Friday, April 30, 2010
warfarin bleedings cystitis ciprofloxacin
Upper Gastrointestinal Tract Hemorrhage, Warfarin, and Urinary Tract Antibiotics
(cotrimoxacin=trimetroprim sulfa (Mijn opmerking)Findings from a population-based investigation indicate that cotrimoxazole increased hemorrhage risk among patients on long-term warfarin therapy.
Hemorrhage is a well-known side effect of long-term warfarin use in older patients. Interactions between warfarin and certain other drugs can increase the risk for this complication. In a recent nested case-control study conducted using healthcare databases from Ontario, Canada, researchers examined the risk for upper gastrointestinal (GI) tract hemorrhage among patients receiving both warfarin and antibiotics commonly used to treat urinary tract infections.
The cohort consisted of 134,637 patients aged 
66 who had been continuously treated with warfarin for 180 days. Of these patients, 45,972 had received a concomitant prescription for an antibiotic of interest. The 2151 patients (1.6%) who were hospitalized for upper GI tract hemorrhage during the study period were considered cases; up to 10 age- and sex-matched controls were selected for each case.
Cases were nearly four times as likely as controls to have received cotrimoxazole (adjusted odds ratio, 3.84; 95% confidence interval, 2.33–6.33). Ciprofloxacin use was also associated with increased bleeding risk (AOR, 1.94; 95% CI, 1.28–2.95). No significant association was seen between hemorrhage and use of amoxicillin, ampicillin, nitrofurantoin, or norfloxacin.
vitamine D dementia
April 29, 2010 (Toronto, Ontario) — Vitamin D deficiency appears to increase the risk for cognitive impairment, a large, population-based study of older women shows.
Presented here at the American Academy of Neurology 62nd Annual Meeting, the cross-sectional study shows older women with serum 25-hydroxyvitamin D (25OHD) levels of less than 10 ng/mL had a 2-fold increased risk of global cognitive impairment compared with their counterparts who were not vitamin D deficient.
"After accounting for all potential confounders, our findings showed an association between vitamin D deficiency and global cognitive impairment. These results are congruent with fundamental research and add to the growing body of evidence in favor of the neurological action of vitamin D," principal investigator, Cédric Annweiler, MD, Angers University Hospital in France, told Medscape Psychiatry.
Dr. Annweiler said he became interested in looking at the potential impact of vitamin D on cognitive function when studying risk factors associated with falling in older women in the Epidemiologie de l'Osteoporose (EPIDOS) study. This large, prospective, observational, multicenter cohort study was designed to evaluate risk factors for hip fracture among more than 7500 healthy, community-dwelling older women.
Typically associated with skeletal disorders, vitamin D deficiency is also associated with neuromuscular disorders in humans and severe coordination disorders in animal research, said Dr. Annweiler.
Specific CNS Effects
A neurosteroid hormone, research shows it has specific effects on the central nervous system (CNS), including regulation of neurotransmission, neuroimmunomodulation, and neuroprotection.
According to Dr. Annweiler, few studies have investigated the association between low serum 25OHD and cognitive impairment. A recent systematic review of the literature conducted by his team produced mixed results (Eur J Neurol. 2009;16:1083-1089).
However, the investigators speculated that these inconclusive findings may be explained by the lack of control for potential confounders.
To determine whether there was an association between vitamin D deficiency and global cognitive impairment, the investigators studied 752 women from the EPIDOS cohort. Participants were 75 years and older and were divided into 2 groups according to serum 25OHD concentration — deficient (<10>
Cognitive impairment was determined using the Pfeiffer Short Portable Mental State Questionnaire (SPMSQ), a validated, 10-item, composite questionnaire used to screen for organic brain diseases. Cognitive impairment was defined as an SPMSQ score of less than 8.
Investigators controlled for a variety of potential confounders, including age, body mass index, number of chronic diseases, current hypertension, current depression, use of psychoactive drugs, education level, regular physical activity, and serum intact parathyroid hormone and calcium.
Rampant Problem in the Elderly
The results showed that compared with women who were not vitamin D deficient (n = 623) their vitamin D deficient counterparts had a lower mean SPMSQ score (P < .001) and were also more likely to have an SPMSQ score of less than 8 (P = .006).
Adjusted analysis revealed that vitamin D was significantly associated with cognitive impairment (odds ratio, 2.03; P = .001).
The clinical implications, said Dr. Annweiler, appear clear — clinicians need to assess and treat vitamin D deficiency in their older patients for a variety of health reasons that may include preservation of cognitive function.
Vitamin D deficiency is common in the general population but is rampant among the elderly. According to Dr. Annweiler, it is estimated that 70% to 80% of individuals older than 75 years are vitamin D deficient.
Currently, adequate intakes of vitamin D for 51- to 70-year-olds are 400 IU per day and 600 IU for those older than 70 years to maintain a 25OHD level of 30 ng/mL or more. However, Dr. Annweiler noted that these recommendations are based primarily on preservation of bone health alone.
The reason the elderly are more vulnerable to vitamin D deficiency than younger individuals are several-fold and include decreased exposure to sunlight and inadequate dietary intake. In addition, said Dr. Annweiler, the skin of older people is not as efficient at synthesizing UV-B rays into vitamin D.
"This study provides more evidence to support [vitamin D] supplementation in our elderly patients to normalize serum concentrations and help sustain good health. Although we are not certain yet, it may be that this will also be a viable way to prevent or treat cognitive impairment and possibly turn out to be a new management strategy for dementia," said Dr. Annweiler.
The study was initially published earlier this year in the January 5 issue of Neurology. At that time, in an accompanying editorial, Joshua W. Mill, PhD, UC Davis Medical Center, Sacramento, California, echoed Dr. Annweiler's clinical recommendation (Neurology. 2010;74:13-15).
What are needed now are placebo-controlled intervention studies to determine whether vitamin D supplements will protect against age-related cognitive decline. In the meantime, neurologists and geriatricians should be aware of the high prevalence of vitamin D deficiency in their patient populations and the possibility that supplementation could be beneficial," Dr. Mill writes.
Dr. Annweiler said his team plans to prospectively follow up the cohort and examine the potential relationship between vitamin D status and incident dementia. In addition, his team is exploring the possibility of conducting a clinical trial to look at the impact of supplementation on cognitive outcomes.
The study was funded by the French Ministry of Health. Dr. Annweiler and Dr. Miller have disclosed no relevant financial relationships.
American Academy of Neurology (AAN) 62nd Annual Meeting: Abstract S34.003. Presented April 14, 2010.
Friday, April 23, 2010
colon kanker statins
Statins Do Not Protect Against and May Increase Risk for Colorectal Adenomas
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April 22, 2010 (Washington, DC) — Statins do not protect patients against colorectal adenomas, the benign precursors of colorectal cancer, and might increase the risk of developing them when used for 3 years or more, according to new research.
However, the increased risk is in need of further study, and not cause for patients to stop taking statins for cardiovascular benefit, said lead researcher Monica Bertagnolli, MD, who presented study results here at the American Association for Cancer Research (AACR) 101st Annual Meeting.
I would hate to take away a life-saving drug for a theoretical risk.
"The clear message is that statins save lives in patients with cardiovascular disease. I would hate to take away a life-saving drug for a theoretical risk," said Dr. Bertagnolli, chief of the Division of Surgical Oncology at Brigham and Women's Hospital and professor of surgery at Harvard Medical School in Boston, Massachusetts. She spoke to Medscape Oncology in the press room at AACR.
The new results come from the Adenoma Prevention with Celecoxib (APC) trial, which was primarily designed to evaluate whether the arthritis drug celecoxib (Celebrex, Pfizer) could be used to prevent colon cancer (N Engl J Med. 2006;355:873-884).
However, about a third of the 2035 patients in the study also took cholesterol-lowering statins.
The new statin results are from a planned secondary analysis of the ACP trial and were published online April 19 in Cancer Prevention Research to coincide with the presentation at the meeting.
The randomized placebo-controlled APC trial was designed to assess the effect of concomitant medications on the development of adenomas and other study end points, Dr. Bertagnolli explained.
To make this assessment, the investigators separated out the 679 placebo users, 221 of whom used statins.
Like the rest of the participants in the trial, the patients on placebo were at high risk for adenomas, and underwent colonoscopic surveillance for 5 years after study enrollment.
After adjustment for covariates, including cardioprotective aspirin use, age, and sex, participants in the placebo group who used statins at any time had no benefit over 5 years, compared with participants who had never used statins (risk ratio, 1.24; 95% confidence interval [CI], 0.99 - 1.56; P = .065)
Statins definitely did not prevent adenomas.
"Statins definitely did not prevent adenomas," said Dr. Bertagnolli.
However, an increased risk for adenomas over the 5-year study period was found in a subset analysis of patients taking statins for more than 3 years (risk ratio, 1.39; 95% CI, 1.04 - 1.86; P = .024).
"We found more adenomas in this group," said Dr. Bertagnolli about the subset analysis. However, the finding was "intriguing only" and was in need of follow-up study, she said.
"We ought to study what happens to patients who take statins for more than 3 years," she said.
Friday, April 09, 2010
AF dementia
From Heartwire
New AF Predicts Diagnosis of Alzheimer's, Other Dementias
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Information from Industry
April 7, 2010 (Murray, Utah) — Onset of atrial fibrillation (AF) in a community population followed for five years predicted development of dementia of any kind during the same period, and it also predicted each of four dementia subtypes independently, including Alzheimer's disease [1].
The relationship of new AF to Alzheimer's was significant only among patients who were younger at baseline, report Dr T Jared Bunch (Intermountain Medical Center, Murray, UT) and colleagues in the April 2010 issue of Heart Rhythm. The arrhythmia was also a predictor of mortality among people who developed dementia.
Of 37 025 patients in the cohort from a regional medical group, who were predominantly white and without preexisting AF or dementia, 27% developed the arrhythmia and 4.1% were diagnosed with some form of dementia over a mean of five years.
Significantly more AF patients than non-AF patients developed each of four types of dementia as defined by ICD-9 codes (p<0.0001>
In multivariate analyses, those developing AF had an odds ratio (OR) of:
- Only 1.06 (p=0.59) for developing Alzheimer's regardless of age, but it was 2.30 (p=0.001) among those <70 years; ORs weren't significant in any older age group by decade.
- 1.44 overall for nonspecific dementia and 2.87 among patients <70 (p<0.0001 p="0.001).">
- 1.39 overall (p=0.005) for senile dementia; it was 3.34 in the <70 group and 1.60 in those aged 70 to 79 (p<0.0001 p="">
Overall, development of dementia independently increased hazard ratio (HR) for mortality, at p<0.0001><70>
Why AF and the different forms of dementia were linked is unknown, Bunch et al observe, but they list a few possible mechanisms. Dementia and AF could share a common predisposing condition, such as central hypertension or microvascular dysfunction. Perhaps heart failure associated with AF compromises cerebral perfusion. Or, the group speculates, "AF independently increases systemic inflammation beyond other cardiac risk factors and may thereby accelerate the inflammation-mediated progressive cognitive decline."
Bunch and coauthors Drs J Peter Weiss, Brian G Crandall, and Jeffrey S Osborn (all of Intermountain Medical Center) report receiving honoraria from Boston Scientific. Dr John D Day (Intermountain Medical Center) reports consulting for Boston Scientific and St Jude Medical.
dementia
From Medscape Medical News
Subjective Memory Impairment an Independent Risk Factor for Dementia
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processing....
Information from Industry
See data on an antipsychotic that significantly improved both positive and negative symptoms of schizophrenia and also reduced the risk of relapse at 1 year.
See it now
April 8, 2010 — Subjective memory impairment (SMI) or mild deficits in memory that may, or may not, worry an individual appear to predict progression to more advanced cognitive impairment and dementia, new research suggests.
A study by investigators at the University of Bonn, Germany, shows that individuals who had memory impairment with concern at the beginning of the study were at the highest risk for conversion to any dementia, or Alzheimer's disease (AD)–related dementia, at either 18-month or 5-year follow-up.
"Subjective memory impairment without worry was independently associated with increased risk for dementia," the study authors, led by Frank Jessen, MD, write. "This risk was roughly doubled by the presence of subjective memory impairment–related worry."
In addition, the results showed that having memory impairment at the beginning of the study and mild cognitive impairment (MCI) at the first follow-up increased the risk for conversion to any dementia or dementia related to AD at the second follow-up; these individuals had the greatest risk of developing dementia.
"Our data support the concept of SMI as a pre-MCI condition in AD. Furthermore, the risk increase associated with SMI-related worry indicates that this early memory decline in AD may vary and may be more subjectively dramatic than memory decline related to other factors such as normal aging even among subjects with equal performance on testing," the investigators write.
The study is published in the April issue of the Archives of General Psychiatry.
Longitudinal, Multicenter Study
The researchers used the German Study on Aging, Cognition and Dementia in Primary Care Patients of the German Competence Network Dementia, a longitudinal investigation of subjects initially without dementia. The subjects, recruited at 6 study sites in Germany, were 75 years or older.
Trained psychologists interviewed subjects at home. To assess SMI, subjects were asked whether they felt as though their memory function was worsening and whether this was a source of worry.
Subjects also completed a battery of neuropsychological tests, including the Structured Interview for Diagnosis of Dementia of Alzheimer’s Type, Multi-infarct Dementia and Dementia of Other Etiology (SIDAM).
The SIDAM interview, including the SIDAM cognitive (SISCO) score (which includes memory and nonmemory domains, such as orientation, language, and perception), and the Geriatric Depression Scale were performed at baseline and 1.5- and 5-year follow-up.
MCI was defined as 1-SD performance below age- and education-adjusted normal ranges in any of 4 SISCO score domains, the absence of dementia, and lack of impact on activities of daily living (ADL). Dementia, which requires cognitive impairment and impaired ADL, was diagnosed according to Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) criteria.
MCI has an annual conversion rate to dementia of 10% to 20%.
From a baseline population of 2415 subjects, researchers tested a variety of different sequences of SMI and MCI at follow-up with regard to the prediction of dementia, including
- No SMI at baseline and no MCI at first follow-up;
- SMI at baseline and no MCI at first follow-up;
- No SMI at baseline and MCI at first follow-up; and
- SMI at baseline and MCI at first follow-up.
The researchers found that SMI with worry (P < .001) and SMI without worry (P = .02) were associated with increased risk for dementia at first and second follow-up.
Age (P = .003), ApoE4 genotype (P = .04), and baseline SISCO score (P < .001) were other significant risk factors. Sex, education, and Geriatric Depression Scale score were not associated with increased risk for dementia.
Incidence dementia in AD at follow-up 1 or 2 was associated with SMI with worry (P < .001), SMI without worry (P = .007), age (P = .003), and baseline SISCO score (P < .001). Sex, education, depression score, and ApoE4 genotype were not associated with incidence dementia.
The sensitivity and specificity for conversion to dementia in AD among subjects having SMI with worry at baseline were 69.0% and 74.3%, respectively
Subjects without SMI at baseline and without MCI at 18-month follow-up served as the reference category in a second analysis. The greatest risk for dementia was in subjects with SMI at baseline and with MCI at first follow-up.
At 5-year follow-up, the risk for conversion to any dementia was increased by an odds ratio (OR) of 8.92, whereas the risk for conversion to dementia in AD was increased by an OR of 19.33.
Worry Doubles Risk
The greatest risk for conversion to any dementia (OR, 29.24) was in subjects with SMI at baseline and with amnestic MCI at first follow-up. The risk was even greater (OR, 60.28) for conversion to dementia in AD at the second follow-up period.
The hazard ratio (HR) of conversion at follow-up 1 or follow-up 2 for SMI without worry at baseline was 1.83 (95% confidence interval [CI], 1.12 – 2.99) for any dementia and 3.04 (95% CI, 1.36 – 6.81) for dementia in AD. For SMI with worry at baseline, the corresponding HRs were 3.53 (95% CI, 2.07 – 6.03) for any dementia and 6.53 (95% CI, 2.82 – 15.20) for dementia in AD.
"Subjective memory impairment without worry was independently associated with increased risk for dementia. This risk was roughly doubled by the presence of subjective memory impairment–related worry," the study authors note.
Overall, these results provide "strong empiric support" for the recently suggested model of SMI as a pre-MCI syndrome in the clinical manifestation of AD, say investigators.
"The present data contribute to the current efforts toward a predementia diagnosis of AD. We suggest that biomarker studies (such as magnetic resonance imaging, positron emission tomography, and cerebrospinal fluid investigations) should address not only MCI but also earlier SMI as performed in some studies," they write.
They added that future evaluation of SMI in conversion to dementia may identify specific profiles of SMI that are particularly predictive.
Red Flag
Commenting on the findings for Medscape Psychiatry, Ronald Petersen, MD, PhD, director of the Mayo Clinic Alzheimer’s Disease Research Center, Rochester, Minnesota, and a member of the American Academy of Neurology, said subjective concerns on the part of patients are very important, especially now that researchers are investigating earlier stages of the disease process.
Although not every patient with a subjective concern is necessarily on the road to MCI and AD, such complaints should not be discarded or chocked up to normal forgetfulness in aging, said Dr. Petersen.
"Subjective memory concern raises a flag that clinicians should not ignore. It doesn’t mean you have to launch a million dollar workup on the patient, but don’t ignore it; explore it a little bit further, see what kinds of memory concerns the patient has, and then if you think this might be a genuine memory problem, then go ahead and pursue it with further evaluation," he said.
Assessing the element of worry may be a bit trickier, said Dr. Petersen. "It behooves the clinician to take it a step further and not only inquire about the type of memory impairment, the quality, but also look at things like anxiety, depression, and melancholy," which may, in fact, explain some subjective memory impairment.
The study authors and Dr. Petersen have disclosed no relevant financial relationships.
Arch Gen Psychiatry. 2010;67:414-422.
B12 folic acid foliumzuur
JAMA. 2009;302(19):2119-2126.
Context Recently, concern has been raised about the safety of folic acid, particularly in relation to cancer risk.
Objective To evaluate effects of treatment with B vitamins on cancer outcomes and all-cause mortality in 2 randomized controlled trials.
Design, Setting, and Participants Combined analysis and extended follow-up of participants from 2 randomized, double-blind, placebo-controlled clinical trials (Norwegian Vitamin Trial and Western Norway B Vitamin Intervention Trial). A total of 6837 patients with ischemic heart disease were treated with B vitamins or placebo between 1998 and 2005, and were followed up through December 31, 2007.
Interventions Oral treatment with folic acid (0.8 mg/d) plus vitamin B12 (0.4 mg/d) and vitamin B6 (40 mg/d) (n = 1708); folic acid (0.8 mg/d) plus vitamin B12 (0.4 mg/d) (n = 1703); vitamin B6 alone (40 mg/d) (n = 1705); or placebo (n = 1721).
Main Outcome Measures Cancer incidence, cancer mortality, and all-cause mortality.
Results During study treatment, median serum folate concentration increased more than 6-fold among participants given folic acid. After a median 39 months of treatment and an additional 38 months of posttrial observational follow-up, 341 participants (10.0%) who received folic acid plus vitamin B12 vs 288 participants (8.4%) who did not receive such treatment were diagnosed with cancer (hazard ratio [HR], 1.21; 95% confidence interval [CI], 1.03-1.41; P = .02). A total of 136 (4.0%) who received folic acid plus vitamin B12 vs 100 (2.9%) who did not receive such treatment died from cancer (HR, 1.38; 95% CI, 1.07-1.79; P = .01). A total of 548 patients (16.1%) who received folic acid plus vitamin B12 vs 473 (13.8%) who did not receive such treatment died from any cause (HR, 1.18; 95% CI, 1.04-1.33; P = .01). Results were mainly driven by increased lung cancer incidence in participants who received folic acid plus vitamin B12. Vitamin B6 treatment was not associated with any significant effects.
Conclusion Treatment with folic acid plus vitamin B12 was associated with increased cancer outcomes and all-cause mortality in patients with ischemic heart disease in Norway, where there is no folic acid fortification of foods.
Thursday, April 08, 2010
endarterectomy carotis
Carotid Stenting vs. Endarterectomy: Coming into Focus Free!
April 7, 2010 | Beat J. Meyer, MD
Findings from a large clinical trial and magnetic resonance imaging substudy strengthen the case for endarterectomy as the preferred treatment for carotid artery stenosis.
Reviewing: ICSS Investigators. Lancet 2010 Mar 20; 375:985
Bonati LH et al. Lancet Neurol 2010 Apr 9:353
Rothwell PM. Lancet 2010 Mar 20; 375:957
Wednesday, April 07, 2010
hart failure vitamine D
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Correlation between Vitamin D and Cardiovascular Events
Overall, the literature points to the observation that a low 25(OH)D concentration is closely associated with CVD. As previously discussed, several mechanisms explain the protective effects of vitamin D on the cardiovascular system: involvement of the vitamin D-PTH axis, the regulation of inflammation with its link to atherosclerosis, the regulation of the RAAS system, and the effect on insulin secretion, insulin sensitivity, and metabolic syndrome. Understanding these mechanisms assists pharmacists and other health care providers in interpreting recent studies that evaluate vitamin D deficiency and adverse cardiovascular events.
A recent investigation of the general U.S. population found that 25(OH)D deficiency (lowest quartile, <17.8>[28] Data from NHANES (2001–2004) revealed that adults with lower 25(OH)D concentrations were more likely to have CVDs such as coronary heart disease, heart failure, stroke, and peripheral arterial disease.[36] It was discussed, however, that lower vitamin D levels might have been observed in patients with heart failure and heart disease due to limited physical activity, leading to decreased sunlight exposure, suggesting that lower vitamin D was a result of CVD, and not vice versa. However, another prospective observational study, with a mean follow-up period of 5.4 years, found that subjects with low vitamin D levels without CVD at baseline had a 53% to 80% higher rate of a CVD end point (fatal or nonfatal myocardial infarction [MI], ischemia, stroke, and heart failure).[30] Additionally, in the Health Professionals Follow-up Study, it was found that men without CVD at baseline but with vitamin D deficiency, defined as 25(OH)D <15>[37]
Although these trials are important stepping-stones to our insight into this widely debated topic in the literature, future research is necessary to reveal the relationship between vitamin D and cardiovascular health.
hypertension bloeddruk vitamine D
Hypertension
Vitamin D deficiency and insufficiency have been observed to upregulate the renin-angiotensin-aldosterone system (RAAS), resulting in hypertension, a well-known risk factor for CVD.[21] In an animal study emulating vitamin D deficiency, vitamin D receptor knockout mouse models showed increased blood pressure, increased serum angiotensin-converting enzyme levels, and tissue renin content.[8,22] Human studies have shown that 1,25(OH)2D has an inhibitory effect on renin synthesis, which decreases blood pressure.[23] It has also been demonstrated that exposure to UVB, but not UVA, radiation on a regular basis both elevated serum 25(OH)D levels above 100 nmol/L and decreased blood pressure by 6 mmHg in hypertensive patients.[24] (In this study, patients were exposed to UVB radiation in a tanning bed, 3 times per week, for a total of 3 months.) Another study in elderly women demonstrated that supplementation with vitamin D and calcium, compared to calcium alone, resulted in a significant increase in 25(OH)D concentrations (P <.01), a decrease in PTH levels (P <.05), a decrease in blood pressure by 9.3% (P <.025), and a decrease in heart rate by 5.4% (P <.025).[25] Furthermore, the NHANES III study found that those individuals with higher serum 25(OH)D concentrations had a self-reported mean systolic blood pressure approximately 3 mmHg lower compared to patients with lower concentrations.[8]
In contrast, several smaller studies noted no such benefits of vitamin D supplementation on blood pressure decline.[5] The Women's Health Initiative study, recently conducted in the U.S., revealed that no blood pressure changes were noted in women randomized to receive vitamin D (400 IU) and calcium at the end of a 7-year follow-up period.[26] It should be noted, however, that the vitamin D dose administered to study subjects was lower than recommended in clinical practice (for adults >70 years, supplementation is recommended to be at least 800 IU daily).[27] In addition, the authors also reported that study subjects had low adherence to the study drug. Nevertheless, these results should not be ignored; further studies are needed to clarify the clinical importance of vitamin D supplementation as an antihypertensive agent.
vitamine D vervolg
Atherosclerosis and Inflammation
Although the association of ESRD and increased CVD risk has been well documented, the effect of elevated PTH levels induced by vitamin D deficiency on CVD risk in the absence of ESRD continues to be under investigation. A recent cross-sectional study evaluated 654 adults between the ages of 55 and 96 years without a history of coronary heart disease, revascularization, or stroke. Results revealed that those with higher concentrations of 25(OH)D had a significantly dose-dependent decrease of the intima-media wall thickness of the carotid artery (P = .036), linking vitamin D deficiency to development of subclinical atherosclerosis.[20] This finding is supported by research stating that vitamin D deficiency increases systemic inflammation, as confirmed by elevated levels of C-reactive protein and interleukin-10.[4,6,9] In addition, the administration of vitamin D analogues has been shown to downregulate the inflammatory markers and reduce plaque production and instability.[8,9]
vitamine D
Vitamin D: The Basics
Vitamin D refers to two biologically inactive precursors: vitamin D3 (cholecalciferol), produced mainly in the skin post exposure to ultraviolet (UV) radiation, and vitamin D2 (ergocalciferol), produced exogenously and entering the circulation solely after gastrointestinal absorption.[3] Both vitamin D2 and D3 require hydroxylation reactions in the liver and kidney, closely regulated by the parathyroid hormone (PTH), to form the biologically active metabolite of vitamin D, 1,25(OH)2D (calcitriol).[4] Vitamin D status is best measured by 25(OH)D concentrations or levels and not calcitriol levels for several reasons, including longer half-life (~3 weeks compared to ~8 hours for calcitriol), higher circulating serum concentrations, and tight regulation of calcitriol by PTH, resulting in falsely elevated calcitriol levels despite vitamin D deficiency.[5] Currently, there is no universally accepted "normal" measure of 25(OH)D levels; however, it has been suggested that concentrations above 30 ng/mL are associated with decreased fracture rates and maximal parathyroid suppression.[6]
Although the classic function of vitamin D has been to increase the intestinal absorption of calcium for proper bone health, its role in health maintenance is beginning to expand with the finding of vitamin D receptors (VDRs) in many cells throughout the body, including cardiomyocytes, vascular smooth muscle, and endothelium.[5,7] Additionally, recent studies have found that individuals with vitamin D deficiency have increased incidence of CVD.[7]
vitamine D
Introduction
Heart disease is a broad term that describes a range of diseases that affect the cardiovascular system and result in approximately 630,000 deaths annually in the United States.[1] Cardiovascular disease (CVD) is the leading cause of death of both men and women above the age of 35 among all racial and ethnic groups.[2] While risk factors such as increased age, male gender, and family history are nonmodifiable, others, such as smoking, high cholesterol, hypertension, physical inactivity, obesity, diabetes mellitus, and stress are preventable.[2] Another possible modifiable risk factor, vitamin D deficiency, has been identified and has caused debates in the literature as the protective role of vitamin D on the cardiovascular system continues to be investigated. This article will expand on this proposed phenomenon, providing deeper insight into recently published literature, as well as discuss the pharmacist's role in preventing vitamin D deficiency.
Monday, April 05, 2010
statines
Very low LDL targets attainable with statin-based therapy
25 March 2010
MedWire News: Very low target levels of low-density lipoprotein (LDL) cholesterol are achievable through statin-based therapy, a study of very-high-risk heart patients has found.
The study authors report that nearly half of patients in a real-world practice attained the LDL cholesterol goal of less than 70 mg/dl (1.81 mmol/l), as recommended in the revised National Cholesterol Education Program guidelines for very-high-risk patients with coronary artery disease (CAD).
The study was a retrospective, cross-sectional analysis of patients in the Kaiser Permanente Colorado healthcare system aged 18 years and above and with CAD and a predetermined LDL cholesterol goal of less than 70 mg/dl (1.81 mmol/l).
In all, 3226 of 7427 patients (43%) attained the goal, report Amy Kauffman (University of Colorado, Denver, USA) and colleagues in the Journal of Clinical Lipidology.
Patients who achieved their LDL goal were significantly more likely to be receiving a statin – either alone or in combination – than were patients not at goal (92.4% vs 81.3%).
Among those who attained the goal, 61.1% were receiving statin monotherapy, 70.7% were taking a moderate-to-high-potency statin, and 87.4% were taking a generic statin.
The remaining patients at goal were taking combination therapy, most often a statin in combination with ezetimibe (70.6%) or niacin (13.1%).
Multivariate analysis revealed several factors that were independently associated with failure to attain a LDL cholesterol of less than 70 mg/dl (1.81 mmol/l): age less than 65 years, female gender, hyperlipidemia diagnosis, and creatine kinase levels in the range 861–2000 IU/l.
Conversely, factors that independently predicted goal attainment were statin therapy (monotherapy or in combination), a history of gout, a higher body mass index, a greater level of cardiovascular risk, and a higher burden of chronic disease.
“Despite reporting a higher percentage of patients attaining a LDL cholesterol of less than 70 mg/dl treatment goal compared to previous studies, under 50% attained goal in a system which includes aggressive implementation and titration of lipid-lowering therapies and close monitoring and follow-up for all patients,” Kauffman and co-authors remark.
They conclude: “These data demonstrate the difficulty in attaining a LDL cholesterol of less than 70 mg/dl in the vast majority of patients with CAD.”
MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2010
J Clin Lipidol 2010; Advance online publication
Saturday, April 03, 2010
dementia
From Reuters Health Information
Modifiable Factors Predict Aggression in Dementia
By Karla Gale
NEW YORK (Reuters Health) Mar 26 - Aggressive behavior in patients with recent-onset dementia is linked with pain, caregiver burden at baseline, and declining quality of the caregiver-patient relationship, prospective study findings suggest.
"Historically, behavioral problems (in patients with dementia), such as aggression, have been treated with tranquilizing medications without regard to what might be causing the behavior," lead author Dr. Mark E. Kunik told Reuters Health. The medications are not particularly effective and often result in side effects, he said.
"By understanding possible causes, we can develop (nonpharmacologic) interventions to prevent the development of aggression or more effectively treat aggression once it develops," he added.
Dr. Kunik, from the Michael E. DeBakey Veterans Affairs Medical Center, Houston, and colleagues studied 215 community-dwelling patients diagnosed in the past year with dementia, and their caregivers. They excluded patients who had shown aggressive behavior since their diagnosis.
All subjects were at least 60 years old; their mean age was 76, and 95% were men.
Every four months for the next two years, the researchers assessed patients for frequency and disruptiveness of aggression (taking into account spitting, cursing and other verbal aggression, physically trying to hurt themselves or others, destroying property, and making inappropriate verbal and/or physical sexual advances).
The research team also analyzed caregiver burden, along with the quality of the patient-caregiver relationship ("mutuality"), including the frequency of communication, positive engaging interactions, attachment, and emotional support.
As they report in a March 9 online article in the Journal of Clinical Psychiatry, 89 patients (41%) developed aggression (0.37 cases per year at risk). Several baseline characteristics were associated with aggression, including dementia severity, lower mutuality score, and higher scores for depression, hallucinations, delusions, and caregiver burden.
On multivariate analysis, higher levels of baseline caregiver burden (p = 0.002), worst pain (p = 0.01), and decline in mutuality over time (p = 0.006) were independently associated with increased risk of aggression.
"Caregivers do play an important role in the onset of aggression, but it is important to not place blame on the caregiver," Dr. Kunik told Reuters Health by email. "Caregiving of patients is extremely stressful and often caregivers feel isolated and have little access to help or resources to help with caregiving."
He advises physicians to carefully screen for and treat pain in dementia patients.
"Pain is difficult to recognize in persons with dementia because of the language problems that are associated with dementia," he said. "Sometimes, the best way to prevent aggression may be the prescription of over-the-counter Tylenol (acetaminophen)." Is hetzelfde als paracetamol
He continued: "Physicians should also evaluate caregiver stress. Providing the number for the Alzheimer's Association can be extremely helpful. The Alzheimer's association has many resources for caregivers that are available online or in person. Some of the resources are educational and others offer direct support such as care consultation and support groups."
The authors note that their study did not differentiate types of dementia, and that it suffered from attrition at all stages of the project and from the large male composition of the population.
Nevertheless, Dr. Kunik concluded, "The identification of causes of aggression and aiming to prevent aggression is a fundamental shift in how aggression is currently managed."
J Clin Psychiatry 2010.
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