum concentration of carotenoids lower than the

reference range of 50 to 250 mg/dL.

The test does not distinguish among the various etiologies of malabsorption.

44
Other Tests of Intestinal Malabsorption
Diminished appetite and dietary intake are usually more severe in patients who have
malabsorption with an intestinal etiology.

Body wasting or cachexia may be severe.

Because loss of albumin into the intestine and diminished dietary intake of protein, a
negative nitrogen balance occurs together with decreased serum total proteins and
albumin.

A serum albumin of less than 2.5 g/dL is much more characteristic of intestinal disease
than of pancreatic disease.

In association with severe disease of the small intestine, deficiencies of fat soluble
vitamins A, D, E, and K occur.
45
Vitamin K deficiency, in turn, causes deficiencies of vitamin K–dependent coagulation
factors II (prothrombin), VII , IX, and X, which are reflected in abnormal prothrombin
time and partial thromboplastin time tests.

In severe small intestinal disease such as celiac sprue, malabsorption of folate and
vitamin B12 can occur, and megaloblastic anemia is common.

Absorption of iron is usually diminished.

Intestinal absorption of calcium is often diminished as a result of calcium binding by

unabsorbed fatty acids and accompanying vitamin D deficiency and decreased serum
magnesium.

Because sodium, potassium, water absorption, and metabolism may also be seriously
deranged, serum sodium and potassium levels are decreased and dehydration occurs.

46