[acb-diabetics] many articles

Patricia LaFrance-Wolf plawolf at earthlink.net
Thu May 13 14:37:06 GMT 2010


1. %% Artificial Pancreas May Help Control T1DM  4/14/10  Automated control
of blood glucose (BG) concentration is a long- sought goal for T1 therapy.

“We have developed a closed-loop control system that uses frequent
measurements of BG concentration along with subcutaneous delivery of both
the fast-

acting insulin analog lispro and glucagon (to imitate normal physiology) as
directed by a computer algorithm.” said the team leader. [11 subjects; 27hr

experiments - lispro] "Near-normal mean BG concentrations without
hypoglycaemia were achieved without feedforward information or pretreatment
for very

high carbohydrate meals in the subjects with faster insulin PKs. In those
with slower insulin absorption, adjustment of algorithm parameters prevented

hypoglycemia at the cost of modestly higher average BG concentrations."
Until there is a cure for insulin- dependent DM  the influence of the
patient on

controlling his or her diabetes will remain significant."

 

2.%%Monofilament Test Helps Predict Long-Term Risk of Diabetic Neuropathy
(Reuters Health) Apr 15 - A sensitive, specific - & simple - monofilament
exam

can help predict patients' long-term risk of diabetic neuropathy [DN]. Most
sensory screening tests diagnose neuropathy when nerve injury has already
occurred.

-- this team  wanted to find a way to identify patients at particularly high
risk for developing neuropathy in the future. [175 neuropathy -free subjects

performed Semmes-Weinstein 10g Monofilament Exams]  This exam uses "a
hand-held calibrated nylon thread that buckles once it has delivered a force
of 10

grams," the authors explain. ".. it provides a standardized measure of a
patient's ability to sense a point of pressure." By the second exam 4yr
later,29%

had developed DN.  The strongest predictor - stronger than gender, disease
duration, height, and BP - was a lower baseline monofilament ".., this study


defines the value of simple tests to predict a person's  subsequent risk of
developing neuropathy.. doctors can focus on potential at-risk patients to

make sure they are meeting treatment guidelines."  Diabetes Care 2010.

 

3.%% Am J Ophth vol 149, 5 May 2010 Four-Year Incidence and Progression of
Diabetic Retinopathy and Macular Edema: The

Los Angeles Latino Eye Study Conclusions The 4-year incidence and
progression of DR and the incidence of macular edema  and clinically
significant ME among

Latinos are high compared to non-Hispanic whites. These findings support the
need to identify and modify risk factors associated with these long-term
complications.

 

4.%% Am J Ophth vol149,5 May 2010 Topical Mecamylamine for Diabetic Macular
Edema   23  patients with chronic DME received 1% mecamylamine topically
twice

daily for 12 weeks,  there were no drug-related safety problems. Conclusions
- This study suggested that administration of topical mecamylamine, a
nonspecific

nACh receptor blocker, may have heterogeneous [different] effects in
patients with DME. Variable expression of receptor subtypes on endothelial
cells that

have different effects on permeability would provide an explanation for
these results and should be investigated.. 

 

5.%% Am J Ophth vol149,5 May 2010  Assessment of Disability Related to
Vision Performance (ADREV) -Based Measure in DM Retinopathy [91 patients
with DR]

.. binocular visual acuity, contrast sensitivity, and better eye visual
field were the best predictors of ADREV performance.  Conclusions - ADREV
performance

measure is a valid instrument for the assessment of disability related to
vision in patients with diabetic retinopathy.

 

6.%% Removable Walker Cast as Effective as Total Contact Cast in Diabetic
Foot Ulcers (Reuters Health) Apr 13 - DM plantar ulcers heal just as well
with

removable walker casts as with non-removable fiberglass total-contact casts.
The removable cast could be a good option when patients can't have a non-

removable total-contact cast, [such as]: those with infection or critical
ischemia, those who are very elderly or have problems with vision or
equilibrium,

and those with a contralateral foot ulcer or varicose veins. [48 patients ]

 

7.%% Glucagon Plus Insulin Reduces Hypoglycemia in Some Type 1 Diabetics
(Reuters Health) Apr 12 -“..we deliver the natural hormone glucagon for the
purpose

of preventing overt Hypo.” the senior author said. "Our computer algorithm
calls for glucagon delivery during impending hypoglycemia." [ 13 adults with

T1] automated glucagon plus insulin reduced the time spent in the
hypoglycemic range by 63% compared to placebo plus insulin. He said the use
of 2sensors

as opposed to one increases the safety of the artificial pancreas system.
"Sometimes a sensor can drift to inaccurate levels, but if 2 sensors are
used

(and the system has the opportunity to switch from the less accurate to the
more accurate), the system works very well with very good control of blood

sugar," Diabetes Care 2010.

 

8.%%MW  Dietary Glycemic Load Linked to Coronary Heart Disease Risk in Women
But Not Men 4/14/10  — High dietary glycemic load and carbohydrate intake

from high- glycemic index foods are associated with an increased overall
risk for coronary heart disease (CHD) in women but not in men." [47,749
subjects;

follow up 7.9 yr] Of 463 patients with CHD identified during follow-up, 158
were women and 305 men.  Compared with women in the lowest quartile
[quarter]

of carbohydrate intake, those in the highest carbo intake quartile had a
significantly greater risk for CHD (RR, 2.00) the  authors write. "We
tentatively

suggest that the adverse effects of a high glycemic diet in women are
mediated by sex-related differences in lipoprotein and glucose metabolism,
but further

prospective studies are required to verify a lack of association of a high
dietary glycemic load with CVD [cardiovascular disease] in men."

 

9.%% Somatostatin Secreted by Islet d-cells Fulfills Multiple Roles as a
Paracrine Regulator of Islet Function 4/14/10; Diabetes. 2010;58(2):. ADA
[mouse

study], .Conclusions —We suggest that d-cell SST exerts a tonic inhibitory
influence on insulin and glucagon secretion, which may facilitate the islet

response to cholinergic activation. In addition, d-cell SST is implicated in
the nutrient-induced suppression of glucagon secretion.

 

10.%% MW Exercising With Visual Impairment: Prescription for Health

Am College Sports Medicine 4/14/10  Regular physical activity can help you
maintain a healthy body weight, boost immunity, reduce stress, sleep better

and feel more energized. Do not let fear or lack of confidence prevent you
from participating in physical activities. The good news is that visual
impairment

generally does not affect the benefits that can be derived from regular
physical activity. The key is to find activities you enjoy and feel
comfortable

doing so that you will stick to your program over the long-term.    Getting
Started  Talk with your health care provider about integrating regular
exercise

into your lifestyle. Choose environments that are comfortable and familiar
to you. To improve cardiovascular fitness, choose low-impact, large- muscle

activities that can be done continuously, such as walking, swimming, and
indoor cycling. If balance is a challenge, use handrails for occasional
support.

If your fitness level is low, start with shorter sessions (10 -15 min) and
gradually build up to 20 - 60 min of aerobic activity, at least three or
more

days per week. At least 2 days per week, follow a strength-training program
with 1-3 sets of exercises for the major muscle groups, (10 -15
repetitions.)

Stretch regularly to improve joint range of motion.

Exercise Cautions - If you have any other conditions, such as heart disease
or hypertension, follow the recommendations specific to that condition.  Do

not hesitate to ask for further explanations about how to perform exercises
properly. Your exercise program should be designed to maximize the benefits

with the fewest risks of aggravating your health or physical condition.
e-mail 

eim at acsm.org 

www.exerciseismedicine.org  

 

11.%% MNTD Diabetic Factors Associated With Gastrointestinal (GI) Symptoms
4/14/10  New research examines GI symptoms in T2DM and to analyze associate 

DM factors. In this well designed study with age-& sex-matched controls, the
frequency of overall GI symptoms, upper GI symptoms and lower GI symptoms

in the 190 patients with DM was 72%, 43% and 58%, respectively. The risk of
only upper GI symptoms showed a statistically significant increase of 1.68

times as many (adjustments for age, gender, smoking and alcohol use) in the
diabetic group. This study also demonstrated that upper GI symptoms appeared

to be independently linked to poor glycemic control as measured by HbA1c
levels. Therefore the team cautiously suggests that chronic upper GI
symptoms

may be reversible with tight

control of blood glucose level.

 

12.%%NREndo 6,241 May 2010  Addition of genetic information to
phenotype-based risk models for the determination of incident cases of
future T2DM  does

not substantially improve the accuracy of risk estimation. [5,535  subjects]
Over 10 years, new-onset T2 developed in 302 participants, but
phenotype-based

risk models were more accurate in discriminating new cases than
genotype-based tests. © 2010 Nature Publishing Group

 

13.%% NREndo 6,242 May 2010 Anti-CD3 antibody therapy for T1DM outcome 4
years after treatment  A short course of anti-CD3 antibody therapy decreases
the

insulin needs of patients with T1 during the first few years after
diagnosis,.. the effects of the antibody therapy are influenced by age and
residual

ß-cell mass at initiation of treatment. Anti-CD3 antibody therapy aims to
restore immune tolerance to target autoantigens in patients with T1DM
without

affecting their responses to other antigens. [80 subjects; random treatment
or placebo] All participants received intensive insulin therapy throughout

the trial. Over the 48 months, insulin requirements were reduced in patients
who received the antibody therapy compared with those of the placebo group.

The difference in insulin requirements between the groups resulted from a
decline in residual ß-cell function in the placebo groupbut maintenance of
this

function for at least 24 months in the antibody group. This apparent
suppression of ß-cell destruction by the antibody therapy thereafter waned.
.. the

metabolic control of younger (12–27 years) but not older (27–39 years)
patients benefited from the therapy. .. patients with early stages of ß-cell
destruction

benefited most from the therapy. Although no long-term adverse effects of
the therapy were reported, transient, flu-like symptoms were noted during
and

shortly after the treatment. A lead author says “It will now be necessary to
define efficacious and safe protocols for antibody administration in
patients

with recent-onset of T1 including children, as well as in individuals at
high risk for this disease.

 

14.%%NREndo 6,243 May 2010  Hearing loss and diabetes mellitus.

Inflammation, hyperglycemia and neuropathic or microvascular factors may
contribute to DM-related hearing loss, [1508 people age 40–69 ] the team
observed

that people with DM were twice as likely to have hearing impairment at low
or mid frequences (500, 1,000 and 2,000 Hz) than people who did not have the

disease when adjusting for factors such as age, sex and occupational noise
exposure. They also found evidence that inflammation, peripheral neuropathy,

cochlear vasculopathy, & hyperglycemia might mediate the relationship
between DM and hearing impairment.

 

15.%% NREndo 6, May 2010 Diabetic nephropathy is prevented using
(ADA)-recommended treatment targets. [1290 T2 Asian patients  received
intensive treatment

to meet ADA targets. They found a significant association between
achievement of ADA goals for HbA1c, systolic BP & HDL cholesterol and
development of

new-onset microalbuminuria.

 

16.%% NREndo 6, May 2010 Pathogenesis of T1DM: interplay between enterovirus
and host  - Enteroviruses such as coxsackievirus B, are believed to
contribute

to the pathogenesis of T1. Enteroviral RNA and/or proteins can be detected
in tissues of patients with T1. Isolation of coxsackievirus B4 from the
pancreas

of T1 patients or the presence of enteroviral components in their islets
strengthens the hypothesis of a relationship between the virus and the
disease.

Enteroviruses can play a part in the early phase of T1DM through the
infection of ß cells and the activation of innate immunity and inflammation.
In contrast

with its antiviral role, virus-induced interferon a can be deleterious,
acting as an initiator of the autoimmunity directed against ß cells.
Enteroviruses,

through persistent and/or successive infections, can interact with the
adaptive immune system. Host genes, such as IFIH1, that influence
susceptibility

to T1DM are associated with antiviral activities. Iincreased activity of the
IFIH1 protein may promote the development of T1. Improved knowledge of the

pathogenic mechanisms of [these]  infections should help to uncover
preventive strategies for T1DM. .

 

17.%% MW An Unfinished Journey: Molecular Pathogenesis to Prevention of Type
1A Diabetes George S. Eisenbarth 4/16/10; Diabetes. 2010;59(4): The Banting

Medal for Scientific Achievement Award is the ADA’s highest scientific award
and honors an individual who has made significant, long-term contributions

to the understanding of diabetes, its treatment, and/or prevention. The
award is named after Nobel Prize winner Sir Frederick Banting, who
codiscovered

insulin treatment for diabetes.

Introduction The majority of individuals, but not all, developing what is
routinely diagnosed as T1DM have the immune-mediated form of the disease
(type

1A)[T1A] that results from T cell–mediated specific ß-cell destruction.
Studies suggest that the root cause of T1 involves germline-encoded
sequences forming

tri-molecular complexes consisting of the insulin peptide B:9-23. Utilizing
genetic, metabolic,  and autoantibody parameters it is now possible to
predict

T1A DM in humans, and immune therapy can delay, but not permanently prevent,
destruction of ß-cells. With an increasing incidence and an estimated 1
million

individuals in the U.S. developing T1A, safe prevention has become a major
international goal. Achieving this goal may come from incremental
modification

of immune therapies currently being tested and/or may involve a deeper
understanding of the autoimmune tri-molecular complexes underlying the
disorder's

pathogenesis.

 

T1A is associated with both devastating chronic complications and acute
life-threatening ketoacidosis and hypoglycemia.  There are multiple pathways
being

pursued to "cure" this disease or at least dramatically ameliorate the
burden it imposes on patients and their families. Continuous glucose
monitoring

is already improving the lives of many patients by providing "real time"
information with alarms for hypo- and hyperglycemia.  Multiple groups are
now

studying devices that will control insulin pumps, in particular turning off
insulin delivery to prevent hypoglycemia. Though many patients do not
consider

such mechanical devices, especially the current "first" generation of
devices, as a true cure, these therapies will set the bar in evaluating
immunologic

therapies considered for prevention of diabetes and ß-cell replacement.
Thus, the bar will be high and hopefully ever higher over the next decade.
At present,

pancreatic (long term)  as well as islet transplantation (short term)  can
cure T1 but, for most patients, with unacceptable risks associated with
immune

suppression. It is likely that autoimmunity, in addition to alloimmunity,
limits the therapeutic potential of either of these forms of
transplantation.

 

Stages of Human T1 Diabetes  In 1986, we proposed a model of chronic
autoimmune development of T1A with disease pathogenesis divided into a
series of stages. 

Technology to directly assess ß-cell mass in humans is still lacking,
Different individuals progress at different rates to overt diabetes, and
decades

can elapse between the development of DM in one monozygotic twin and the
development of islet autoantibodies in their twin mate.

Stage 1: Genetic Susceptibility - Type 1A diabetes is usually polygenic
[caused by many genes] in etiology, but there are two highly informative
rare "monogenic"

autoimmune syndromes associated with this disease: APS-1 (autoimmune
polyendocrine syndrome type 1)  and IPEX syndrome (Immune Dysregulation,
Polyendocrinopathy,

Enteropathy, X-linked) IPEX syndrome results from mutations of the FoxP3
gene, that is essential for  development of regulatory T cells.  In the
absence

of FoxP3, children develop overwhelming autoimmunity, and it is estimated
that 80% develop T1. Diabetes can present as early as the first days of
life.

This syndrome clearly demonstrates the crucial role played by regulatory T
cells and that most humans would develop T1 unless pathogenic T cells are
held

in check. Bone marrow transplantation, by providing dominant regulatory T
cells, is a consideration for children diagnosed with this fatal autoimmune
syndrome.

..

APS-1 is more common than IPEX syndrome but still rare, The syndrome is
characterized by.., Addison's disease, and hypopara thyroidism and results
from

mutations of the AIRE  (autoimmune regulator) gener. In combination, these
two syndromes illustrate extremes of genetic determination of autoimmune DM 

when one or more pathways that are essential to maintenance of tolerance are
disrupted. The genome of humans favors the development of T1 when mutations

in genes controlling tolerance override the normal polygenic prevention of
autoimmunity.  

APS-2 syndrome is much more common than APS-1. [and] is characterized by the
occurrence of multiple autoimmune disorders in the same individual (e.g.,

T1A,, Addison's disease, thyroiditis, celiac disease, etc.).  It has a
complex inheritance similar but not identical to T1A. Siblings of a patient
with

T1 have a DM risk that is several-fold that of offspring..Given the dramatic
protection provided by certain specific HLA alleles, the question has been

raised as to whether provision of such alleles might be considered
therapeutically or assessed in family planning. The alleles protecting and
determining

risk are presumably "normal" HLA alleles determining the targeting of
specific self-molecules. . haplotype that provides dominant protection from
T1A is

the highest risk haplotype for multiple sclerosis.

 

Stage II: Triggering-environment  The least amount of knowledge gains over
the past 2 decades has been made in defining environmental factors
contributing

to the development of T1 It is nevertheless clear that environmental
determinants are important

given the remarkable doubling of T1 incidence in most Western countries over
the past 20 years.  This is too rapid a change for a common genetic disorder

to be ascribed to genetic alteration (alone) of the population. A leading
hypothesis to explain such an increase

in incidence is the "hygiene" hypothesis, positing decreased infections
increasing multiple immune-mediated disorders including asthma and diabetes.
Both

the NOD mouse and BB rat, when raised in a germ-free environment, have been
reported to alter diabetes, with recent studies suggesting that intestinal

microbiota in animal models modulates development of DM. ..certain
medications clearly induce development of T1 .. interferon therapy is
associated with

DM in animal models, and in humans this treatment can induce islet
autoantibodies and accelerate diabetes progression .  Methimizole,
penicillamine, and

lipoic acid  (i.e., sulfhydryl-containing drugs) can induce autoantibodies,
with titers of the antibodies, at times, high enough to influence metabolism

..Other contenders for environmental factors are dietary, with reports that
cows milk,  early introduction of cereals,  decreased levels of n-3 fatty
acids,

and vitamin D contribute to diabetes risk.  Large current trials and
prospective observational studies will hopefully rigorously test these
hypotheses.

%%Stage III: Active Autoimmunity The immunocytochemical (ICA) assay measures
a combination of autoantibodies .. The clearest indication of the presence

of islet autoimmunity is the expression of

islet autoantibodies.. It is estimated that 10% of children with diabetes
lacking all islet autoantibodies have definable monogenic forms of DM..At
present,

the insulin autoantibody is the most difficult

for laboratories to master..

Stage IV: Progressive Metabolic Abnormalities There are multiple ways to
assess metabolic progression of patients developing DM  One of the most
specific

is the intravenous glucose tolerance test. Oral glucose tolerance testing
with measurement of glucose is also highly predictive of deterioration.  In
studies

such as DAISY, we now utilize fingerstick measurement of A1C, with the great
majority (but not all) of children developing DM  demonstrating a gradual

rise of A1C in the normal range within the 1 - 2 years prior to overt DM.

Stage V: Overt Diabetes The development of overt type 1A diabetes is often
acute. It is likely that the majority of patients presenting with T1A have
had

[it] for months to a year prior to diagnosis; they present with high A1C and
at times glucose >1,000 mg/dl.  Once diabetes has developed, loss of
C-peptide

secretion is the primary parameter to follow further disease progression.

Stage VI: Insulin Dependence.. Most of the pancreases from patients with
long-term childhood-onset diabetes have no ß-cells within islets.
Approximately

10% have limited areas with insulin containing ß-cells. 

 

Trials for Prevention of ß-cell Destruction   Though multiple interventions
have failed to prevent either progression to T1or loss of ß-cell function
postdiagnosis,

we are entering an era where several

immunotherapies can almost certainly ameliorate ß-cell loss,  with several
phase III trials underway or planned. Key information nevertheless remains
lacking

in terms of the long-term efficacy and safety and each therapeutic pathway,
thus necessitating the need for further study. fic.. Confirmatory studies of

GAD65 vaccination are underway, including a new-onset TrialNet study, with
plans for a prevention study.

%%To date none of the aforementioned therapies have demonstrated long-term
permanent arrest of disease progression. It is remarkable that despite being

such a slow destructive process, the autoimmunity underlying type 1A
diabetes is so resistant to immunotherapy. It is likely that the therapies
showing

promise to date in the above trials do not eliminate the underlying T cell
memory driving ß-cell destruction, and that multiple courses of therapy or
combinatorial

therapies will need to be developed to achieve long-term immunologic
remission.   That said, long-term continuous immunosuppression is almost
certainly

not an option as a therapy for T1 North American patients with new-onset
diabetes and relatives of patients with T1 can be evaluated for islet
autoantibodies

and participation in trials by calling 1-800-HALT-DM1 or accessing the
TrialNet Web site 

www.diabetestrialnet.org

 Banting Lecture 2009:

 

18.%% Exenatide May Be Useful in Adolescent Diabetics (Reuters Health) Apr
16 - Adjunctive exenatide therapy was safe and effective

in a small pilot study of adolescents with T1 .The glucagon-like peptide
(GLP)-1 inhibitor is known to reduce post-prandial hyperglycemia in adults
with

T2 but "there are few studies using exenatide in T1 and none in
adolescents," said senior author.  Their study tested the effect of two
doses of exenatide

(1.25 or 2.5 mcg) given along with pre-breakfast insulin in 8 teenaged
volunteers.

Compared to insulin monotherapy, both exenatide doses significantly reduced
post-prandial hyperglycemia. Gastric emptying was significantly delayed with

both doses. Diabetes Care 201

 

19.%% MW Antidepressant Pharmacotherapy in Adults with T2DM 4/19/10;
Diabetes Care. 2010;33(3):  [387 patients who received up to 16 weeks of
bupropion

or sertraline] Conclusions:  In patients with T2 poor initial response to
antidepressant medication is predicted by multiple factors. Auxiliary
treatment

of pain and impairment may be required to achieve better outcomes.

 

20.%% Metformin-induced Vitamin B12 Deficiency Presenting as a Peripheral
Neuropathy  4/22/10; South Med J. 2010;Abstract

Chronic metformin use results in vitamin B12 deficiency in 30% of patients.
Exhaustion of vit B12 stores usually occurs after 12-15 years of absolute
vit

B12 deficiency. Vitamin B12 deficiency, which may present without anemia and
as a peripheral neuropathy, is often misdiagnosed as diabetic
neuropathy..Failure

to diagnose the cause of the neuropathy will result in progression of
central and/or peripheral neuronal damage which can be arrested but not
reversed

with vit B12 replacement. .  Metformin is now recommended as initial therapy
for T2DM  Because of this, metformin used either [alone] or in combination

with other antidiabetic oral agents and insulin has become the most widely
utilized antidiabetic oral agent. Metformin's best known and most feared
side

effect, (lactic acidosis) almost never occurs if the drug is not used
appropriately.  The common side effects of metformin are GI and can be
overcome by

[includes] initiating metformin therapy at a lower dose and by giving
metformin after meals.. However, a common, potentially damaging, and
well-documented

complication of metformin - vit B12 malabsorption is poorly recognized and
not screened for or treated prophylactically by the majority of physicians
who

prescribe metformin. This is unfortunate since a correctable cause of
irreversible damage to the central and peripheral nervous system may be
overlooked.

.

 

21.%% NIH news 4/27/10  Comparative-effectiveness Study Confirms New
Treatment for Diabetic Macular Edema [DME] Ranibizumab [lucentis] Injections
Plus

Laser Therapy Results in Dramatic Visual Improvement  Laser treatment alone
has been the standard care for the past 25 years. But nearly 50% of patients

who received this new treatment experienced substantial visual improvement
after one year, compared with 28% who  received the standard laser
treatment.

[52 clinical sites] supported by NEI and the National Institute of Diabetes
and Digestive and Kidney Diseases,"Eye injections of ranibizumab with prompt

or deferred laser treatment should now be considered for patients with
characteristics similar to those in this clinical trial." Diabetic
retinopathy is

the most common cause of vision loss in working-age Americans. This
condition damages the small blood vessels in the eye's light-sensitive
retinal tissue.

When these damaged blood vessels begin to leak fluid near the center of the
retina, known as the macula, macular edema [ME]occurs. The macula provides

detailed central vision used for activities such  as reading, driving, and
distinguishing faces. In ME the retinal tissue swells, which can lead to
vision

loss if left untreated.   ..recent small short-term studies have revealed
the visual benefits of  eye injections of medications that block a chemical
signal

that stimulates blood vessel growth, known as vascular endothelial growth
factor (VEGF) and that repeated doses of anti-VEGF medications, such as
ranibizumab,

may prevent blood vessels from leaking fluid and causing ME. [854 eyes of
691 people, with T1 or 2 & DME.]After one year, nearly 50% of eyes treated
with

ranibizumab and prompt or deferred laser treatment showed a substantial
visual improvement. People could read at least two additional lines on an
eye chart

with the treated eye, or letters that were at least one-third smaller than
they could read before the study treatment. In contrast, about 30% of eyes
that

received laser treatment alone or triamcinolone plus laser showed a visual
improvement of two or more lines on an eye chart, while 13-14%  of eyes in
these

groups had a visual loss of 2 or more lines.    About 30% of people in the
triamcinolone group developed high eye pressure that required medications,
and

about 60 % developed cataracts that at required surgery.  Few participants
who received eye injections of [lucentis] had eye-related complications,
such

as an infection inside the eye likely caused by the injections, or worsening
of a retinal detachment that existed prior to beginning treatment. The study

found that eye injections of ranibizumab were not associated with any
serious risks such as heart attack or stroke.

 

22.%% NYTimes 4/27/10 A Genentech Eye Treatment Is Found to Help Prevent
Vision Loss in Diabetics [more re above announcement] The drug Lucentis can
improve

eyesight being lost to diabetes, “This is the first new treatment for people
with diabetic macular edema in a quarter of a century,” the  clinical
director

of NEI said. the study group leader said said a two-line improvement in
vision would allow some people to read normal-size print or to drive again.
Lucentis

is not approved as a treatment for macular edema. But it is approved for
another eye disease, AMD. So doctors can  -and some already do  use the drug
off-label

for the diabetic condition. With this successful Phase 3 trial, insurers
will now be more likely to pay for such off-label use. Some doctors
criticized

the organizers of the trial for testing Lucentis rather than another
Genentech drug, Avastin, which works in the same way as Lucentis. Although
it is a

cancer drug, Avastin is often used off-label for eye diseases because it is
far cheaper than Lucentis, costing only $20 to $100 a dose, compared with
$2,000

for Lucentis. Organizers of the trial conceded that a major reason Lucentis
was chosen was that Genentech, which is now owned by Roche, agreed to
provide

the drug free of charge and to contribute $9 million in additional financing
— but only if Lucentis were used.. But he said there were other factors as

well, like a belief that Lucentis might have been the better drug. Dr. P
Rosenfeld ( U of Miami) said the decision was “clearly a case of pay to
play”

since Genentech’s money dictated the choice of drugs.

 

23.%%  Heartwire  Diabetes Associated With Increased Risk of Atrial
Fibrillation 4/27/10   Results from a new analysis suggest that diabetics
are at an

40% increased risk of developing atrial fibrillation [AF] & that this risk
was higher among patients with a longer duration of treated DM and poorer
glycemic

control. "People with diabetes– specifically, those who are taking
medications for DM --are at a substantially higher risk of developing AF
than people

that don't have diabetes at all," said lead investigator. This study,
emerged from her group's earlier research examining the association between
obesity

and AF In which obesity was shown to be a risk factor for developing the
arrhythmia..researchers accumulated evidence that suggested DM wasn't the
cause

of atrial fibrillation in obese patients but might be an independent risk
factor. [1410 subjects & 2203 controls ] they found a significant 40%
increased

risk of AF among those with treated DM  even after adjustment for body-mass
index, among other variables. The risk of atrial fibrillation was increased

3% for each additional year they were treated for DM and was doubled among
patients with HbA1c levels >9% compared with people without diabetes. "We
know

that diabetes is associated with inflammation throughout the body, and we
also know that inflammation itself can lead to AF.... but we don't know
exactly

why--if it's the inflammation, the diastolic dysfunction, or something else.
It could also be through an increased risk of sleep apnea. We have all these

ideas, but there is no smoking gun for why this happens."

 

24.%% MW Diabetes Is Leading Cause of Attributable Cases of Hepatocellular
Carcinoma 4/28/10  Which risk factor for hepatocellular carcinoma (HCC) is
associated

with the largest proportion of cases of the disease in the US? If you
answered hepatitis C (HCV), hepatitis B (HBV), or alcohol-related disease,
you would

be wrong. However, more cases of HCC overall are attributable to diabetes
than any other risk factor, the presenter said.   the new study sheds light
on

the risk factors for HCC and their incidence. They found that DM was
associated with the greatest percentage of cases (33.5%), followed by
alcohol-related

disorders (23.9%), HCV infection (20.7%), HBV infection (5.7%), rare
metabolic disorders (3.1%), and obesity (2.7%).

"Overall, controlling diabetes might have a greater impact than any other
single factor on reducing the incidence of hepatocellular carcinoma in the
US,"

[5607 subjects]

 

- Abbreviations:  DM - diabetes Mellitus;T1DM - type 1 diabetes mellitus
T2DM - type 2; DME - diabetic macular edema; GDM gestational diabetes;PDR -
proliferative

diabetic retinopathy;   FPG - fasting plasma glucose; BP - blood pressure;
CVD - cardio-vascular disease; MI -myocardial infarction or heart attack
;HTN

- hypertension or high BP; OCT - optical coherence tomography; VA - visual
acuity  -ADA - Amer Diabetes Ass & ADA Professional Resource Online; JHA -
Johns

Hopkins Alerts ; MW Medscape Web MD; NIH - Nat Institutes of Health;  MNTD-
Medical News Today  NREndo;Nature Reviews Endocrinology

Definitions via online Medical dictionaries.  Disclaimer, I am a BSN RN but
not a diabetic or diabetic educator. Reports are excerpted unless otherwise

noted. This project is done as a courtesy to the blind/visually impaired and
diabetic communities. Dawn Wilcox BSN RN Coordinator The Health Library at

Vista Center; an affiliate of the Stanford Hospital Health Library.
contact above e-mail or 

thl at vistacenter.org     

           

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