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Number 620 HEALTHNET NEWS June 20, 2005
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This weekly bulletin is supported by generous charitable
contributions from individuals and institutions
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COMMENTARY by Malcolm Bryant, MD, MPH
CHILDHOOD CANCER
1. Saving the children - Improving childhood cancer treatment
in developing countries
CARDIOLOGY
2. Vascular risk factors and diabetic neuropathy
3. Low-grade microalbuminuria predicts hypertension
4. Pentoxifylline for heart failure: A systematic review
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EDITORS: Ramnik Xavier, MD Malcolm Bryant, MD, MPH
Harvard Medical School Management Sciences for Health
Jill Durocher Leela McCullough, Ed.D
SATELLIFE SATELLIFE
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Dear Colleagues,
We are all very aware of the dangers that cigarette smoke poses
to the respiratory tract but how many of us take on board the
serious effects of indoor air pollution on respiratory function?
More than half of the worlds population relies on dung, wood,
crop waste or coal to meet their most basic energy needs. Cooking
and heating with such solid fuels on open fires or stoves without
chimneys leads to indoor air pollution. This indoor smoke
contains a range of health-damaging pollutants including small
soot or dust particles that are able to penetrate deep into the
lungs. In poorly ventilated dwellings, indoor smoke can exceed
acceptable levels for small particles in outdoor air 100-fold.
Exposure is particularly high among women and children, who spend
the most time near the domestic hearth. Every year, indoor air
pollution is responsible for the death of 1.6 million people - one
death every 20 seconds.
The WHO has assessed indoor air pollution as the 8th most
important contributor to the global burden of disease, accounting
for 2.7% of the total burden, and in many countries it is the most
lethal killer after malnutrition, unsafe sex and lack of safe
water and sanitation. Indoor air pollution has been associated
with a wide range of health outcomes, and there is strong,
consistent evidence that exposure to indoor air pollution
increases the risk of pneumonia among children under five years,
and chronic respiratory disease and lung cancer (in relation to
coal use) among adults over 30 years old. There is also good
evidence for a link with lung cancer from exposure to biomass
smoke, and for a link with asthma, cataracts and tuberculosis.
Measures to reduce indoor air pollution and associated health
effects range from switching to cleaner alternatives, such as
gas, electricity or solar energy, to improved stoves or hoods
that vent health-damaging pollutants to the outside, to behavioral
changes. There is an urgent need to investigate which
interventions work and how they can be implemented in a
successful, sustainable and financially viable way.
Acting to deal with this situation is not easy however. In the
end it is only going to be by addressing the Millennium
Development Goals in the context of household energy will we see
a long-term difference. Specific is linked to achieving the
Millennium Development Goals, relate to reducing child mortality
(Goal 4), to promoting gender equality and empowering women
(Goal 3), to opening up opportunities for income generation and
eradicating extreme poverty (Goal 1), and to ensuring
environmental sustainability (Goal 7).
Malcolm Bryant, MD, MPH
Management Sciences for Health
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CHILDHOOD CANCER
1. Saving the children - Improving childhood cancer treatment
in developing countries
AU: RC Ribeiro, Ching-Hon Pui
SO: New England Journal Medicine 2005 May 26; 352(21): 2158-60.
http://content.nejm.org/cgi/content/full/352/21/2158
PERSPECTIVE
Unprecedented gains have been made in the cure rates for childhood
cancer during the past four decades. This progress reflects steady
improvement in treatment protocols, a multidisciplinary approach
to patient care, adequate hospital infrastructure, and
psychosocial and economic support for affected families. Perhaps
the greatest success has been the 80 percent cure rate among
children with acute lymphoblastic leukemia who are treated in a
modern center. Most of these survivors have long, productive
lives, are well integrated into their communities, and make
substantial contributions to society. (1) But this story of
medical achievement is tempered by the harsh reality that more
than 60 percent of the world's children with cancer have little
or no access to effective therapy, and their survival rates are
predictably inferior to those in countries with advanced health
care systems. The geographic inequality in cancer treatment poses
challenges that have only begun to be addressed.(2,3)
Perhaps the most compelling case to be made against investing in
better cancer treatment for children in poor countries is that
millions of deaths may be prevented by focusing instead on
relatively inexpensive strategies for combating infectious
diseases. Indeed, the World Health Organization and many
international charities have committed their resources to reducing
mortality from infectious diseases by two thirds during the next
decade. Not surprisingly, noncommunicable diseases and chronic
childhood disorders are not among the priorities of these
organizations. Although the marshaling of resources to fight
infectious diseases clearly has the potential to save the most
children in developing countries, we would argue that alternative
support mechanisms are also needed to ensure wider access to
effective cancer treatment. This argument is not grounded solely
in humanitarian considerations; it also addresses the rapidly
changing profile of causes of illness and death among children in
countries with limited resources.
Although pediatric human immunodeficiency virus infection and AIDS
remain a critical health priority in sub-Saharan Africa, cancer is
emerging as a major cause of childhood death in developing regions
of Asia, South and Central America, northwest Africa, and the
Middle East, as a result of reduced mortality from preventable
infectious diseases.(3) For example, in 1960, the rate of death
among infants in China was 150 per 1000 live births; among
children under five years of age, the death rate was 225 per 1000
live births. By 2002, the rates had decreased to 31 per 1000 and
39 per 1000, respectively. As the population of Chinese children
nears 300 million, a conservative projection of 45,000 new cases
of pediatric cancer each year can be made.
At the Shanghai Children's Medical Center, which serves the only
Chinese city in which health insurance for catastrophic diseases
is offered, 234 children with acute lymphoblastic leukemia were
admitted for treatment between October 1998 and June 2003.
According to Dr. J.Y. Tang of the medical center, therapy for 66
of these children (most of whom did not live in Shanghai) had to
be abandoned, apparently for financial reasons, and another 52
children died of leukemia or treatment-related complications,
leaving only 116 in continuous complete remission. This problem is
much worse elsewhere in the country, especially in rural
areas: only about 10 percent of Chinese children under 14 years of
age who have acute leukemia receive protocolbased therapy,
according to Dr. L.J. Gu, also of the Shanghai center.
What, if anything, can be done to bring the benefits of modern
cancer treatment to more children? The most immediate and
substantial results will probably come from expanded access to
treatment, the elimination of reasons for abandoning treatment,
and better control of complications of infections. Possible
approaches to achieving these goals are admirably covered in the
recent book Cancer in Developing Countries: The Great Challenge
for Oncology in the 21st Century. One strategy, described in the
chapters by Masera et al. and Cavalli, emphasizes a partnership
('twinning') between institutions in developed countries and
those in underdeveloped countries, an approach that seems most
likely to have long-term success.
Examples of the twinning approach to childhood cancer treatment
have been in place in Central and South America, northwest Africa,
and southeast Asia for as long as 10 years.(3,4) These programs
have reduced the rates of abandonment of treatment, relapse, and
death due to toxic effects of treatment, and the investments
they have attracted have led to improvements in access to
treatment and hospital infrastructure.
Briefly, twinning fosters interactions between public hospitals in
developing countries and established cancer treatment centers,
with the goal of improving survival rates among children with
cancer. The best results have been obtained when local oncologists
were recruited as program directors and asked to promote the idea
of a strong pediatric oncology unit among their peers and
coordinate the training of providers. Although at first the
partner institution in the more affluent country may subsidize the
costs of treatment, these and other expenses are eventually met
with funds raised by charitable groups in the community. Such
alliances have generated sufficient momentum to allow some
hospitals in Central and South America to begin sharing their
expertise with other oncologists in the developing regions of
Latin America, by developing joint treatment protocols and
consulting about problems in the management of childhood cancer.
Can twinning be effective in countries that lack even rudimentary
health care systems? We believe that a low level of development
does not pose an insurmountable obstacle to a productive
partnership. In parts of Africa, for example, it may be possible
to cure children of Burkitt's lymphoma by treating them with
cyclophosphamide alone, and there is evidence from Malawi that
even a simplified twinning program can save lives.(5) Thus, a
modified program concentrating on education, training, and the
treatment of the most responsive cancers could be quite effective.
Most progress in pediatric cancer treatment has been stimulated by
research involving children in Western countries. Since the
susceptibility to and pathogenesis of cancer are heavily
influenced by genetic background, environmental exposure, and
lifestyle, we must broaden research to include cases in developing
countries. It will be easier to do so if the development of
pediatric-cancer units in poor countries leads to the evolution of
international banks of cells and tissue and of cancer registries
that collect long-term follow-up data.
It has been said that if we are to preserve civilization, we must
make certain its benefits are available to the many, not reserved
for the few. The development of curative treatment for children
with cancer is a benchmark for medical progress, and such
treatment must not be sequestered within the borders of a few
countries. The strategy we describe is only a start, but it could
ignite a spirit of achievement that may ultimately reach even the
least privileged nations.
References are available upon request at info@healthnet.org
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What are your thoughts or questions on this issue?
Send a message to your colleagues at hnn-chat@healthnet.org
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CARDIOLOGY
2. Vascular risk factors and diabetic neuropathy
Summary by: Ronan J. Walsh, MB, BCh
SO: Journal Watch Neurology May 5, 2005
CO: Massachusetts Medical Society 2005
www.jwatch.org
Summary: Other than tight glycemic control, no evidence-based
treatments currently exist that prevent or ameliorate diabetic
neuropathy. These authors studied the effects of potentially
modifiable vascular risk factors on the development of distal
symmetric polyneuropathy and autonomic neuropathy in patients with
type 1 diabetes from 31 centers. The authors assessed patients for
evidence of neuropathy at baseline and an average of 7.3 years
later, using clinical evaluation, quantitative sensory testing,
and autonomic function tests. Neuropathy was diagnosed based on
the presence of two or more of four measures: one or more
symptoms, absence of ankle or knee reflexes, abnormal vibration
perception threshold, and abnormal autonomic function or autonomic
symptoms.
Among 1172 patients without baseline neuropathy who completed
follow-up, neuropathy developed in 23.5%. As in previous studies,
the cumulative incidence of neuropathy was related to the
glycosylated hemoglobin value and the duration of diabetes. In
multivariate logistic-regression models (adjusted for glycosylated
hemoglobin and diabetes duration), baseline risk factors that were
significantly higher in patients who developed neuropathy were
total and low-density lipoprotein cholesterol and triglyceride
levels, body-mass index, von Willebrand factor level, and urinary
albumin excretion rate. Hypertension and current or former smoking
were also independently associated with the incidence of
neuropathy. After complications of diabetes were added to the
model, cardiovascular disease was a significant risk factor, but
retinopathy, hypertension, and increased triglycerides were not.
Comment: Cardiovascular risk factors appear to accelerate the
adverse effects of hyperglycemia on peripheral nerves. A
randomized double-blind controlled trial, along the lines of the
landmark Diabetes Control and Complications Trial, is required to
address the question of whether aggressively treating these
modifiable risk factors will reduce the development of neuropathy
in type 1 diabetes (N Engl J Med 1993; 329:977).
Source: Tesfaye S et al. for the EURODIAB Prospective
Complications Study Group. Vascular risk factors and diabetic
neuropathy. N Engl J Med 2005 Jan 27; 352:341-50.
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3. Low-grade microalbuminuria predicts hypertension
Summary by: Kirsten E. Fleischmann, MD, MPH
SO: Journal Watch May 10, 2005
CO: Massachusetts Medical Society 2005
www.jwatch.org
Summary: Microalbuminuria, a marker for glomerular hyperfiltration
and endothelial dysfunction, is often seen in patients with
diabetes or hypertension. Researchers from the Framingham Heart
Study followed 1499 people without diabetes or hypertension to see
whether microalbuminuria might predict blood pressure progression
and incident hypertension.
After a mean of 2.9 years, 230 study subjects (15%) had developed
hypertension, and 499 (33%) had progressed to worse BP categories
as defined by standard guidelines. In multivariate analyses, the
ratio of albumin to creatinine in the urine predicted incident
hypertension. Patients in the highest quartile of albumin
/creatinine ratio at baseline had approximately double the risk
for hypertension of those in the lowest quartile.
Comment: Although levels of microalbuminuria measured in this
study were generally low, they did predict incident hypertension
and worsening blood pressure. The authors hypothesize that
glomerular endothelial dysfunction, manifested as low-level
microalbuminuria, is potentially both a precursor of essential
hypertension and an identifier of patients at increased risk for
BP progression. Whether measuring microalbuminuria and instituting
early intervention can change outcomes remains to be determined.
Source: Wang TJ et al. Low-grade albuminuria and the risks of
hypertension and blood pressure progression. Circulation
2005 Mar 22; 111:1370-6.
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4. Pentoxifylline for heart failure: A systematic review
AU: K Batchelder, BM Mayosi
SO: South African Medical Journal 2005 Mar; 95(3):171-5.
http://www.ajol.info/viewarticle.php?id=20296&jid=76&layout=abstract
ABSTRACT
BACKGROUND: Recent trials have indicated a beneficial effect of
pentoxifylline on measures of inflammation and markers of cardiac
dysfunction in people with heart failure. However, it is
uncertain whether pentoxifylline should be used routinely in the
management of heart failure.
OBJECTIVE: To determine the effectiveness of pentoxifylline in
heart failure. DESIGN: Systematic review of randomised
controlled trials.
METHODS: We searched MEDLINE (1 January 1966 - 20 November 2004),
the Cochrane Controlled Trials Register (issue 4, 2004), and
reference lists of related papers, for randomised controlled
trials of pentoxifylline in the treatment of heart failure.
Prospective, randomised, double-blind controlled trials were
sought for inclusion in the study. The two reviewers independently
assessed trial quality and extracted data, which were analysed
using RevMan statistical software. The following outcome measures
were evaluated: (i) New York Heart Association (NYHA) functional
class; (ii) left ventricular ejection fraction (LVEF); (iii)
frequency of hospitalisation; and (iv) death from all causes.
RESULTS: Four studies with a total of 144 participants met the
inclusion criteria. Statistical pooling (or meta-analysis) was
not performed owing to the significant clinical heterogeneity and
differences in reporting of the outcomes in the included studies,
instead, the trials were analysed separately for the outcomes of
interest. The four studies tested the use of pentoxifylline versus
placebo in patients with heart failure of varying aetiology
(idiopathic dilated cardiomyopathy, 3 studies; ischaemic
cardiomyopathy, 1 study). In 2 of the idiopathic dilated
cardiomyopathy studies, patients were classified as NYHA class II
or III, while the study population in another idiopathic
cardiomyopathy study was in NYHA class IV. The trial of patients
with ischaemic cardiomyopathy included patients in NYHA functional
classes I - IV. The use of pentoxifylline was associated with
significant improvement in symptoms (i.e. NYHA functional class)
and cardiac function (i.e. LVEF) in 3 out of 4 studies. The
beneficial effect on symptoms of heart failure and cardiac
function was seen in all grades of severity of heart failure and
in patients with ischaemic and idiopathic dilated cardiomyopathy.
All 4 studies showed a trend towards reduction of mortality, but
this effect was not statistically significant. The effect of
pentoxifylline on the frequency of hospitalisation has not been
tested in randomised controlled trials.
INTERPRETATION: Pentoxifylline may have a beneficial effect on
NYHA functional class, ejection fraction and mortality in heart
failure, but published trials are too small to provide conclusive
evidence. There is a need for large, placebocontrolled trials of
pentoxifylline in heart failure, involving a diverse group of
patients with regard to cause and severity of heart failure.
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