Læknablaðið : fylgirit - 01.05.1978, Qupperneq 136

THERAPY PHA-P 1000>jg/ml ConA 100pg/ml PWM 5/jg/ml
AZATHIOPRINE 73812 i 15370 1 16893 i
n = 2 28863 939 4617
53343 t 21656 i 14133 1
D-PENICILLAMINE
n=5 16501 12604 10066
CHLOROQUINE 42310 t 19788 i 6101 i

n=2 23596 16530 8046
GLUCOCORTICO- 625931 17354 í 9916 t
STEROIDS
n=4 14114 5065 4651
TOTAL * 576601 18385 t 11676 i
n=13 18849 10509 7503
UNTREATED 495391 20883i 7557 1
PATIENTS**
n=12 29650 16440 7420
INDOMETHACIN * 7/13 ;~0/12 counts per minute S ♦ SD
MITOGEN INDUCED3H-THYMIDINE UPTAKE OF LYMPHOCYTES
INNORMAL POOL-SERUM. 25 PATIENTS WITH RHEUMATOID
ARTHRITIS WITH DIFFERENT TREATMENT
Slide 5 .
PHA-P SERUM
1000/jg/ml NATIVE HEATHNACTIVATED (56°C FOR 30MIN )
RHEUMATOID ARTHRITIS n«10 53364 ♦ 5358 36111 ♦16756
BLOOD DONORS n= 5 56460 ♦9496 54406 ♦9017
ConA lOO^ig/ml
RHEUMAT0ID ARTHRITIS n«10 21990 ♦ 5381 10984 ♦7750
BL00D D0N0RS n = 5 26222 ♦ 4561 20343 t 3745
PWM
5>jg/ml
RHEUMATOID 7378 4675
ARTHRITIS ♦2200 ♦3423
n=10
BLOOD 13290 14279
D0N0RS n=5 ♦4246 •1890
counts per mmute 8 *SC
DIFFERENCE STATISTICALLY SIGNIFlCANTp<0.05
MITOGENINDUCED 3H-THYMIDINE UPTAKE OF LYMPHOCYTES
FROM ONE HEALTHY DONOR IN NATIVE AND HEATHNACTIVATED
SERA FROM RA-PATIENTS AND BLOOD DONORS
Slide 6.
relationship of rheumatoid factors, of the severity
of the disease and of the drug therapy to the
depressed stimulation response of RA-lymphocytes
to mitogens. (3. Slide). The lymphocyte stimula-
tion in autologous serum from rheumatoid factor
(RF) positive patients with rheumatoid arthritis
did not differ from the results in the RF-negative
patients. (4. Slide). More advanced seemed to
have lower stimulation results with all mitogens
used, but the difference could not be confirmed
by statistical analysis using splitplot-analysis of
variance. The experiment has to be repeated
(5. Slide) in a larger series of patients. . Nearly
all patients were treated with antirheumatic drugs
at the time of examination. Because of the smail
groups of patients treated with one certain drug,
patients under therapy with Azathioprine,
D-peniciilamine, Chloroquine and Glucocorticos-
teroids were comprised. The lymphocyte response
in patients treated with these drugs (listed up
here) did not differ from the response of untreated
patients. About 2/3 of the patients in both groups
received indomethacin.
In a second experiment we studied the effect of
native or heat-inactivated serum from patients with
RA or from blood donors on the stimulation response
of blood donor lymphocytes to PHA, Con A and
Pokeweed mitogen.
The results are documented in the next slide.
(6. Slide).
The split-plot analysis of variance was carried
out separately for each mitogen because of
interactions between the factors serum treatment
and mitogen. Compared with the controls the LC-
response in the sera from patients with RA was
lower, if the lymphocytes were stimulated with
Con A, or PWM. The use of heat-inactivated
sera produced a decrease of PHA- or Con A-
stimulation of the donor lymphocytes. This
effect is also demonstrable with normal sera
but is more pronounced with RA sera. The
results from this experiment has to be recon-
firmed using other LC-donors, because in the
first experiment there was no evidence for serum
factors influencing the mitogen dependent
lymphocytes response.
C onclusions:
The first experiment has shown a cefl depend-
ent depression of the lymphocyte response to all
mitogens tested. Two interpretations are poss-
ible:
1) Different lymphocyte subpopulations have a
different responsiveness to certain mitogens.
A low LC-response may be caused by a
diminuition of the LC-subpopulation sensitive
for a certain mitogen. In RA however
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