WASHINGTON – Climate change could increase exposure to water-borne diseases originating in oceans, lakes and coastal ecosystems, and the impact could be felt within 10 years, US scientists told a conference here Saturday.Several studies have shown that shifts brought about by climate change make ocean and freshwater environments more susceptible to toxic algae blooms and allow harmful microbes and bacteria to proliferate, researchers from the National Oceanic and Atmospheric Administration said.In one study, NOAA scientists modeled future ocean and weather patterns to predict the effect on blooms of Alexandrium catenella, or the toxic “red tide,” which can accumulate in shellfish and cause symptoms, including paralysis, and can sometimes be deadly to humans who eat the contaminated seafood.”Our projections indicate that by the end of the 21st century, blooms may begin up to two months earlier in the year and persist for one month later compared to the present-day time period of July to October,” said Stephanie Moore, one of the scientists who worked on the study.But the impact could be felt well before the end of this century — as early as 2040, she said at the annual meeting of the American Association for the Advancement of Science (AAAS).”Changes in the harmful algal bloom season appear to be imminent. We expect a significant increase in Puget Sound (off the coast of Washington state where the study was conducted) and similar at-risk environments within 30 years, possibly by the next decade,” said Moore.In another study, NOAA scientists found that desert dust that is deposited into the oceans from the atmosphere could also lead to increases of harmful bacteria in seawater and seafood.Researchers from the University of Georgia found that adding desert dust, which contains iron, to seawater significantly stimulated the growth of Vibrios, a group of ocean bacteria that can cause gastroenteritis and infectious diseases in humans.”It is possible this additional input of iron, along with rising sea surface temperatures, will affect these bacterial populations and may help to explain both current and future increases in human illnesses from exposure to contaminated seafood and seawater,” the researchers said.”Within 24 hours of mixing weathered desert dust from Morocco with seawater samples, we saw a huge growth in Vibrios, including one strain that could cause eye, ear and open wound infections, and another strain that could cause cholera,” said Erin Lipp, who worked on the study.the amount of iron-containing dust that is deposited in the sea has increased over the last 30 years and is expected to continue to rise, based on precipitation trends in western Africa which are causing desertification.meanwhile, researchers at the University of Wisconsin-Milwaukee warned that an increase in severe rainstorms could cause more sewage overflows, which would release disease-causing bacteria, viruses and protozoa into drinking water and onto beaches.the researchers in this study used climate models to show that spring rains are expected to increase in the next 50 years, and with that increase, ageing sewer systems are more likely to overflow because the ground is frozen and rainwater can’t be absorbed.

Berries may offer sweet hope in reducing the risk of Parkinson’sdisease, Harvard researchers are reporting.

The Harvard School of Public Health examined the effect onParkinson’s disease of flavonoids, a dietary component found incitrus fruits, chocolate and berries. The study was released lastSunday, and will be presented at the American Academy ofNeurology’s 63rd Annual Meeting in Honolulu in April.

The exact reason people develop Parkinson’s is not clear, thoughsome genetic and environmental factors are thought to beresponsible.

“The study opens up a whole area of potential future studiesexamining other types of environmental effects on Parkinson’s,”said Dr. Anna Hohler, a neurologist and professor of neurology atBoston University who was not involved with the study.

The study found that the top 20 percent of males who consumedthe most flavonoids were 40 percent less likely to developParkinson’s than the bottom 20 percent of men who consumed theleast amount of flavonoids. In women, there was no correlationbetween overall flavonoid consumption and Parkinson’s.

However, a subclass of flavonoid called anthocyanins, which areprimarily found in berries, were associated with reduced risk ofdeveloping Parkinson’s, said study author Dr. Xiang Gao, researchscientist at Harvard.

“These components we found to have neuroprotective effects,” hesaid. “Anthocyanins are a kind of pigment in food. for example, ina blackberry or a strawberry, when you see the different colors inthese berries, that’s because of anthocyanin.”

The study examined 129,617 individuals – 49,281 men and 80,336women. Participants were followed for 20 to 22 years, and wereasked to periodically fill out questionnaires about their foodconsumption habits. During that period, 805 participants developedParkinson’s. when the study started, the average age of maleparticipants was about 55, and the average age of femaleparticipants was about 51, Gao said.

Parkinson’s is a neurodegenerative disorder that affectsmovement. Most people with the disease start to get symptoms intheir sixties, though some people get it much earlier, Hohlersaid.

An estimated 60,000 Americans are diagnosed with Parkinson’sdisease each year, and as many as one million Americans live withParkinson’s, according to the Parkinson’s Disease Foundation in NewYork.

The study did not track the consumption of all types of berries,but looked specifically at strawberries and blueberries.

“We asked about a number of different dietary items – howfrequently they were eaten and the intake per month of each item,”Gao said. “That means we could only list the most consumedfoods.”

Participant’s questionnaires were then stored in a databasewhere researchers could later revisit answers and calculateaverages.

A strength of the study is the fact that people’s eating habitswere tracked before any of them had Parkinson’s, Gao said.

“Otherwise, if you do a kind of study called a case-controlstudy, in which you start with a group of people who already haveParkinson’s disease and ask them to recall their dietary intakefive years later, there may be some error,” he said. “This way wereduce this kind of memory bias.”

Gao said the link between flavonoid consumption on Parkinson’sand gender could not be confirmed until further studies takeplace.

“Our study is the first prospective study in humans,” he said.”So our observations need to be confirmed by other studies to seeif there is a difference. and if the other studies find some sortof gender, the next step is to do some more studies to understandthe mechanism.”

The study raises further questions about the consumption ofanthocyanin as well.

“Future research needs to find out in terms of quantity, howmuch do you need to consume to have a beneficial effect and in whatperiod of time,” Hohler said.

Although Gao agreed that more research must be done before anystrong conclusions are made, he said there is certainly no harm ineating more berries.

“Although it’s too early to recommend eating berries to reduceParkinson’s risk, think about the other beneficial effects ofberries,” he said. “If you only eat one cup of berries a month,maybe you can increase to another one.”

Hohler plans to discuss the study with Parkinson’s patients.

“When a study comes out like this, we say, ‘There is one studyso far which is interesting and may suggest that this might besomewhat neuroprotective,’ but that further studies need to be doneto clarify,” she said. “Parkinson’s patients are very eager to trythings that might decrease their chance of developing [thedisease].”

New Research Shows That Thinking Skills are better for MS Patients on Colder Days

Feb. 17, 2011 — As one of the most brutally cold winters on record drags on, most of us are pining for summer. but for many patients with multiple sclerosis, hotter temperatures may not be so welcome because they bring worsening symptoms.

Now new research finds this may be especially true for some of the least well understood symptoms of the disease — thinking and memory problems.

When researchers tested the memories and information processing abilities of MS patients and people without the disease at different points during the year, they found that the MS patients performed worse on the cognitive tests in warmer seasons.

No seasonal difference was seen in test performance among people without multiple sclerosis.

The study is the first to document the impact of hotter temperatures on memory and thinking function in MS patients, say neuropsychologist and study co-author James F. Sumowski, PhD, of the Kessler Foundation Research Center in West Orange, N.J.

The study will be presented in April at the 63rd annual meeting of the American Academy of Neurology in Honolulu.

MS Worse in Hot Weather

Each week in the United States about 200 people are diagnosed with MS, according to the National MS Society.

Numbness, limb weakness, and problems with balance and vision are among the most widely known symptoms of the disease, but problems with thinking and memory are also very common.

Neurologist Barbara Giesser, MD, says the link between hot weather and worsening MS symptoms has been recognized for more than 100 years.

“At the turn of the 20th century, long before we had MRIs and fancy diagnostics, one way of diagnosing MS was the ‘hot bath’ test,” she says. “They would put the patient in a tub of very hot water and if their symptoms worsened, the diagnosis was confirmed.”

Although not all MS patients have worse symptoms in hot weather, Giesser says the vast majority have some degree of heat sensitivity.

The newly reported study included 40 MS patients and 40 people without the disease matched to the patients for age, sex, and education level.

All the participants underwent tests designed to measure memory function and information acquisition and processing.

Overall, the MS patients performed 70% better on the thinking tests when the tests were given in colder months compared to warmer ones.

The researchers did not measure the patients’ body temperatures or record how long they spent outside before taking the tests.

MS Lesions More Common in Summer

It is not clear if hot weather affects the progression of MS or just causes temporary worsening of symptoms.

A brain imaging study published last summer by researchers at Harvard University showed that MS-associated brain lesions actually occur more often in warmer months than in colder ones.

Heat appears to slow down nerve impulses that are already impaired by the disease, Giesser says.

“Basically nerves are electrical cables,” she says. “MS damages the insulation and short circuits the nerves so that they don’t conduct signals as efficiently. if you heat up a damaged nerve, that causes further problems.”

Giesser recommends her heat-sensitive patients try cooling strategies like drinking something cold or sucking on ice during warm weather.

This study will be presented at a medical conference. the findings should be considered preliminary as they have not yet undergone the “peer review” process, in which outside experts scrutinize the data prior to publication in a medical journal.

SAN ANTONIO—Oxytocin, a hormone with a rosy reputation for getting people to love, trust and generally make nice with one another, can get down and dirty, according to evidence presented on January 28 at the annual meeting of the Society for Personality and Social Psychology.

This brain-altering substance apparently amplifies whatever social proclivities a person already possesses, whether positive or negative, says psychologist Jennifer Bartz of Mount Sinai School of Medicine in new York City.

Previous work has shown that a nasal blast of the hormone encourages a usually trusting person to become more trusting (SN Online: 5/21/08), but now Bartz and her colleagues find that it also makes a highly suspicious person more uncooperative and hostile than ever.

“Oxytocin does not simply make everyone feel more secure, trusting and prosocial,” Bartz says.

These new results raise concerns about plans by some researchers to administer oxytocin to people with autism and other psychiatric conditions that include social difficulties, she adds.

Her team studied 14 people diagnosed with borderline personality disorder and 13 volunteers with no psychiatric conditions. Symptoms of borderline personality disorder include severe insecurity about relationships, fears of abandonment and constant, needy reassurance-seeking from partners.

Borderline personality disorder usually occurs in women, but Bartz’s sample included four men. her group of healthy participants included seven men.

Members of each group played a computer game with an experimenter posing as a research volunteer. in each of three rounds, volunteers had to predict whether their partner would cooperate with them so that each player could make $6 or if the partner would leave the game in order to claim $4 alone.

Volunteers who suspected the partner of bad intent could leave the game early and claim $4 for themselves.

Borderline personality players of both sexes left the game early far more often after receiving an oxytocin nasal spray than after whiffing a placebo spray. Inhaling the hormone prodded their already high levels of hostile suspicion and depleted minimal reserves of trust, Bartz suggests.

Psychiatrically healthy players became more cooperative in the money game after getting oxytocin, relative to their placebo responses.

Nasally inhaling oxytocin also magnifies men’s memories of their mothers as being either supportive or not, Bartz says. her team had 31 men fill out surveys on the quality of their relationships with their mothers up to age 16.

Those who described good maternal relationships remembered mom as substantially more caring and supportive after receiving oxytocin, compared with after inhaling a placebo spray. those whose early home life had been troubled remembered mom as much less caring and supportive after oxytocin, versus placebo.

Bartz’s team initially described oxytocin’s two-sided influence on men’s maternal memories in the Dec. 14 Proceedings of the National Academy of Sciences.

These findings underscore that “oxytocin is not a love hormone; its effects vary in different people,” remarks psychologist Greg Norman of Ohio State University in Columbus.

Norman and his colleagues have found that oxytocin stimulates the heart to beat more in sync with the breathing cycle in people with healthy social lives, but not in people who report constant loneliness.

Other researchers have recently reported that oxytocin stimulates greater trust of members of one’s own ethnic group and greater suspicion of other ethnicities.

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Another sleepless night; another round with Restless Legs Syndrome (RLS) is keeping you awake. RLS is often associated with menopause, but in fact, the two are not interconnected. This first of a two-part series looks at RLS and its causes.Restless Legs Syndrome (RLS) definedDr. John W. Winkelman of Brigham & Women?s Hospital in Boston recently discussed RLS at the 21st Annual Meeting of the North American Menopause Society (NAMS). His focus is to draw greater attention to RLS as a largely misunderstood sleep disturbance. Winkelman lists the four main criteria, known as URGE, in this neurological disorder:*Urge to move limbs especially the legs*Rest or inactivity worsens symptoms*Getting up and/or moving around improves the sensations*Evening and night time bring on worsening symptomsRLS patients complain of uncomfortable sensations in the legs or limbs described as throbbing, pulling, creeping or crawling when sitting or lying down. Smaller numbers of patients may experience RLS in their arms, heads or torsos. These sensations can occur in one or both sides of the body. RLS sufferers have anywhere from 100 to 300 movements during the night.RLS vs. PLMSRestless Leg Syndrome should not be confused with Periodic Leg Movement Syndrome (PLMS). PLMS is a similar disorder that affects up to 80% of RLS sufferers; but not all PLMS patients will have RLS. PLMS is the involuntary twitching of legs during sleep, usually every 15 to 40 seconds, which causes sufferers to wake up. The main difference between the two is that RLS occurs when a patient is awake, preventing one from falling and staying asleep, while PLMS occurs during sleep and causes one to wake up repeatedly during the night.causes of RLS:RLS strikes at night or during prolonged periods of sitting or inactivity. Patients find that walking around or moving the legs while sitting or in bed helps to alleviate those unpleasant feelings. Generally, there is no real known cause, but these are the most common traits in RLS patients:*Genetics: RLS tends to run in families*Low iron levels in the brain: serum Ferritin levels lower than 40 may indicate an iron deficiency or the brain?s inability to transmit iron though the cells*Dopamine abnormalities: dopamine is a chemical found in the brain and controls muscle activity; dopamine keeps muscle movements smooth versus jerky; any disruptions in dopamine transmission patterns may increase the risk of developing RLS. For example, those with Parkinson?s disease have abnormal dopamine function in brain and often develop RLS. however, this does not mean that RLS sufferers are more prone to developing Parkinson?s disease itself.*Some chronic diseases such as kidney failure (End Stage Renal Failure) and diabetes*Certain medications: antinausea drugs (prochlorperzine, metoclopramide), antipsychotic drugs (haloperidol, pehnothiazine derivatives), antidepressants that increase serotonin levels and some cold and allergy medications that contain sedating antihistamines *Pregnancy: particularly in the last trimester; usually RLS symptoms should disappear within 4 weeks after birthRLS and menopause: is there a connection?Winkelman points out around 5% of Americans experience some degree of RLS ?at a clinically significant rate of occurrence.? Moreover, the National Institute of Neurological Disorders and Stroke (NINDS) supports these statistics, reporting that as many as 10% of Americans have RLS. around two or three percent of those patients have moderate to severe symptoms while five percent have mild symptoms. This means roughly five million adults and one million children suffer from RLS. so is there a connection to menopause?Women tend to associate RLS with menopause and perimenopause since RLS may strike around age 40. but neither perimenopause nor menopause and fluctuating hormone levels are to blame or as Winkelman says, ?menopause and RLS are not interconnected. indeed RLS does affect more men than women ? almost double ? for reasons that are not always clear. he continues by pointing out that women have a greater chance of developing RLS in their 70s, long after menopause, than in their 40s.why is this important?Winkelman notes, ?Some doctors who are unfamiliar with sleep disturbances may miss a proper diagnosis because they are not asking the right questions.? This often leads to doctors and patients associating RLS to menopause, nervousness, insomnia, stress, arthritis, muscle cramps, and simple aging. Winkelman suggests that RLS should ?be the tip of the iceberg to find the underlying cause for proper treatment options and patient relief. in the past, RLS was often mistaken for leg cramps but the two conditions are not related and each requires a different course of treatment.?In part two, learn more about why RLS is a concern and the treatment options available.?Restless Legs Syndrome in Women at the Menopause? as presented by John. W. Winkelman, MD, PhD, Brigham & Women?s Hospital, Boston, MA at the NAMS 21st Annual Meeting menopause.orgNational Institute of Neurological Disorders and Stroke ninds.nih.gov

Findings Demonstrate LATUDA 80 and 160 mg/day Significantly more Effective than Placebo

MARLBOROUGH, Mass.–(BUSINESS WIRE)–Sunovion Pharmaceuticals Inc. (Sunovion) today announced the results of the PEARL 3 study, the third phase 3 worldwide clinical trial of Latuda® (lurasidone HCl) tablets, a once-daily atypical antipsychotic agent recently approved by the U.S. Food and Drug Administration (FDA) for the treatment of patients with schizophrenia. In this six-week, placebo-controlled trial, both fixed doses of LATUDA 80 and 160 mg once-daily, demonstrated statistically significant improvement in symptoms of schizophrenia versus placebo across both primary and secondary efficacy measures. LATUDA was also well tolerated with a relatively low discontinuation rate. the LATUDA 160 mg/day dose has not been reviewed or approved by FDA. the study was presented today at the American College of Neuropsychopharmacology (ACNP) 49th Annual Meeting in Miami, Florida.

“the PEARL 3 results are an important addition to the LATUDA clinical database, and our fifth placebo-controlled trial demonstrating efficacy in schizophrenia”

“The recent FDA approval of LATUDA provides an additional treatment option for patients with schizophrenia. the PEARL 3 study data demonstrating clear efficacy coupled with weight and metabolic properties similar to placebo add to our understanding of the future role of LATUDA in managing the debilitating symptoms that can be challenging to treat,” said Steven G. Potkin, M.D., professor, department of psychiatry and human behavior, University of California, Irvine and presenting author of the study.

the PEARL 3 study (Program to Evaluate the Antipsychotic Response to Lurasidone) was part of an extensive worldwide clinical development program involving more than 2,900 subjects, which evaluated the safety and efficacy of LATUDA for the treatment of adult patients with schizophrenia.

Schizophrenia is a chronic, disabling and serious brain disorder that affects approximately 2.4 million American adults or 1 in 100 people. Schizophrenia is characterized by symptoms such as hallucinations, delusions, disorganized thinking, lack of emotion, lack of energy, as well as problems with memory, attention and the ability to plan, organize and make decisions.

PEARL 3 Key Study Findings

the PEARL 3 study was a double-blind, fixed-dose, placebo-controlled, six-week clinical trial involving 488 patients with schizophrenia and was conducted at 64 sites worldwide. the study had three active treatment arms: LATUDA 80 mg/day and 160 mg/day, and quetiapine extended-release (XR)* 600 mg/day. the use of quetiapine XR was intended to establish assay sensitivity; the study was not designed to directly compare the efficacy of quetiapine and LATUDA. Patients were diagnosed with schizophrenia (using DSM-IV criteria) and were required to have an acute exacerbation of psychotic symptoms with a PANSS [the Positive and Negative Syndrome Scale] total score of 80 or higher at study baseline.

LATUDA 80 and 160 mg once daily were significantly more effective than placebo (-22.2 and -26.5 vs. -10.3 placebo) at Week 6 in the treatment of patients with schizophrenia, with improvements seen as early as day four on the PANSS, the primary efficacy measure. a total of 65% of patients on LATUDA 80 mg/day and 79% of patients on LATUDA 160 mg/day demonstrated a 20% or more improvement on the PANSS total score from baseline versus 41% on placebo at Week 6/Last Observation Carried forward (LOCF) endpoint.

In addition, both LATUDA dose groups were significantly more effective than placebo on the Clinical Global Impressions Severity scale (CGI-S), the key secondary efficacy endpoint, as early as week one. CGI-S score changes from baseline for LATUDA 80 and 160 mg/day versus placebo were -1.5 and -1.7 vs. -0.9, respectively, at Week 6.

Based on the results of this study, the overall safety profile of the drug is not changed. LATUDA 80 and 160 mg/day treatment was well tolerated with a lower overall discontinuation rate than placebo (29% and 23%, respectively vs. 39% placebo), while adverse event-related discontinuations were comparable to placebo (4% and 3%, respectively vs. 4% placebo). the most commonly reported adverse events for LATUDA 80 and 160 mg/day (greater than 5% and at least twice the rate of placebo) were akathisia (8.0% and 7.4% vs. 0.8% placebo); nausea (8.0% and 6.6% vs. 3.3% placebo); parkinsonism (5.6% and 6.6% vs. 0% placebo); dizziness (4.8% and 5.8% vs. 1.7% placebo); and somnolence (4.0% and 6.6% vs. 0.8% placebo).

the effect of both LATUDA doses (80 and 160 mg/day) on weight was similar to placebo: mean weight change was 0.6 kg (1.3 lbs) for both doses compared to 0.1 kg (0.2 lbs) for placebo, at Week 6/LOCF endpoint. Median changes in total cholesterol and other lipid measurements for both LATUDA doses (80 and 160 mg/day) were also similar to placebo: total cholesterol -4.0 mg/dL and -7.5 mg/dL as compared to -7.0 mg/dL placebo; and triglycerides -2.0 mg/dL and -9.0 mg/dL as compared to -9.0 mg/dL placebo, respectively, at Week 6/LOCF endpoint.

“The PEARL 3 results are an important addition to the LATUDA clinical database, and our fifth placebo-controlled trial demonstrating efficacy in schizophrenia,” said Antony Loebel, M.D., executive vice president, Clinical Research and Medical Affairs at Sunovion Pharmaceuticals Inc. “In this study once-daily LATUDA was given in the evening with food. This regimen was well-tolerated at the doses studied.”

Quetiapine XR Key Study Findings

Quetiapine XR 600 mg/day produced significantly greater improvements than placebo at Week 6 on both the PANSS total score (-27.8 vs. -10.3 placebo) and CGI-S (-1.7 vs. -0.9 placebo). a total of 79% of patients on quetiapine XR demonstrated a 20% or more improvement on the PANSS total score from baseline versus 41% on placebo at Week 6/LOCF endpoint. Quetiapine XR was associated with an overall discontinuation rate of 19% vs. 39% placebo. the most commonly reported adverse events for quetiapine XR (greater than 5% and at least twice the rate of placebo) were dizziness (13.4% vs. 1.7% placebo), somnolence (13.4% vs. 0.8% placebo), increased weight (6.7% vs. 0.8% placebo), constipation (6.7% vs 2.5% placebo); dry mouth (7.6% vs. 0.8% placebo); arthralgia (5.9% vs. 0.8% placebo) and, ?upper respiratory tract infection (5.0% vs. 0.8% placebo).

Patients given quetiapine XR reported a 2.1 kg (4.6 lbs) increase in mean weight gain vs. 0.1 kg (0.2 lbs) placebo, at Week 6/LOCF endpoint. Patients treated with quetiapine XR had a greater increase in lipid parameters versus placebo (median change: cholesterol 6.0 mg/dL vs. -7.0 mg/dL placebo; and triglycerides 8.0 mg/dL vs. -9.0 mg/dL placebo at Week 6/LOCF endpoint).

About Latuda® (lurasidone HCl) tablets

LATUDA is an atypical antipsychotic indicated for the treatment of patients with schizophrenia. the efficacy of LATUDA in schizophrenia was established in four 6-week controlled studies of adult patients with schizophrenia. the effectiveness of LATUDA for longer-term use, that is, for more than 6 weeks, has not been established in controlled studies. therefore, the physician who elects to use LATUDA for extended periods should periodically re-evaluate the long-term usefulness of the drug for the individual patient.

Dosage and Administration

the recommended starting dose of LATUDA is 40 mg once daily. LATUDA should be taken with food. Initial dose titration is not required. LATUDA has been shown to be effective in a dose range of 40 mg/day to 120 mg/day. In the 6-week controlled trials, there was no suggestion of added benefit with the 120 mg/day dose, but there was a dose-related increase in certain adverse reactions. therefore, the maximum recommended dose is 80 mg/day.

the LATUDA 160 mg/day dose has not been reviewed or approved by FDA.

IMPORTANT SAFETY INFORMATION FOR LATUDA

WARNING: INCREASED MORTALITY IN ELDERLY PATIENTS WITH DEMENTIA-RELATED PSYCHOSIS

Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death. Analyses of 17 placebo-controlled trials (modal duration of 10 weeks), largely in patients taking atypical antipsychotic drugs, revealed a risk of death in the drug-treated patients of between 1.6 to 1.7 times that seen in placebo-treated patients. Over the course of a typical 10-week controlled trial, the rate of death in drug-treated patients was about 4.5% compared to a rate of 2.6% in the placebo group. Although the causes of death were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature. LATUDA is not approved for the treatment of patients with dementia-related psychosis.

Contraindications: LATUDA is contraindicated in any patient with a known hypersensitivity to lurasidone HCl or any components in the formulation. LATUDA should not be used in combination with a strong CYP3A4 inhibitor or inducer.

Cerebrovascular Adverse Events: In placebo-controlled trials with risperidone, aripiprazole, and olanzapine in elderly subjects with dementia, there was a higher incidence of cerebrovascular adverse reactions (cerebrovascular accidents and transient ischemic attacks) including fatalities compared to placebo-treated subjects. LATUDA is not approved for the treatment of patients with dementia-related psychosis.

Neuroleptic Malignant Syndrome (NMS): NMS, a potentially fatal symptom complex, has been reported with administration of antipsychotic drugs, including LATUDA. NMS can cause hyperpyrexia, muscle rigidity, altered mental status, irregular pulse or blood pressure, tachycardia, diaphoresis, and cardiac dysrhythmia. Additional signs may include elevated creatine phosphokinase, myoglobinuria (rhabdomyolysis), and acute renal failure. Management should include immediate discontinuation of antipsychotic drugs and other drugs not essential to concurrent therapy, intensive symptomatic treatment and medical monitoring, and treatment of any concomitant serious medical problems.

Tardive Dyskinesia (TD): the risk of developing TD and the potential for it to become irreversible may increase as the duration of treatment and the total cumulative dose increase. however, the syndrome can develop, although much less commonly, after relatively brief treatment periods at low doses. Prescribing should be consistent with the need to minimize TD. If signs and symptoms appear, discontinuation should be considered.

Hyperglycemia and Diabetes Mellitus: Hyperglycemia, in some cases associated with ketoacidosis, hyperosmolar coma, or death, has been reported in patients treated with atypical antipsychotics. Patients with risk factors for diabetes mellitus who are starting treatment with atypical antipsychotics should undergo fasting blood glucose testing at the beginning of and during treatment. Any patient treated with atypical antipsychotics should be monitored for symptoms of hyperglycemia including polydipsia, polyuria, polyphagia, and weakness. Patients who develop symptoms of hyperglycemia during treatment with atypical antipsychotics should also undergo fasting blood glucose testing. In some cases, hyperglycemia has resolved when the atypical antipsychotic was discontinued; however, some patients required continuation of antidiabetic treatment despite discontinuation of the antipsychotic drug.

Weight Gain: In short-term schizophrenia studies, there were differences in mean weight gain between LATUDA-treated and placebo-treated patients. the mean weight gain was 0.75 kg for LATUDA-treated patients compared to 0.26 kg for placebo-treated patients. the proportion of patients with a ?7% increase in body weight was 5.6% versus 4.0% for placebo-treated patients. In longer-term studies (primarily open-label extension studies), LATUDA was associated with a mean change in weight of -0.38 kg at week 24 (n = 531), -0.47 kg at week 36 (n = 303) and -0.71 kg at week 52 (n = 244).

Orthostatic Hypotension, Syncope, and other Hemodynamic Effects: LATUDA may induce orthostatic hypotension and syncope. LATUDA should be used with caution in patients with known cardiovascular disease, cerebrovascular disease, or conditions that predispose them to hypotension and in the elderly. LATUDA should be used cautiously when treating patients who receive treatment with other drugs that can induce hypotension, bradycardia, respiratory or central nervous system depression. Monitoring of orthostatic vital signs should be considered in all such patients, and a dose reduction should be considered if hypotension occurs.

Leukopenia, Neutropenia, and Agranulocytosis: In clinical trial and postmarketing experience, events of leukopenia/neutropenia have been reported temporally related to antipsychotic agents. Patients with a preexisting low white blood cell count (WBC) or a history of leukopenia/neutropenia should have their complete blood count (CBC) monitored frequently during the first few months of therapy, and LATUDA should be discontinued at the first sign of a decline in WBC in the absence of other causative factors.

Hyperprolactinemia: Like other drugs that antagonize dopamine D2 receptors, LATUDA can elevate prolactin levels, and the elevation can persist during chronic administration. Galactorrhea, amenorrhea, gynecomastia, and impotence have been reported in patients receiving prolactin-elevating compounds.

In short-term placebo-controlled studies, the median change from baseline to endpoint in prolactin levels for LATUDA-treated patients was 1.1 ng/mL and was -0.6 ng/mL in the placebo-treated patients. the increase in prolactin was greater in female patients. In the longer-term studies (primarily open-label extension studies), LATUDA was associated with a median change in prolactin of -1.9 ng/mL at week 24 (n = 188), -5.4 ng/mL at week 36 (n=189) and -3.3 ng/mL at week 52 (n = 243).

Seizures: LATUDA should be used cautiously in patients with a history of seizures or with conditions that lower seizure threshold (eg, Alzheimer’s dementia).

Dysphagia: Esophageal dysmotility and aspiration have been associated with antipsychotic drug use. Aspiration pneumonia is a common cause of morbidity and mortality in elderly patients, in particular those with advanced Alzheimer’s dementia. LATUDA is not indicated for the treatment of dementia-related psychosis, and should not be used in patients at risk for aspiration pneumonia.

Potential for Cognitive and Motor Impairment: Somnolence and sedation were reported in patients treated with LATUDA. Patients should be cautioned about performing activities requiring mental alertness, such as operating hazardous machinery or operating a motor vehicle, until they are reasonably certain that LATUDA therapy does not affect them adversely.

Body Temperature Regulation: appropriate care is advised when prescribing LATUDA for patients who will be experiencing conditions that may contribute to an elevation in core body temperature, e.g., exercising strenuously, exposure to extreme heat, receiving concomitant medication with anticholinergic activity, or being subject to dehydration.

Suicide: the possibility of suicide attempt is inherent in psychotic illnesses. Close supervision of high-risk patients should accompany drug therapy. Prescriptions for LATUDA should be written for the smallest quantity of tablets in order to reduce the risk of overdose.

Alcohol: Patients should be advised to avoid alcohol while taking LATUDA.

Commonly Observed Adverse Reactions (?5% and at least twice that for placebo): the most commonly observed adverse reactions associated with the use of LATUDA versus placebo in short-term clinical studies were somnolence, akathisia, nausea, parkinsonism, and agitation.

before prescribing LATUDA, please read the full Prescribing Information, including Boxed Warning.

About Sunovion Pharmaceuticals Inc. (Sunovion)

Sunovion is a leading pharmaceutical company dedicated to discovering, developing and commercializing therapeutic products that advance the science of medicine in the central nervous system (CNS) and respiratory disease areas and improve the lives of patients and their families. Sunovion’s drug development program, together with its corporate development and licensing efforts, has yielded a portfolio of pharmaceutical products including LATUDA® brand lurasidone HCl, LUNESTA® brand eszopiclone, XOPENEX® brand levalbuterol HCl Inhalation Solution, XOPENEX HFA® brand levalbuterol tartrate inhalation aerosol, BROVANA® brand aformoterol tartrate inhalation solution, OMNARIS® brand ciclesonide nasal spray and ALVESCO® brand ciclesonide HFA inhalation aerosol.

Sunovion, an indirect, wholly-owned subsidiary of Dainippon Sumitomo Pharma Co., ltd., is headquartered in Marlborough, Mass. more information about Sunovion Pharmaceuticals Inc. is available at sunovion.com.

About Dainippon Sumitomo Pharma Co., ltd. (DSP)

DSP is a multi-billion dollar, top-ten listed pharmaceutical company in Japan with a diverse portfolio of pharmaceutical, animal health and food and specialty products. DSP aims to produce innovative pharmaceutical products in the CNS field, which has been designated as the key therapeutic area and will also focus in on other specialty disease categories with significant unmet medical needs, which are designated as frontier therapeutic areas. DSP is based on the merger in 2005 between Dainippon Pharmaceutical Co., ltd., and Sumitomo Pharmaceuticals Co., ltd. Today, DSP has more than 7,000 employees worldwide. Additional information about DSP is available through its corporate website at ds-pharma.com.

LATUDA® is a registered trademark of Dainippon Sumitomo Pharma Co., ltd. LUNESTA, XOPENEX, XOPENEX HFA and BROVANA are registered trademarks of Sunovion Pharmaceuticals Inc. OMNARIS and ALVESCO are registered trademarks of Nycomed GmbH.

* Manufactured by AstraZeneca.

for a copy of this release or any recent release,

visit Sunovion’s web site at sunovion.com.