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Monday, August 11, 2014

More Natural Light in Workplace contributes to Good Sleep and Healthy Life

Sleep plays an important role in synchronizing body and mind, maintaining the body’s circadian clock that up keeps correct rhythm.
Inadequate sleep and sleep deprivation contribute to;
  1. Heart disease,
  2. Diabetes,
  3. Depression,
  4. Accidents,
  5. Impaired cognition,
  6. Irritability and
  7. A poor quality of life.
While normal changes due to ageing interfere with the quality of sleep, some disease conditions and medications used by older adults compromise sleep patterns. Now, researchers have come out with evidence that light in work environment also contribute positively to the sleep pattern.

A study published in The Journal of Sleep Medicine authored by Mohamed Boubekri, Ivy N. Cheung, Kathryn J. Reid, Chia-Hui Wang, Phyllis C. Zee, conclude that  exposure to light, during the day, particularly in the morning, is beneficial to health via its effects on mood, alertness and metabolism.
Employees with windows in the workplace received 173 percent more white light exposure during work hours and slept an average of 46 minutes more per night than employees who did not have the natural light exposure in the workplace, the study shows.
There also was a trend for workers in offices with windows to have more physical activity than those without windows. The quality of sleep was measured by Pittsburgh Sleep Quality Index (PSQI) that differentiates “poor” from “good” sleep by measuring seven domains: subjective sleep quality, sleep latency, sleep duration,habitual sleep efficiency, sleep disturbances, use of sleep medication, and daytime dysfunction over the last month.
The client self rates each of these seven areas of sleep. Scoring of the answers is based on a 0 to 3 scale, whereby 3 reflects the negative extreme on the Likert Scale. A global sum of “5”or greater indicates a “poor” sleeper.
Good design of house and office with adequate number of windows not only saves power, but also allows the users to enjoy a healthy life.

Sunday, July 13, 2014

Flatus Gas (H2S) may have Protective Effect on Progression of Various Diseases in Human

Hydrogen sulphide (H2S) is a colourless gas with an odour of rotten eggs, long familiar to the students who worked in Chemistry Laboratories.
It is increasingly coming into light that, in fact, H2S can prevent cell damage in human from the noxious effect following myocardial infarction, brain stroke, traumatic brain injury, diabetes, atherosclerosis, Alzheimer’s disease and kidney injury etc.. This gas, in minute quantities, which is yet to be quantified, may actually protect mitochondria the power house of body. 
Photo Credit: Mail Online Health

It is produced in the human gut, mostly in colon by fermentation of food from bacterial action. Cystathioneine-lyase (CSE) and cystathionine-synthase are the two enzymes that regulate H2S levels in mammals (including humans).
CSE is found in the liver and vascular smooth muscle cells, but cystathioinine-synthase produces H2S in the brain.
Garlic can be transformed into H2S by enzymatic action in the body, so that some of its claimed medicinal properties can be traced to H2S.
It has been seen to be an important mediator of gastrointestinal (GI) mucosal defence and contributes significantly to repair of damage and resolution of inflammation. Synthesis of H2S increases markedly after mucosal injury, and inhibition of H2S in such circumstances leads to delayed healing and exacerbated inflammation.
The beneficial effects of H2S may be attributable to its ability to elevate mucosal blood flow, prevent leukocyte-endothelial adhesion, reduce oxidative stress, and stimulate angiogenesis.
Thus novel H2S -based therapies have been shown to be effective anti-inflammatories that can promote the resolution of inflammation and accelerate the healing of GI ulcers. Encouraging results have already been seen experimentally with a mesalamine derivative and with H2S -releasing derivatives of non-steroidal anti-inflammatory drugs.
Researchers at Johns Hopkins University, in Maryland, found that the H2S gas is produced in the cells lining blood vessels by CSE that relaxes the blood vessels, may have a role in regulating blood pressure.
In neurotoxin-induced Parkinson’s disease animal models, it has been seen that sodium hydrogen sulphate (NaHS), an H2S donor, reversed dopaminergic neuron loss via its anti-oxidant, anti-inflammatory and anti-apoptotic effects.
It has been found that the characteristic memory deficiency in Alzheimer’s disease (AD) may be related to reduced H2S and administration of NaHS could provide a therapeutic approach for AD.  Sufficient evidence has accumulated in support of H2S acting as a signalling molecule in the mammalian Central Nervous System (CNS).
Its beneficial effect in Alzheimer’s disease in animal models has also been substantiated. It has been seen that NaHS inhibited formation of amyloid β , which is a major component of the neuritic plaques by down-regulation of β-amyloid precursor protein (APP) expression and suppression of the activity of β-secretase, a β-site APP cleaving enzyme 1 (BACE1).
Abnormal accumulation of tau protein, a neuronal microtubule-associated protein that causes paired helical fragments (PHF) in Alzheimer’s disease is inhibited by NaHS through hyperphosphorylation, polymerization and aggregation.
Hydrogen sulfide has recently been found decreased in chronic kidney disease. A hydrogen sulfide donor (sodium hydrogen sulfide) inhibited renal fibrosis by attenuating the production of collagen, extracellular matrix, and the expression of α-smooth muscle actin.
At the same time, the infiltration of macrophages and the expression of inflammatory cytokines including interleukin-1β, tumor necrosis factor-α, and monocyte chemoattractant protein-1 in the kidney were also decreased.
In cultured kidney fibroblasts, a hydrogen sulfide donor inhibited the cell proliferation by reducing DNA synthesis and down-regulating the expressions of proliferation-related proteins including proliferating cell nuclear antigen and c-Myc.
Further, the hydrogen sulphide donor blocked the differentiation of quiescent renal fibroblasts to myofibroblasts by inhibiting the transforming growth factor-β1-Smad and mitogen-activated protein kinase signaling pathways. Thus, low doses of hydrogen sulphide or its releasing compounds may have therapeutic potentials in treating chronic kidney disease.
Experiments with mice have shown that H2S can reduce their ability to metabolize oxygen, reducing their heart rate and breathing rate, lowering their body temperature, and creating a state of deep hibernation. By flushing with air, the mice can be restored to normal without apparent behavioural effects.
The possibility of using H2S in heart surgery or treating badly injured soldiers is being studied. By studying roundworms (C. elegans) it has been shown that 50 parts per million of H2S can extend their lives by 70 percent. This "fountain of youth" phenomenon seems to be connected to the gene SIR-2, which had previously been related to life span regulation. 
These preliminary findings are very exciting and may lead to medical advances. H2S appears to be another example of a "gasotransmitter" such as the hormone NO. Researchers speculates that H2S may be involved in the hibernation of certain animals.
Now researchers have come up with a new compound named AP39 to assist the body in producing just the right amount of hydrogen sulphide. 
They believe that it will help prevent or reverse mitochondrial damage, which is a key strategy in treating conditions such as stroke, heart failure, diabetes, arthritis, dementia and ageing.

The past few years demonstrated its role in many biological systems and it is becoming increasingly clear that H2S is likely to join nitric oxide (NO) and carbon monoxide (CO) as a major player in mammalian a cardioprotectant for treating ischaemic heart diseases and heart failure.
H2S treatment represents a novel therapeutic strategy to prevent acute lung injury induced by high tidal volume (HVT) ventilation. Moreover, it is pivotally involved in the control of important functions in the central nervous system (CNS).
H2S facilitates the induction of hippocampal long-term potentiation by enhancing the activity of N-methyl D, L-aspartate (NMDA) receptors. H2S induces Ca2+influx in astrocytes that propagates to the surrounding astrocytes as Ca2+ waves.
In stroke, H2S appears to act as a mediator of ischemic injuries and thus inhibition of its production has been suggested to be a potential treatment approach in stroke therapy.
Cerebral oedema has been reported to be one of the major factors leading to the high mortality and morbidity associated with patients with traumatic brain injury (TBI).
 A recent study interestingly showed that H2S at a low concentration significantly attenuated the injury in a mild focal cerebral ischemia rat model.
It was observed that low concentration of H2S is neuro-protective, whereas higher concentrations of H2S have been shown to magnify cerebral damage.
H2S may serve as a neuroprotectant to treat TBI-induced brain injury via anti-apoptosis and suppression of excessive activation of autophagy therefore has potential clinical therapeutic value for treatment of TBI.
This field is still in its infancy and much will be learnt in the near future about the central roles play by H2S in health and disease


Sunday, July 6, 2014

“Hospital Infection Control Committee” must address the issue of “Antibiotics Policy” with reference to the emerging “Antibiotics Resistance” and “Gloomy” days ahead

In India, if chief of a medical institution talks about the emerging “Microbial Resistance” and constitutes an "Hospital Infection Control Committee" to take up the issue and to recommend an “Antibiotic Policy”, most of the doctors become skeptical about it; and think it to be an endeavour to curtail their liberty to prescribe the antibiotic of their choice, which might have been influenced by the Pharmaceutical Company's strategy to promote their product adopting whatever means.
It is estimated that drug-resistant strains of bacteria are responsible for 5,000 deaths a year in the UK and 25,000 deaths a year in Europe; as usual the statistics from India may be poor or incorrect.
If this trend of practising medicine continues unabated, we are likely to face a situation, which is variously described as, “Time Bomb”, “Leading to Dark Ages” and “Gloomy Days Ahead” etc. 

English: Magnified 20,000X, this colorized sca...
English: Magnified 20,000X, this colorized scanning electron micrograph (SEM) depicts a grouping of methicillin resistant Staphylococcus aureus (MRSA) bacteria. See PHIL 617 for a black and white view of this image. These S. aureus bacteria are methicillin-resistant, and are from one of the first isolates in the U.S. that showed increased resistance to vancomycin as well. Note the increase in cell wall material seen as clumps on the organisms’ surface. (Photo credit: Wikipedia)

Recently, the concern of the Prime Minister of UK Mr. David Cameron may be seen here.
India has shown its' concern in the Chennai Declaration, but the effect is yet to be felt in the grass root level and more is needed to be done to further the actions to achieve the targets of the declaration.
Antibiotic resistance is the ability of a microorganism to withstand the effects of an antibiotic on it, administered to kill or arrest its' growth.
Antibiotic resistance evolves naturally via natural selection through random mutation, but it could also be engineered by applying an evolutionary stress on a population. Once such a gene is generated, bacteria can then transfer the genetic information in a horizontal fashion (between individuals) by plasmid exchange.
If a bacterium carries several resistance genes, it is called multi-resistant or, informally, a super-bug.
Other factors contributing towards resistance include incorrect diagnosis and treatment with an antimicrobial, unnecessary prescriptions, improper use of antibiotics, self medication by patients, and the use of antibiotics as livestock food additives for growth promotion.
Earlier in May 2014, a Government body, NICE (National Institute for Health & Care Excellence) said that one in 16 patients are developing infections on NHS (National Health Service) wards because of poor hygiene among staffs. NICE said 800 patients a day, the equivalent of 300,000 a year, are infected by a member of staff or by dirty equipment. It is estimated the infections cause 5,000 deaths annually and contribute to another 15,000.
According to WHO, in 2012, there were about 450 000 new cases of multidrug-resistant tuberculosis (MDR-TB). Extensively drug-resistant tuberculosis (XDR-TB) has been identified in 92 countries.MDR-TB requires treatment courses that are much longer and less effective than those for non-resistant TB. Resistance to earlier generation antimalarial drugs is widespread in most malaria-endemic countries. Further spread, or emergence in other regions, of artemisinin-resistant strains of malaria could jeopardize important recent gains in control of the disease.
There are high proportions of antibiotic resistance (ABR) in bacteria that cause common infections (e.g. urinary tract infections, pneumonia, bloodstream infections) in all regions of the world.
A high percentage of hospital-acquired infections are caused by highly resistant bacteria such as methicillin-resistant Staphylococcus aureus (MRSA) or multidrug-resistant Gram-negative bacteria.
Treatment failures due to resistance to treatments of last resort for gonorrhoea (third-generation cephalosporins) have now been reported from 10 countries. Gonorrhoea may soon become untreatable as no vaccines or new drugs are in development.
Apart from these, there has been resistance to microbes like HIV, Fungus (Candida), C. Difficile and Campylobacter etc.
It will be better to discuss the pattern of developing resistance by a bacterium called Saphylococcus aureus (colloquially known as "Staph aureus" or a Staph infection) that has become a serious concern world-wide.
This bacterium can cause a large number of infection in human starting from skin and soft tissue infection to bloodstream infection, and has become resistant a host of antibiotics.
Found on the mucous membranes and the skin of around a third of the population, it is extremely adaptive to antibiotic pressure. It was the first bacterium in which penicillin resistance was found—in 1947, just four years after the mass production of the drug started.
Methicillin was then the antibiotic of choice, but has since been replaced by oxacillin due to significant kidney toxicity. MRSA (methicillin-resistant Staphylococcus aureus) was first detected in Britain in 1961 and is now "quite common" in hospitals. MRSA was responsible for 37% of fatal cases of blood poisoning in the UK in 1999, up from 4% in 1991.
Half of all S. aureus infections in the US are resistant to penicillin, methicillin, tetracycline and erythromycin. This left vancomycin as the only effective agent available at a time.
However, strains with intermediate (4-8 ug/ml) levels of resistence, termed GISA (glycopeptide intermediate Staphylococcus aureus) or VISA (vancomycin intermediate Staphylococcus aureus), began appearing the the late 1990s. The first identified case was in Japan in 1996, and strains have since been found in hospitals in England, France and the US.
The first documented strain with complete (>16ug/ml) resistence to vancomycin, termed VRSA (Vancomycin-resistant Staphylococcus aureus) appeared in the United States in 2002.
A new class of antibiotics, oxazolidinones, became available in the 1990s, and the first commercially available oxazolidinone, linezolid, is comparable to vancomycin in effectiveness against MRSA. Linezolid-resistance in Staphylococcus aureus was reported in 2003.
Now, only a few arsenals are there with us to treat multi-drug resiatance Staphylococcus Aureus, perhaps drugs like quinupristin-dalfopristin, daptomycin, teicoplanin and tigecycline etc.; and these hopes are fast fading away with reports of resistance coming in.
CA-MRSA (Community-acquired MRSA) has now emerged as an epidemic that is responsible for rapidly progressive, fatal diseases including necrotizing pneumonia, severe sepsis and necrotizing fasciitis.
Methicillin-resistant Staphylococcus aureus (MRSA) is the most frequently identified antimicrobial drug-resistant pathogen in US hospitals. The epidemiology of infections caused by MRSA is rapidly changing. In the past 10 years, infections caused by this organism have emerged in the community. The 2 MRSA clones in the United States most closely associated with community outbreaks, USA400 (MW2 strain, ST1 lineage) and USA300, often contain Panton-Valentine leukocidin (PVL) genes and, more frequently, have been associated with skin and soft tissue infections.
Outbreaks of community-associated (CA)-MRSA infections have been reported in correctional facilities, among athletic teams, among military recruits, in newborn nurseries, and among active homosexual men. CA-MRSA infections now appear to be endemic in many urban regions and cause most CA-S. aureus infections.
However, the U.S. Food and Drug Administration on May 23, 2014, approved Dalvance (dalbavancin), a new antibacterial drug used to treat adults with skin infections.
Dalvance is intended to treat acute bacterial skin and skin structure infections (ABSSSI) caused by certain susceptible bacteria like Staphylococcus aureus (including methicillin-susceptible and methicillin-resistant strains) and Streptococcus pyogenes. The treatment is administered intravenously.
Dalvance is the first drug designated as a Qualified Infectious Disease Product (QIDP) to receive FDA approval. Under the Generating Antibiotic Incentives Now (GAIN) title of the FDA Safety and Innovation Act, Dalvance was granted QIDP designation because it is an antibacterial or antifungal human drug intended to treat serious or life-threatening infections.
Dalvance is marketed by Chicago-based Durata Therapeutics. However, The situation is not very much encouraging and no quick solution seems to be within reach, except a much needed cohesive effort from all the stake-holders; from which the medical community can play a major and important role.
To elaborate on the causes of microbes developing resistance, the following are important ones;

Inappropriate use:
  • not completing a course of antibiotics as prescribed
  • skipping doses of antibiotics
  • not taking antibiotics at regular intervals
  • saving some for later

Inappropriate prescribing includes:

  • unnecessary prescription of antibiotics
  • unsuitable use of broad-spectrum antibiotics
  • wrong selection of antibiotics and inappropriate duration or dose of antibiotics


MRSA - Patients infected with MRSA (methicillin-resistant Staphylococcus aureus) are 64 per cent more likely to die than those with a non-resistant form of S. aureus.
People infected by resistant superbugs are also likely to stay longer in hospital and may need intensive care, pushing up costs.

C. difficile - This bacteria produces spores that are resistant to high temperatures and are very difficult to eliminate. It is spread through contaminated food and objects and can cause blood poisoning and tears in the large intestine.
E. coli - this now accounts for one in three cases of bacterial infections in the blood in the UK and a new strain is resistant to most antibiotics. It is highly contagious and could cause more than 3,000 deaths a year.
Acinetobacter Baumannii - a common bacteria which is resistant to most antibiotics and which can easily infect patients in a hospital. It can cause meningitis and is fatal in about 80 per cent of patients.

CRKP (carbapenem-resistant Klebsiella pneumoniae) - this is a bacterium that is associated with extremely difficult to treat blood infections and meningitis. It is resistant to nearly all antibiotics and is fatal in 50 per cent of cases.

Multi-drug resistant tuberculosis is estimated to kill 150,000 people globally each year.
NDM-1 - a bacteria detected in India of which some strains are resistant to all antibiotics.

Therefore, a policy need to be evolved on practicing antibiotics in all the hospitals in a locality, for which a sub-division may be taken as an unit. Much expected from the Government in India to lead the way with co-operation from the private hospitals. World leaders also think seriously over the emerging threat.

Sunday, June 22, 2014

Does Your Mammogram Report mentions anything about Dense Breast Parenchyma?

You should not get swayed by your mammogram report that does not mention anything about the density of breast parenchyma, in spite of all normal findings.

Breast implant: Mammographs: Normal breast (le...
Breast implant: Mammographs: Normal breast (left) and cancerous breast (right). (Photo credit: Wikipedia)

According to legislation passed in Connecticut, the radiologist is expected to mention about the density of breast tissue. “Dense parenchyma” that “lowers the sensitivity of mammography”.
where applicable, such report shall include the following notice:
"If your mammogram demonstrates that you have dense breast tissue, which could hide small abnormalities, you might benefit from supplementary screening tests, which can include a breast ultrasound screening or a breast MRI examination, or both, depending on your individual risk factors. A report of your mammography results, which contains information about your breast density, has been sent to your physician's office and you should contact your physician if you have any questions or concerns about this report."
The Legislation can be viewed here.
This legislation was passed because of Nancy Cappello, a 61-year-old Connecticut woman. Her breast cancer had spread to her lymph nodes by the time it was diagnosed, even though she had had normal mammograms every year.
Ms. Cappello, the woman who started the movement to inform patients, began having yearly mammograms at age 40. In 2004, when she was 51, her doctor felt a lump in her breast, only six weeks after a mammogram had looked normal. Even after the lump was detected, mammography still could not find it. Only then, Ms. Cappello was told that she had dense breast tissue. The cancer had already spread to 13 lymph nodes. She needed a mastectomy, chemotherapy, radiation and hormone treatment.
Mammograms are scored on a five-point scale, using the following American College of Radiology Breast Imaging Reporting and Data System (BI-RADS) categories:
  1. Negative;
  2. Benign finding;
  3. Probably benign finding, short follow-up interval suggested;
  4. Suspicious abnormality, biopsy should be considered; and
  5. Highly suggestive of malignancy.
After this, the density of breast tissue has to be mentioned. Laws requiring disclosure of density have been passed in Connecticut, Texas and Virginia, and most recently in California and New York.
“Dense” breasts have a relatively high proportion of glandular or connective tissue, which blocks X-rays used in mammography. Non-dense breasts have more fat through which X-rays penetrate easily.
Over all, about 40percent of women who have mammograms have dense breast tissue. It is not abnormal, just one of nature’s variations. Younger women are more likely to have dense tissue, but as many as 25 percent of older women have it. Density cannot be judged by touch; it shows up only on mammograms.
In dense breast tissue, there is chance that abnormality may remain unnoticed.  Something like, trying to see ice through ground glass. However,mammogram is gold standard, should not be ignored.
If it is a dense parenchyma, there is option for ultrasonogram (USG) and magnetic resonance imaging (MRI). USG and MRI are more sensitive than mammogram, but problem is that more often those give false positive results. False positivity may lead to unnecessary anxiety in patient and warrant more interventions like biopsy.
However, those are useful tool in case of dense breast parenchyma and indicated in case, there exist the risk factors for breast cancer, like strong family history and BRCA 1 or 2 mutation etc..
MRI may be used in women for evaluating;
  • The integrity of silicone breast implants,
  • Assessing cancers associated with silicon breast implant
  • Assessing palpable masses following surgery or radiation therapy,
  • Assessing for occult breast cancer in patients with axillary nodal    metastasis found in mammogram or USG,
  • Preoperative planning for some patients with known breast cancer.
  • It has been promoted as a screening test for breast cancer among women at elevated risk of breast cancer based on BRCA1/2 mutation carriers, a    strong family history of breast cancer, or several genetic syndromes such as Li-Fraumeni or Cowden disease.
Mammography is still the "gold standard" for the detection of breast cancers and the first screening test to be undertaken. Very importantly, it allows for the detection of microcalcifications which may sometimes be the only sign of a very early breast cancer. Microcalcifications are not visible on other types of imaging studies. Digital and 3D Mammograms are more sensitive than screen/film mammogram. The mammogram also helps determine the need for additional studies, such as MRI or sonography.
That is why your radiologist must mention about density of breast parenchyma, if not, you should ask for it.

Sunday, June 15, 2014

Evolving Newer Treatments for Rosacea, Ivermectin Cream

Redness over central face area? Comes and goes? Later on turns to permanent uneven, hard, rough and red skin?
It may be rosacea. Rosacea looks like several acnes concentrated in a small area of face but, it is not. The biggest difference is that rosacea may have acne, while acne does not have the extra blood vessels (called telangiectasias) found in rosecea.
Rosacea typically first appears after 30 years of age as a sustained flush, blush or redness on the cheeks, nose, forehead or chin that may come and go.
Over time, the redness becomes ruddier and more persistent, and telangiectasia (visible blood vessels) may appear. Some cases, red domed papules (small bumps) and pustules, red gritty eyes, burning and stinging sensations, and in some advanced cases, a red lobulated nose (rhinophyma), may develop. Rosacea, when have acne with it, called acne rosacea.
There are four forms of rosacea, which are defined by the following range of symptoms:
1. Mild (Erythematotelangiectatic) The main symptoms are facial flushing and redness that may come (Flares) and go. In addition, there may some swelling, burning and stinging, roughness, and visible red blood vessels.
2. Moderate (Papulopustular) This is a more advanced form of rosacea that is marked by persistent redness and pimplelike bumps (often mistaken for acne), as well as burning and stinging.
3. Severe (Phymatous) In some individuals, rosacea may affect the nose, causing the skin tissue to thicken (giving an enlarged appearance) and become bumpy. This advanced form of rosacea is called rhinophyma.
4. Ocular rosacea In addition to skin symptoms, rosacea may also affect the eyes and eyelids. It may cause redness to the surrounding skin tissue but also burning or stinging, dryness, light sensitivity, blurred vision, and watery, bloodshot eyes.
Rosacea is a chronic, inflammatory and vascular disorder affecting the face, with facial erythema (redness) being a prominent characteristic.
While the exact cause of rosacea is unknown; it may run in families, but genetic predisposition has not been established. Small Intestinal Bacterial Overgrowth (SIBO) by Helicobacter specis) is also thought to be one of the causes.
Several triggers have been identified that may make the condition worse.
These include; identifying and avoiding those can be a useful way of controlling the symptoms.
  • Exposure to sunlight
  • Stress
  • Strenuous exercise
  • Cold weather (wind)
  • Heat, hot and humid weather
  • Menopause
  • Certain medications, such as vasodilator drugs
  • Hot drinks
  • Alcohol and caffeine
  • Spicy foods
  • Dairy products
Download Rosacea Trigger Tracker for you from Canadian Dermatology Association.
Recently, some researchers attribute rosacea to a tiny spider-like 8 legged bug (A mite) called demodex folliculorum that appears from the pores of the skin and crawls over the face to mate, as we sleep. It is just 0.01mm to 0.04mm long and is harmless to most people.

About 70 per cent of adults aged 50 plus have been shown to have the mite, but previous studies have found that rosacea sufferers have up to ten times more demodex mites on their skin than unaffected carriers.
When it dies, the creature releases a bacteria, bacillus bacterium, which triggers inflammation in patients who have rosacea, leading to the most severe form of the condition, papulopustular rosacea.
There has been no perfect cure for this condition. Some time back, in February, 2014, one more topical gel Mirvaso® (brimonidine) was approved by European Commission for marketing in Europe.
Recently, there has been strong evidence that Ivermectin that kills the demodex mite has a role to play in the treatment of rosacea through 12 weeks.
Studies have concluded that Ivermectin 1% cream was effective and safe in treating inflammatory lesions of papulopustular rosacea.
There has been several other treatment options with varying results;
  1. Metronidazole cream or gel (topical metronidazole)
  2. Azelaic acid that helps unblock pores and reduce inflammation (redness and swelling).
  3. Antibiotics like tetracycline and Erythromycin
  4. Laser and intense pulsed light (IPL) treatment
  5. Thickened skin (rhinophyma) may require the attention of a plastic surgeon.

  1. Choose products that are non-drying, free of alcohol or astringents.
  2. Use a mild cleanser and do not rub or scrub skin.
  3. Make a habit of using sunscreen (SPF 30 or higher) every day.
  4. Moisturize your skin, especially during the colder months when the air is dry.

Don't s:

  1. Do not try acne creams because may dry out and irritate your skin even more.
  2. Alcohol consumption. Alcohol is a known trigger, so, it can worsen symptoms in individuals with rosacea.
  3. Use medications for blood pressure thinking that the flush is due to high blood pressure.
  4. Over cleansing with an idea that rosacea results from unclealiness.
  5. Assume that you have sunburned skin.

    There are so many celebrities living with this condition. Let us try ivermectin inrosacea, which has manifold use; from treating scabies, nematodes, lice and immunomodulation to its' potential role as angiogenesis inhibitor in cancer treatment.

Sunday, June 1, 2014

It is Beer, Not Wine among the Alcoholic Beverages that may Increase your Uric Acid Level

Uric acid (UA) is the end product of purine metabolism in humans, and increased serum uric acid concentrations may lead to gout.
Purine is a nitrogenous base and an important component of DNA; DNA is composed of two types of nitrogenous base pairs called purines and pyrimidines.
Purine is metabolised in liver and gut to uric acid in human and higher mammals; excreted via kidney (Approximately 75%) and faeces (25%). In contrast, birds and reptiles excrete most of uric acid in feces. Purines are also synthesized from degradation of adenosine triphosphate (ATP) to adenosine monophosphate (AMP).
The average serum uric acid level in male is 416 µmol/L (Approximately 7 mg/dl) and in female is 340 µmol/L (approximately 5.7 mg/dl); {conversion factor, 1 mg/dL=59.48 µmol/L}. In case of male it ranges from 4-8.5 mg% and 2.5- 7.5 mg% in female. check here.
Rise in serum uric acid level is an important risk factor for gout and has other significant associations with human disorders, such as cardiovascular diseases like hypertension and renal diseases like uric acid stones.
Apart from many other risk factors like heredity, members of metabolic syndrome like obesity, diabetes mellitus; liver and kidney disease, alcohol consumption is an important risk factor for high uric acid level.
In a recent article published in The PlosOne, it has been seen by the researchers that beer among alcoholic beverage is associated with increased uric acid level, whereas wine is not.
This is because Beer is an alcoholic beverage with high purine content, whereas wine contains a minimal amount of purines and several nonalcoholic components, including antioxidants, vasorelaxants and stimulants of anti-aggregatory mechanisms.

English: Cervantez, wine of Spain
English: Cervantez, wine of Spain (Photo credit: Wikipedia)
Thus, the effect of the purines ingested from beer on the serum uric acid (UA) concentrations may be sufficient to augment the hyperuricemic effect of alcohol itself. Whereas, the absence of an effect of wine may result from non-alcoholic components with antioxidant properties, such as polyphenols, which may mitigate the impact of alcohol on the serum UA concentration.
The accelerated synthesis of UA from adenosine, which is produced after the degradation of adenosine triphosphate to adenosine monophosphate, and reduced urinary excretion due to the elevation of blood lactate caused by the oxidation of ethanol may contribute the rise if UA in blood.
UA is the end product of purine metabolism in humans and higher primates; in contrast, other mammals further metabolize urate to allantoin. The absence of the hepatic enzyme uricase (urate oxidase) and/or efficient renal UA reabsorption contributes to the ten-fold higher UA blood levels in humans compared to those of other mammals.
UA is a powerful scavenger of peroxyl radicals, hydroxyl radicals and singlet oxygen in human biological fluids.

The balance between UA production and excretion determines serum UA concentrations; the daily production of urate is approximately 1000 mg (6 mmol) in adults. Approximately 75% of UA excretion occurs via the kidney, and the gastrointestinal tract eliminates 25%.
In the human kidney, urate handling involves urate glomerular filtration followed by a complex array of re-absorptive and secretory mechanisms taking place in the proximal tubule. The renal excretion of UA depends on the balance between filtration, secretion and re-absorption. As a result, approximately 10% of the UA filtered through the glomerular membranes is finally excreted.
The foods with high purine content include meat, especially the internal organs like liver and kidney, anchovies, mackerel, sardines, beef kidneys, brains, meat extracts (e.g., Oxo, Bovril), herring, game meats, sweetbreads, beer (from the yeast) and gravy.
In general, plant-based diets are low in purines. A moderate amount of purine is also contained in asparagus, cauliflower, spinach, mushrooms, green peas, lentils, dried peas, beans, oatmeal, wheat bran, wheat germ, and hawthorn. Purines are also created through the natural process of cell breakdown in the body.
You may like to know, how to keep a check to your rising serum uric acid level; please read more in Mayoclinic.
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