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October
2001
H.
Pylori and Gastric Cancer
Studies have linked Helicobacter pylori (H. pylori) infection
with the development of gastric (stomach) cancer. H. pylori is
a spiral-shaped bacterium that lives in the stomach and duodenum (the
section of intestine just below the stomach). It has the ability to adjust
to the harsh conditions in the stomach. H. pylori is believed
to be transmitted orally.
Recently, researchers
in Japan sought to clarify this association and explore which, if any,
gastrointestinal conditions increase a person's risk of developing
gastric cancer. The results of this study appeared in the September
13, 2001, issue of the New England Journal of Medicine.
The participants
had duodenal (in the duodenum) ulcers, gastric ulcers, gastric hyperplasia
(abnormal cell growth), or nonulcer dyspepsia (stomach pain). They
underwent endoscopy — for the early detection of cancer — at
enrollment and again during the next three years. Of the 1,526 who
took part in the study, 1,246 had H. pylori infection and 280
did not.
Thirty-six of
the H. pylori-infected patients developed gastric cancer versus
none of the uninfected patients. Patients with H. pylori and
significant gastric disorders had a significantly higher risk of developing
gastric cancer. However, no gastric cancer was found in people with
duodenal ulcers
— despite being H. pylori-positive. This supports the notion
that duodenal ulcers are related to a low risk of gastric cancer.
Results of the
study — supported by a 1998 study in which 98% of patients with
gastric cancer were H. pylori-positive — suggests gastric
cancer develops almost exclusively in people infected with the bacterium.
October 2001 Update
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Angiotensin-II-receptor
Antagonists for Diabetic Nephropathy
Anyone with type 2
diabetes knows about the host of complications that can result
if blood sugar is not kept under tight control. One complication
is diabetic nephropathy, or kidney damage. When functioning
normally, our kidneys keep proteins and other beneficial substances
in the blood and filter out waste products, which the body excretes
as urine. Diabetes can interfere with this process. As a result,
waste products remain in the blood and protein is excreted into
the urine (proteinuria).
Angiotensin-converting-enzyme (ACE) inhibitors have been shown
to slow the progression of renal, or kidney, disease
in patients with type 1 diabetes. ACE inhibitors are widely
given to patients with type 2 diabetes for the same purpose,
even though there's less evidence they are effective. A set
of studies published in the September 20, 2001 New England
Journal of Medicine examined the effects of a different
class of drugs, called angiotensin-II-receptor antagonists on
nephropathy caused by type 2 diabetes.
The first study involved 1,715 patients with type 2 diabetes,
above-normal blood pressure, urinary protein excretion of at
least 900 mg per day, and serum creatinine levels (a marker
of kidney damage) between 1-3 mg/dL. Each day, the patients
took either 300 mg of the angiotensin-II-receptor antagonist
irbesartan, 10 mg of the calcium-channel blocker amlodipine,
or a placebo. After an average of 2.6 years, significantly
fewer patients receiving irbesartan experienced a doubling
of serum creatinine, end-stage renal disease, or death than
patients taking either amlodipine or placebo (33% vs. 41% vs.
39%).
In another study, which involved a similar patient group, investigators
studied the effects of the angiotensin II-receptor antagonist
losartan versus the effects of a placebo. At the end of 3.4
years, patients taking losartan had a 25% risk reduction in
the incidence of serum creatinine doubling and a 28% risk reduction
of end-stage renal disease compared to patients taking a placebo.
However, losartan did not have any effect on the rate of death.
An editorial accompanying the NEJM articles suggests
that although angiotensin-II-receptor antagonists performed
well in these trials, they are still far from effective in
all patients. In addition, this study did not compare the performance
of angiotension-II-receptor antagonists to that of the widely
used ACE inhibitors.
October 2001 Update
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Inhalers
Lead to Hip Bone Loss
Medications
commonly used for the long-term treatment of asthma may lead to hipbone
loss in premenopausal women.
Researchers at Brigham and Women's Hospital in Boston found bone
mass in the hip and trochanter decreased in women taking inhaled
glucocorticoids, a type of steroid used for treating asthma. The
rate of bone loss also increased with the rate of dosage. The three-year
prospective study involved 109 women aged 18 to 45. Bone density
was measured at the beginning of the study, after six months of treatment
and at one, two, and three years.
Bone density was found to decline 0.00044 grams per square centimeter
per puff of medicine per year of treatment. Although that's a small
amount, it can be significant in the long run. If a woman with asthma
is treated with six puffs of triamcinolone acetonide (the glucocorticoid
studied) twice a day for 20 years, she could expect to have 0.106
grams per square centimeter less bone in her hip than she would have
had without the treatment, according to this study. That degree of
bone loss has been associated with a risk of hip fractures more than
double that of normal women 65 and older.
Besides the hip, measurements were also taken at the spine and femoral
neck, but no changes were found there. The rate of decline also varied
between patients in the same dosage group and no reason for that
could be found.
Though osteoporosis is a major health problem for women, the study's
authors admit that inhaled glucocorticoids are among the most effective
and safest medicines for asthma. They suggest doctors prescribe the
lowest effective dose and patients using high doses should ask their
doctors to periodically assess their bone density.
The results of previous, less extensive studies on inhaled steroids
and bone density have been mixed.
October 2001 Update
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H.
pylori Infection May
Aggravate GI Injury in Patients Taking Low-dose Aspirin
Doctors commonly prescribe low-dose aspirin for the prevention of heart
disease, but it may also be responsible for some potentially serious
side effects when taken frequently. Among the most common of these are
gastrointestinal erosions and ulcers.
A recent study
in The American Journal of Gastroenterology sought to determine
whether certain people taking low-dose aspirin — specifically,
people infected with Helicobacter pylori, a common bacterium
that can cause ulcers — are more susceptible to gastrointestinal
erosions and ulcers than people who are not infected with H. pylori.
Researchers from
the University of Texas Southwestern Medical School and Baylor College
of Medicine recruited 61 healthy volunteers between the ages of 18
and 61. Of these, 29 volunteers were infected with H. pylori.
Forty-six of the volunteers were then randomly selected to receive
low-dose aspirin (either 81 mg daily or 325 mg every three days), while
15 received a placebo.
After 46 days
of treatment, an upper GI endoscopy was performed on each subject to
determine the extent of gastrointestinal injury. The researchers did
not detect any injury in the stomach or duodenum (upper intestine)
of the patients taking placebo. In the subjects taking aspirin, those
patients who were infected with H. pylori were significantly
more likely to have gastrointestinal injury than those who were not
infected (50% vs. 16%).
However, there
was no difference between the groups in complaints of pain, nausea,
vomiting, indigestion, or heartburn. In addition, the difference in
outcomes between patients taking 81 mg of aspirin daily and 325 mg
every three days was not statistically significant.
The researchers caution that the results of this study may not hold for
older people or those with gastrointestinal diseases such as peptic ulcer
disease, because the volunteers were healthy and aged 61 or younger.
However, this study does suggest eradicating H. pylori infection
may help prevent gastrointestinal erosions and ulcers in patients taking
low-dose aspirin on a long-term basis.
October 2001 Update
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Statins
Associated With Lower Dementia Risk
Most people who develop dementia - poor memory and intellectual functioning
that often accompanies old age - have Alzheimer's disease. But a small,
yet sizable group of people appear to develop dementia from a narrowing
of the arteries supplying the brain. The lack of blood can lead to many
small areas of damage to the brain; each too small to be noticeable as
a "stroke," but collectively devastating in their effect. This syndrome
is called "vascular dementia" to differentiate it from Alzheimer's disease
and other types of dementia.
Presumably because high cholesterol levels contribute to the damage of
brain's blood vessels, researchers have looked for evidence that people
who use statins might have a lower rate of dementia. Statins are the
most widely used cholesterol-lowering drugs. In addition to protecting
the brain's arteries from atherosclerosis, some scientists believe statins
may also help protect the brain against non-vascular forms of dementia,
including Alzheimer's disease.
A recent study examined the relationship between statin use and types
of dementia among people living in the United Kingdom. The researchers
identified 284 people with dementia, and matched them with 1,080 "control"
subjects of similar age and sex, but without dementia. After adjusting
statistically for a wide range of clinical information, the researchers
found statin use was associated with a 71% reduction in dementia risk.
Could statins really cut the risk for dementia by two-thirds or more?
It seems unlikely, since other studies haven't suggested protective effects
of this size. On the other hand, this study adds to several other laboratory
and epidemiological investigations that suggest statins might provide
some benefit in the protecting the brain - if for no other reason than
lower cholesterol levels lead to healthier brain arteries. No one should
start taking statins as a strategy for preventing dementia, but these
data do provide another reason for people with elevated cholesterol levels
who are on these medications to be sure they take them as prescribed.
October 2001 Update
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