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Saturday, May 28, 2016

How much low Salt in Diet might be Safe

Posted by Prahallad Panda on 10:53 AM Comments


General advice to patients suffering from hypertension is to consume low salt diet. But, how much less is safe for the patient has not been clearly defined. Generally, it is advised to remain below 2.3 gms/day. Some say 1.5 gms/day.
A large worldwide study has found that, contrary to popular thought, low-salt diets may not be beneficial and may actually increase the risk of cardiovascular disease (CVD) and death compared to average salt consumption. The study suggests that the only people who need to worry about reducing sodium in their diet are those with hypertension (high blood pressure) and have high salt consumption.
The study, involving more than 130,000 people from 49 countries, was led by investigators of the Population Health Research Institute (PHRI) of McMaster University and Hamilton Health Sciences.
Current intake of sodium in Canada is typically between 3.5 and 4 grams per day. Some guidelines suggest to consume salt below 2.3 grams per day, a level that fewer than five per cent of Canadians and people around the world consume.
Only about 10 per cent of the population in the global study had both hypertension and high sodium consumption (greater than 6 grams per day).
Low sodium intake reduces blood pressure modestly, compared to average intake, but low sodium intake also has other effects, including adverse elevations of certain hormones which may outweigh any benefits.
This new study shows that the risks associated with low-sodium intake -- less than three grams per day -- are consistent regardless of a patient's hypertension status.
"An approach that recommends salt in moderation, particularly focused on those with hypertension and high salt intake, appears more in-line with current evidence."
The study was funded from more than 50 sources, including the PHRI, the Heart and Stroke Foundation of Canada and the Canadian Institutes of Health Research.
The article was published in the ScienceDaily, can be accessed here.
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Sunday, April 24, 2016

Metformin can be used to Treat certain Type II Diabetes Patients with Mild to Moderate Impaired Kidney Function

Posted by Prahallad Panda on 10:48 AM Comments


Traditionally, use of metformin is contraindicated in patients with renal failure due to concern about lactic acidosis.
Metformin 500mg tablets
Metformin 500mg tablets (Photo credit: Wikipedia)
In December of 2014, a seminal paper critically looked at the evidence for the use of metformin in mild to moderate renal failure and concluded that, “Metformin levels generally remain within the therapeutic range and lactate concentrations are not substantially increased when used in patients with mild to moderate chronic kidney disease (estimated glomerular filtration rates, 30-60 mL/min per 1.73 m2).”
The paper suggested that given the benefit of metformin to patients with diabetes, of whom up to one-quarter have some degree of renal failure, and the lack of evidence of harm, metformin should be able to be used in this group.
The paper recommended dose adjustments of metformin with maximum total daily dose in patients with mild renal insufficiency (GFR 45-60) of 2000 mg per day and in patients with moderate renal insufficiency (GFR 30-35) not to initiate therapy but that one may continue metformin with maximum daily dose of 1000 mg daily.
English: Physiology of Nephron
English: Physiology of Nephron (Photo credit: Wikipedia)
Now, the US Food and Drug Administration (FDA) is requiring labeling changes regarding the recommendations for metformin-containing medicines for diabetes to expand metformin’s use in certain patients with reduced kidney function. The current labeling strongly recommends against use of metformin in some patients whose kidneys do not work normally.

After reviewing a number of medical studies, the FDA concluded that metformin can be used safely in patients with mild impairment in kidney function and in some patients with moderate impairment in kidney function and is requiring changes to the metformin labeling to reflect this new information while providing the following specific recommendations on the drug’s use in patients with mild to moderate kidney impairment:
• FDA recommends that healthcare professionals follow the latest recommendations when prescribing metformin-containing medicines to patients with impaired kidney function.
• Patients should talk to their health care professionals, if they have any questions or concerns about taking metformin.
The labeling recommendations on how and when kidney function is measured in patients receiving metformin will include the following information: 
  • Before starting metformin, obtain the patient’s eGFR.
  • Metformin is contraindicated in patients with an eGFR below 30 mL/minute/1.73 m2.
  • Starting metformin in patients with an eGFR between 30-45 mL/minute/1.73 m2 is not recommended.
  • Obtain an eGFR at least annually in all patients taking metformin. In patients at increased risk for the development of renal impairment such as the elderly, renal function should be assessed more frequently.
  • In patients taking metformin whose eGFR later falls below 45 mL/minute/1.73 m2, assess the benefits and risks of continuing treatment.  Discontinue metformin, if the patient’s eGFR later falls below 30 mL/minute/1.73 m2.
  • Discontinue metformin at the time of or before an iodinated contrast imaging procedure in patients with an eGFR between 30 and 60 mL/minute/1.73 m2; in patients with a history of liver disease, alcoholism, or heart failure; or in patients who will be administered intra-arterial iodinated contrast. Re-evaluate eGFR 48 hours after the imaging procedure; restart metformin, if renal function is stable.
Generally, 90-120 ml/minute/1.73 m2 of eGFR is taken as normal value. Levels below 60 mL/min/1.73 m2 for 3 or more months are a sign of chronic kidney disease. A GFR lower than 15 mL/min/1.73 m2 is a sign of kidney failure and requires immediate medical attention.
Hence, in addition to the level of serum creatinine, it is recommended to have the eGFR estimated in patients of T2DM before starting of Metformin or metformin in combination; also periodically measure, while on the medication.
The article was published in FDA Web site, April 8, 2016. US Food and Drug Administration. Metformin-containing drugs: Drug safety communication – revised warnings for certain patients with reduced kidney function.
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Wednesday, April 13, 2016

Acetaminophen makes it Harder to recognize Errors

Posted by Prahallad Panda on 6:53 AM Comments


Dan Randles and researchers from the University of British Columbia researched in a first neurological study to look at the potential of acetaminophen to inhibit the brain response associated with making errors.
It is a well established fact that physical pain and social rejection share a neural process that can be traced to the same part of the brain..
Recent research has begun to show how exactly acetaminophen inhibits pain, while behavioural studies suggest it may also inhibit evaluative responses more generally. Randles own past research has found that people are less reactive to uncertain situations when under the effect of acetaminophen.
In the research, two groups of 30 were given a target-detection task called the Go or No Go. Participants were asked to hit a Go button every time the letter F flashed on a screen but refrain from hitting the button if an E flashed on the screen. "The trick is you're supposed to move very quickly capturing all the GOs, but hold back when you see a No Go," says Randles.
The activity of brain of person was mapped through electroencephalogram (EEG) during the experiment. The researchers were looking for a particular wave called Error Related Negativity (ERN) and Error Related Positivity (Pe). Essentially what happens is that when people are hooked up to an EEG and make an error in the task there is a robust increase in ERN and Pe.
One group, which was given 1,000 mg of acetaminophen -- the equivalent of a normal maximum dose -- showed a smaller Pe when making mistakes than those who didn't receive a dose, suggesting that acetaminophen inhibits our conscious awareness of the error.
Cognitive control is an important neurological function because people are constantly doing cognitive tasks that flow automatically like reading, walking or talking. These tasks require very little cognitive control because they are well mapped out neurological processes, notes Randles.
"Sometimes you need to interrupt your normal processes or they'll lead to a mistake, like when you're talking to a friend while crossing the street, you should still be ready to react to an erratic driver," explains Randles.
"The task we designed is meant to capture that since most of the stimuli were Go, so you end up getting into a routine of automatically hitting the Go button. When you see a No Go, that requires cognitive control because you need to interrupt the process."
The study was double blind, so neither the researcher running the study nor the participant knew whether they had been given a placebo or acetaminophen.
An unexpected and surprise finding that Randles plans to explore more closely is that those who received an acetaminophen dose appeared to miss more of the Go stimuli than they should have. He plans on expanding on the error detection aspect of the research to see whether acetaminophen is possibly causing people to "mind wander" and become distracted.
"An obvious question is if people aren't detecting these errors, are they also making errors more often when taking acetaminophen? This is the first study to address this question, so we need more work and ideally with tasks more closely related to normal daily behaviour."
The research is published in the current edition of the journal Social Cognitive and Affective Neuroscience.
The news published in the Sciencedaily can be accessed here.
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Sunday, April 10, 2016

Cyclodextrin for Treatment of Atherosclerosis

Posted by Prahallad Panda on 11:34 AM Comments


Cardiovascular disease from atherosclerosis is one of the most common causes of death worldwide. Inflammation plays a crucial role in atherosclerosis and cholesterol crystals are considered to be main culprit.

Researchers have found out that cyclodextrin dissolves cholesterol crystals and reduces atherosclerotic plaques. This is a promising therapeutic approach for treating atherosclerosis. Their find was published in Science Translational Medicine.
Micrograph of an artery that supplies the hear...
Micrograph of an artery that supplies the heart with significant atherosclerosis and marked luminal narrowing. Tissue has been stained using Masson's trichrome. (Photo credit: Wikipedia)
Cyclodextrin works by reprogramming macrophages so that they do not cause such a strong inflammatory response in blood vessels that contain cholesterol crystals. The cyclodextrin also dissolves cholesterol crystals so that the cholesterol can be excreted from the body in urine. The result is prevention of plaque formation and even atherosclerotic plaque reduction in mice. Furthermore, when researchers used cyclodextrin to treat biopsies of plaques from human carotid arteries, they found similar results.
he study points to cholesterol crystals as a target for treatment of atherosclerosis, meaning that using cyclodextrin to dissolve the crystals could affect how the disease is treated.
The original idea for the test of cyclodextrin came from Chris Hempel, an American mother whose twin daughters are affected by a rare illness called Niemann-Pick Type C disease, in which cholesterol accumulates in the body. The children are being treated with cyclodextrin with promising results.
Hempel read about previous research on cholesterol crystals conducted by senior researcher Eicke Latz from the University Hospital Bonn and his colleagues from the Center of Molecular Inflammation Research (CEMIR) at the Norwegian University of Science and Technology (NTNU) in Trondheim. She contacted Dr. Latz to suggest that they test cyclodextrin as a possible treatment for atherosclerosis.
It was published in Sciencedaily, can be accessed here .

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Saturday, September 26, 2015

Dosing Blood Pressure Control Medicines at Bed Time Reduces the risk of Stroke and T2 Diabetes Mellitus

Posted by Prahallad Panda on 9:12 PM Comments



We all prescribe medications for control of Hypertension. Most common among those are the ACE (Angiotensin Converting Enzyme) inhibitors, ARBs (Angiotensin Receptor Blocker) and Third generation β-Blocker like Nebivolol. But, seldom we advise the patients which is the preferred time to take these groups of medications. Most of the patients, conventionally, take these medicines after awakening, in the morning.
It has been observed that most susceptible people get heart attack towards dawn or early morning. One of the factors can possibly be due to the fact that blood pressure starts rising from 03 to 04 AM and gradually rises till 12 Noon.
Normally, there is a fall of systolic blood pressure more than 10% of mean day time BP reaching the zenith from 12 Mid-Night to 03-04 AM, regulated by circadian rhythm. This phenomenon is called as “Dipping.”
Alterations in these intrinsic circadian rhythms can result in the absence of the nocturnal BP decline (non-dipping). This altered pattern is commonly seen in patients with essential hypertension, several forms of secondary hypertension and disorders of the autonomic nervous system.
The clinical relevance of this phenomenon lies in the fact that non-dipping has been associated with increased frequency of hypertensive target organ damage (brain, heart and kidney), as well as cerebrovascular and cardiovascular events in hypertensive patients.
Circadian rhythms typically originate in “master oscillators” located in the suprachiasmatic nuclei (SCN) of the anterior hypothalamus. How this hypothalamic rhythm is translated into changes in blood pressure is not entirely known, but the autonomic nervous system is suspected to play a role; sympathetic activity is also modulated by hypothalamic centers, and follows a circadian pattern similar to that of blood pressure.
Patients are categorized, usually based on systolic blood pressure, as extreme dippers (night–day blood pressure ratio ≤ 0.8), dippers (0.8 < ratio ≤ 0.9), non-dippers (0.9 < ratio ≤ 1.0) and reverse dippers or risers (ratio > 1.0). Reverse dipper are particularly in the risk of developing end organ damages.
A new research article published in The Diabetologia by Ramón C. Hermida, Diana E. Ayala, Artemio Mojón and José R. Fernández of University of Vigo, Campus Universitario, Vigo, Pontevedra 36310, Spain, titled as”Bedtime ingestion of hypertension medications reduces the risk of new-onset type 2 diabetes: a randomised controlled trial” has concluded that in hypertensive patients without diabetes, ingestion of 1 BP-lowering medications at bedtime, mainly those modulating or blocking the effects of angiotensin-II, compared with ingestion of all such medications upon awakening, results in improved ambulatory BP (ABP) control (significant further decrease of asleep BP) and reduced risk of new-onset diabetes.
Renin angiotensin pathway or RAAS.
Renin angiotensin pathway or RAAS. (Photo credit: Wikipedia)
Drugs that target angiotensin include angiotensin receptor blockers (ARBs), ACE inhibitors and beta blockers. These medications act through blockade of the RAAS (Rennin-Angiotensin-Aldosterone System) in kidney that causes blood vessels to constrict and blood pressure to rise. 
Angiotensin, Aldosterone and adrenaline also contribute to increased glucose (sugar) release from the liver and decreased insulin sensitivity. These factors can lead to Type 2 diabetes.
 The researchers conducted a prospective, randomised, open-label, blinded endpoint trial of 2,012 hypertensive patients without diabetes, 976 men and 1,036 women, 52.7±13.6 years of age. Patients were randomised, using a computer-generated allocation table, to ingest all their prescribed hypertension medications upon awakening or the entire daily dose of 1 of them at bedtime.
During a median follow-up of 5.9 years, 171 participants developed type 2 diabetes. Patients in the bedtime, compared with the morning-treatment group, showed a significantly lower asleep mean BP and a greater sleep-time relative BP decline.
In the bedtime treated group, there was a lower-prevalence of a phenomenon known as 'non-dipping' -- in which patients' night time BP falls by less than 10% compared to daytime BP. Non-dipping occurred in 32% of bedtime-treated patients and 52% of those getting their treatment in the morning.
There was also a 57% decrease in the risk of developing new-onset type 2 diabetes in the bedtime-treated group after adjustment for the potential confounders of fasting glucose, waist circumference, mean asleep systolic BP, dipping classification and chronic kidney disease.
Specifically, the odds of type 2 diabetes dropped 61 percent for people taking angiotensin receptor blockers at bedtime compared to morning. For those on ACE inhibitors at night, the odds went down 69 percent. People on beta blockers reduced their odds of the blood sugar disease by 65 percent when they took their medicine at night, the researchers reported.
All three classes of medication were associated with a reduced risk of type 2 diabetes when taken at bedtime as the effect will be much more on liver/kidney in comparison to the waning effect at night when taken in the morning.
Let us remember to advise our hypertensive patients to take their anti-hypertensive medications at bed time, especially ARBs, ACE-Inhibitors and Nebovolol for better effect and delaying development of T2DM.



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