[acb-diabetics] multiple articles

[Patricia LaFrance-Wolf]

1. %% M 5/2/11 FDA Approves New Drug for T2 -linagliptin (Tradjenta)
either as a stand-alone or in combo. with other therapies. Tradjenta which
comes in tablet form, boosts the level of hormones that stimulate the
release of insulin after a meal by blocking an enzyme called dipeptidyl
peptidase-4. Eight double-blind, placebo- controlled clinical trials showed
the drug is safe and effective in pts with T2. However, the combination of
linagliptin & insulin has not been studied. Clinicians should not prescribe
linagliptin for pts with T1 or those who have DM ketoacidosis. The drug's
most common adverse effects are upper respiratory tract infection, stuffy or
runny nose, sore throat, muscle pain, headache.

2.%% M 4/28/11 New Diabetes Guidelines Address Gap in Compre-hensive Care In
an effort to address the dangerous conditions that often accompany DM as
well as the symptoms of the disease itself, The (AACE) has released new
clinical practice guidelines for T1 & T2 emphasizing individualized,
comprehensive healthcare for pts with DM. statistics show that DM patients
suffer complications such as heart attack.. 3-7 times more often than those
without diabetes, Unfortunately, many patients with DM do not have the most
common complications of the disease - high lipids & high BP, in addition to
high blood sugar under control. The new guidelines also address but also
underrecognized problems affecting pts with DM , such as depression & sleep
apnea.. The guidelines recommend a blood glucose target of an HbA1c level of
6.5% if it can be achieved safely- a level more stringent than that
recommended by the ADA which recommends 6.9% or below.

3.%% [deleted]
4.%% Is Glucose Self-Monitoring Beneficial in Noninsulin Therapy?
4/22/11 Structured Self-Monitoring of Blood Glucose Significantly Reduces
A1C Levels in Poorly Controlled, Noninsulin-Treated T2 [12-m; 483pt]

5.%% MP Structured Exercise Programs Help Lower Blood Sugar, 5/3/11- A
structured EX program helped people with T2 lower their blood sugar level
more effectively than just receiving advice about getting more physical
activity. [47 randomized clinical trials; 8500pts] "If these pts can perform
training for more than 150 min per wk, this would be more beneficial
concerning their glucose control. However, if they cannot reach this level,
lower exercise amounts are also beneficial." The studies used hemoglobin A1C
(HbA1C) to assess a particular Rx’s effectiveness. HbA1C, sometimes just
A1C, is a measure of long-term blood sugar control. It provides an average
of blood sugar levels over a 2-3 month period. ADA recommends that people
with DM strive to lower their HbA1C levels to less than 7%.

6.%% 4/28/11 Joslin Diabetes Medication Misconceptions T1 &T2 One of the
most pervasive myths about DM --both forms--is that it can be treated by
simply refining your diet or exercising more. While this is certainly an
option for some people with T2, it is absolutely untrue for people with type
1. T1 is an auto-immune disease that occurs when the body’s disease fighting
system, the immune system, destroys all your body's insulin- producing
cells. Insulin is a vital agent that your body needs to convert food into
energy. If your body is not producing insulin, you must take it by injection
or a pump to live. Insulin currently cannot be taken by mouth because the
digestive juices will break down the insulin before it has a chance to get
into your bloodstream to do its job. 
If you have T2, you may or may not need insulin injections. insulin
injections are not for people with DM who have been "bad" instead, taking
insulin is a reflection of insulin production by the pancreas. People just
diagnosed with T2 generally are still producing some insulin- but their
cells may also be resistant to the effects of insulin, so they need more
than a person without DM. Sometimes oral DM drugs are needed to help your
body produce more insulin or use it more efficiently. People who have had T2
for many years may ultimately discover that despite their best efforts, the
oral drugs, along with diet & EX, no longer keep their blood glucose in a
healthy range. This is not unusual - your insulin-producing cells may just
be depleted from having to produce extra insulin to overcome insulin
resistance for an extended period of time. At this time, insulin injections
may be required to continue to keep your blood glucose in the healthy range
to avoid long-term diabetes complications.

7.%% M 5/4/11 Stress Predicts Development of Impaired Glucose Metabolism
Perceived stress and stressful life events predict the development of
impaired glucose metabolism (IGM) over 5 years in previously normoglycemic
[normal level of blood glucose] people
The study showed that perceived stress increased the risk for incident IGM
by between 1.0-1.06. "The effect size sounds quite small but for every point
increase there is a 4% increased risk of developing IGM, so stress is quite
a strong risk factor for IGM," presenter said.. "..we think stress
management should be incorporated into health behavioral interventions for
the most effective prevention and management of DM

8.%% M Comprehensive Review of the Effects of Diabetes on Ocular Health
repub 5/4/11 DM afflicts 23.6 million people in the USA, & an additional ..
57mil exhibit prediabetic symptoms. Conclusion - It is clear that pts with
uncontrolled DM are at risk of developing a wide range of ocular pathology.
While treatment of sight-threatening retinal disease is paramount in these
pts, visual morbidity can also result from DM-induced infection as well as
damage to optic nerve, cornea, uveal tract, orbital tissues & lids, cranial
nerves that innervate the [eye] muscles, & lens. Recent advancements in the
Rx of some of these complications, such as the use of VEGF inhibitors
&intravitreal steroid injections, have improved the visual outcome in pts.
However, other advances in eyecare such as LASIK have presented DM pts with
new challenges. The most important approach to the prevention of ocular
complications in DM patients remains the maintenance of tight glycemic
control. [References of over - 300 deleted]

9.%% Vista Center 5/2/11 New T1 clinical trials at UCSF Diabetes Centre
From: S. E. Gitelman, M.D. The purpose of my letter is to inform you about 2
new exciting clinical research studies currently underway at UCSF for pts
with recent onset T1. --Treatment of T1with Polyclonal Tregs Phase I study,
the researchers will take T Regulatory cells (Tregs) from the pt’s blood,
multiply them in the lab, & infuse them back into the pt to determine which
dose of multiplied Tregs is the safest in humans & if they can prevent
further beta cell destruction. --Reversing T1 After it is Established with
Thymoglobulin (ATG) & Neulasta (GCSF) a randomized, placebo- controlled
Phase I/II study designed to determine the safety of using a combo therapy
(ATG + GCSF), & test its ability to retain/ enhance beta cell function in
pts with established T1.Basic criteria: • Recent onset T1 [age 16 - 44 yrs]
recruitment coordinator Kathleen Fraser 415-353-9084 or
kfraser at diabetes.ucsf.edu for more info 

10.%% Oph 118 May 2011 Is Diabetic Retinopathy Related to Subclinical
Cardiovascular Disease? Persons with DM retinopathy (DR) have an increased
risk of clinical CV events.[927 pts] measures assessed included high
coronary artery calcium score; ankle-brachial index.. Conclusions In persons
with DM without a history of clinical CVD, the presence of advanced-stage DR
is assoc with subclinical coronary artery disease. These findings emphasize
the need to be careful about the use of anti–vascular endothelial growth
factor [VEGF] for the treatment of DR.

11.%% Oph 118 May 2011 Incidence of Nonarteritic Anterior Ischemic Optic
Neuropathy: Increased Risk Among Diabetic Patients [25515pts] randomly
selected Conclusions -DM significantly increased the risk of NAION.
incidence of NAION among pts aged 67 + may be higher than previously
reported.

12.%% ADA 4/28/11 Insulin Pumps - Insulin pumps replace the need for
periodic injections by delivering rapid-acting insulin continuously
throughout the day using a catheter. They offer many advantages that can
simplify DM management. Switching to a pump requires some adjustment, so
discuss the options with your health care team before making a decision. By
using an insulin pump, you can match your insulin to your lifestyle rather
than adjusting your lifestyle to your body's response to insulin injections.
People of all ages with T1 use insulin pumps, & people with T2 have started
to use them as well.

13.%% MTD 5/3/11 Insomnia Linked To High Insulin Resistance In DM Lead
author said "People who have a hard time controlling their blood glucose
[BG] levels have a greater risk of complications, reduced quality of life, &
reduced life expectancy." [40pt;6 nights] poor sleepers had 23% higher BG in
the morning, & 48% higher blood insulin levels. poor sleepers with DM had
82% higher insulin resistance than normal sleepers with DM. The next step is
to see if treating poor sleep can improve long-term outcomes and quality of
life for diabetics.


14.%% MTD 4/30/11 Researchers study Way To Make Insulin Cells
.. A UCLA team shows that chemical tags called "methyl groups" bind to DNA,
where they act like a volume knob, turning up or down the activity of
certain genes. This is crucial to understanding how cells can be converted
into insulin- secreting beta cells. . the basis for this conversion depends
not on genetic sequences but on modifications to the DNA that dictates how
the it is wrapped within the cell,"

15.%% Nat Med 5/2011 B cells promote insulin resistance through modulation
of T cells & production of pathogenic IgG antibodies . Chronic inflammation
characterized by T cell & macrophage [large white blood cell which takes in
foreign material] infiltration of visceral adipose [abdominal fat] tissue
(VAT) is a hallmark of obesity- assoc. IR & glucose intolerance. B cells
accumulate in VAT in obese mice, but those mice lacking Bcells are protected
from disease despite weight gain. .Rx with a B cell– depleting antibody
decreases disease.. Moreover, insulin resistance in obese humans is assoc
with a unique profile of IgG auto- antibodies. These results establish the
importance of B cells & adaptive immunity in IR & suggest new therapeutic
modalities for managing the disease.

16.%% Nat Endo 7, (June 2011) Endocrine disruptors in the etiology of T2DM
Abstract - The etiology of T2 involves the induction of IR along with the
disruption of pancreatic ß-cell function & the loss of ß-cell mass. In
addition to a genetic predisposi tion, lifestyle factors seem to have an
important role. Epidemiological studies indicate that the increased presence
of endocrine disrupting chemicals (EDCs) in the environment may also play an
important part in the incidence of metabolic diseases. Widespread EDCs, such
as dioxins, pesticides & bisphenol A, cause insulin resistance and alter
ß-cell function in animal models. These EDCs are present in human blood &
can accumulate in and be released from adipocytes [fatcells]. After binding
to cellular receptors & other targets, EDCs either imitate or block hormonal
responses. Many of them act as estrogens in insulin-sensitive tissues & in ß
cells.. exposure in mice produces IR & other metabolic alterations; during
pregnancy, EDCs alter glucose metabolism in female mice. .. evidence already
exists to consider exposure to EDCs as a risk factor in the etiology of T2..

17.%% MAP 5/24/11 Long-term benefit of sustained-delivery fluocinolone
acetonide (FA) [steriod] vitreous inserts for diabetic macular edema. [716pt
] Conclusions: Both FA inserts significantly improved best corrected visual
acuity in pts with DME over 2 years, This is the first pharmacologic
treatment that can be administered by an outpatient injection to provide
substantial benefit in patients with DME for at least 2 years.

18. %% ADA -- Aerobic exercise alone or combined with resistance
training significantly improves cardiovascular (CV) risk factors including H
A1c, systolic blood pressure (SBP), triglycerides, & waist circumference in
pts with T2. meta-analysis -34 studies pub 1970-09. Aerobic EX alone or in
combo with resistance training, significantly improved H A1c levels & SBP.
Triglyceride levels & waist circum also improved significantly, but these
were measured in fewer studies.. Resistance training alone, or in combo with
other forms of EX, was not associated with a significant impact on CV
markers.”

19.%% ADA 5/10/11 Creatine supplementation improves glucose tolerance ..
[25subjects;12wk; randomized, double-blind, placebo- controlled] Creatine, a
natural amine in the human body, is partly synthesized by kidneys, pancreas,
& liver as well as ingested from food- meat & fish..In summary, we reported
a novel therapeutic role of creatine supplementation on metabolic control in
T2 pts. .creatine supplementation might modulate glucose uptake in these pts
mainly via an increase in GLUT-4...

20.%% ADA 5/11 Insulin resistance precedes mitochondrial dysfunction in T2DM
It has long been known that people with T2 often suffer from dysfunctions in
their mitochondria [M], organelles contained within cells that produce
energy. However, it was not known whether these M irregularities were the
cause of IR & DM, or whether a single preexisting difference accounted for
both IR & impaired M function. The team examined people born with genetic
defects in their insulin receptors- a dysfunction mimicking symptoms of T2.
tests showed that insulin signaling dysfunction & insulin resistance are the
root cause of M dysfunctions. Showing that IR is the cause of mitochondrial
dysfunction rather than the other way around, could provide direction to
researchers who are looking to solve the health consequences that can result
from either condition. Aside from health complications assoc. with T2, M
dysfunction can lead to muscle weakness, hearing loss, & loss of vision. 

21.%% MAP 5/24/11 Vegetarian diet improves insulin resistance and oxidative
stress markers more than conventional diet in subjects with Type?2 diabetes.
[note some authors are now using ? Like this & also re beta-cells]
[74pt;24-wk] randomized, to veg. or “conventional DM diet” Both diets were
calorie restricted. All meals were provided. The second 12wk of the diet
were combined with aerobic EX. Conclusions A calorie- restricted vegetarian
diet had greater capacity to improve insulin sensitivity than conventional
DM diet over 24 weeks. The greater loss of visceral fat & improvements in
plasma concentrations of adipokines & oxidative stress markers with this
diet may be responsible for the reduction of IR. The addition of EX training
further augmented the improved outcomes.

22. MAP 5/24/11 Losing weight may not be required to lower a person's risk
for DM, Rather, ..small dietary changes can make a big difference in risk,
even without weight loss & particularly among blacks. [69 pts] lower-fat
group consumed a diet comprised of 27 % fat & 55 % carbs. The low-carb
group's diet was 39% fat & 43 % carbs. "At 8wks, the group on the lower-fat
diet had significantly higher insulin secretion, better glucose tolerance
and tended to have higher insulin sensitivity," The findings were stronger
among black participants. the results suggest that attention to diet
quality, not quantity, can make a difference in risk for T2

23.%% MP 5/15/11 Scientists find "master switch" gene for obesity
..a gene linked to DM & cholesterol is a "master switch" that controls other
genes found in fat in the body.. .. & since fat plays an important role in
susceptibility to metabolic diseases like obesity, heart disease & DM, this
regulating gene could be target for drugs to treat such illnesses..
Scientists have already identified a gene - KLF14 -as being linked to T2 &
cholesterol levels, but until now they did know what role it played. [20,000
genes from fat under the skin of 800 pt] They found a link between the KLF14
gene & levels of many other genes found in fat tissue. genes controlled by
KLF14 are linked to a range of metabolic traits, including body mass index,
obesity, cholesterol, insulin & glucose levels. "KLF14 seems to act as a
master switch controlling processes that connect changes in the behavior of
subcutaneous fat to disturbances in muscle & liver that contribute to DM and
other conditions,"

24.%% MP 5/13/11 More signs DM drug linked to bladder cancer - A review of
official reports of drug reactions is revealing more signs that people
taking Actos are at higher risk of developing bladder cancer. Between 2004 &
2009, there were 138 instances of bladder cancer in pts taking at least one
of more than 15 different anti-DM drugs. However, more than a fifth of those
bladder cancers were in pts on Actos (pioglitazone)a "disproportionate risk"
in comparison with other anti-diabetics, ..these findings do not show Actos
increases the risk of bladder cancer, the author cautioned - just that
researchers should look into it further. Actos is in the same class of drugs
as Avandia, which has not been associated with bladder cancer but has been
linked to heart risks. FDA has said patients should not stop taking Actos
unless told to do so by their doctor.

25.%% Diabetes.co.uk 5/24/11 Computed tomography (CT) scan, could help
predict early death in patients suffering from T2. The study also revealed
that diabetics were at an increased risk of developing heart & vascular
disease. [1500pt;13yr]The team used a high coronary artery calcium (CAC)
score to assess the risk of coronary heart disease being present in the
blood vessels of the heart. For people with DM, there is a typically a wide
range of calcified plaque that has built up in the heart & arteries. ..a
significant risk of dying earlier was found in those with highest levels of
calcified plaque in their blood vessels. .

26.%% M Can DM Meds Treat Depression? 5/15/11 The insulin- releasing
properties of suphonylureas [SU] may include antidepres- sant effects. In
study, DM pts prescribed a SU alone had the lowest likelihood for concurrent
co-prescription with an antidepressant The presenter,in 2007 proposed a new
hypothesis for the pathophysiology of depressive disorder, - that it might
be a "diabetes of the brain"- an attenuated cerebral glucose metabolism in
astroglia [type of brain cell]. [3.4mil persons’s data] ".SUs,"the only
group of oral antidiabetic drugs directly stimulating insulin release
(probably also in the brain as the drug has access to cerebral tissues), are
associated with a significantly lower concurrent anti-depressant use...this
data support the idea that there is a compensatory increased activity of
brain insulin in depression. "..it is important to realize that the glucose
absorption of astroglia is influenced by insulin, whereas in neurons insulin
does not have this effect."

27.%% 5/17/11Breakthrough on insulin sensitivity and cholesterol .. removal
of cholesterol by an enzyme (CEH) can reduce inflammation & slow development
of T2. The team used a mouse model to assess the part CEH plays in
regulating the removal of cholesterol from cells & making it available to
high-density lipo protein (HDL), sometimes known as "good cholesterol".
..when the CEH transgene is expressed, the mice showed improved insulin
sensitivity, despite equal weight gain. Diabetes.co.uk 

28.%% MAP 5/17/11 Influence of diabetes on endothelial cell response during
sepsis. [infection] observational cohort study [207pts] Conclusions: During
septic shock, pts with DM had higher levels of circulating biomarkers of
endothelial cell adhesion & VEGF signalling (sFLT-1). Future studies should
address whether enhanced activation of the endothelium [inner cell layer of
blood vessels] places pts with DM at increased risk for the development of
sepsis and worsening morbidity and mortality.

29.%% Another Anti-VEGF Drug Showing Promise for Diabetic Macular Edema
(DME) (Reuters Health) 5/16/11 -.. intravitreal injections of a fusion
protein called VEGF Trap-Eye proved superior to focal/grid laser treatment.
The anti-VEGF drugs ranibizumab (Lucentis) and bevacizumab (Avastin), have
recently been shown to be effective in reducing swelling in the retina and
improving vision in these pts. But the team- Wilmer Eye Institute, Johns
Hopkins - says VEGF Trap-Eye has some theoretical advantages over [lucentis
& avastin] including a longer half-life in the eye, a higher binding
affinity to VEGF-A, & the capacity for binding placental growth factors 1 &
2. [52-wk; 221 pts;randomly assigned to 1 of 5 groups] VEGF Trap-Eye led to
significantly better mean visual acuity outcomes compared with laser
therapy..results suggest it may be possible to prolong the retreatment
interval from 4 wks to 8 wks. Local adverse events were ..consistent with
those seen with other intravitreal anti-VEGF agents," study sponsored by
Regeneron Pharmaceuticals, 

30.%% M Immunology and Immunogenetics, Joslin DM Center 5/11 T1 affects 1 in
300 people & the incidence of the disease is rising worldwide. T1 is caused
by chronic autoimmune destruction of the insulin-producing cells. Exact
etiology & primary auto- antigen are not yet known. The autoimmune, chronic,
& progressive nature of DM raises the possibility of intervention,
preferably by slowing down or stopping the destruction of the ?-cells. Since
the 1980s, several attempts have been made to maintain ?-cell function using
immuno-suppressive agents, immune modulation such as plasmapheresis,
cytokine therapy, or antibody treatment. These agents were not DM s
specific; the occasionally observed beneficial effect did not compensate for
the often very severe side effects. According to the latest assumption, the
administration of diabetes- specific auto- antigens can elicit tolerance,
which can prevent the destruction of the ?-cells, hopefully without serious
side effects...In T1 pts, not only these special cells, but the entire CD4 +
T-cell population is down- regulated affecting [includes] cell cycle, key
immune functions, & electron transport. There are 3 stages at which the
process leading to T1 can be intercepted. In the first stage auto- immunity
has not yet started - primary prevention The second stage is when the
subject has already developed auto- antibodies signaling the presence of
ongoing autoimmunity. The goal here is to prevent the onset of the clinical
disease. These studies target those individuals at risk of developing DM,
such as relatives of T1 pts carrying genetic markers, ..or showing an
abnormal handling of glucose (but not yet diabetic). The third stage is when
clinical T1 is already present but there is still a residual ?-cell function
to preserve. If the autoimmune process is inhibited, there is a chance of
regeneration of the ?cells. ..Glucocorticoids have been widely used as
immunosuppressive treatments. Unfortunately several serious adverse effects
can follow chronic Rx, including weight gain, dyslipidemia, & even steroid-
induced DM. Cyclosporine & tacrolimus have an temporary immuno-suppressive
effect & have toxic effects on kidney, liver, & nervous system Attempts to
use plasmapheresis to maintain ?-cell function in T1 pts did not have any
beneficial effects.. 
The anti- CD20 (rituximab) used in Rx of B-cell lymphomas, decreases the
amount of CD20+ B cells & thus can also reduce auto-antibody production. The
team recently completed a double- blind, placebo- controlled phase I
clinical trial with insulin B chain. The vaccinated pts developed a vigorous
insulin- specific humoral & T-cell response. Summary - There are many
successful Rxs & prevention methods using NOD mice, but those failed to
yield the same results in humans, The pathogenesis of T1 is different in
humans & NOD mice. Using dogs or monkeys, is not feasible for ethical &
financial reasons. Among the prevention & intervention studies, the most
promising are those based on re-establishment of immune tolerance to
DM-specific self-antigens. .increasing data indicate that the primary
auto-antigen in humans is insulin or proinsulin. It is conceivable that
combination therapies may need to be used to tackle autoimmunity; 

31.%% M 5/12/11 How Does Type 1 DM Develop? The Notion of Homicide or ?-Cell
Suicide Revisited Despite decades of acknow ledging that a loss of
insulin-producing pancreatic ?-cells is central to the disorder now referred
to as T1, the specific roles for genetic susceptibility, environmental
factors, the immune system, and ?-cells themselves in the pathogenic
processes underlying the disorder remain unclear...Many reasons exist with
respect to why we are in this knowledge void, including the exceedingly
complex nature of T1, the likelihood that this disorder may represent a
disease with more than one etiology, as well as the complex interplay of
genetics, the immune system, & environment. One limitation in solving
important pathogenic questions in T1 has likely been suboptimal cross-talk
among geneticists, epidemiologists, endocrinologists, &others. [long very
technical discussion of research] .. the onset of T1 may not be solely a
consequence of irreversible ?-cell death. Loss of insulin production more
likely results from a combo of ?-cell destruction alongside partially
reversible loss of ?-cell function caused by inflammatory cytokines. .. back
to the question, is the death of a ?-cell in the pathogenesis of DM homicide
or suicide? given what we have learned about the immune response & the
?-cell, our belief is that T1 appears to be a case of (immune) self-assisted
homicide. 

32.%% ADA Enzyme may increase IR and T2 risk Higher levels of an enzyme
known as PKC-delta may lead to greater insulin resistance & a higher risk of
developing T2, IR is one of the first steps in the development of T2. It
occurs when tissue no longer responds to the hormone, which is responsible
for removing glucose from the blood & converting it to energy. The findings
showed that mice susceptible to IR had a gene that caused levels of the
PKC-delta enzyme to rise. When these mice were fed a high-fat diet, enzyme
levels increased at about the same rate as insulin resistance. However, when
the team eliminated the gene from the mice, they were much less likely to
develop IR.

33.%% ADA 5/20/11 Men with T2DM are more likely to suffer cardio-vascular
complications than women [1123 subjects] while just 1.7% of women suffered a
heart attack during the study period, 3.8% of the men did. Author concluded
that regular MPI screening [myocardial perfussion imaging] is not
recommended for women with T2 due to their relatively low rate of heart
attack. However, the procedure may help men who are at the highest risk of
suffering a MI.

34.%% Vitamin D Levels, Microvascular Complications, & Mortality in T1DM
[227 pts] Conclusions—In patients with T1, severe vitD deficiency
independently predicts all-cause mortality but not development of
microvascular complications in the eye & kidney. Whether vitD substitution
in T1 patients can improve the prognosis remains to be investigated.

35. %% MP 5/25/11 Combo of Paxil, Pravachol May Raise Blood Sugar
Taken in combination, 2 commonly prescribed drugs, the antidepres sant Paxil
& the cholesterol-lowering medication Pravachol, appear to significantly
raise blood sugar levels..the increase is most apparent -- & concerning --
among diabetics. It's possible that the blood sugar spike triggered a
diagnosis of T2 in some pts, Altman (Stanford) said. Neither drug alone
raises blood sugar, & he said they can't yet explain the effect of the
combination. Also, combos of other antidepressants & cholesterol-lowering
drugs do not boost glucose levels. "It is not what we would call a 'class'
effect," Paxil(paroxetine) is in a class of drugs called selective serotonin
reuptake inhibitors (SSRIs), & Pravachol (pravastatin) is a statin. The team
used data from the FDA Adverse Event Reporting System, plus data from
Stanford, Harvard & Vanderbilt to identify associations that would not be
apparent to doctors treating individual pts. They found 135 non-DM pts on
both drugs whose blood sugar increased 19 mg per deciliter after starting Rx
&104 diabetics whose blood sugar increased an average of 48 mg/dl while
taking both drugs. People with blood sugar levels of 126 mg/dl or higher on
2 tests are considered diabetic. The team believes that of 33 million people
currently taking Paxil or Pravachol, 500,000 - 1million take them
together... Goldberg [U of Miami] thinks it's too early to change clinical
practice based on this study alone. "This needs to be confirmed in a
clinical trial," he said.

36.%% M 5/26/11 Diabetic men are significantly more likely to require
invasive second- and third-line therapies to manage erectile dysfunction
(ED) than nondiabetic men, including surgical intervention. Data from a
large medical-claims database found that DM men were more than 50% more
likely than nondiabetic men to progress to secondary therapies, such as
penile suppositories or injectables, within 5 years of an ED diagnosis. "Our
results suggest that ED among diabetics may be less responsive to primary
treatment with oral agents, more rapidly progressive than ED not associated
with diabetes, or both," Am Urological Assoc. 2011 

37.%% 5/27/11 'ultra-bad' cholesterol present in elderly & people with T2.
Scientists have discovered a new form of ‘ultra-bad’ cholesterol that
increases the risk of heart disease. The ultra-bad form, called MGmin-LDL,
has sugary molecules that are smaller and denser than those of normal LDL.
The altered shape readily sticks to artery walls, providing a starting point
for the build-up of dangerous fatty plaques. As the deposits grow, they
narrow arteries and reduce blood flow. Eventually they can rupture,
triggering a blood clot that causes a heart attack or stroke. ..U.S. Halts
'Good Cholesterol' Study a drug that boosts people’s good cholesterol did
not go on to prevent heart attacks or strokes, leading officials to abruptly
halt a major study yesterday. The disappointing findings involve
super-strength niacin, a type of B vitamin that many doctors already
prescribe as potential heart protection. The failed study marks the latest
setback in the quest to harness good cholesterol to fight the bad kind.
Mailonline UK


AACE -American Association of Clinical Endocrinologists (AACE) 20th 
Annual Meeting and Clinical Congress.
Abbreviations: fup-follow up; pt - patients; DM - diabetes Mellitus; T1DM -
type 1 diabetes mellitus T2DM - type 2; DME - diabetic macular edema;DR -
diabetic retinopathy; IR-insulin resistance;EX-exercise; FPG - fasting
plasma glucose; BP - blood pressure; Rx-treatment ;NV- neovascularization;
CVD - cardiovascular disease; MI -myocardial infarction/ heart attack ; OCT
- optical coherence tomography; BCVA - best corrected visual acuity ;ADA -
Am Diab Ass & ADA Prof; M- Med scape Web MD; MAP- Medline Abstract &Plus;
MTD- Med News Today;NEI - Nat Eye Institute; Definitions via online Medical
dictionaries. Disclaimer, I am a BSN RN but not a diabetic or diabetic
educator. Reports are excerpted unless otherwise noted. [translations,
explanations by thl] This project is done as a courtesy to the
blind/visually impaired and diabetic communities. Dawn Wilcox RN BSN
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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