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The prevalence of colorectal
adenomas in Māori and New Zealand Europeans parallels colorectal
cancer rates
Graeme Dickson, Chris W Cunningham, Susan Parry
New Zealand has a high incidence of colorectal cancer with
an age standardised incidence (non-Māori, 2005) of 51.9 per
100,000.1,3 However, the rate amongst the
Māori population appears to be approximately half that of the
non-Māori population.3 Despite this
difference the CRC mortality rate for Māori is no better than
non-Māori.2,3,17 This is partially
explained by a greater proportion of Māori presenting at a more advanced
stage.2 Correspondingly there is poorer
survival from diagnosis for Māori. The documented lower CRC incidence rate
for Māori remains unexplained. One potential explanation is incomplete
recording of ethnicity at the time of diagnosis.
To minimise the influence of any confounding factors we
decided to study the prevalence of adenomatous polyps which are the precursors
of colorectal cancer.4 The differences in
prevalence between ethnicities should reflect the differences in cancer
incidence.5
MethodsWe performed a retrospective review of all
colonoscopies recorded on the Middlemore Colonoscopy Audit Database between
1/7/01 and 31/12/05. Demographics, patient self-identified ethnicity, polyp
details and indication for colonoscopy were recorded. Indications which were
associated with a low prevalence of polyps (e.g. inflammatory bowel disease) or
a high prevalence (e.g. previous polyps, family history of cancer or abnormal
radiology) were excluded. The endoscopy database, Endoscribe, was used to
determine polyp location, number and size. Polyp histology was checked from case
notes and presence of high risk features (high grade dysplasia, tubulovillous,
size>1cm or >3 adenomas) documented.
Statistical analysis: Continuous data
was expressed as the mean ± standard deviation. A p value<0.05 was
considered statistically significant. Statistical analysis was carried out using
Graphpad.15 Proportions were analysed using
Fisher’s exact test and continuous variables with an unpaired
t-test.
Results2842 (2842) colonoscopies were performed for accepted
indications (2523 European, 319 Māori). The average age of the European
group (64.7±21.1) was significantly older than the Māori group
(55.8±14.2; p=0.0001). Accordingly to ensure parity we selected and
analysed only the 40-59 years age bracket as the majority of CRC occurs after
the age of 50 years, with precursor adenomas developing 5- 10 years previously.
This age bracket also had the highest number of patients identified as
Māori.
Average ages were not significantly different (Māori
50.2±6.3, European 50.4±6.3; p=0.72) and the sex ratio was also
comparable (Māori 44% male, Europeans 40.6%; p=0.46). At colonoscopy,
polyps were found in 213 Europeans (33.1%) but only 35 Māori (23.5%;
p=0.029). At histology, the adenomatous polyp rate in Europeans was 16.7%
compared to 8.7% in Māori (p=0.019; 8% difference, CI=2.3-13.9%).
Table 1 Polyps and colorectal cancer in the
40-59 year old age band
Amongst patients with adenomas, the percentage showing high
risk features was not significantly different (European 39.3%, Māori 38.5%;
p=1.0). There was also no difference in the average number of adenomatous polyps
per person (European 1.7±1.3, Māori 1.9±1.4; p=0.59) or location
in the colon (right colon in 41% European and 52% Māori; p=0.39).
Table 2. Adenomatous polyp characteristics,
location and number in the 40–59yr age band
DiscussionDifferences in the incidence of CRC, between ethnicities,
are likely to result from a combination of genetic and environmental factors.
Epidemiology suggests that colorectal cancer is highly
dependent on the environment. This dependence is illustrated by the high rates
of CRC in the offspring of Japanese immigrants to USA compared to the low rates
of CRC for Japanese in Japan.1 It is unlikely
that genetic predisposition to CRC would change so quickly.
Within the United States of America, African Americans have
an increased incidence of CRC compared to the White
population.6 The reasons for the higher
incidence are not known but environmental factors such as diet, exercise and
smoking have been implicated.7,8 Some
biological differences have also been noted. There is evidence of a more
proximal distribution of cancers and adenomatous polyps in African
Americans.9 Also, the rates of microsatellite
instability (MSI) in sporadic cancers are much higher in African Americans (45%)
than would be expected from the literature
(12-17%).10 MSI-high often implies a better
prognosis in CRC patients but its effect on the outcome of African Americans is
not clear. Overall, ethnic differences have led to the recommendation that CRC
screening starts 5 years earlier in African Americans (45yrs old).
However, recognised environmental risk factors do not appear
to explain the differences in incidence of CRC between Māori and NZ
Europeans.11 Factors associated with higher
risk of CRC are paradoxically more prevalent in Māori who are more likely
to be overweight and have higher intakes of fat, energy and alcohol than NZ
Europeans.12,13,16 Although vegetable intake is
similar in Māori and NZ Europeans, it has been suggested that the different
types of vegetables consumed may be
protective.14 Māori commonly eat
watercress, puha (sow thistle), melon, kumara and silverbeet in greater
quantities than NZ European. However evidence for the presence of
anticarcinogens in these particular foods is lacking.
An explanation for the reported difference in incidence of
CRC in Māori and the NZ European remains illusive. Our study contributes
usefully by showing that the prevalence of colorectal adenomas,
the precursor lesions in CRC, in Māori is approximately half that found in
NZ Europeans. This mirrors the reported difference in CRC incidence between
these groups.3 In addition, amongst patient
with adenomas there was no significant difference in the number of adenomas or
percentage of adenomas displaying high risk features between Māori and
European . Accordingly the poorer outcome for Māori with this disease may
reflect a lack of timely access to quality diagnosis and treatment, rather than
an adverse biologic predilection per se.
Further research comparing the biology and histology of
colorectal cancer between these groups would be required to strengthen this
conclusion. However, if timely access to quality medical
services is a concern the importance of health initiatives to improve outcomes
for CRC in Māori would be reinforced.
We recognise that the sample population in this study were a
symptomatic group and may not represent the general population. However, there
are limited opportunities to study the general (asymptomatic) population due to
the low autopsy rate and the absence of a CRC screening program in New Zealand.
Additionally, the number of adenomas in the Māori group was small and could
be associated with a type 2 error.
ConclusionThe prevalence of colorectal adenomas in Māori is
approximately half that found in NZ Europeans. This finding mirrors the reported
difference in colorectal cancer incidence and supports this being a real
finding. There were no significant differences between Māori and NZ
Europeans in the proportion of high risk adenomas, the total number of polyps
found and the location in right or left colon. This is potentially a positive
health finding for Māori as improvements in diagnosis and management of
colorectal cancer could see mortality rates halve.
Competing interests: None known.
Author Information: Graeme Dickson,
Research Fellow, Department of Gastroenterology, Middlemore Hospital, Auckland;
Chris Cunningham, Professor of Māori Health and Director, Research Centre
for Māori Health & Development, Massey University, Wellington; Susan
Parry, Gastroenterologist, Department of Gastroenterology, Middlemore Hospital,
Auckland
Correspondence: Dr Susan Parry,
Gastroenterologist, Department of Gastroenterology, Middlemore Hospital,
Auckland, New Zealand. Email: sparry@middlemore.co.nz
References:
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