section VI.1
Serum Protein Electrophoresis
arthritis, uncontrolled diabetes, intravenous feeding (the
hypoalbuminemia is due to a deficiency of amino acids in
portal blood), and dietary deficiency of proteins containing
essential amino acids.
Hypoalbuminemia also occurs in the acute stress re-
action. The sharp drop of albumin is essentially due to
adrenocortical stimulation, which gives rise to enhanced
catabolism of albumin and sodium retention. The latter is
responsible for hemodilution and expansion of extracel-
lular fluid. The oq- and oq-globulin fractions (see below)
are also increased in the acute stress reaction. The im-
-fraction) do not undergo significant al-
terations during the acute phase of a stress reaction but are
elevated during the chronic phase. Some examples of situ-
ations in which acute stress patterns may be seen are acute
infections in early stages, tissue necrosis (myocardium,
renal, tumor), severe burns, rheumatoid disease of acute
onset, surgery, and collagen disorders.
is a rare autosomal recessive disorder.
Affected individuals do not exhibit serious clinical symp-
toms, not even edema. The lack of clinical edema is pre-
sumably due to osmotic compensation by the mildly ele-
vated globulins. Osteoporosis in analbuminemia has been
corrected by the administeration of human serum albu-
min. Affected females exhibit minimal pretibial edema,
mild anemia, normal liver function tests, absence of pro-
teinuria, lowered blood pressure, elevated serum choles-
terol levels, and lipodystrophy. Despite elevated plasma
cholesterol levels, severe atherosclerosis was not present.
Bisalbuminemia is due to albumin polymorphism.
Upon serum electrophoresis, a double albumin band is
seen. These double peaks are due either to differences
in electrical charge
( 1 1
electrophoretically distinct forms
have been reported) or to albumin dimers. Both forms
are expressed as autosomal dominant traits and apparently
present no significant clinical abnormalities. However, ac-
quired bisalbuminemia may be associated with diabetes
mellitus, the nephrotic syndrome, hyperamylasemia, and
penicillin therapy. In these instances, the bisalbuminemia
disappears after correction of the underlying disorder.
The proteins that migrate in this region are aq-
antitrypsin (which accounts for 70-90% of the
a \
a i-acid glycoprotein, or orosomucoid (which accounts
1 0
2 0
% of the a i-peak),
a \
-lipoprotein, prothrom-
bin, transcortin, and thyroxine-binding globulin. In acute
phase reactions, elevation of the
a \
-peak is due to in-
creases in a i -antitrypsin and
a \
-acid glycoprotein, the two
principal constituents of the peak,
a \
-Peak elevations are
also seen in chronic inflammatory and degenerative dis-
eases and are highly elevated in some cancers. When the
a i-peak is depressed,
i -antitrypsin deficiency (Chap-
) must be ruled out by direct measurements us-
ing sensitive quantitative methods. The presence of aq-
fetoprotein (AFP) in nonfetal serum is of clinical sig-
nificance because of its close association with primary
carcinoma of the liver. However, during pregnancy, AFP
synthesized by the fetus gains access in small but mea-
surable amounts to maternal circulation. Measurement of
maternal serum AFP (MSAFP) levels during the second
trimester is widely used to detect fetal abnormalities. In
neural tube defects, MSAFP levels are elevated, and in
Down’s syndrome, they are decreased (Chapter 38). Rou-
tine serum electrophoresis seldom gives such sensitive in-
formation, and specific immunochemical methods should
be employed to detect
i -fetoprotein in the serum.
globulin, aq-microglobulin, ceruloplasmin, erythropoi-
etin, and cholinesterase. Haptoglobin is nonspecifically
increased in the acute stress reaction in the presence of
inflammation, tissue necrosis, or destruction. A function
of haptoglobin is to combine with hemoglobin to remove it
from the circulation. Thus, during an episode of intravas-
cular hemolysis, haptoglobin is depleted and may require
a week or more to return to normal serum levels. Hap-
toglobin levels in these instances should be quantitated
by immunochemical procedures. oq-Macroglobulin func-
tions as a protease inhibitor (Chapter
). In the nephrotic
syndrome, there is a characteristic elevation of both
and /3 peaks with hypoalbuminemia (Figure VI-Id).
The elevation in
a 2
and /3 fractions is due to higher
very-low-density lipoprotein (VLDL) and low-density
nephritic syndrome include proteinuria (>3.5 g per
24 hours), hypoalbuminemia (<3 g/dL), hyperlipidemia
with elevated triglyceride and cholesterol levels, and
lipiduria and generalized edema. The exact mechanism
for the higher VLDL and LDL levels is not understood. In
part, these elevations may be due to increased synthesis
of VLDLs in the liver and then conversion to LDLs in
the peripheral circulation (Chapter 20), as well as their
decreased catabolism. It is thought that the decreased
plasma oncotic pressure due to hypoalbuminemia may
stimulate increased hepatic synthesis of VLDLs.
Increased glomerular permeability for protein due to
derangement in capillary walls is an early event in the
nephrotic syndrome that has several causes, as listed below
with examples:
1. Primary glomerular disease: membranous
glomerulonephritis, lipid nephrosis
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