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	<title>Pharmatite &#187; Diseases and Treatment</title>
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	<link>http://pharmatite.com</link>
	<description>Satisfy your Pharma Appetite</description>
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		<title>USFDA Approval: Teriflunomide for Relapsing Multiple Sclerosis</title>
		<link>http://pharmatite.com/2012/10/usfda-approval-teriflunomide-for-relapsing-multiple-sclerosis/</link>
		<comments>http://pharmatite.com/2012/10/usfda-approval-teriflunomide-for-relapsing-multiple-sclerosis/#comments</comments>
		<pubDate>Thu, 25 Oct 2012 10:29:48 +0000</pubDate>
		<dc:creator>ANTS4U</dc:creator>
				<category><![CDATA[Breaking News]]></category>
		<category><![CDATA[Diseases and Treatment]]></category>

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		<description><![CDATA[The US Food and Drug Administration (FDA) has approved teriflunomide to treat relapsing forms of multiple sclerosis (MS), making it the second oral agent approved for this indication. (Fingolimod was the first oral treatment approved in September 2010 for relapsing MS. Since then, changes have been made to the label to reflect FDA concerns about [...]]]></description>
				<content:encoded><![CDATA[<p>The US Food and Drug Administration (FDA) has approved teriflunomide to treat relapsing forms of multiple sclerosis (MS), making it the second oral agent approved for this indication. (Fingolimod was the first oral treatment approved in September 2010 for relapsing MS. Since then, changes have been made to the label to reflect FDA concerns about cardiovascular effects of the drug after the first dose.)</p>
<p>It is also used to treat rheumatoid arthritis, and there are a total of approximately 2.1 million patient-years of exposure in patients with this condition, suggesting an excellent safety and tolerability profile.</p>
<p>Teriflunomide is a once-daily, orally available immunomodulator that reversibly inhibits the mitochondrial enzyme dihydroorotate dehydrogenase, which plays an important role in pyrimidine synthesis needed for DNA replication. By hindering T- and B-cell proliferation and function in response to autoantigens, the drug functions as a disease-modifying therapy for MS. However, it does not affect the replication and function of hematopoietic cells, memory T cells, or other cells living on their pyrimidine pool through the salvage pathway.</p>
<p>The boxed warning points out that, based on animal studies, the drug may be teratogenic, important because many patients with MS are women of childbearing age.</p>
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		<title>WHO  recommends honey as a nighttime treatment for coughing</title>
		<link>http://pharmatite.com/2012/08/who-recommends-honey-as-a-nighttime-treatment-for-coughing/</link>
		<comments>http://pharmatite.com/2012/08/who-recommends-honey-as-a-nighttime-treatment-for-coughing/#comments</comments>
		<pubDate>Tue, 07 Aug 2012 20:19:49 +0000</pubDate>
		<dc:creator>ANTS4U</dc:creator>
				<category><![CDATA[Breaking News]]></category>
		<category><![CDATA[Diseases and Treatment]]></category>

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		<description><![CDATA[Honey may be a preferable treatment of cough and sleep difficulties associated with childhood URI]]></description>
				<content:encoded><![CDATA[<p>The World Health Organization recommends honey as a nighttime treatment for coughing in young children with URIs.</p>
<p>In the current study, children with URIs and nocturnal cough were given either 1 of 3 different honey products or a placebo 30 minutes before bedtime, based on a double-blind randomization plan. The primary outcome evaluated was a subjective change in cough frequency, based on parent surveys. Secondary outcomes measured included a change in cough severity, the effect of the cough on sleep for both the child and the parent, and the combined score on the pre- and postintervention surveys.</p>
<p>Herman Avner Cohen, MD, from the Pediatric Ambulatory Community Clinic, Petach Tikva, Israel, and colleagues compared symptom scores for each treatment group before and after the intervention and found that patients in all 3 honey groups demonstrated significant improvement compared with patients treated with placebo. There were no significant differences among the different types of honey.</p>
<p>&#8220;The results of this study demonstrate that each of the 3 types of honey (eucalyptus, citrus, and labiatae) was more effective than the placebo for the treatment of all of the outcomes related to nocturnal cough, child sleep, and parental sleep,&#8221; the authors write.</p>
<p>The researchers enrolled 300 children with URIs, aged 1 to 5 years, who were seen at 1 of 6 general pediatric community clinics between January 2009 and December 2009. Patients were eligible if they had a nocturnal cough attributed to the URI. Children were excluded if they had symptoms of asthma, pneumonia, laryngotracheobronchitis, sinusitis, and/or allergic rhinitis. Patients who used any cough or cold medication or honey in the previous 24 hours were also excluded.</p>
<p>Parents were asked to evaluate the children the day of presentation, when no medication had been given, and then again the day after a single dose of 10 g of eucalyptus honey, citrus honey, labiatae honey, or placebo (silan date extract) had been administered before bedtime. Pre- and postintervention subjective assessments were obtained using a 5-item Likert-scale questionnaire regarding the child&#8217;s cough and sleep difficulty. Only those children whose parents rated severity as at least a 3 (on a 7-point scale) for at least 2 of the 3 questions related to nocturnal cough and sleep quality on the preintervention questionnaire were included.</p>
<p>Of the 300 patients enrolled, 270 (89.7%) completed the single-night study. The median age of these children was 29 months (range, 12 &#8211; 71 months). There was no significant age difference among the treatment groups. Symptom severity was also similar among all 4 treatment groups.</p>
<p>Adverse events were reported for 5 patients and included stomachache, nausea, and vomiting and were not significantly different between the groups.</p>
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		<title>Glaucoma &amp; Preventive Measures</title>
		<link>http://pharmatite.com/2012/05/glaucoma-preventive-measures/</link>
		<comments>http://pharmatite.com/2012/05/glaucoma-preventive-measures/#comments</comments>
		<pubDate>Wed, 16 May 2012 12:23:49 +0000</pubDate>
		<dc:creator>Shivani Prashar</dc:creator>
				<category><![CDATA[Diseases and Treatment]]></category>
		<category><![CDATA[Health topics]]></category>
		<category><![CDATA[Study Material]]></category>
		<category><![CDATA[alpha lipoic acid]]></category>
		<category><![CDATA[disease]]></category>
		<category><![CDATA[eye]]></category>
		<category><![CDATA[glaucoma]]></category>
		<category><![CDATA[intra ocular pressure]]></category>
		<category><![CDATA[Omega 3 fatty acid]]></category>

		<guid isPermaLink="false">http://pharmatite.com/?p=292</guid>
		<description><![CDATA[GLAUCOMA ???? Glaucoma is an eye disorder in which internal eye pressure (Intraocular pressure-IOP) is very high. In this condition, eye has too much aqueous humor pressure either because of over production of fluid or of improper draining. This leads to damage of optic nerve results in Vision loss. This nerve acts like an electric [...]]]></description>
				<content:encoded><![CDATA[<p><strong>GLAUCOMA ????</strong></p>
<p>Glaucoma is an eye disorder in which internal eye pressure (Intraocular pressure-IOP) is very high. In this condition, eye has too much aqueous humor pressure either because of over production of fluid or of improper draining. This leads to damage of optic nerve results in Vision loss. This nerve acts like an electric cable with over a million wires. It is responsible for carrying images from the eye to the brain.<br />
According to World Health Organization, Glaucoma is the second leading cause of blindness (behind cataracts).</p>
<p><strong>GLAUCOMA SYMPTOMS:</strong><br />
Glaucoma, known as<strong> “silent thief of sight”</strong> as it causes no pain and shows no symptoms in early stages and quietly causes vision loss. As no symptoms occur, the best way to diagnose this form of glaucoma is by periodic eye examination. Onset of any of symptoms like blurred vision, severe eye pain, red eyes, headache, nausea and vomiting is the warning alarm for eyes.</p>
<p><strong>GLAUCOMA CAUSE:</strong><br />
A clear fluid flows in and out of the space at the front of the eye, nourishing nearby tissues. Glaucoma causes the fluid to pass through too slowly or to stop draining altogether. As the fluid builds up, the pressure inside the eye increases, causing damage to the optic nerve and vision loss.</p>
<p><strong>RISK FACTORS:</strong><br />
<strong>Age:</strong> Glaucoma is more common among older people. People above 40 are 6 times more likely to get glaucoma.<br />
<strong>Family History:</strong> The most common type of glaucoma, primary open angle glaucoma, is hereditary. Family history of glaucoma increases the risk of glaucoma four to nine times.<br />
<strong>Indiscriminate use of Steroids:</strong> Studies indicate Steroids increase intraocular pressure. These could be in the form of Oral medications, Steroid Inhalers and Steroid Eye Drops used for long periods of time.<br />
<strong>Injury to Eye:</strong> Injury to the eye may cause secondary open angle glaucoma. This type of glaucoma can occur immediately after the injury or years later.</p>
<p><strong>CARE, NUTRITION AND SUPPLEMENTS:</strong><br />
Glaucoma is controlled and treated if detected in early stages. Early detection of Glaucoma save the patient form vision loss and eye damage. Glaucoma is control with Medicines (Oral and eye-drops) and Laser Surgery.</p>
<p>Other than Medicines and Surgery, following care, nutrition and supplements are required to keep eye healthy and free from eye problems:</p>
<p><strong>1. Exercise:</strong> Regular physical activity can lower intra ocular pressure by a little bit.</p>
<p><strong>2. Food &amp; Diet:</strong> Carrots, Spinach, Green leafy vegetables, citrus fruits, blueberries, cherries, tomatoes, whole milk, egg, lean meat and seafood should be taken to keep eye healthy and full of vision. And should limit the intake of caffeine, alcohol and smoking.</p>
<p><strong>3. Nutritional Supplements:</strong> There are few supplements known to improve the clinical condition of Glaucoma.</p>
<p><strong>A. Alpha Lipoic Acid (ALA):</strong> Alpha Lipoic Acid (ALA) is very powerful antioxidant and this antioxidant property is helpful in improving eye conditions like glaucoma, cataract and diabetic retinopathy. Clinical studies shows that, regular intake of 150 mg of Alpha Lipoic acid improves visual acuity and colour perception by 45- 47% in glaucoma patients. ALA shows strong neuroprotective properties which significantly prevent ischemic optic nerve damage and improves fluid discharge.</p>
<p><em>Ref.: Filina AA, et al. Lipoic acid as a means of metabolic therapy of open-angle glaucoma. Vestn Oftalmol 1995; 111:6-8.</em></p>
<p><strong>B. Omega-3 Fatty Acids:</strong> Studies show direct association between Omega 3 fatty acid and eye health. Omega 3 fatty acid is helpful in inflammatory and intraocular pressure (IOP) conditions. It is studied that with the regular consumption of Omega 3 fatty acid leads to decrease in IOP with age by increasing the aqueous outflow in glaucoma patients. Omega 3 fatty acid helps to decrease the eye inflammation by reducing the production of inflammatory cellular signaling molecules.</p>
<p><em>Ref.: 1. Cellini M, Rossi A &amp; Moretti M. The use of polyunsaturated fatty acids in ocular hypertension. Acta ophtalmol Scand 1999;77 (suppl. 229):54-55</em><br />
<em> 2. Dietary omega 3 fatty acids decrease intraocular pressure with age by increasing aqueous outflow. Invest Ophthalmol Vis Sci. 2007.</em></p>
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		<title>Questionable use of Statins in Primary Prevention</title>
		<link>http://pharmatite.com/2012/04/questionable-use-of-statins-in-primary-prevention/</link>
		<comments>http://pharmatite.com/2012/04/questionable-use-of-statins-in-primary-prevention/#comments</comments>
		<pubDate>Wed, 18 Apr 2012 20:06:45 +0000</pubDate>
		<dc:creator>ANTS4U</dc:creator>
				<category><![CDATA[Discussions]]></category>
		<category><![CDATA[Diseases and Treatment]]></category>
		<category><![CDATA[In Practice]]></category>

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		<description><![CDATA[By taking statins, one or more patients will develop diabetes and 20% or more will experience disabling symptoms, including muscle weakness, fatigue, and memory loss

]]></description>
				<content:encoded><![CDATA[<p>For every 100 patients with elevated cholesterol levels who take statins for five years, a myocardial infarction will be prevented in one or two patients. Preventing a heart attack is a meaningful outcome.</p>
<p>However, by taking statins, one or more patients will develop diabetes and 20% or more will experience disabling symptoms, including muscle weakness, fatigue, and memory loss</p>
<p>&nbsp;</p>
<p>Ref: <em>JAMA</em> 2012; 307: 1489-4532</p>
]]></content:encoded>
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		<title>Antihypertensive Drugs More Effective When Taken at Night</title>
		<link>http://pharmatite.com/2011/11/antihypertensive-drugs-more-effective-when-taken-at-night/</link>
		<comments>http://pharmatite.com/2011/11/antihypertensive-drugs-more-effective-when-taken-at-night/#comments</comments>
		<pubDate>Thu, 24 Nov 2011 02:51:19 +0000</pubDate>
		<dc:creator>ANTS4U</dc:creator>
				<category><![CDATA[Breaking News]]></category>
		<category><![CDATA[Diseases and Treatment]]></category>
		<category><![CDATA[In Practice]]></category>

		<guid isPermaLink="false">http://pharmatite.com/?p=163</guid>
		<description><![CDATA[Taking antihypertensive medications at bedtime rather than in the morning has been shown to be associated with an increase in bedtime blood pressure (BP) decline toward a dipping pattern and better BP control and reduction in urinary protein excretion. Nocturnal hypertension is more common among patients with chronic kidney disease (CKD) who may thus experience greater effects of time medications for hypertension.]]></description>
				<content:encoded><![CDATA[<p>According to the current study by Hermida and colleagues, taking antihypertensive medications at bedtime rather than in the morning has been shown to be associated with an increase in bedtime blood pressure (BP) decline toward a dipping pattern and better BP control and reduction in urinary protein excretion. Nocturnal hypertension is more common among patients with chronic kidney disease (CKD) who may thus experience greater effects of time medications for hypertension.</p>
<p>This randomized controlled, open-label trial compares the effect of bedtime vs morning administration of BP medications on a composite of cardiovascular disease (CVD) outcomes and BP control.</p>
<p>According to Dr. Hermida and colleagues, &#8220;treatment at bedtime is the most cost-effective and simplest strategy of successfully achieving the therapeutic goals of adequate asleep BP reduction and preserving or re-establishing the normal 24-hour BP dipping pattern.&#8221;</p>
<p>The authors suggest that a potential explanation for the benefit of nighttime treatment may be associated with the effect of nighttime treatment on urinary albumin excretion levels. &#8220;We previously demonstrated that urinary albumin excretion was significantly reduced after bedtime, but not morning, treatment with valsartan,&#8221; they note. In addition, this reduction was independent of 24-hour changes of BP, but correlated with a decline in BP during sleep.</p>
<p>Refer: <em>J Am Soc Nephrol</em>. Published online October 24, 2011</p>
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		<item>
		<title>PPI linked to fracture risk</title>
		<link>http://pharmatite.com/2011/05/ppi-linked-to-fracture-risk/</link>
		<comments>http://pharmatite.com/2011/05/ppi-linked-to-fracture-risk/#comments</comments>
		<pubDate>Sat, 21 May 2011 08:21:53 +0000</pubDate>
		<dc:creator>ANTS4U</dc:creator>
				<category><![CDATA[Breaking News]]></category>
		<category><![CDATA[Diseases and Treatment]]></category>
		<category><![CDATA[Drug Comparisons]]></category>
		<category><![CDATA[In Practice]]></category>

		<guid isPermaLink="false">http://pharmatite.com/?p=140</guid>
		<description><![CDATA[PPI use is linked to fracture risk]]></description>
				<content:encoded><![CDATA[<p><strong>Proton pump inhibitor (PPI) use is linked to fracture risk</strong>, according to the results of a meta-analysis reported in the May/June issue of the Annals of Family Medicine.</p>
<p>&#8220;[PPIs] and histamine 2 receptor antagonists (H2RAs) are the most popular [acid-suppressive drugs] available, and millions of individuals currently take these medications on a continuous or long-term basis,&#8221;</p>
<p>These potent drugs are used to treat various disorders, and indications for long-term maintenance therapy with this drug class continue to expand. The relationship between [acid-suppressive drug] use and bone health remains unclear</p>
<p>The final analyses included 5 case-control studies, 3 nested case-control studies, and 3 cohort studies selected from 1809 articles meeting the initial inclusion criteria. With use vs nonuse of PPIs, the pooled odds ratio (OR) for fracture was 1.29 (95% confidence interval [CI], 1.18 &#8211; 1.41) compared with 1.10 (95% CI, 0.99 &#8211; 1.23) for use vs nonuse of H2RAs.</p>
<p><strong>Risk for any fracture and for hip fracture was increased with long-term use of PPIs </strong>(adjusted OR, 1.30 [95% CI, 1.15 - 1.48]; adjusted OR, 1.34 [95% CI, 1.09 - 1.66], respectively). <strong>Vertebral fracture risk was also increased by 54% with PPI use. In contrast, long-term use of H2RA was not significantly associated with fracture risk.</strong></p>
<p>&#8220;We found possible evidence linking PPI use to an increased risk of fracture, but no association between H2RA use and fracture risk,&#8221; the study authors write. &#8220;Widespread use of PPIs with the potential risk of fracture is of great importance to public health. Clinicians should carefully consider their decision to prescribe PPIs for patients already having an elevated risk of fracture because of age or other factors.&#8221;</p>
<p>It is not necessary to treat patients to the point of an achlorhydric state to resolve acid reflux symptoms, so we recommend that drug doses be chosen thoughtfully with consideration of what is necessary to achieve desired therapeutic goals,&#8221; the study authors conclude.</p>
<p>PPIs have clear benefits in patients that require them, and they should not be denied to patients who are likely to benefit from them,&#8221; the editorialists write. &#8220;On the other hand, long-term PPI exposure may lead to other unwanted effects and should be reserved for patients likely to benefit from them. They should not be used long-term for undifferentiated dyspepsia, but neither should they be denied for patients with established persistent [gastroesophageal reflux disease], [nonsteroidal anti-inflammatory drugs] risk, and hypersecretory states, while aiming for the lowest effective maintenance dose.&#8221;</p>
<p><em>Ann Fam Med</em>. 2011;9:257-267, 200-202</p>
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		<item>
		<title>Probiotic May Help Prevent Recurrent Urinary Tract</title>
		<link>http://pharmatite.com/2011/04/probiotic-may-help-prevent-recurrent-urinary-tract/</link>
		<comments>http://pharmatite.com/2011/04/probiotic-may-help-prevent-recurrent-urinary-tract/#comments</comments>
		<pubDate>Fri, 29 Apr 2011 05:47:30 +0000</pubDate>
		<dc:creator>ANTS4U</dc:creator>
				<category><![CDATA[Diseases and Treatment]]></category>
		<category><![CDATA[Study Material]]></category>

		<guid isPermaLink="false">http://pharmatite.com/?p=109</guid>
		<description><![CDATA[InfectionApril 20, 2011 &#8211; In a randomized, double-blind phase 2 study, an intravaginal probiotic composed of Lactobacillus crispatus CTV-05  reduced the rate of recurrent urinary tract infection (rUTI) in UTI-prone women by roughly one half, which compares favorably with historical data on antimicrobial prophylaxis, the researchers say. They add that larger trials are warranted to [...]]]></description>
				<content:encoded><![CDATA[<p>InfectionApril 20, 2011 &#8211; In a randomized, double-blind phase 2 study,<strong> an intravaginal probiotic composed of <em>Lactobacillus crispatus</em> CTV-05  reduced the rate of recurrent urinary tract infection (rUTI) in UTI-prone women by roughly one half,</strong> which compares favorably with historical data on antimicrobial prophylaxis, the researchers say.</p>
<p>They add that larger trials are warranted to see whether use of vaginal <em>Lactobacillus</em> could replace long-term antimicrobial preventive treatments in women susceptible to rUTI<strong>.</strong></p>
<p>UTIs are common in women and frequently recur, Ann Stapleton, MD, from the University of Washington in Seattle, and colleagues note in their report. It has been shown, they add, that women with rUTIs often have alterations in vaginal microbiota, including depletion of lactobacilli.</p>
<p>A phase 1 study of <em>Lactobacillus crispatus</em> CTV-05 showed that the probiotic can be given as a vaginal suppository with minimal adverse effects to healthy women with a history of rUTI. In the phase 2 study, 100 premenopausal women (median age, 21 years) with a history of rUTI received antimicrobials for acute UTI and then were randomly assigned to receive either <em>Lactobacillus crispatus</em> CTV-05 or placebo vaginal suppository gelatin capsules administered once daily for 5 days, followed by once weekly for 10 weeks.</p>
<p>&#8220;We found that Lactin-V reduced the risk of rUTI approximately as effectively as antimicrobial prophylaxis, achieved high-level vaginal colonization in most women, and was well tolerated,&#8221; Dr. Stapleton and colleagues report.</p>
<p>According to the investigators, culture-confirmed rUTI occurred in 7 (15%) of 48 of women who received <em>Lactobacillus crispatus</em> CTV-05 compared with 13 (27%) of 48 women who received placebo (relative risk [RR], .5; 95% confidence interval [CI], .2 &#8211; 1.2).</p>
<p>A high level of vaginal colonization with <em>L crispatus</em> throughout follow-up was associated with a significant reduction in rUTI only among women receiving <em>Lactobacillus crispatus</em> CTV-05 (RR for Lactin-V, .07; RR for placebo, 1.1; <em>P</em> &lt; .01).</p>
<p>The safety profile of the probiotic mirrored that seen in the phase 1 study. Adverse effects were reported by 56% of women receiving <em>Lactobacillus crispatus</em> CTV-05 and 50% of those receiving placebo. The most common adverse effects included vaginal discharge or itching or moderate abdominal discomfort.</p>
<p>A novel aspect of this study, the authors say, is the application of quantitative polymerase chain reaction to assess vaginal microbiota after UTI. This enabled them to define sentinel changes in vaginal microbiota with or without the <em>Lactobacillus crispatus</em> CTV-05 probiotic.</p>
<p>Using quantitative polymerase chain reaction to assess <em>L crispatus</em> colonization in women in both study groups, the researchers say, allowed them to distinguish the natural recovery of the vaginal microbiota after UTI, as may have potentially occurred in the placebo group, from specific effects attributable to the probiotic.</p>
<p>What was &#8220;striking,&#8221; the investigators add, was that placebo-treated women often had high concentrations of vaginal <em>L crispatus</em> during follow-up, yet this failed to protect them from rUTI (RR, 1.1; 95% CI, .4 &#8211; 3.1). In contrast, women who received <em>Lactobacillus crispatus</em> CTV-05 and achieved high colonization were protected from rUTI (RR, .07; 95% CI, .02 &#8211; .3; <em>P</em> &lt; .01).</p>
<p>&#8220;Lactin-V after treatment for acute UTI,&#8221; they conclude, &#8220;confers a significant advantage over repopulation of the vaginal microbiota with endogenous <em>L. crispatus</em>.&#8221;</p>
<p>&#8220;Ongoing studies in our group are directed at understanding the mechanisms of protection in vivo and optimizing this prophylactic regimen,&#8221; they note.</p>
<p><em>The study was supported by the National Institute of Diabetes and Digestive and Kidney Diseases and the Office of Research in Women&#8217;s Health at the National Institutes of Health. Results of the trial also were presented at the 48th Annual Interscience Conference on Antimicrobial Agents and Chemotherapy/46th Annual Meeting of the Infectious Diseases Society of America, Washington, DC, and the 47th Annual Meeting of the Infectious Diseases Society of America, Philadelphia, Pennsylvania. The authors have disclosed no relevant financial relationships.</em></p>
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		<title>Escitalopram for Hot Flashes</title>
		<link>http://pharmatite.com/2011/04/escitalopram-for-hot-flashes/</link>
		<comments>http://pharmatite.com/2011/04/escitalopram-for-hot-flashes/#comments</comments>
		<pubDate>Thu, 21 Apr 2011 04:28:16 +0000</pubDate>
		<dc:creator>ANTS4U</dc:creator>
				<category><![CDATA[Diseases and Treatment]]></category>
		<category><![CDATA[Study Material]]></category>
		<category><![CDATA[Escitalopram]]></category>
		<category><![CDATA[Hot Flashes]]></category>

		<guid isPermaLink="false">http://pharmatite.com/?p=106</guid>
		<description><![CDATA[This multicenter, 8-week, randomized, double-blind, placebo-controlled, parallel group trial of 205 women (95 African American, 102 white, 8 other) examined efficacy and tolerability of 10 to 20 mg/day escitalopram, a selective serotonin reuptake inhibitor (SSRI), in alleviating frequency, severity, and bother of hot flashes between July 2009 and June 2010. Frequency and severity of hot [...]]]></description>
				<content:encoded><![CDATA[<p>This multicenter, 8-week, randomized, double-blind, placebo-controlled, parallel group trial of 205 women (95 African American, 102 white, 8 other) examined efficacy and tolerability of 10 to 20 mg/day escitalopram, a selective serotonin reuptake inhibitor (SSRI), in alleviating frequency, severity, and bother of hot flashes between July 2009 and June 2010. Frequency and severity of hot flashes were primary outcomes, while secondary outcomes were hot flash bother and clinical improvement. Outcomes were recorded with daily diaries. Mean daily hot flash frequency was 9.78 at baseline. Among women taking escitalopram, mean difference in hot flash frequency reduction was 1.41 (95% CI, 0.13-2.69) fewer hot flashes per day at week 8 (<em>P </em>&lt; .001). There were mean reductions of 4.60 (95% CI, 3.74-5.47) hot flashes per day in the escitalopram group and 3.20 (95% CI, 2.24-4.15) hot flashes in the placebo groups. At the 8-week follow-up, 55% of women in the escitalopram group versus 36% in the placebo group reported a decrease of at least 50% in hot flash frequency (<em>P </em>= .009), with reductions in hot flash severity scores significantly greater in the escitalopram group. Race did not significantly modify the treatment effect (<em>P </em>= .62). <strong>Use of escitalopram compared with placebo resulted in fewer, less severe hot flashes in healthy women at 8 weeks of follow-up.</strong></p>
<p><em>Refer: JAMA 2011;305:267-274.</em></p>
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		<title>Pathogenesis of Rheumatoid arthritis and Osteoarthritis</title>
		<link>http://pharmatite.com/2011/02/rheumatoid-arthritis-and-osteoarthritis/</link>
		<comments>http://pharmatite.com/2011/02/rheumatoid-arthritis-and-osteoarthritis/#comments</comments>
		<pubDate>Fri, 18 Feb 2011 04:44:17 +0000</pubDate>
		<dc:creator>ANTS4U</dc:creator>
				<category><![CDATA[Diseases and Treatment]]></category>
		<category><![CDATA[Health topics]]></category>
		<category><![CDATA[In Practice]]></category>
		<category><![CDATA[Study Material]]></category>

		<guid isPermaLink="false">http://pharmatite.com/?p=72</guid>
		<description><![CDATA[Irreversible bone erosion occurs in RA, whereas subchondral bone sclerosis with synovial joint remodeling is typically characteristic of OA]]></description>
				<content:encoded><![CDATA[<p>A well-accepted view holds that the pathogenesis of rheumatoid arthritis (RA) and osteoarthritis (OA) differs. However, recent evidence has also indicated that similar focal and systemic alterations exist in RA and OA, leading us to postulate that there may well be a &#8216;final common pathway&#8217; for arthritis. Thus, synovial tissue and articular cartilage responses to activated T and B cells, NF-κB and AP-1 activation, proinflammatory cytokines, growth hormone, chemokines, matrix metalloproteinases and hydrolytic cathepsins often act concurrently and synergistically to generate RA and OA pathology in which articular cartilage destruction is uncoupled from cartilage repair. However, there are also several critical areas in which RA and OA differ. These include the prominent involvement of synovial tissue angiogenesis and fibrin deposition in RA and, most notably, in the timing and extent of subchondral bone responses. Thus, irreversible bone erosion occurs in RA, whereas subchondral bone sclerosis with synovial joint remodeling is typically characteristic of OA.</p>
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		<title>Drugs And Pregnancy</title>
		<link>http://pharmatite.com/2011/02/drugs-and-pregnancy/</link>
		<comments>http://pharmatite.com/2011/02/drugs-and-pregnancy/#comments</comments>
		<pubDate>Sun, 13 Feb 2011 09:27:31 +0000</pubDate>
		<dc:creator>ANTS4U</dc:creator>
				<category><![CDATA[Diseases and Treatment]]></category>
		<category><![CDATA[Health topics]]></category>
		<category><![CDATA[In Practice]]></category>

		<guid isPermaLink="false">http://pharmatite.com/?p=60</guid>
		<description><![CDATA[Drugs can have harmful effects on mother and foetus at any time during the pregnancy. Use of medications during pregnancy requires a careful assessment of risks and benefits for them. During the first trimester teratogenic effects are frequent. There is higher risk from third to eleventh week of gestation. During the second and third trimester [...]]]></description>
				<content:encoded><![CDATA[<p>Drugs can have harmful effects on mother and foetus at any time during the pregnancy. Use of medications during pregnancy requires a careful assessment of risks and benefits for them. During the first trimester teratogenic effects are frequent. There is higher risk from third to eleventh week of gestation. During the second and third trimester drugs may affect the growth and functional development of the foetus or have toxic effect on the foetal tissues. Drugs administered shortly before term or during labour may have adverse effects on mother or on neonate. The FDA has established five categories (A, B. C, D, X) which indicate the potential of a systemically absorbed drug causing birth defects. These categories are indicative of the level of risk to the foetus. The category X includes the drugs for which there is enough data to implicate their teratogenecity and the risk vs benefit ratio does not support the use of the drug and hence these are contraindicated during pregnancy. A few drugs present variable risk to the foetus depending on the time and duration of their use. These drugs have been assigned double categories. The categories of risk involved are as under:</p>
<p>A: adequate studies in pregnant women have not demonstrated a risk to the foetus in the first trimester of pregnancy and there is no evidence of risk in later trimesters.</p>
<p>B: animal studies have not demonstrated a risk to the foetus but there are no adequate studies in pregnant women or, animal studies have shown an adverse effect, but adequate studies in pregnant women have not demonstrated a risk to the foetus during the first trimester of pregnancy and there is no evidence of risk in later trimesters.</p>
<p>C: animal studies have shown an adverse effect on the foetus but, there are no adequate studies in humans; the benefits from the use of the drug in pregnant women may be acceptable despite its potential risks or there are no animal reproduction studies and no adequate studies in humans.</p>
<p>D: there is evidence of human foetal risk, but the potential benefits from the use of the drug in pregnant women may be acceptable despite its potential risks.</p>
<p>X: studies in animals or humans demonstrate fetal abnormalities or adverse reaction reports indicate evidence of foetal risk; the risk of use in a pregnant woman clearly outweighs any possible benefit.</p>
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