Philip Morris
Helicobacter Pylori Infection and Coagulation in Healthy People
Fields
- Author
- Duca, P.
- Imbesi, V.
- Maconi, G.
- Parente, F.
- Poggio, M.
- Porro, G.B.
- Rossi, E.
- Sangaletti, O.
- Imbesi, V.
- Type
- PSCI, PUBLICATION SCIENTIFIC
- BIBL, BIBLIOGRAPHY
- Area
- CARCHMAN,RICHARD/OFFICE
- Litigation
- Iwoh/Produced
- Characteristic
- EXTR, EXTRA
- MARG, MARGINALIA
- Site
- R530
- Named Organization
- Takeda Farmaceutici
- Author (Organization)
- Bmj
- L Sacco Univ Hospital
- Papers
- Univ of Milan
- L Sacco Univ Hospital
- Named Person
- Porro, G.B.
- Master ID
- 2063633486/4072
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Document Images
Papers
without major electrocardiographic abnormalities at
baseline (47% v 35%; difference 12.7% 5.1% to 20.7%).
Comment
On cross sectional analysis we found no association
between Hpflor/seropositivity and cardiovascular dis-
eases (assessed in several ways) in our 624 elderly sub-
ject~ Because H pflori seroposidvity did not predict
total or cardiovascular mortality during a five year fol-
low up, our results offer no evidence for an association
between Hpy/ar/infection and coronary heart disease,
and they differ from those reported recendy in
younger subjects.~ Our results do not exclude the
possibility that chronic Hpy/od infection acquired early
in life may increase the lifelong risk of coronary heart
disease. By analogy with serum cholesterol concentra-
don in elderly m~bject& controlled intervention studies
may be needed to a~certain whether eradicating
Hpylori infection in certain subgroups is worthwhile.
Funding: Ragnar Ekbetg Fotm.dation and YrjO Jahnsson
Foundation, Helsinki, Huland. Conflict of im~ None
Patel R Mendall MA. Carrington D, Smtchan D, Leatham E, Molineaux N,
a a/. Atu~:iation of Helicobacter pylori and Chhmydia pneumoniae
infections with coronary heart disease and cardiovavxdar risk factm-t
BMJ 1995",31 h711-4.
2 Murray LJ, Bamford KB, O'Reilly DPJ, McCrum EE, Evam AE.
Helkobacter pylori infection: reladon with cardiovasodar risk factort,
hdaaemic heart dttea~, and uxdal ciatt Br Heart.[ 1995;74:497-501.
S Kommen TU, HOOk J, Rantetin HI, Myllyla G. Age-dependent increate of
Campylobacter pylori anu]3odiet in blood donor~ S~andf
1989;24:110.4.
4 Lindroo$ M, Kupari M, HeikkiRt J, T'dvis RS. Pre~ence of aor6c valve
abnormalities in the elde~: an eehocardiographic study of a random
population sample.JAm Co//~ 1993;21:1220-5.
(acrtpud 15 Nomnk, r Z 996)
Helicobacter pylon infection and coagulation in healthy
people
Fabrizio Parente, Giow2nni Maconi, Venerina Imbesi, Omella Sangaletti, Marina Poggio,
Edoardo Rossi, Piergiorgio Duca, Gabriele Bianchi Porto
0
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Department of
Gastroenterology,
L S~ U~i~
Hospi~ Wm G B
G~ 74, 20157
M~ t~
F~o ~t~
Gio~ M~
V~ ~
G~fide B~
Po~
~of~
~tol~, L
S~ U~
Ho~i~ ~
D~t ~
M~ S~
~d Biome~,
U~v~i~ of ~
Co~nd~ce
~f~r
BMJ 1997'314:1318-9
Helicobaaer pylori infection has recendy been associ-
ated with an increased risk of developing ischaemic
heart disease.' * It has been suggested that chronic gas-
tritis related to Hpylori infection may increase, through
inflammatory mediators, the concentration of certain
coagulation factors such as fibrinogen,~ which are pre-
dictors of ischaemic heart disease2 We investigated the
potential assodadon between H py/or/infection and
abnormalities of plasma coagulation in healthy people,
with particular emphasis on the poss~ility of H py/or/
inducing a tendency tox~rards coagniadon, thereby
influencing the risk of ischaemic heart disease.
Subjects, methods, and results
Initially, 368 comecutive asymptomatic blood donors
(unpaid volunteers) were recruited for this study.
Exclusion criteria were age > 51 years, any chronic
drug treatment, recent intake of drugs interfering with
blood coagulation, use of oral contraceptives, previous
treatment for H pflor/infection, pregnancy or breast
feeding, and previous diagnosis of ischaemic heart dis-
ease, peptic ulcer, or any systemic chronic illnes,s.
Dietary habits, alcohol and cigarette consumption, and
sodoeconomic status were determined. A total of 300
subjects (229 men) aged 20-51 (mean 34.7) years
fulfilled the inclusion criteria and were enrolled into
the study. A resting venous blood sample was taken in
all subjects and was analysed for concentratiom of total
cholesierol, C reactive protein, plasma tibrinogen,
factor VII C, arid haemoglobin; erythrocyte sedimenta-
tion rate; prothrombin time; partial thromboplastin
time; and platelet and leucocyte count. Prothrombin
cleavage fragment (factors I and ID, an index of
prothrombin activation,~ was also assayed. IgG
anffbodies specific to H py/or/ were determined by
using a commercial ELISA kit (Helori test, Eurospital,
Trieste, Italy); a cut off value of 19% was used, based on
previous analysis of 200 patients (semidvity compared
with histology, 92%; spedfidty, 94%0). Student's t test
and the X~ test were used to compare characteristics of
subjects and values of haemostadc factors in subjects
with and without Hpy/or/irYection; multiple regression
was used to assess the effects ofcovariates.
The overall prevalence of H py/or/infection was
53% (158/300). Table 1 shows that subjects positive for
Hpy/or/were significantly older than those negative for
Hpy/or~ The groups did not differ significandy in other
characteristics or in values for plasma fibrinogen,
cholesterol, leucocyte and platelet count, erythrocyte
sedimentation rate, prothrombin time, partial throm-
boplastŁn time, and C reactive protein. However,
concentrations of factor VII C and prothrombin cleav-
age fragment were significandy higher in positive than
in negative subjects, though the association disap-
peared after adjustment by muldple logisdc regression
for age, sex, and sodal dass~
Comment
As plasma fibrinogen and total leucocyte count, which
are well known risk factors for ischaemic heart disease, ~
are increased in patients infected with H py/or/,' the
increased risk of ischaemic~heart disease in people
posidve for H py/or/may be mediated through raised
plasma fibrinogen concentrations. However, a large
cross sectional population survey failed to find a
significant association between H py/or/ and
fibrinogen.~ These studies may be biased because the)"
included patients with ischaemic heart disease, a
condition which could be associated with increased
concentrations of coagulation factors irrespective of
patients' Hpy/or/status. Comparing the concentladons
of circulating coagulation factors in healthy people
1318
I~MJ VOLL,%tESl4
3 MAY I997

Papers
Table 1 Mean (SD) age and circulating coagulation factors in healthy people with and without
Helicobacter pylori infection, and
multiple regression analysis using concentrations of factor VII C and prothrombin cleavage fragment
{factors I and II) as dependent
variables and H pylori status, smoking habits (0=no; 1=yes), sex (0=female; 1=male), and age (in
years) as independent variables
(ita14~)
(ea151) Olfleflllce or ˘on'M|tion co|fficleM (96% CI)
Vedeld~
Age (yeas) 32.2 (7.4) 37.0
(7.9) -4.8 (-6.54 to -3.06)
Ptatalet count (xl0S/1) 216.7 (42.9)
210.2 (50.9) 6.5 (-4.26 to 17.26)
Lelcoc'/ta count (x 108/1) 6.41 (1.6)
8.41 (1.8) 0 (-0.39 to 0.39)
Eq/t~ sedimentation rata 5.81 (4.2) 5.57 (5.2) 0.24 (-0.84 to
1.32|
C rzact~ protein (mg/1) 8.0 (6.0)
9.1 (7.0) -1.1 (-2.5 to 0.5)
Pto~rombin time (ratio) 0.93 (0.1)
0.93 (0.2) 0 (-0.04 to 0`04)
P'art~ thromboplastin time (ratio) 1.53 (0.2) 1.00 (0.2) 0`03
(-0.02 to 0`08)
Factor Vll:C (%) 84.6 (18,4) 89.3 (17.7) -4.7 (-6.80 to -0.60)
Rbrino~n (g/1) 3.36 (8.5) 3.42 (8.7) -0`06 (-2.20 to 1.90)
Factors 1 + 2 (nmoVl) 0.89 (0.3) 1.00 (0`4) -0.11 (-0.19 to -0.03)
Multiple ~egression
Prct~rombin cleavage fragment (/:1~0.54):
H pylon' status
0.002 (-0.05 to 0.59)
Smoking 0.075 (0.020 to
0.130)
Sex 0.080 (-0.145 to
-0.015)
Age 0.018 (0.014 to 0.022)
(Co~'tont) 0.318 (0.196 to 0.440)
Factor VII C (Re0.40):
H py/od status
1.209 (-2.768 to 5.188)
Smoking 8.017 (4.138 to
11.896)
Sea 4.748 (-9.332 to
-0.104)
Age 0.710 (0.458 to 0`9ei)
(Constant) 61.955 (53.390 to
70.520)
with and without H py/or/infection, we found that/-/
py/or/ infection is not associated with increased
circulating concentmtious of fibrinogen, factor VII:C,
or prothrombin cleavage fragment, or with other hae-
mostatic factors, which does not support the possibility
of this infection inducing a tendency towards a proco-
agulant state. Thus it seems unlikely that Hpy/or/infec-
tion predisposes the development of ischaemic heart
disease through effects on the coagulation system.
Funding: VI is partly funded by a grant from Takeda Farma-
ceudci Italia.
Conflict of interest: Non~
Mendall MA, Goggin PM, Molineaux N, LevyJ, Toosy T, Strachan D, a aL
Relation of Helicotmcm- wlori infecfon and coronary heart disease. Br
Hmrq 1994;71:4~7-9.
Murray LJ, Bamford KI~ O'Rcflly DP, McCrum EE, E~r~ AE.
Heiicobacm" pylori infection: retaken with cantiova.scul~ risk factors,
itchaemic heart dfneas~ and sodal ~ Br HmrtJ 1995;74:49%50L
Pa~ P, MendaIl MA, Carringy.on D, Strachan DP, Leatham E, Mo]ineaux
N, ~ a/. ~n of He~cobacter pylod and Chlamydia pr~umoniae
infecdom with coronary heart disease and cardiovasogar risk factors.
~ 1995;311:711-4.
PJ, a a~ F~rinogen, viscosity, and white blood cell count am major risk
favors for isc.haemic hear t disease. C/rcu/at/on 199 I'~3.'8~>44.
Mannucd PM, Tripodi A, Bottasso B, Baudo F,F'ma2zi G, De Stefano V, e*
a/. Marke~ of procoagulant imbahace in patient~ wlth inherited throm.
bo~c syndrom~ T'an~nbos/s and Ha,-ta0sta~/s 1992,'67:200-2.
(~ 29 No~J~r Z 996)
A memorable book
From magic to science
I graduated in Prague, Czechoslovakia, in 1939 one month before
the Czech capital was occupied by the Nazis. I was lucky to escape
to Palestine, where I joined the Czechoslovak Axmy, later to be
transferred to the Royal Army Medical Corps. In order to
acquaint myself with the British pharmacopoeia--somewhat
different from the cenwal European one--I looked up in the
hospital's small l~rary a textbook of clinical pharmacology. Itwas
in fact American--by Harry Beckmann-
Here I must point out that not only pharmacology but the
whole concept of medicine at that time was different on the
continent than in the Angio-Saxon world During our studies we
were inculcated with the deepest admiration for our elders, whose
views were not to be disputed. Traditions were sacred; the doctor's
social status was maintained by a pompous gravi~. Sceptical
questioning was frowned on, and even a trace of humour was
sacrileg~
Now I opened a book written in a highly readable, enterta/ning
style often spiced with humour. Drugs were evaluated with
caution. I still remember the following story. For many years acute
cholecystitis used to be treated by a drug, I forget its name as k
has been long forgotten by alL A few researchers in the United
States examined the bile from postoperative blliary fistulas after
having administered the drug. Not a trace of it or its metabolites
was found on analys~. A tenet of decades was destroyed in a
matter of weeks.
The iconoclastic questioning, the constant search for proof of
every hypothesis, has been the hallmark of medicine in the
Anglo-Saxon world. That is what I discovered in the booL Even
after 50 years living in England I are still filled with gratitude and
joy at having found out what turned medicine from magic to
science. Of course there are still small pockets of the old "sacred
cow" attitude here as much as ehewhere, but in general the
critical spirit of evidence guided medicine has taken firm root on
the continent It is up to politicians and economists to detibemte
whether Britain needs Europe. In medicine, however, Europe
certainly needs Britain.
Jan Pollen is a retired chest physician in lwndon
0
0
BM]" VOLUMESI4 SMAY 1997
1319
