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In the study, one week of dosing CRx-170 demonstrated a statistically significant mean percentage improvement (increase) in FEV1 from the treatment baseline of the study of approximately 6% (p=0.045). Neither low dose nortriptyline as a single agent nor low dose budesonide as a single agent showed significant improvement in FEV1 from the separate study baseline used to evaluate the single agents (approximately 2% decrease for low dose nortriptyline, p=0.466; approximately 5% decrease for low dose budesonide, p=0.251). In the wheal and flare skin test, otherwise known as the Late Allergen Response (LAR), CRx-170 decreased the area of LAR by more than 50% (p=0.053). CRx-170 did not show a modulation of the inflammatory marker CD163 from the treatment baseline, although nortriptyline clearly did decrease CD163 on its own. Analysis of additional measurements and the final analysis of these data is ongoing. The most common adverse events related to CRx-170 were dry mouth, drowziness, constipation and headache; known effects of nortriptyline.
“The observed effect of CRx-170 in such a short period of dosing, as measured by FEV1, the most clinically relevant endpoint and generally accepted measure of clinical activity, suggests that CRx-170 may have potential as a novel agent for the treatment of pulmonary diseases such as asthma and COPD,” said Dr. Jan Lessem, Chief Medical Officer of CombinatoRx. “Given these signals of clinical activity and observed immunological activity, CRx-170 certainly merits further clinical studies.”
“This proof of concept trial provides another successful translation of our discovery technology into positive clinical results” commented Alexis Borisy, President and CEO of CombinatoRx. “We are pleased to see the activity of CRx-170 where the low doses of these individual agents have not shown clinical activity, and we look forward to the continuing development of the CombinatoRx pipeline.”
About the Trial Design
This clinical trial was conducted over an approximately 17-week per patient period and was a single center, single blind, dose de-escalation study. The proof-of-concept phase 2 study was primarily descriptive in design, with a change in circulating monocyte CD163, an inflammatory marker, designated as its primary endpoint. Secondary endpoints of the study included clinical measures such as spirometry (i.e., FEV1), evening peak expiratory flow, and the use of rescue medication and reduction in other inflammatory markers including wheal and flare response.
Patients were sequentially treated with decreasing oral doses of nortriptyline and budesonide as single agents, with washout periods between each treatment, followed by 1-week treatment with nortriptyline and 1-week with CRx-170. During the nortriptyline alone and budesonide alone phases, changes in FEV1 were measured versus study baseline, which was set on the first day of dose de-escalation of nortriptyline as a single agent. During the CRx-170 treatment phase, changes in FEV1 were measured from treatment baseline, which was set following the last washout from the single agent dosing period. During the treatment period with CRx-170, patients were given 3 mg of budesonide orally and the lowest dose of nortriptyline from the de-escalation phase.
Patients with mild allergic asthma were enrolled in the trial. To be eligible, patients had to have a history of bronchial asthma for at least 6 months as defined by ATS criteria, a positive wheal and flare skin test response to allergens, and FEV1 greater than or equal to 60% of the predicted FEV1. Of the nineteen patients enrolled, seventeen completed treatment.
About CRx-170
CRx-170 is a novel, orally available syncretic drug candidate in Phase 2 clinical development. A syncretic drug comprises two compounds that are designed to act synergistically through multiple pathways to provide a novel therapeutic effect which neither component alone can achieve. CRx-170 contains a low dose of the steroid budesonide and a low dose of nortriptyline. The target product profile for CRx-170 is to selectively amplify certain elements of budesonide’s anti-inflammatory and immunomodulatory activities, without replicating its side effects. CRx-170 was discovered using the CombinatoRx proprietary combination High Throughput Screening (cHTS(TM)) technology. We plan to develop CRx-170 in a unique formulation for the treatment of pulmonary or additional immuno-inflammatory diseases. CRx-170 is one of a portfolio of six product candidates that CombinatoRx is currently testing in phase 2 clinical trials.

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In addition, the invesigators found that venlafaxine given in high doses (225-300 mg/day) had a slightly better side-effect profile than nortriptyline (25-50 mg/day).
COPYRIGHT 2003 International Medical News Group
COPYRIGHT 2008 Gale, Cengage Learning

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However, 29 (60%) of the 48 smokers in the nortriptyline group with a high level of nicotine addiction quit smoking, which was significantly higher than 4 (7%) of 57 similar smokers in the placebo group.
COPYRIGHT 2002 International Medical News Group
COPYRIGHT 2008 Gale, Cengage Learning

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Only 7% of patients with Parkinson’s disease and depression are on a tricyclic antidepressant, noted Dr. Menza, professor of psychiatry and neurology at the University of Medicine and Dentistry of New Jersey, Newark.
More research is needed to confirm these pilot results and to provide guidance to clinicians on treating depression in Parkinson’s disease, he added.
The National Institute of Neurological Disorders and Stroke funded the study. Dr. Menza has been a consultant or speaker or received research grant support from Eli Lilly & Co., which makes a brand of nortriptyline, and for GlaxoSmithKline, which makes paroxetine CR and provided the drug and matching placebo for the study.
The study randomized patients to 8 weeks of blinded treatment with nortriptyline, paroxetine CR, or placebo. Approximately a third of the patients in each group discontinued treatment before the end of the trial, including 29% on nortriptyline, 39% on paroxetine CR, and 35% on placebo. Of those who completed the study, the average dose by the end of 8 weeks was 63 mg/day nortriptyline, 32 mg/day paroxetine CR, or two pills of placebo.
The nortriptyline group showed better results on the two primary end points–Hamilton Depression Rating Scale (HAM-D) scores and the proportion that showed a response to therapy, Dr. Menza and his associates reported.
Scores on the HAM-D changed by about 11 points in the nortriptyline group, 7 in the paroxetine CR group, and 3 in the placebo group. The differences between the nortriptyline and paroxetine groups were significant at weeks 2 and 4, with a trend toward significance at week 8. Scores in the nortriptyline group were significantly different from those in the placebo group at all visits.
The proportion of patients who responded to therapy was 53% in the nortriptyline group, 11% in the paroxetine group, and 24% in the placebo group. The nortriptyline response rate was significantly higher, compared with the paroxetine group, but not compared with placebo.
The total number of side effects did not differ significantly between groups, but the nortriptyline group had more anticholinergic effects, including constipation and dry mouth. No worsening in cognition or movement was seen.
Among the patients who showed an improvement in depression scores, 20 continued therapy in a 4-month blinded extension period after the 8 weeks ended. Two measures suggested that quality of life improved in these patients, whose depression improved, compared with baseline, he said.
The study excluded patients with dementia, psychosis, or motor fluctuations. Patients averaged 62 years in age and had had Parkinson’s disease for 6 years on average. The cohort included 25 women and 27 men.
From 40% to 50% of the approximately 1 million U.S. residents with Parkinson’s disease have a major depressive disorder or dysthymia. Depression often precedes motor impairment in the disease.
In two small previous trials of 12 and 37 patients with Parkinson’s disease, an SSRI showed no advantage over placebo in treating depression, he said. A few double-blind trials of other antidepressive agents were poorly designed, with significant methodological problems, he added.
BY SHERRY BOSCHERT San Francisco Bureau
COPYRIGHT 2008 International Medical News Group
COPYRIGHT 2008 Gale, Cengage Learning

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This finding comes on the heels of evidence that bupropion, a dopamine-enhancing drug but not a tricyclic, also increases abstinence in those trying to quit cigarettes (SN: 11/15/97, p. 319). Bupropion, which is more expensive than nortriptyline, has been approved by the Food and Drug Administration for use in programs to help people stop smoking.
“The outcome data suggest that nortriptyline is a useful adjunct to smoking cessation efforts,” Hall and her coworkers conclude in the August Archives of General Psychiatry.
Through public service and newspaper ads, the scientists recruited 199 men and women, all of whom smoked 10 or more cigarettes daily. None exhibited symptoms of major depression, but 65 had been diagnosed with it previously.
Volunteers were randomly assigned to nortriptyline or placebo treatment. All attended eight weekly group sessions that focused either on monitoring abstinence efforts or promoting positive thoughts and activities linked to a nonsmoking way of life. These group sessions took place during the last 2 months of treatment, allowing nortriptyline the several weeks required to begin exerting its effects.
Abstinence was confirmed by urine analyses at the end of treatment and at three points during the following year.
Among participants with no history of depression, slightly more than 40 percent of those who received nortriptyline remained abstinent after 1 year. Around one-quarter of those who received placebos ended up cigarette-free. In neither case was there a difference attributable to which group sessions participants had attended.
Among previously depressed volunteers, the type of group sessions made a difference. About one-third of those who attended sessions that emphasized mood-boosting strategies were abstinent after 1 year in both the nortriptyline and placebo groups. Those who attended the other type of sessions achieved much lower abstinence rates, regardless of which type of pill they had received.
Self-reported mood in the first 3 days after quitting cigarettes was brighter for those who took the antidepressant, which may have increased their likelihood of achieving short-term abstinence.
However, it’s tough to give up cigarettes for good. A majority of participants, including those given nortriptyline, resumed smoking after 1 year.
Scientists need to look for specific dopamine-enhancing actions of nortriptyline and bupropion that influence smoking abstinence, holds psychiatrist Alexander H. Glassman of Columbia University in a commentary accompanying Hall’s findings. Indirect evidence for a dopamine role comes from three unpublished clinical trials, conducted several years ago, which found that Prozac and related serotonin boosters offer no help to those trying to quit cigarettes, Glassman says.
Drugs such as nortriptyline may help cigarette smokers negotiate the long process of dumping their habit, which typically includes seven or eight unsuccessful attempts, comments psychiatrist John R. Hughes of the University of Vermont in Burlington.
“Nortriptyline and bupropion treatment may prompt more quitting attempts by smokers,” Hughes says. “Every time someone quits and fails, they learn something about their cigarette cravings that makes them more likely to quit for good on the next try.”
COPYRIGHT 1998 Science Service, Inc.
COPYRIGHT 2008 Gale, Cengage Learning

With failed dieting and cardio workout, the diet pills remain the most preferred approach for the bulky ones. The weight loss pills like Phentermine act as appetite suppressants and have reported great results. Before knowing the nitty-gritty of the drug, the patients buy Phentermine online. The cheap Phentermine available with online pharmacies lure the patients and in the process, they become a victim of their own follies. Phentermine is a prescription pill used for short-term treatment of obesity. Consequently, a proper physical examination by a qualified doctor is a vital pre-requisite before buying Phentermine.

Your doctor needs to know his patient better in order to prescribe an effective treatment plan. Before taking Phentermine, your doctor must know the following particulars about his patient -
His agitated states,
Any allergy to sympathomimetic amines,
Any anxiety disorder,
The existence of arteriosclerosis (hardening of the arteries),
If breast-feeding,
Any cardiovascular disease,
If diabetic,
Any emotional problems,
Epilepsy or another seizure disorder,
Glaucoma,
Any heart disease,
High blood pressure,
History of drug abuse,
Hyperthyroidism,
Pregnancy,
Any thyroid problems

The doctor also needs to know if you are taking any of the following medicines -
Amitriptyline
Amoxapine
Clomipramine
Desipramine
Doxepin
Furazolidone
Guanethidine
High blood pressure medicine
Imipramine
MAO inhibitors
Monoamine oxidase
Nortriptyline
Phenelzine
Protriptyline
Selegiline
Tranylcypromine
Tricyclic antidepressant

A common man might not have the knowledge about the generic drugs. The safe bet is to tell your doctor every medicine you are taking or have taken in the recent past or planning to take.

In case of consultation regarding side effects, tell your doctor if you experience any of the following reactions so that proper medical attention could be diverted in order to minimize the side effects -
Anxiety
Chest pain
Breathing difficulties
Constipation
Diarrhea
Difficulty urinating
Dizziness
Headache
Mood changes
Nervousness, restlessness or tremor
Swelling
Impotence or changes in your sex drive.

The importance of a doctor in the use of prescribed medicines can never be overstated. He is the appropriate and legal agony aunt for your Phentermine problems.

The various options for the treatment of depression varies from medication to psychotherapy to self help. Study suggests relaxation techniques may improve symptoms of depression (definitely in the case of mild depression).

Talking to someone close to you can go a long way in keeping away the blues. Your spouse/partner, your parents, your siblings or your close friends can be your pillar of strength during this depressive phase. Always remember those who love you, will not judge you based on your weaknesses and will definitely give you the support you need.

The biggest problem with depression is how it affects the lives of those who live or work with the person with the condition; now after many years of research, medicine has recognized a number of types all with slightly different symptoms. Even though there are number of types, they are all based around some issue in the life of the affected person that has never been resolved; almost every person will suffer from it (usually to a lesser degree) from time to time during their lives.

Depressive illnesses make you feel exhausted, worthless, helpless and hopeless. Such negative thoughts and feelings make some people feel like giving up. It is important to realize that these negative views are part of the depression and typically do not accurately reflect your situation. Negative thinking fades as treatment begins to take effect.

In a therapy process, the person is exposed to a therapist who advices the patient to balance his thoughts. The depressed person can also consult a doctor and prescribe suitable drugs to deal with different cases of depression. People are often hospitalized so that they do not hurt themselves being influenced by their own depression. Proper care is taken for them. In severe cases shock treatment is also used. The patient is given electric shocks to let out the internal shocks which are caused by the depression.

If there is no obvious cause for the depression, or if reactive depression persists longer than might be expected, or if you are having suicidal thoughts, more aggressive therapy is needed. This means drug therapy and, possibly, hospitalization. The mainstay of drug treatment has long been a group of medications called tricyclic antidepressants, including amoxapine (Asendin), clomipramine (Anafranil), desipramine (Norpramin), imipramine (Tofranil), and nortriptyline (Aventyl, Pamelor). These drugs do not take effect immediately, so a test period of at least two weeks is necessary to determine whether they are working.

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Introduction
Post-herpetic neuralgia (PHN) is a painful and debilitating disease. Despite major advances in its treatment and prevention, management of PHN patients remains a challenge. In this clinical review of PHN, we will examine recent advances in treating and preventing PHN. We will also focus on early treatments of herpes zoster (HZ) and the exciting varicella vaccines for children and adults.
What Is Post-Herpetic Neuralgia?
PHN is a complication of infection by the varicella zoster virus (VZV). During an early infection by primary varicella, some of the virus latently infects sensory ganglia. Later reactivation of the dormant virus, called HZ, results in shingles and sometimes severe and debilitating pain. Viral reactivation is more common in the immunocompromised and elderly, but the specific triggers are unknown.
HZ is a significant medical problem with 500,000 to 1,000,000 cases annually in the US. Age is a risk factor for HZ; the majority of patients are older than age 50. The age-related decline in cell-mediated immunity to the latent VZV is a likely factor. Age is also an important risk factor for PHN. In one report, at least 40% of HZ patients over age 50 and 75% of those over age 70 developed PHN. (1) Interestingly, HIV, which leads to immunocompromise, increases the incidence of HZ but not of PHN.
HZ results when latent VZV is reactivated in neurons and spreads to the skin through the peripheral nerves. The pain associated with HZ and PHN begins with peripheral nerve injury. Peripheral nerves have low activation thresholds and exhibit exaggerated responses to stimuli. The resulting peripheral nerve damage increases activity in the central nervous system pain transmission neurons, so that both peripheral and central pathophysiological mechanisms contribute to PHN pain. The pain can be paroxysmal or steady, deep aching, burning, stabbing, shooting, or electric shock-like. Hyperalgesia, allodynia, and severe pruritus, with or without pain, may also occur.
Surprisingly, PHN lacks a standard definition in the literature. A frequently cited definition is pain lasting longer than 3 months after the acute inflammatory phase of HZ. (2) Other definitions include pain that persists or develops after the lesions of HZ have healed or pain lasting one month to 6 months after the onset or healing of lesions. Some advocate replacing the term PHN with “zoster-aggravated pain,” which describes any pain associated with HZ. (3) I suggest that PHN is a common and intractable neuropathic pain after HZ.
Treatment
Topical, systemic, and nonpharmacologic therapies have been used to treat PHN. The major therapeutic advances have been the 5% lidocaine patch, opioid analgesics, nortriptyline and amitriptyline, and gabapentin. All of these therapies have been based on the results of randomized controlled trials. (4)
Topical and Local Therapies
Topical therapy is considered when the disease is mild or systemic therapy is contraindicated, or as an adjuvant therapy to systemic treatment. Historically, topical aspirin and nonsteroidal anti-inflammatory preparations (NSAIDS) were used, but they were of limited benefit because studies did not show them to be superior to placebo. More recently, capsaicin and topical anesthetics have been used, including a eutectic mixture of local anesthetics (EMLA), 5% lidocaine patch, and local anesthetics via subcutaneous, intravenous, epidural, and intercostal routes.
Capsaicin is the active principle of hot chili peppers (5) and causes initial release and subsequent depletion of substance P, which is a transmitter of painful stimuli in C fibers. Recommended use is 4 to 5 times daily for 4 to 5 weeks. Patients experience some initial burning and hyperalgesia from the first release of substance P. The pain causes 30% of patients to discontinue its use. However, pretreatment with EMLA can decrease these symptoms and, with repeated treatments, the burning and hyperalgesia are replaced with hypogeusia, as substance P is depleted. In one study, after 6 weeks of treatment, 50% of patients experienced 40% pain relief. (6)