Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

VII. Interpretation of Serum Protein Profiles
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process, fluids and proteins move into the tissues, inducing
edema and contributing to a decrease in plasma albumin.
Hemorrhage or massive exudation with large external losses
of plasma is followed by a rapid movement of interstitial
fluid (without protein) into the plasma compartment to
induce an acute hypoproteinemia. Conversely, dehydration
leads to hemoconcentration through reduction in fluid volume
and consequent hyperproteinemia. During splenic contraction
in the horse, a large mass of erythrocytes moves into
the circulation with little or no change in the serum protein.
B . The Dysproteinemias
The current method of choice for the overall evaluation of
protein status remains SPE on cellulose acetate or agarose
gel. The SPE profile and the absolute values of the individual
fractions provide an excellent basis for presumptive
diagnoses and for additional studies of the patient. The A:G
ratio derived from chemistry panels or from the SPE is the
basis on which the SPE can be interpreted.
Classification of the SPE profile in conjunction with
the A:G ratio provides a systematic approach to the interpretation
of protein dyscrasias. Table 5-5 gives such a classification
of the SPE results based on the A:G ratio and the
nature of the profile. This table provides a useful vehicle
for alerting the clinical biochemist and the clinician to the
underlying significance of the specific dysproteinemia.
1 . Normal A:G—Normal Profi le
a . Hyperproteinemia
Simple dehydration with water loss is essentially the only
instance when a simple hyperproteinemia without change
in profile or A:G occurs. In this case, all protein fractions
increase proportionately, including albumin, because only
water has been removed from the system.
b . Hypoproteinemia
Overhydration through vigorous fluid therapy or excess
water intake is a common cause of simple hypoproteinemia.
This is simply a dilution of the system. In other instances,
for example, after acute blood loss, interstitial fluid moves
rapidly into the plasma compartment, thus diluting the system.
This dilution may be further intensified by the ingestion
of water to satisfy the thirst commonly seen in acute blood
loss. Similarly, after acute plasma loss, whether internal or
external, by exudation or extravasation, simple hypoproteinemia
occurs because movement of interstitial water into the
plasma compartment rapidly replaces the water losses.
2 . Decreased A:G—Abnormal Profi le
a . Decreased Albumin
Decreased albumin is a common form of dysproteinemia.
Fundamentally, the decrease can be attributed to either
albumin loss or failure of albumin synthesis. Depending
on the stage of the disease, it can be associated with either
slight hyperproteinemia (acute stage), normoproteinemia
(progressive stage), or, in its advanced stages, hypoproteinemia.
Therefore, the total serum protein is not a reliable
index of albumin status and albumin must be determined.
Because of its small size and osmotic sensitivity to fluid
movements, albumin is selectively lost in renal disease
( Grauer, 2005 ), gastrointestinal disease, ( Kaneko et al. ,
1965 ; Meuten et al. , 1978 ), and in intestinal parasitism
( Dobson, 1965 ). The hypoalbuminemia of intestinal parasitism
is aggravated by increased albumin catabolism
( Cornelius et al. , 1962 ; Halliday et al. , 1968 ; Holmes et al. ,
1968 ). Furthermore, because of the sensitivity of albumin
synthesis to protein and nitrogen loss such as that occurring
in some forms of gastrointestinal disease, albumin
loss impairs albumin synthesis and further compounds
the hypoalbuminemia. Because of this same sensitivity
of albumin synthesis to protein and nitrogen availability,
decreased albumin concentration precedes the development
of generalized hypoproteinemia in dietary protein
deficiencies. Classic human protein-calorie malnutrition,
kwashiorkor, is characterized by hypoalbuminemia and
hypoproteinemia.
The liver is the only site of albumin synthesis, and
hypoalbuminemia is an important feature of chronic liver
disease and when accompanied by marked decrease in total
protein is indicative of terminal liver cirrhosis ( Sevelius
and Andersson, 1995 ). In the horse, a unique postalbumin
shoulder with or without a hypoalbuminemia suggests liver
disease. Additionally, albumin is a negative APP and extensive
inflammation accompanying any of the aforementioned
conditions may compound the hypoalbuminemia.
b . Increased Globulins
i . α -Globulins α 1 -Globulin but mainly α 2 -globulin
increases are commonly found and are of diagnostic
significance. Many of the APPs (Section VI.B) migrate
in the α 1 - and α 2 -globulin regions ( Table 5-5 ) so that
increases in these globulins are a common finding in
acute inflammatory diseases and represent an acute phase
response. Increases in α -globulins can be accompanied
by increased β - or γ -globulins ( Fig. 5-9a and 5-9c ). In the
nephrotic syndrome, α 2-globulins increase due in part to
increases in α 2 -macroglobulin and the lipoproteins. The triad
of azotemia, hypoalbuminemia, and hypercholesterolemia
is a characteristic of the nephrotic syndrome. Increased α -
globulin, identified as α 1 -antitrypsin, and Hp have been
described in dogs with chronic liver disease, many of which
recovered ( Sevelius and Andersson, 1995 ).
ii . β -Globulins Increases in β-globulins alone are
infrequent in most species and found in association with
active liver disease, suppurative dermatopathies, and in the