Læknablaðið : fylgirit - 01.05.1978, Síða 121

Det.i r)i te Def H-SUStt . Controls Controls
(N-18) (N =24) Icel. N=182 Denmark
lfet locus
HLA-Al HL-Al) 17$ (3) 17$ (4) 20,7$ 31,1$
HLA-A2 HL-A2 ) 72$ (13) 79$ (19) 52,6$ i 53,6$
HLA-A3 HL-A3) 11$ (2) 13$ (3) 31,9$ 26,9$
HLA-A9 HL-A9) 50$ (9) 46$ (11) 22,4$ 17,3$
HLA-A10 HL-AIO) 11$ (2) 8$ (2) 6,1$
HLA-All HL-All) 11$ (2) 8$ (2) 14,7$
HLA-Aw25 HLA-Aw26 W 25) W 26) }l7$ (3) } 17$ (4) 3,8$ 5,9$
2nd locus HLA-B7 HL-A7) 22$ (4) 29$ (7) 40,0$ 26,8$
HLA-B8 HL-A8) 39$ (7) 29$ (7) 16,5$ 23,7$
HLA-B12 (HL-A12) 17$ (3) 13$ (3) 23,5$ 25,2$
HLA-B27 (W 27) 44$ (8) 42$ (10) 6,9$ 8,6$
HLA-Bwl5 (W 15) 6$ (1) 13$ (3) 19,1$ 17,9$
HLA-Bw35 (W 5) 22$ (4) 17$ (4) 7,1$ 13,1$
HLA-Bw40 (W 10) 33$ (6) 33$ (8) 20,9$ 17,9$
HLA-B18 (W 18) 10,4$ 7,1$
HLA-B18 Fudger 11$ (2) 8$ (2)
Table5: The HL-A ántipen frequencies in Icelandic SLE-patier.ts
Group tested
Uefinite SLE (N=18)
Def.+susp. SLE (N=24)
Control, Iceland (l>487)
F-^S FF_________FS SS______FS^
0 0 22$ (4) 78‘/»(14) 0
4$ (1) 4?í (1) 25$ (6) 67$(16) 0
0,62$ 2,1$ 29$ '66,3$ 0,21$
Table 6: Frequency of properdin factcr B pher.otypes in Icelandic
SLE-patients.
figures 29,7 from Halmstadt in 1964 -76 6) t and
from San Fransisco in 1965-’73^) are, however,
remarkably higher. The unusually high San Fran-
sico figure may perhaps be explained in part by
the fact that it stems from a closely controlled
group, members of the Kaiser Foundation Health
Plan.
The incidence of definite SLE in Iceland seems
to have risen over the last 10 years. The cases
are quite few, however, and thus not highly
statistically significant. The question is: If the
incidence has risen, then why? Increasing
awareness against SLE and better diagnostic
techniques might be a part of the explanation.
Regarding the age at the time of diagnosis,
relatively many seem to have been in the age
10-19. For comparison, Eyrich & al.6) had no
case below the age of 20 at the onset of symptoms.
The frequency of the ARA-criteria among the
definite cases shows obvious similarities to the
results of Cohen & al.6). The ARA-criteria
were initially based on those results. However,
some deviations are noted, e.g. our incidence of
leucopenia seems a bit high. This is perhaps
related to the observation that the average WBC
in the Icelandic population seems definitely lower
than in the American one. Yet we used 4000/
mm3 as the lower limit of normal.
The results of the HL-A typing on our SLE-
patients agree fairly well with those of the control
groups. There is, though, a statistically signifi-
cant (p< 0,001) increase in HLA-B27 compared
with the Icelandic control and a questionable
increase (0,05> p > 0,02) in HLA-A9.
A part of the explanation of this might be the
observation that a group of three near relatives
in our SLE-popuIation all had both HLA-B27 and
HLA-A9. Also, out of these 24 definite and
suspected SLE-cases a total of nine had both
HLA-A9 and HLA-B27. Does this say that these
patients all have a common ancestor from whom
they have got these antigens and some predis-
position for SLE has travelled along with the
HL-A antigen-combination ?
The hitherto published results concerning
association between SLE and any particular HL-A
<*
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