From www.bloodjournal.org by guest on June 18, 2017. For personal use only.
Carbonic
Anhydrase
and
Fetal
Hemoglobin
in Thyrotoxicosis
By
LIE-INJo
LUAN
I
N A RECENT
REPORT
acterized
by a deficiency
of carbonic
anhydrase.
This
fetal
fetal
proof
were
hemoglobin,
hemoglobin,
of hereditary
caused
by
syndrome
rather
findings
These
had not
findings
than
hemoglobin.
\Ve
as
a specific
states,
now
with
disease
before.
to study
especially
report
the
thyrotoxicosis,
electrophoresis
of hemoglobin
amount
of
entity,
as
such
a combination
carbonic
with
occurrence
several
of
had
levels
increase
carbonic
of
anhydrase
an
of
anhydrase
unexplained
of whom
of Wilbur
method
the
H2C03
rate
in
red
the
blood
enzyme
required
and
by
is given
of
fetal
deficiency
increase
of HbF
level
cells
in
of
was
per
to reduce
units
the
method
the
upper
out
the
on
pH
the
blood
is based
is measured
enzyme.
measured
milligram
the blank
limit
of
normal.
diethylaminoethyl
Quantitative
(DEAE)
analysis
cellulose
of
column
and Dozy.7
red
which
METHODS
in starch
gel’ and in agar gel.5 Alkali denaturaof Singer
et al.,’ and 2 per cent of the total
of Huisman
of
presence
by
as
Anderson,8
change
the
carried
activity
and
AND
performed
taken
was
anhydrase
method
enzyme
done
was
by the method
Carbonic
arbitrary
was
components
chromatography
packed
was
hemoglobin
hemoglobin
value
FUDENBERG
1 described
a condition
char..
112 (also designated
B and C)
associated
with
a high
level
of
erythrocyte
those
MATERIALS
to
HUGH
blood.
hemoglobin
tion
H.
AND
Lie-Injo
and
of both
types
I and
deficiency,
though
been
described
prompted
us
disease
in the
HOLLANDER
was not due to hemoglobinopathy,
hereditary
persistence
of
or any of the known
types
of thalassemia.
Because
of lack of
basis
and uncertainty
whether
the changes
in the patient
a specific
etiology,
the condition
was
designated
as a new
in different
in patients
L.
ENG,
was
that
when
Enzyme
in
cells
on
two
CO2
of
by
Roughton
and
in
activity
different
estimated
solution
in
in
the
H20
hemolysates
concentrations
quantitative
Booth.’
By
is
prepared
and
from
expressed
Hb. A unit of activity
is defined
as that
reaction
time under
the stated
conditions
this
converted
in
amount
of
to
its
half
formula:’
From
the G. W. looper
Foundation
and the Section
of Hematology
and Immunology,
Department
of Medicine,
University
of California
Medical
Center,
San Francisco,
Calif ornia,
and the Permanente
Medical
Group,
Oakland,
California.
This study
was
supported
by Research
Grant
ROl HE 10486-10
GEN
from
the NIH,
USPHS;
by the University
of California
international
Center
for Medical
Research
and
Training
(Ilooper
Foundation,
San Francisco
School
of Medicine)
with
Research
Grant
TW 00144
from
the Office
of international
Research,
NiH,
USPHS;
by a grant
front the
University
of California
School
of Medicine
Committee
on Research;
and by a hematology
Training
Grant,
HE 05677,
NiH,
USPHS.
First submitted
Feb. 29, 1967;
accepted
for publication
April
7, 1967.
LIE-INJo
LUAN
ENG,
M.D., PH.D.,
D.T.M.
& H.: Associate
Research
Hematologist,
Tile
G. W. Ilooper
Foundation,
University
of California
San
Francisco
Medical
Center,
San
Francisco,
Calif.
L. HOLLANDER,
M.D.:
Chief,
Department
of internal
Medicine,
Permanente
Medical
Group,
Oakland,
Calif. 11. HUGH
FUDENBERG,
M.D.:
Professor
of Medicine,
Section
of Hematology
and immunology,
Department
of Medicine,
University
of California
San Francisco
Medical
Center,
San Francisco,
Calif.
442
BLOOD,
VOL.
30,
No.
4 (OcTonEli),
1967
From www.bloodjournal.org by guest on June 18, 2017. For personal use only.
CARBONIC
ANHYDRASE
AND
SA
FETAL
443
hEMOGLOBIN
F
Pat.
L.R.
before
treatment
.-
Pat
#{149}
L
#{149}
after
.R
treatment
Father
Son
L.
Fig.
showing
F after
1.-Agar
significant
treatment.
gel
electrophoresis
amount
of Hb
Carbonic
buffer
pH
9.5
of
which
gel
was
the
lowed
Hiiusler’s
pH
6.2
Mrs.
L.R.,
the
and
hemolysate
of
strongly
reduced
absence
of enzyme.
patient
L.R.,
amount
of Hb
the
-
was
Haut
et
rates
in the
qualitatively
al.’#{176}
and
stained
with
units
presence
and
visualize(l
pH
at
amido
8.6
by
with
black.
starch-gel
electrophoresis
Tris-HC1-boric
Specific
using
acid-EDTA
staining
for
buffer,
carl)onic
the
after
aiiliydrase
fol-
method.”
CASES
and
of
F before
________
R
=
.
R
anhydrase
major
R -R.
Activity
11 and
Thalassernia
a 44-v(ar-old
nervousness
of long
Negro
duration.
STUDIED
woman,
complained
She
a past
had
of
history
loss
of
of
weight,
anemia
fatigue,
one
year
irritability,
previously,
for
she was treated
with iron
and
vitamin
B12 injections.
When
examined
on January
17,
1966,
she was found
nonanemic
and
without
jaundice.
11cr
thyroid
was
moderately
and
diffusely
enlarged,
and
she had
clinical
signs of thyrotoxicosis.
Laboratory
findings:
lib 12.6 Cm./100
ml., \VBC
and
platelet
counts
normal.
Sickling
test of the red 1)100(1 cells was positive.
Alkali-resistant
hemoglobin
was 17 per cent of total.
On electrophoresis
in cellulose
acetate,
lIb
S was
30 per cent
of the
total
hemoglobin.
No
other
abnormal
hemoglobin
was
detected.
Bone marrow
was
normal
with
normal
amount
of iron. Protein-bound
iodine
was
10.2 pg. per cent.
Serum
iron
was
normal.
Findings
in
the
first
half
of February,
1966
were:
lIb 13.9 Cm./100
ml.; PCV 41.5 per cent;
\VBC
and
platelet
counts
normal.
Differential
count
of the white
blood
cells
normal.
hemoglobin
analysis:
Hb
F 19.0
per
cent,
lib
5 31.9
per
cent,
Hb
A 46.0
per
cent,
and
Hb
A2 3.1
per
cent.
The
presence
of Jib
S was
confirmed
by a positive
sickling
test,
i)y starch-gel
which
and
agar-gel
by agar-gel
showed
electrophoresis;
the
electrophoresis
that
Hemoglobin
hib F ranging
tile
fetal
analysis
from
(see
hemoglobin
repeated
19
presence
Fig.
to 20
was
on
per
1).
two
cent
of
The
Hb
F
was
acid-elution
technic
heterogeneously
different
of the
distributed
days
total
shown
gave
hemoglobin.
essentially
by
alkali
of
denaturation
Klcihauer
in
the
the
same
and
red
1)100(1
pattern,
and
Betke’2
cells.
vitii
From www.bloodjournal.org by guest on June 18, 2017. For personal use only.
444
LIE-IN
JO
LUAN
ENG
ET
AL.
Thalassemia
Pat.
L.R.
after
Pat.
L.R.
before
treatmer.
treatmel.
Normal
Norn].
Fig.
2.-Starch
gel
carbonic
anhydrase
was
drawn
on the
This
hemoglobin
known
patterns
thought
the
anhydrase
level
was
types,
B and
it
been
diminished.
Since
test
her
pattern
it
not
into
red
(I
C
was
the
be
patient
possibility,
red
cell
carbonic
16,
1966,
thyrotoxic,
was
suitable
cells
Hb
F;
then
lib
On
43.1
6.6
ve
28
Hb
cent.
normal,
62.9
1 grain
of
January
7,
elevated,
goiter.
an
enlarged
of
1967.
per
August
and
A
Hb.
Because
and
carbonic
cent
of
the
showed
a paternal
paternal
uncle
2),
4.4
the
signs
of
Hb
but
had
per
the
March
35 per
S was
patient
this daily dosage
when
level
was normal,
but
the
was
on
cent
level
of
further
anhydrase
on
cent,
patient
seen
dropped
carbonic
hypothyroidism
pg.
anhydrase
of Hb F
cent,
February
obviously
The
carbonic
level
On
an increase
of
A2 was normal.
when
and
To
her
still
14.5
deficient.
cent
erythrocyte
per
tendency
to
had
been
hospitalized
had
paternal
parents,
a son,
without
enlargement
the
limits
of
Tile
and
each
normal
normal.
per
11
PB!,
Hb
was
27,
was
hemoglobin;
improvement
carbonic
measured
with
clinical
F
she
weight.
still
to
to
level
then
was
was
given
we saw her again
on
Jib F was still slightly
hemoglobin.
physically
lower
the
Another
we
carbonic
led
unchanged
showed
still
a strong
aunt
more
of
anhydrase
total
lost
was
July
of
was
the
hemoglobin.
treatment.
14,
higher,
was
have
after
March
essentially
Hb
F
and
On
amount
Fig.
JIb
day
Her
thyroid.
examined
(see
had
total
On
of
indeed
possibly
slightly
euthyroid.
30,
per
history
the
and
normal
1-131.
was
half
anhydrase;
might
during
of
and
hemoglobin.
was
8 mc.
although
solution
units/mg.
grandfather
for
below
carbonic
any
Therefore,
an increase
of fetal
hyperthyroidism
and carefully
hemoglobin
of
fit
combinations.
to
for
analysis
appeared
thyroid
family
fetal
of
condition
patient
did
their
showing
controls
deficient.
While
in 70 normal
controls
a
the patient’s
erythrocyte
carl)onic
anhydrase
of the
two
different
carbonic
anhydrase
separately
; however,
from the electrophoretic
primarily
(lecreased,
type
C might
also
have
indirectly,
tachycardia,
Lugol’s
On
6.0
this
dose
level,
she
units/mg.
The
and
oral
definitely
study
was
or
Hemoglobin
amount
B
the
with
the
estimated
directly
an
and
or
definitely
type
anhvdrase
total
per
was
not
treated
received
with
for
thyrotoxicosis,
anhydrase
April
was
and,
S was
treated
the
had
increased.
carbonic
)
II
unusual,
Hb was found,
The
activity
although
hyperkinetic
still
The
and
deficiency
she
distinctly
hemoglobinopathy,
blood
that
this
We
black,
normal
would
seems
anhydrase
of
amido
of the
of 38.4 to 70.9 units/mg.
only
20 units/mg.
Hb.
pattern,
31.
with
blood
of thalassemia,
patient
in
electrophoresis
pH 9.5
stained
before
and
after
treatment.
The
same
dates
as those
of the patient.
aunt
and
two
of
father,
(lied
a large
paternal
who
disease.
years
appeared
but
of
her
after
respiratory
thyroid
uncles
thyroid
of
patients
The
previously
because
had
the
thyroid
several
but
the
Hb
physically
paternal
an
operation
difilculty
no
clinical
patient.
level
The
and
normal
due
to
symptoms.
mother
PCV
without
was
were
at
clear
From www.bloodjournal.org by guest on June 18, 2017. For personal use only.
CARBONIC
Table
ANHYDRASE
AND
1.-Erythrocyte
Carbonic
44
24
23
32
27
36
7
F
14
8
10
M
M
F
14
50
63
11
F
71
12
F
37
13
F
17
9
CA
Carbonic
=
Carbonic
increase.
The
were
at the
was
otherwise
difficult
activity
son
entirely
Hb F level
sponse
to
anhydrase
symptoms
studied
in
Thyrotoxicosis
CA
units/mg.
Hb
Hb
F
+
+
20.0
17.0
5.1
+
30.3
+
+
+
30.6
0.7
1.6
1.1
0.5
1.2
1.8
0.7
19.5
27.1
31.8
50.0
16.5
24.1
-
+
+
59.5
0.8
±
47.7
31.9
2.9
0.8
+
29.5
1.6
+
-
in
70
normal
We
borne
normal.
healthy
therapy.
levels
in
normal
persons
red
limits.
the
blood
from
anhydrase
deficiency
Twelve
instituted.
for
Nine
had
were
ranges
also
him,
from
had
of
complaints
whom
and
1 that
38.4
to
70.9
who
the
units
results
not
low
enzyme
normal
globin
limits,
in one
in one
patient
with
was
radioactive
levels
were
not
was drawn.
In the three
tests gave normal
results
but radioactive
patient
with
normal
the one
studied
patients
in two;
when
enzyme
level
whose
PBI was
it
was
normal
blood
with
in the
to this
for
but
carbonic
function
lead
tests
to carof fetal
family
were
and
Hb F levels.
only after treatment
carbonic
his
in re-
the
increase
In
had
anhydrase
patients
with low enyzme
in six showed
a definite
borderline.
The other
two
for
carbonic
normal
enzyme
third
the PBI
to 2.9 per
test showed
anhydrase
levels,
thyroid
test was within
remained
elevated.
was
increased
to
increased
but the
S trait,
thyroid
may
of erythrocyte
iodine
uptake
enzyme
deficiency
disappeared
of
related
anhydrase
available
had normal
enzyme
levels.
In seven
of the nine
levels
thyroid
function
tests
were
carried
out. Tests
increase
of thyroid
function;
in one the results
were
estimation
function
had
to an
three
hospitalized
Hb
thyrotoxicosis
were
deficiency
been
the
we examined,
or indirectly,
erythrocyte
carbonic
for such studies
were
a definite
who
a carrier
his
normal
directly
patients
uncle,
was
relatives
in Case
and,
other
examined
opportunities
patient’s
cells
findings
paternal
thyroid,
we saw
all the
In
postulated
hemoglobin.
other
to an enlarged
normal.
By the time
was
therefore
most cases
The
due
iodine
within
with
F Levels
enlargement,
was
a carrier
of Hb
S trait,
and
his Hb S was definitely
Fetal
hemoglobin
was 2.4 per cent,
representing
a slight
unexplained
was
physically
normal,
had no Hb 5, and his hemoglobin
level and PCV
limits of normal.
One paternal
uncle
was a carrier
of the Hb S trait but
lower
breathing
been
Hb
Hb.
evidence
of thyroid
below
50 per cent.
were
and
Anhydrase
anhydrase
mg.
Activity
Clinical
when
F
M
F
M
M
M
1
2
3
4
5
6
iir
Anhydrase
Age
No.
445
HEMOGLOBIN
Sex
Case
*
FETAL
Fetal
hemo5.1 per cent;
cent.
This
latter
a high uptake
of
iodine.
DIscussIoN
The
hemoglobin
pattern
in
the
first
patient
was
unusual-consisting
of an
Hb
From www.bloodjournal.org by guest on June 18, 2017. For personal use only.
446
LIE-INJO
S level
of
less
normal
Hb
than
50
A2 level,
per
and
cent,
the
a high
rest
Hb
Hb
A-and
patterns
found
in hemoglobinopathies,
homozygous
sickle-cell
anemia,
one
F level
of
did
follow
not
thalassemia
would
expect
LUAN
about
ENG
19
any
ET
per
AL.
cent,
a
of the
known
or their
combinations.
the hemoglobin
to be
almost
in
all Hb 5, with a small
amount
of Hb F and no Hb A. In Hb S-beta
thalassemia
one would
expect
an Hb S level of more
than
50 per cent and an increase
Hb A2; also,
no evidence
of beta
thalassemia
was found
in either
parent
of
of
this
in
patient.
In
Hb
Hb S associated
exceeds
50 per
geneous,
while
plained
high
of the
and
S-alpha
level
of fetal
concomitant
the
normal
caused
in the
in nine
toxicosis
toxicosis
there
hemoglobin
the
thyroid
results
in erythrocyte
treatment,
the carbonic
erythrocytes.
carbonic
all
led
to
anhydrase
The finding
function
In
the
for
tests
the
thyroid
per
to 4.4
anhydrase
the
cent)
per
that
deficiency
and
of an erythrocyte
the
F. Also
Hb S usually
cells is homoThe
unex-
before
treatment
after
treatment,
cent
level,
conclusion
deficient
before
thyrotoxicosis
increase
carbonic
were
normal,
one.
In
this
last
may
Increased
require
the
(3)
The increase
with an enzyme
postulate
that
red
of the
anhydrase
and
probably
of fetal
anhydrase
hemoglobin
deficiency
for
carbonic
becomes
reached
level
unexplained
for
and
carbonic
anhydrase
substances
elevated.
Hb
was
anhydrase
F level
An
the
patient
normal
points
The
anhydrase
borderline
presence
or
the
deficient
carbonic
Thyrotoxic
substances
of metabolism
in
amount
of CO2.
anhydrase
in the
lead
This
red
to depletion
depress
the
production
may
thyro-
is accompblood
cells.
of the
avail-
of carbonic
in the first patient
and in two others,
one
without,
is hard
to explain.
It is tempting
to
hemoglobin
is a compensatory
mechanism
normal.
after
(1)
increase
may
may
hepatospleno-
carbonic
two
and
method),
antithyroid
microsomal
LATS
activity
(bioassay)
showed
of an increased
long
after
her carbonic
anhydrase
elevation
of her Hb F level
while
the enzyme
an
the time
we estimated
clinical
symptoms
and
erythrocyte
results
slightly
cells are possible:
activity.
(2) An
of fetal hemoglobin
deficiency
and one
the increase
of fetal
level
was
had
F was
enzyme
Thyrotoxic
by chronic
carbonic
is 100 to 120 days,
however,
Hb
(agglutination
method),
disposal
help
demand
able enzyme.
anhydrase.
she
At
from
carbonic
anhydrase
or Hb F levels.
relating
to the mechanism
of
anhydrase
activity
in the
inhibit
carbonic
anhydrase
with
but
one
of antithyroglobulin
(fluorescent
antibody
toxicosis
continuously.
she was free
three
patients
with
normal
function
tests
gave
normal
no correlation
with
Several
explanations
caused
cytes
of Hb
other
cases
of hyperthyroidism
also supports
the assumption
that thyroleads
to carbonic
anhydrase
deficiency.
Of the three
cases
of thyrowith
normal
carbonic
anhydrase
level,
one patient
had thyrotoxicosis
absence
antibody
lished
increase
1 (19.5
decrease
from
childhood
but had been
treated
her carbonic
anhydrase
and fetal
Hb,
megaly.
level,
is no
in Case
thyrotoxicosis,
changes
after
thalassemia
with
hereditary
persistence
of fetal
hemoglobin,
cent and the distribution
of Hb F in the red blood
in this patient
the distribution
was heterogeneous.
deficiency.
may
still
Hb
had
be
F level
been
Since
the
present
of
level
had
returned
she was taking
the
more
4.4
treated
to a direct
lifespan
when
the
per
cent
for
about
to normal.
thyroid
drug
influence
of erythrocarbonic
in
Case
5 months,
The
and
of the
slight
while
thyroid
1,
From www.bloodjournal.org by guest on June 18, 2017. For personal use only.
CARBONIC
ANHYDRASE
hormone
on the
AND
FETAL
increase
of Hb
F. Also,
the
who
was not deficient
in erythrocyte
theory
that deficiency
of the enzyme
the possibility
that thyrotoxic
substances
production,
even
Furthermore,
elevation
without
carbonic
the possibility
of fib F, together
may represent
and independent
What part,
symptoms
increase
anhydrase
remains
Addendum:
Dr.
B carbonic
deficiency,
J. \Veatherall
D.
hyperthyroidism.
Dr.
by the
uncertain.
has
deficiency
warrants
\Veatherall
thyroid
further
Hb
plays
study.
F production
in producing
since
clinical
the
disease
is
rate, the disposal
of increased
If so, further
studies
of the
appear
clearly
warranted.
informed
us
Dr.
believes
father,
the persistent
slight
of fetal hemoglobin
Nevertheless,
he and
F in the
does not fit into the
increase.
Therefore,
of fetal hemoglobin
involving
an increased
metabolic
tissues
may be necessary.
deficiency
in thyrotoxicosis
anhydrase
of Hb
in mind
that
slight
elevation
some
type of genetic
defect
directly
of thyrotoxicosis.
if any, carbonic
anhydrase
deficiency
in thyrotoxicosis
depressed
slight
carbonic
anhydrase,
was the cause
of the
lead to an increase
must
be kept
with the father’s
a condition
associated
with
amounts
of CO2 from the
role of carbonic
anhydrase
type
447
HEMOGLOBIN
that
the
B. F. Rieder
that
type
patient,
whose
described,
13
B carbonic
had
anhydrase
is
hormones.
SUMMARY
An
adult
patient
deficiency
and
with
an
of the hyperthyroidism,
and the level
of Hb
and
not
under
an
related
increase
had
high
level
erythrocyte
of fetal
the erythrocyte
carbonic
F dropped.
Twelve
other
to
treatment.
this
Nine
of fetal
hemoglobin,
thyrotoxicosis
abnormally
index
had
case
were
hemoglobin.
erythrocyte
anhydrase
patients
studied.
erythrocyte
The
of
possible
treatment
them
were
deficiency;
of increase
anhydrase
relationship
anhydrase
anhydrase
After
level became
normal
with
hyperthyroidism
Most
carbonic
carbonic
carbonic
hemoglobin.
deficiency
and
already
two had
of fetal
thyrotoxicosis
is
discussed.
SUMMARIO
Un
patiente
carbonic
adulte
e anormalmente
thyroidismo,
le
hemoglobina
similemente
esseva
con
jam
alte
nivello
descendeva.
studiate.
Nulle
de
de
carente
nivellos
hemoglobina
anhydrase
Dece-duo
tractamento.
e duo habeva
un augmento
augmento
de hemogiobina
habeva
niveilos
erythrocytic
fetal
sub
IN INTERLINGUA
thyrotoxicosis
fetal.
carbonic
altere
de illes
esseva
Novem
manifestava
del
carentia
de
anhydrase
tractamento
del
normal,
con
consanguineo
Es
le
deveniva
patientes
de hemoglobina
fetal.
fetal, carentia
erythrocytic
erythrocytic
Post
e le
hyper-
nivello
hyperthyroidismo
probando.
Le
erythrocytic
de
commentate
de anhydrase
majoritate
del
anhydrase
le relation
carbonic,
de
esseva
12
carbonic,
possibile
inter
e thyrotoxicosis.
ACKNOWLEDGMENT
We wish to thank
all colleagues
who
provided
blood
especially
Dr. A. Blum of the Thyroid
Clinic,
University
Center,
the
who
Section
also
carried
out
of Hematology
the
LATS
activity
and
Immunology,
and
Tarail,
samples
(bioassay)
who
from
thyrotoxicosis
of California
San
studies,
carried
out
the
and
thyroid
patients,
Francisco
Dr.
K.
Medical
Wuepper
antibody
studies.
Nature
(London)
of
REFERENCES
1.
Lie-Injo
Carbonic
persistence
Luan
Eng
anhydrase
of
foetal
deficiency
haemoglobin:
R.:
new
with
syndrome.
211:47,
A
2.
Tashian,
1966.
R.
E.,
and
Shaw,
M.
W.:
In-
From www.bloodjournal.org by guest on June 18, 2017. For personal use only.
448
LIE-LNJO
heritance
of
esterase
variant
Hum.
3.
an
Genet.
Rickli,
E.
bons,
E.,
bonic
anhydrases
rocytes:
Preparation
two
enzymes.
J.
4.
S. A. S., GibJ. T.: Carfrom human
erythand properties
of
Biol.
Chem.
9.
239:
10.
A. R.,
P.,
and
Robson,
Zuelzer,
M.,
W.
Harrison,
W.:
A
1957.
Singer,
K.,
L.:
Studies
Blood
Huisman,
by
The
effect
pH
and
on
abnormal
means
of
alkali
6:413,
1951.
T. H. J., and
Studies
on
hemoglobin.
E.,
12.
in
von
heterogeneity
The
use
A. M.:
292,
of
of
tris
aminomethanethe anion-exchange
of hemoglobins.
13.
C.
R.,
Cartwright,
M.
Carboanhy-
im
Modellversuch
Gewebsschnitten
1:29,
E.,
and
von
1:29,
1958.
Betke,
Anwendung
Hb F-haltigen
Ratten-
1958.
des
Zellen
Internist
K. I.:
Prak-
Nachweises
in
fixierten
(Berlin)
1:
1960.
Rieder,
R. F., and Weatherall,
D. J.:
A variation
in the
electrophoretic
pattern
of human
erythrocyte
carbonic
J.
acBio-
1946.
Wintrobe,
Histochemie
Kleihauer,
tische
disor-
the
anhydrase.
histochemischen
Blutausstrichen.
IX.
in
and
Histochemie
sickle-cell
upon
carbonic
M.: The
nonhemoglobin
erythrocytic
proteins,
studied
by electrophoresis
on starch
gel. J. Clin. Invest.
41:579,
1962.
H#{228}usler,C.: Zur Technik
und Spez-
nieren.
denaturation.
the
(hydroxymethyl)
HCL
buffers
chromatography
Singer,
AL.
concentration,
factors
drasenachweises
hemoglobins.
Dozy,
substrate
chem.
J. 40:319,
Haut,
A., Tudhope,
ifit#{228}tdes
50:745,
A. I., and
of
other
of
und
Chemoff,
I. Their
demonstration
in
anemia
and other hematologic
ders
11.
new
of hemo-
ET
Chromatogr.
19:160,
1965.
K. M., and Anderson,
N. C.:
Electrometric
and
colorimetric
determination
of carbonic
anhydrase.
J.
Biol. Chem.:
176:147,
1948.
Roughton,
F. J. W., and Booth,
V. H.:
G.
1959.
Robinson,
ENG
Wilbur,
tivity
technique
for differentiation
globin.
J. Lab.
Clin.
Med.
7.
8.
Edsall,
Smithies,
0.:
An improved
procedure
for starch-gel
electrophoresis:
further
variation
in the serum
proteins
of
normal
individuals.
Biochem.
J. 71:
A.
6.
J.
1964.
585,
5.
acetyl-
Ghazanfar,
B. H., and
1065,
erythrocyte
in man.
Amer.
14:295,
1962.
LUAN
1964.
anhydrase.
Nature
203:1364,
From www.bloodjournal.org by guest on June 18, 2017. For personal use only.
1967 30: 442-448
Carbonic Anhydrase and Fetal Hemoglobin in Thyrotoxicosis
LIE-INJO LUAN ENG, L. HOLLANDER and H. HUGH FUDENBERG
Updated information and services can be found at:
http://www.bloodjournal.org/content/30/4/442.full.html
Articles on similar topics can be found in the following Blood collections
Information about reproducing this article in parts or in its entirety may be found online at:
http://www.bloodjournal.org/site/misc/rights.xhtml#repub_requests
Information about ordering reprints may be found online at:
http://www.bloodjournal.org/site/misc/rights.xhtml#reprints
Information about subscriptions and ASH membership may be found online at:
http://www.bloodjournal.org/site/subscriptions/index.xhtml
Blood (print ISSN 0006-4971, online ISSN 1528-0020), is published weekly by the American Society of
Hematology, 2021 L St, NW, Suite 900, Washington DC 20036.
Copyright 2011 by The American Society of Hematology; all rights reserved.