Helicobacter pylori and cancer among adults in Uganda

Article (PDF Available)inInfectious Agents and Cancer 1(1):5 · November 2006with71 Reads
DOI: 10.1186/1750-9378-1-5 · Source: PubMed
Abstract
Data from Africa on infection with Helicobacter pylori (H. pylori) are sparse. Therefore, as part of an epidemiological study of cancer in Uganda, we investigated the prevalence and determinants of antibodies against H. pylori among 854 people with different cancer types and benign tumours. Patients were recruited from hospitals in Kampala, Uganda, interviewed about various demographic and lifestyle factors and tested for antibodies against H. pylori. In all patients combined, excluding those with stomach cancer (which has been associated with H. pylori infection), the prevalence of antibodies was 87% (723/833) overall, but declined with increasing age (p = 0.02) and was lower among people who were HIV seropositive compared to seronegative (p < 0.001). Otherwise, there were few consistent epidemiological associations. Among those with stomach cancer, 18/21 (86%) had anti-H. pylori antibodies (odds ratio 0.8, 95% confidence intervals 0.2-2.9, p = 0.7; estimated using all other patients as controls, with adjustment for age, sex and HIV serostatus). No other cancer site or type was significantly associated with anti-H. pylori antibodies. The prevalence of H. pylori reported here is broadly in accord with results from other developing countries, although the determinants of infection and its' role in the aetiology of gastric cancer in Uganda remain unclear.
BioMed Central
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Infectious Agents and Cancer
Open Access
Short report
Helicobacter pylori and cancer among adults in Uganda
Robert Newton*
1,3
, John L Ziegler
2,8
, Delphine Casabonne
3
,
Lucy Carpenter
4,9
, Benjamin D Gold
5
, Marilyn Owens
5
, Valerie Beral
3
,
Edward Mbidde
2
, D Maxwell Parkin
6
, Henry Wabinga
2
, Sam Mbulaiteye
2
,
Harold Jaffe
7
and the Uganda Kaposi's Sarcoma Study Group
9
Address:
1
Epidemiology and Genetics Unit, Dept. of Health Sciences, First Floor, Seebohm Rowntree Building, University of York, Heslington,
York, YO10 5DD, UK,
2
Uganda Cancer Institute and Makerere University Medical School, Kampala, Uganda,
3
Cancer Research UK Epidemiology
Unit, University of Oxford, Richard Doll Building, Roosevelt Drive, Oxford, OX3 7LF, UK,
4
MRC Programme on AIDS, Uganda Virus Research
Institute, PO Box 49, Entebbe, Uganda,
5
Division of Pediatric Gastroenterology and Nutrition, Department, Pediatrics, Emory University School
of Medicine, 2040 Ridgewood Dr., NE, Atlanta, GA 30322, USA,
6
International Agency for Research on Cancer, 150 Cours Albert Thomas, Lyon,
France,
7
Centers for Disease Control and Prevention, 1600 Clifton Road, Atlanta, Georgia, 30333, USA,
8
Dept. of Veterans Affairs and the
University of California, San Francisco, to the International Agency for Research on Cancer, France and
9
Dept. of Public Health, Oxford University,
to the MRC Programme on AIDS, Entebbe, Uganda
Email: Robert Newton* - Rob.Newton@egu.york.ac.uk; John L Ziegler - ziegler@itsa.ucsf.edu;
Delphine Casabonne - delphine.casabonne@ceu.ox.ac.uk; Lucy Carpenter - lucy.carpenter@nuffield.ox.ac.uk;
Benjamin D Gold - ben_gold@oz.ped.emory.edu; Marilyn Owens - ben_gold@oz.ped.emory.edu; Valerie Beral - pa.valerie.beral@ceu.ox.ac.uk;
Edward Mbidde - mbidde1@infocom.co.ug; D Maxwell Parkin - ctsu0138@herald.ox.ac.uk; Henry Wabinga - cancer-reg@infocom.co.uk;
Sam Mbulaiteye - mbulaits@mail.nih.gov; Harold Jaffe - Harold.Jaffe@dphpc.ox.ac.uk; the Uganda Kaposi's Sarcoma Study
Group - Rob.Newton@egu.york.ac.uk
* Corresponding author
Abstract
Data from Africa on infection with Helicobacter pylori (H. pylori) are sparse. Therefore, as part of an
epidemiological study of cancer in Uganda, we investigated the prevalence and determinants of
antibodies against H. pylori among 854 people with different cancer types and benign tumours.
Patients were recruited from hospitals in Kampala, Uganda, interviewed about various demographic
and lifestyle factors and tested for antibodies against H. pylori. In all patients combined, excluding
those with stomach cancer (which has been associated with H. pylori infection), the prevalence of
antibodies was 87% (723/833) overall, but declined with increasing age (p = 0.02) and was lower
among people who were HIV seropositive compared to seronegative (p < 0.001). Otherwise, there
were few consistent epidemiological associations. Among those with stomach cancer, 18/21 (86%)
had anti-H. pylori antibodies (odds ratio 0.8, 95% confidence intervals 0.2–2.9, p = 0.7; estimated
using all other patients as controls, with adjustment for age, sex and HIV serostatus). No other
cancer site or type was significantly associated with anti-H. pylori antibodies. The prevalence of H.
pylori reported here is broadly in accord with results from other developing countries, although the
determinants of infection and its' role in the aetiology of gastric cancer in Uganda remain unclear.
Background
The work described in this report was part of an epidemi-
ological study of cancer in Kampala, Uganda [1-7]. Data
from Africa on infection with Helicobacter pylori (H. pylori)
Published: 07 November 2006
Infectious Agents and Cancer 2006, 1:5 doi:10.1186/1750-9378-1-5
Received: 04 May 2006
Accepted: 07 November 2006
This article is available from: http://www.infectagentscancer.com/content/1/1/5
© 2006 Newton et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0
),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Infectious Agents and Cancer 2006, 1:5 http://www.infectagentscancer.com/content/1/1/5
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are sparse. Therefore, we examine here the role of antibod-
ies against H. pylori in relation to the risk of cancer and
investigate the prevalence and determinants of infection
among 854 people with different cancer types and benign
tumours.
Materials and methods
Full details of the methods are provided elsewhere [1,2].
Briefly between 1994 and 1998, we recruited adults 15
years or older with a new diagnosis of cancer from the
wards and out-patient clinics of the main hospitals in
Kampala, Uganda. After informed consent and counsel-
ling, patients were interviewed and tested for infection
with HIV-1 using the Cambridge Bioscience Recombigen
ELISA (Cambridge, MA) on sera or the GACELISA method
(Murex, Dartford, UK) on saliva. Cancer diagnoses were
established by histology or other laboratory investigation,
where possible. Diagnoses made on clinical grounds
alone were reviewed by the investigators. The study was
approved by the Committee on Human Research (VA
Medical Centre and University of California San Fran-
cisco) and by the Uganda National Council for Science
and Technology.
Following HIV testing, remaining sera were stored at
minus 80 Celsius and were later shipped on dry ice to the
Centres for Disease Control and Prevention, Atlanta, USA,
for H. pylori testing. Assays were performed by a single
investigator who was blind to the diagnosis of the patient
from whom the blood was obtained. Briefly, H. pylori
organisms were grown overnight in brucella broth
(GIBCO Laboratories, Madison, WS) with 10% fetal
bovine serum (Sigma, St. Louis, MO), 5 μg/ml trimetho-
prim and 10 μg/ml vancomycin (Sigma). H. pylori antigen
extraction and protein isolation were done by gentle
freeze-thaw sonication (Heat System, Farmingdale, NY)
[8,9]. A standard protein assay (Pierce, Rockford, IL) was
used to determine the accurate and reproducible quantity
of solid-phase antigen for our microtitre research ELISA
[10]. Cross-reactivity and specificity of H. pylori whole-cell
antigens has been described previously [9,10]. Optical
density (OD) values at a wavelength of 492 nm were
determined in triplicate for each biopsy-confirmed con-
trol patient sera, using a standard 96-well microtiter plate
ELISA spectrophotometer (Fisher Scientific, Pittsburgh,
PA). The mean OD values were then calculated. The ELISA
cut-off values were derived using known H. pylori-positive
and negative control sera as previously described [9,11].
In previous validation studies the assay has demonstrated
a high and reproducible sensitivity and specificity in Afri-
can patients as compared to upper endoscopy and biopsy;
sensitivity >88%, specificity >90% [9,11].
Serological results were available for 50 people with non-
malignant manifestations of HIV disease, recruited from
the out-patient department of Mulago hospital and for
804 patients with cancer or benign tumours, for whom a
stored blood sample was available for testing. The latter
group comprised people with cancers of the oral cavity
(26), oesophagus (38), stomach (21), liver (52), skin
(22), breast (69), cervix (190), ovary (22), prostate (10),
penis (14), eye (63), and non-Hodgkin's lymphoma (46),
Hodgkin's disease (24), Kaposi's sarcoma (46), other can-
cer sites or types (126) and benign tumours (35).
Data were computerised by trained clerks using EPI-INFO
software (CDC, Atlanta) and statistical analyses were con-
ducted using STATA (STATA Corporation, Texas). Only a
small proportion of those tested were seronegative for
antibodies against H. pylori (optical density <0.9) or had
an indeterminate result (optical density 0.9–1.3). In all
analyses, those with indeterminate results were consid-
ered to be seronegative. In order to examine potential con-
founding factors, the risk of being seropositive for
antibodies against H. pylori was examined in relation to
various social and demographic factors among all patients
combined (but excluding stomach cancer, which has been
associated with H. pylori infection). Odds ratios (OR) were
estimated using unconditional logistic regression model-
ling with adjustment for sex, age group (<30, 30–45, 46+)
and HIV serostatus. When calculating odds ratios in rela-
tion to anti-H. pylori antibodies, for each cancer site or
type, the comparison group included all other patients
with the exception of stomach cancer. Tests for association
used the χ
2
test for linear trend on one degree of freedom
and all p values are 2-sided. Risk factors for high titres of
antibodies against H. pylori were examined amongst all
patients combined (excluding stomach cancer), but no
clear associations were identified and the data are not
shown.
Results
H. pylori antibody status was available for 854 people;
87% (741) were seropositive, 4% (38) were seronegative
and 9% (75) had an indeterminate result. Table 1 shows
the association between H. pylori serostatus and selected
social and demographic factors among all patients exclud-
ing those with stomach cancer. The prevalence of antibod-
ies did not vary with sex, but declined with increasing age
(χ
2
1
= 5.1, p = 0.02) and was lower among people who
were HIV seropositive compared to seronegative (χ
2
1
=
16.2, p < 0.001). No other factor examined was associated
with antibodies against H. pylori with the exception of reli-
gion: the prevalence of antibodies was higher among Mus-
lims than among Christians (χ
2
1
= 5.6, p = 0.02).
Table 2 shows the association between anti-H. pylori anti-
bodies and specific cancer sites or types, together with the
proportion of cancers with a laboratory verification of
diagnosis. Overall, 62% of cancers were diagnosed on the
Infectious Agents and Cancer 2006, 1:5 http://www.infectagentscancer.com/content/1/1/5
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basis of histology or other laboratory investigation, but
the figure varied by cancer site or type, being lowest for
prostate cancer (44%) and highest for Kaposi's sarcoma
(91%). Of those people with stomach cancer, 90% (19/
21) had the diagnosis confirmed by a laboratory investi-
gation.
Among 21 cases with stomach cancer, one was HIV serop-
ositive, 13 were women, one was aged <30 years, three
Table 1: Odds ratios (OR) for H. pylori seropositivity according to various social and demographic factors among all patients (excluding
those with stomach cancer)
Variable Number positive/
total
OR (95% CI)
1
Variable Number positive/
total
OR (95% CI)
1
Sex Time to market
Male 247/284 1.0 <30 minutes 323/375 1.0
Female 476/549 0.9 (0.6–1.3) 30+ minutes 278/320 1.0 (0.7–1.6)
χ
2
1
= 0.5, p = 0.5 χ
2
1
= 0.0, p = 0.9
Age group Size of community
<36 years 269/309 1.0 >100 houses 220/262 1.0
36–50 years 250/282 1.0 (0.6–1.6) 10–99 houses 421/482 1.3 (0.9–2.1)
51+ years 204/242 0.5 (0.3–0.9) <10 houses 51/57 1.6 (0.6–4.1)
χ
2
1
= 5.1, p = 0.02 χ
2
1
= 1.0, p = 0.3
HIV serostatus Ever travel from
home
Negative 514/574 1.0
Positive 201/250 0.4 (0.3–0.6) Yes 91/109 1.0
χ
2
1
= 16.2, p<0.001 No 599/688 1.4 (0.7–2.5)
χ
2
1
= 1.0, p = 0.3
Region of residence Household size
Kampala 161/188 1.0 <6 people 357/410 1.0
Rest of Uganda 560/643 1.0 (0.6–1.6) 6+ people 354/411 0.8 (0.5–1.2)
χ
2
1
= 0.0, p = 0.9 χ
2
1
= 1.6, p = 0.2
Tribe Number of siblings
Baganda 349/410 1.0 <6 siblings 379/438 1.0
Other 374/423 1.2 (0.8–1.8) 6+ siblings 333/384 0.9 (0.6–1.4)
χ
2
1
= 0.8, p = 0.4 χ
2
1
= 0.1, p = 0.8
Religion Number of
children
Muslim 95/100 1.0 <7 children 341/397 1.0
Christian 619/723 0.3 (0.1–0.8) 7+ children 290/329 1.1 (0.7–1.8)
χ
2
1
= 5.6, p = 0.02 χ
2
1
= 0.1, p = 0.8
Occupation Tobacco
consumption
Cultivator 334/387 1.0
Other 382/439 1.1 (0.7–1.9) Never smoker 562/647 1.0
χ
2
1
= 0.1, p = 0.8 Past smoker 81/92 1.2 (0.6–2.5)
Current smoker 68/82 0.7 (0.4–1.4)
χ
2
1
= 0.5, p = 0.5
Education level Alcohol
consumption
No school 153/175 1.0
Primary 361/415 0.9 (0.5–1.6) Never 391/443 1.0
Secondary/tertiary 191/225 0.7 (0.4–1.4) About once/week 134/157 0.8 (0.5–1.4)
χ
2
1
= 1.0, p = 0.3 2–4 days/week 91/106 0.9 (0.5–1.6)
Most days 93/113 0.7 (0.4–1.2)
χ
2
1
= 1.6, p = 0.2
Household Income
(Ug. Sh.)
Lifetime number of
sexual partners
15,000+ 464/533 1.0 1–2 partners 182/204 1.0
<15,000 196/230 0.9 (0.6–1.5) 3–9 partners 305/352 0.9 (0.5–1.5)
χ
2
1
= 0.1, p = 0.8 10+ partners 196/232 0.7 (0.4–1.3)
χ
2
1
= 1.2, p = 0.3
1. Odds ratios adjusted for age group (<30, 30–45, 46+), sex and HIV serostatus
Infectious Agents and Cancer 2006, 1:5 http://www.infectagentscancer.com/content/1/1/5
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were aged between 30–45 years and 17 were aged 46+
years. Among those with stomach cancer, 86% (18/21)
were seropositive for antibodies against H. pylori antigens,
compared to 87% (761/871) of the comparison group
(odds ratio = 0.8, 95% confidence intervals 0.2–2.9; χ
2
1
=
0.1, p = 0.7). Nor was there a statistically significant asso-
ciation between anti-H pylori antibodies and any other
cancer site or type examined.
Discussion
Here we report the first data from Uganda on the seroprev-
alence of antibodies against H. pylori. The prevalence of
87% was broadly comparable to that reported from other
hospital series elsewhere on the African continent: 79% in
Algeria [12], 71% in Côte d'Ivoire [12], 79% in the Dem-
ocratic Republic of Congo [13], 85% in Nigeria [14] and
86–93% in South African blacks [15,16]. In the only other
study of H. pylori from Uganda, Wabinga [17] identified a
high frequency of colonisation in gastric endoscopic biop-
sies from people with upper gastrointestinal symptoms.
Data on the determinants of infection with H. pylori in
Africa are scant. The prevalence of infection has been
found to rise through childhood, reaching over 70% in
early adulthood [15] and has been associated with mark-
ers of Hepatitis A infection [15], premastication of infant's
food [18] and low social class in some studies, but not
others (reviewed in reference [19]). In this study, few con-
sistent associations between either the prevalence or titre
of anti-H. pylori antibodies and any of the risk factors
examined were identified. The reasons for the lower prev-
alence identified in this study among people aged over 50
years and among HIV infected people are unclear. Simi-
larly, since no consistent differences between religious
groups have been identified to date in this study [1-7], it
is likely that the differences in the prevalence of anti-H.
pylori antibodies observed here, between Christians and
Muslims, arose by chance.
It is recognised that serum antibodies against H. pylori
may decline because of the development of gastric
changes, such as malignancy, that can suppress or kill the
infection [20]. Case-control studies have therefore shown
inconsistent associations between antibodies against H.
pylori and gastric cancer (reviewed in reference [21]). The
lack of an association in this study and in the only other
from Africa in which serum antibodies were measured
[22] is, therefore, unsurprising. The lack of statistical
power in this study (based on only 21 cases of stomach
cancer) and the incomplete diagnostic verification may
have further reduced the ability to detect an association.
Indeed, the only study from Africa to find an association
between gastric cancer and H. pylori involved assessment
of infection status microscopically in tissue taken from
areas adjacent to disease and included only six people
with the tumour [23].
The apparent increase in the incidence of gastric cancer
seen in Uganda since the 1960s [24], though not statisti-
cally significant, may have been influenced by improve-
Table 2: H. pylori serostatus for different cancer sites or types and non-malignant conditions, together with the percentage of each
cancer with laboratory verification of diagnosis
Cancer site or type Percentage with laboratory
verification of diagnosis
Number anti-H. pylori anti-
body positive/total
Odds ratio (95% CI)
1
χ
2
1
and p value
Stomach 90% 18/21 0.8 (0.2–2.9) χ
2
1
= 0.1, p = 0.7
All controls
2
- 723/833 1.0 -
Oral 56% 21/26 0.6 (0.2–1.7) χ
2
1
= 0.9, p = 0.4
Oesophagus 45% 37/38 5.1 (0.7–38) χ
2
1
= 2.5, p = 0.1
Liver 56% 44/52 0.7 (0.3–1.6) χ
2
1
= 0.8, p = 0.4
Skin 77% 18/22 0.6 (0.2–1.9) χ
2
1
= 0.8, p = 0.4
Breast 62% 62/69 1.4 (0.6–3.5) χ
2
1
= 0.6, p = 0.4
Cervix 50% 173/190 1.6 (0.9–2.8) χ
2
1
= 2.1, p = 0.2
Ovary 73% 20/22 1.1 (0.3–5.0) χ
2
1
= 0.0, p = 0.9
Prostate 44% 7/10 0.3 (0.1–1.4) χ
2
1
= 2.4, p = 0.1
Penis 57% 12/14 0.9 (0.2–4.3) χ
2
1
= 0.0, p = 0.9
Conjunctiva 66% 33/38 1.3 (0.5–3.5) χ
2
1
= 0.3, p = 0.6
Other eye 52% 22/25 1.1 (0.3–3.9) χ
2
1
= 0.0, p = 0.9
Non-Hodgkin's
lymphoma
76% 39/46 0.8 (0.3–1.8) χ
2
1
= 0.4, p = 0.5
Hodgkin's lymphoma 83% 20/24 0.6 (0.2–1.9) χ
2
1
= 0.7, p = 0.4
Kaposi's sarcoma 91% 36/46 0.7 (0.3–1.6) χ
2
1
= 0.9, p = 0.4
1. Odds ratios adjusted for age group (<30, 30–45, 46+), sex and HIV serostatus
2. The comparison group for the calculation of odds ratios includes all other cancers and non-malignant conditions, excluding stomach cancer
Note: H. Pylori serostatus: negative – optical density (O.D.) 0.0–0.8; indeterminate – O.D. 0.9–1.3; positive – O.D. 1.4–4.0. For the purposes of this
analysis, those with an indeterminate result were considered to be seronegative.
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Page 5 of 5
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ments in diagnosis and is at odds with the decline seen
throughout much of the rest of the world. The role of H.
pylori and other factors in the aetiology of gastric cancer in
Uganda and elsewhere in Africa remains unclear.
Acknowledgements
Support for this work was provided by Mulago Hospital and Makerere Med-
ical School, Kampala, Uganda, the Imperial Cancer Research Fund (now
Cancer Research UK), the United States Centers for Disease Control and
Prevention (interagency agreement with the Department of Veterans
Affairs) and the International Agency for Research on Cancer, World
Health Organisation, Lyon.
The Uganda Kaposi's Sarcoma Study Group includes named authors and V
Sembajwe, M Kalinaki, R Byansi, C Rwatooro, S Nambooze, B Tushemeir-
erwe, N Byabazaire (deceased), E Bitamazire, E Katabira, J Mugerwa
(deceased), D Tindyebwa, C Ateenyi-Agaba, L Marum, J Whitworth, B Rich-
ardson, G Reeves, R Weiss and K de Cock.
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    • "These regions have high prevalences of H. pylori but lower than expected rates of gastric cancer (although we found in one hospital in Kenya introduction of endoscopy led to a rapid rise in diagnoses [33]. Despite this, there are still places from the poorer regions of the world such as Africa [34,35], India [36] and China [37], where studies of the relationship between H. pylori and gastric cancer have yielded null results. In explanation of these patterns, methodological, host and pathogenic differences have been proposed. "
    [Show abstract] [Hide abstract] ABSTRACT: Stomach cancer is one of the leading causes of cancer death worldwide, despite its incidence and mortality falling in many places. The discovery in 1984 that a bacterial infection with Helicobacter pylori could cause stomach and duodenal ulcers prompted work in its role in causing gastritis, and led to the first prospective study in 1991 by Forman et al., showing that infection with H.pylori increased the risk of stomach cancer in those infected by almost three-fold. Prior to then, it was hypothesized that stomach was caused by poor diets. While diets may still play a role, the falls in stomach cancer incidence have been associated with reductions in population prevalence of H. pylori. Discovery of the link was accelerated by the use of stored sera from other unrelated studies, and the use of serological assays. Since those discoveries the treatment landscape of gastric disorders has changed significantly, with a rapid uptake of antibiotic and proton pump inhibitors (triple) therapies in those who are H. pylori positive. Over time we have seen falls in gastric cancer, peptic and duodenal ulcers and in many of the procedures previously used to cure peptic ulcer disease, such as vagotomies and gastrectomies. Further still, an oral vaccine against H. pylori, first trialled in China, holds much promise of being the third vaccine against a cancer causing infection. If successful this would lead to a further reduction in H. pylori related conditions, and ultimately gastric cancer, an otherwise lethal disease.
    Article · Feb 2016
    • "We detected a lower prevalence in children aged 9- < 12 years compared to 6- < 9 years. This finding is not comparable with, for instance, the prevalence found in the Ugandan study from Newton et al [34] in adults, where the prevalence of Helicobacter pylori in adults suffering from different kinds of cancer, except gastric cancer, was 87%. Our study population was distinctly different as all our participants were apparently healthy and children. "
    [Show abstract] [Hide abstract] ABSTRACT: Helicobacter pylori is one of the most common causes of bacterial infection in human beings. Studies have showed a high prevalence of Helicobacter pylori among people in low-income countries and colonization early in life. A monoclonal antigen test, performed on faeces, HpSA ImmunoCardSTAT, has a high sensitivity, specificity and accuracy and the faecal test can be performed in all ages, also in resource-limited settings. The main objective of this study was to determine the prevalence and factors associated with Helicobacter pylori colonization in apparently healthy children aged 0-12 years in urban Kampala, Uganda. We tested 427 apparently healthy children, age 0-12 years (211 males, 216 females), in a cross sectional survey for Helicobacter pylori colonization using HpSA ImmunoCardSTAT. A short standardized interview with socio-demographic information and medical history was used to assess risk factors. The overall prevalence of Helicobacter pylori in the 427 children was 44.3% (189 out of 427). Early colonization was common, 28.7%, in children younger than 1 year of age. The age specific rates were 46.0% in children age 1- < 3 years, 51.7% in children age 3- < 6 years, 54.8% in children age 6- < 9 years and 40.0% in children age 9- < 12 years. There was a significant difference in prevalence by gender; female 38.5% versus male 49.8% and by type of housing; permanent house 38.5% versus semi-permanent house 48.6%. Congestive living and education level of the female caretaker showed a clear trend for a difference in prevalence. Factors independently associated with Helicobacter pylori colonization included: drugs taken last three months, using a pit latrine, sources of drinking water and wealth index. The prevalence of Helicobacter pylori colonization among urban Ugandan children is high at an early age and increases with age. The impact of Helicobacter pylori colonization on children's health in Uganda needs to be further clarified.
    Full-text · Article · Jun 2010
  • [Show abstract] [Hide abstract] ABSTRACT: Incidence rates of different cancers have been calculated for the population of Kyadondo County (Kampala, Uganda) for a 16-year period (1991-2006). This period coincides with continuing social and lifestyle changes and the peak and subsequent wane of the epidemic of HIV-AIDS. There has been an overall increase in the risk of cancer during the period in both sexes, with the incidence rates of cancers of the breast and prostate showing particularly marked increases (4.5% annually). Prostate cancer is now the most common cancer in men. The incidence of cancer of the esophagus, formerly the most common cancer in men and second in frequency in women, has remained relatively constant, whereas the incidence of cancer of the cervix, the most common malignancy in women, continues to increase. Since the early 1990s the incidence of Kaposi sarcoma (KS) in men has declined, and while remaining relatively constant in women, it has been diagnosed at progressively later ages. The rates of pediatric KS have declined by about 1/3rd. The incidence of squamous cell cancers of the conjunctiva has also declined since the mid 1990s. Cancer control in Uganda, as elsewhere in sub-Saharan Africa, involves meeting the challenge of emerging cancers associated with westernization of lifestyles (large bowel, breast and prostate); although the incidence of cancers associated with poverty and infection (liver, cervix, esophagus) shows little decline, the residual burden of the AIDS-associated cancers remains a major burden.
    Article · Nov 2009
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