Læknablaðið - 01.12.1978, Blaðsíða 70

204
LÆKNABLAÐIÐ
when we found his postulate confirmed
which tended to obscure the important
positive findings. We confirmed what
others had found, that when one member
of a family was affected, the incidence in
the family members was much increased.
Subsequently, this was shown for sibs in
Boston13 to be by a factor of five for sibs
of discordant sex and by a factor of nine
for sibs of concordant sex, surely a very
important pointer to an environmental fac-
tor in causation and to the importance of
very close personal contact.
But in the family cases53 we found two
other significant facts; firstly, that mem-
bers of the same family tended to develop
the same histologic subtype of H.D. which
suggests that the subtype developed might
depend on genetic factors. The other thing
noted previously is that where sibs lived
in the same house, the interdiagnostic inter-
val was one year (Mean 1.2, Range, 0.2—2
years), but if they lived in separate houses,
the interval was 3.4 years (Mean 4.1,
Range 0.8—8.7 years), surely also a very
significant feature.
It is now clear that the major deter-
minant in H.D. are the socio-economic
circumstances under which people live in
poor economic circumstances especially
with overcrowding the disease hits child-
ren, with high mortality, unfavourable
histologic subtypes, but with relatively
few cases in early adult life. We see this
in the U.S. in black/hite differentials,34 50
the blacks getting the disease chiefly in
childhood, of poor subtypes with few cases
in young adults, but the death rates in
adults far below that in whites. But this
pattern is also seen in U.S. whites living in
poor economic circumstances.
All the evidence I have tried to present
to you suggests at the very last, H.D. is
due to some agent in the environment. I
would also suggest that it points to an in-
fective cause. Every feature that in classi-
cal epidemiology was regarded as pointing
to an infective cause of a disease can be
demonstrated in H.D. Indeed we have
found that when close contacts of H.D.
patients migrate to other areas, then fresh
foci of the disease develop. True there is
a paucity of marital cases but this was
true of tuberculosis,30 true there has been
an inability to find children of parents
with H.D. affected.20 But the positive evi-
dence has steadily mounted.
Let me return to Uddstromer’s classic
paper47 in which he felt that the case re-
ported by Sisto was trying to tell us
something. The unfortunate surgeon had
removed a lymph node from a patient with
H.D. and in cutting open the node, he sliced
into his hand. He developed rapid involve-
ment of his axillary lymph nodes and died
of acute H.D. In the volume of the Rose
Research on Lymphadenoma from St.
Bartholemews Hospital in London,20 Lord
Horder referred to a surgeon who grinding
up tumour tissue crushed his fingers and
he forthwith developed and died rapidly
of acute H.D. These two cases seem to be
the only such in the world’s medical litera-
ture and they would seem to be telling us
something though in Lord Horder’s in-
stance, he did not state that the tumour
the surgeon was grinding was H.D. tissue
and enquiries made of Horder’s colleagues
and successors has not yielded further in-
formation. What could they be telling us?
Well it so happens that two further cases
have fallen within my personal experience.
The one case was drawn to our attention
by the wife of the affecteed individual
who, as a medical student, cut his finger
while dissecting the corpse of an individual
who had died of H.D. The wound dit not
heal and he developed axillary and servi-
cal glands and some neurologic lesions.
The gland removed showed typical H.D.
lesions and this has been confirmed by
many pathologists who have seen the slide.
With comprehensive treatment all evi-
dence of the disease remitted and the
patient is now well.
The second case was a young man who
was hoping to become a medical student,
so, as a medical corpsman in the US navy,
he assisted pathologists in a Navy Hospital
at autopsies. He too cut his finger at an
autopsy on a H.D. patient. He developed
fever, enlarged lymph nodes and died
rapily of what was called acute H.D. Now
here we have Sisto’s patient, and the two