Related Results

Metoclopramide and akathisiaA case of metoclopramide-induced oculogyric crisis in a 16-year-old girl with…Migraine role seen for metoclopramideMetoclopramide works well for adult migraineMetoclopramide may suppress Tourette’s tics

The average dose after 8 weeks was 32.9 mg. Adverse events were mild; the most common was increased appetite, but weight gain did not differ significantly from that in the placebo group. One patient had a 30-fold increase in prolactin levels that resolved with discontinuation of the drug at the study’s end.
COPYRIGHT 2005 International Medical News Group
COPYRIGHT 2008 Gale, Cengage Learning

Related Results

Metoclopramide and akathisiaA case of metoclopramide-induced oculogyric crisis in a 16-year-old girl with…Migraine role seen for metoclopramideMetoclopramide works well for adult migraineMetoclopramide treats Tourette’s

Both typical and atypical antipsychotic agents generally are highly effective at suppressing tics. Their usefulness, however, is severely limited by numerous adverse effects, including cognitive dulling, anxiety, depression, and affective flattening.
Since patients with Tourette’s syndrome do not have psychotic symptoms, a more specific therapy would be welcome, Dr. Acosta said.
Although metoclopramide usually is thought of as a gastric motility agent, it is classified as a neuroleptic but is seldom used in psychiatric practice.
Even at a substantial dose of 1,000 mg/day, the drug is only minimally effective at reducing psychotic symptoms.
Metoclopramide has a propensity to produce extrapyramidal side effects but seems to be relatively sparing of cognitive and prefrontal circuits. This striking anatomic selectivity is what led Dr. Acosta and her associates to consider metoclopramide as a potential tic-suppressing agent with possible advantages over the typical and atypical antipsychotics.
The drug was well tolerated in the open-label study Nine of the 10 patients were younger than 18 years of age.
They were titrated to a mean effective dose of 39.5 mg/day given b.i.d. or t.i.d. At that dose, side effects consisted of transient sleepiness in a total of four patients.
COPYRIGHT 2002 International Medical News Group
COPYRIGHT 2008 Gale, Cengage Learning

Related Results

Metoclopramide and akathisiaA case of metoclopramide-induced oculogyric crisis in a 16-year-old girl with…Migraine role seen for metoclopramideMetoclopramide works well for adult migraineMetoclopramide treats Tourette’s

Dr. Singh and his associates at the University of Missouri-Columbia have used this technique on 750 patients and have diagnosed gastroparesis–defined as a gastric emptying half-time of over 100 minutes-in 168.
After measuring each patient’s baseline gastric emptying halftime, they administered a 10-mg IV dose of metoclopramide and measured the gastric emptying half-time again. The mean gastric emptying half-time went from 348 minutes to 104 minutes, with 81% of patients experiencing more than a 50% decrease in gastric emptying half-time following the metoclopramide injection.
The overall response to metoclopramide was excellent in men and women, but men had a slightly better response, Dr. Singh reported.
A poor response, defined as a gastric emptying half-time decrease of less than 34%, was noted in 16% of the patients.
These patients were not considered candidates for metoclopramide therapy.
Dr. Singh suggested a gastric emptying half-time reduction of 50% or more as the guiding criterion for determining whether a patient is likely to have a good response to treatment with metoclopramide.
COPYRIGHT 2002 International Medical News Group
COPYRIGHT 2008 Gale, Cengage Learning

Related Results

Metoclopramide and akathisiaA case of metoclopramide-induced oculogyric crisis in a 16-year-old girl with…Metoclopramide works well for adult migraineMetoclopramide treats Tourette’sMetoclopramide may suppress Tourette’s tics

The drug was almost three times as effective as placebo for pain and nausea reduction, but not as effective as other phenothiazine antiemetics (prochlorperazine and chlorpromazine). Metoclopramide compared favorably with ibuprofen and sumatriptan, but there was not enough evidence to determine relative effectiveness, the investigators said (BMJ 2004;329:1369-73).
The combination studies suggested that metoclopramide might also be effective as an adjunctive treatment. Several of those studies showed that metoclopramide combinations were similarly, and more, effective for pain relief than were the comparison regimens.
“Given its nonnarcotic and antiemetic properties, metoclopramide should be considered as a primary agent in the treatment of acute migraine in emergency departments,” they said.
COPYRIGHT 2005 International Medical News Group
COPYRIGHT 2008 Gale, Cengage Learning

Related Results

Metoclopramide and akathisiaA case of metoclopramide-induced oculogyric crisis in a 16-year-old girl with…Migraine role seen for metoclopramideMetoclopramide works well for adult migraineMetoclopramide treats Tourette’s

The other patient, a 74-year-old man with a history of diabetes and CVA, took metoclopramide for gastrointestinal discomfort. After six months, metoclopramide was discontinued; within 12 hours, he experienced anxiety, restlessness, sleep disturbance, and hallucinations. After three days of these symptoms, he underwent a psychiatric evaluation. Once again, risperidone was prescribed and his psychosis symptoms ended.
COPYRIGHT 2003 Vegetus Publications
COPYRIGHT 2003 Gale Group

Dr. Sirgo has over 25 years pharmaceutical industry experience
spanning clinical drug development, executive management, business
development, marketing and sales. He currently serves as President and
Chief Executive Officer of BioDelivery Sciences International
(NASDAQ:BDSI), and previously held positions with Arius
Pharmaceuticals, Pharmaceutical Product Development (PPD) and
GlaxoSmithKline. Dr. Sirgo received his BS in Pharmacy from The Ohio
State University and his Doctorate from Philadelphia College of
Pharmacy and Science.

“We are very pleased to welcome Mark to the Salix Board,”
commented John Chappell, Chairman, Salix Pharmaceuticals. “Mark’s
depth and breadth of experience and skills, particularly his proven
abilities in the oversight and execution of clinical development,
should serve the Board and Company well. We look forward to Mark’s
contributions.”

Salix Pharmaceuticals, Ltd., headquartered in Raleigh, North
Carolina, develops and markets prescription pharmaceutical products
for the treatment of gastrointestinal diseases. Salix’s strategy is to
in-license late-stage or marketed proprietary therapeutic drugs,
complete any required development and regulatory submission of these
products, and market them through the Company’s gastroenterology
specialty sales and marketing team.

Salix markets COLAZAL(R) (balsalazide disodium) Capsules 750 mg,
XIFAXAN(R) (rifaximin) tablets 200 mg , OSMOPREP(R) (sodium phosphate
monobasic monohydrate, USP and sodium phosphate dibasic anhydrous,
USP) Tablets, MOVIPREP(R) (PEG 3350, Sodium Sulfate, Sodium Chloride,
Potassium Chloride, Sodium Ascorbate and Ascorbic Acid for Oral
Solution), VISICOL(R) (sodium phosphate monobasic monohydrate, USP,
and sodium phosphate dibasic anhydrous, USP) Tablets, PEPCID(R)
(famotidine) for Oral Suspension, Oral Suspension DIURIL(R)
(Chlorothiazide), AZASAN(R) Azathioprine Tablets, USP, 75/100 mg ,
ANUSOL-HC(R) 2.5% (Hydrocortisone Cream, USP), ANUSOL-HC(R) 25 mg
Suppository (Hydrocortisone Acetate), PROCTOCORT(R) Cream
(Hydrocortisone Cream, USP) 1% and PROCTOCORT(R) Suppository
(Hydrocortisone Acetate Rectal Suppositories) 30 mg. Current
development projects include balsalazide tablet,
metoclopramide-Zydis(R), encapsulated mesalamine granules, vapreotide
acetate, and rifaximin for additional indications.

For full prescribing information on Salix products, please visit
www.salix.com or contact the Company at 919 862-1000.

Salix trades on the NASDAQ Global Select Market under the ticker
symbol “SLXP.”

For more information please visit our web site at www.salix.com.
Information on our web site is not incorporated in our SEC filings.

Please Note: This press release contains forward-looking
statements regarding future events. These statements are just
predictions and are subject to risks and uncertainties that could
cause the actual events or results to differ materially. These risks
and uncertainties include risks of regulatory review and clinical
trials, potential generic and other competition, market acceptance for
approved products, intellectual property risks, the need to acquire
additional products and management of rapid growth. The reader is
referred to the documents that the Company files from time to time
with the Securities and Exchange Commission.

Zingiberaceae

Common Trade Names

Multi-ingredient preparations: Cayenne Ginger, Gingerall, Ginger Ease, Ginger Peppermint Combo, Ginger Power, Ginger Root Alcohol Free, Ginger Trips, Low Alcohol Misty Ginger Blend

Common Forms

Capsules, liquid, powder: 100 mg, 465 mg

n
Extract: 250 mg

Root: 530 mg

Tablets (chewable): 67.5 mg Also available as teas.

Source

Ginger (Zingiber officinale) is a perennial that grows in India, Jamaica, and China. The plant produces green-purple flowers that resemble orchids. The rhizome (root) is found underground and usually the most valued part of the plant.

Chemical Components

The root contains both volatile and nonvolatile compounds. The nonvolatile constituents, which include the gingerols and gingerol-like compounds, are thought to be responsible for ginger’s flavor, aromatic properties, and any pharmacologic activity. The volatile oil contains zingiberol, zingeberene, curcumene, farnesene, bis-abolene, sesquiphellandrene, and several monoterpenes (linalool, borneol, neral, geraniol, and others). Other compounds present are zingibain (a proteolytic enzyme), oleoresins, fats, waxes, carbohydrates, vitamins, and minerals.

Actions

Human studies have shown that ginger inhibits platelet aggregation induced by adenosine diphosphate and epinephrine . Other studies have demonstrated a lack of effects on platelet aggregation . Ginger extracts have documented anti-inflammatory effects in rodent models . Specific components of ginger produce varying CV effects. Methanolic extracts of ginger have shown positive inotropic effects in a guinea pig model.

Other studies in animals have suggested that components in ginger may be gastroprotective against various chemical insults and stressors. The GI protective action is postulated to be promoted by increased mucosal resistance and potentiation of the defensive mechanism against chemicals or alterations in prostaglandins, providing more protective effects. A study of acetone extracts in mice found them to have similar stimulatory effects on GI motility as those seen with metoclopramide and domperidone .

Reported Uses

Claims for ginger include its use as an antiemetic, an anti-inflammatory useful for arthritis treatment, an antioxidant, an antitumorigenic drug, a CV stimulant, and a GI protectant and as a therapy for microbial and parasitic infestations.

The antiemetic effects of ginger have been extensively studied in humans for morning, motion, and sea sickness and for postoperative nausea and vomiting; most findings provided support for this action. Doses and duration of therapy varied considerably with each study. The antiemetic properties of ginger probably result from local effects on the GI tract rather than the CNS. Increased gastric peristalsis has been shown in animals, but any mechanism in humans is considered speculative.

Ginger has provided relief from pain and swelling in patients with muscle discomfort, osteoarthritis, or rheumatoid arthritis . A proposed mechanism is that it inhibits prostaglandin, thromboxane, and leukotriene biosynthesis.

Dosage

Dosage forms and strength vary with each disease state. As an antiemetic, studies used 500 to 1,000 mg of powdered ginger P.O., or 1,000 mg of fresh ginger root P.O.

Adverse Reactions

CNS: CNS depression (with overdose).

CV: arrhythmias (with overdose).

GI: heartburn.

Interactions

Anticoagulants: Increased risk of bleeding. Avoid administration with ginger.

Contraindications And Precautions

Ginger is contraindicated in pregnant patients; effects are unknown. Some components of ginger have been determined to be mutagenic, whereas others appear to exert an antimutagenic effect. The net effect of these components is unknown . Use only under medical supervision in patients receiving anticoagulants because it may affect bleeding time by inhibiting platelet function.

Special Considerations

Advise women to avoid excessive use of ginger during pregnancy.

Instruct the patient to watch for signs of bleeding when taking ginger.

No consensus exists with respect to dosing and monitoring.

Commentary

Although some data support the use of ginger as an antiemetic in humans, results from several trials have conflicted. Recommendation of ginger for use as an antiemetic, an anti-inflammatory, or a gastroprotective agent, before long-term, controlled, pharmacologic studies of its constituents have been conducted, is premature. Pregnant women should probably avoid excessive consumption of ginger until the effects of all its constituents are understood.

Since the gene that is altered is carried on a mothers X chromosome, her sons have a 50 percent chance of inheriting the disorder and her daughters have a 50 percent chance of being a carrier. Some women who carry the genetic mutation may have symptoms of the disease.

As is expected in X-linked disorders, males with deleterious mutations have little-to-no residual a-Gal A activity. Therefore, these patients experience the full spectrum of disease symptoms. Because of random X inactivation (lyonization), the disease presentation in female carriers is more variable and depends on the normal-to-mutant ratio of a-Gal A in the different tissues. A significant number of female carriers may develop Fabry diseaserelated symptoms, including acroparesthesias, GI symptoms, renal and cardiac disease, and/or stroke.

Symptoms include anhidrosis, fatigue, and red spots on skin. Some of the most common pathological symptoms includes skin lesions (angiokeratomas), and a burning pain of the extremities. This pain can become very intense, especially when one has a fever. Angiokeratomas are tiny, painless papules that appear at any region of the body, but are predominant on the thighs, buttocks, lower abdomen, and groin. Ocular involvement may be present showing cornea verticillata (also known as vortex keratopathy); this corneal whorling does not have any effect on vision or eye function. Symptoms are typically first experienced in early childhood and can be very difficult to understand; the rarity of Fabry disease to many clinicians sometimes leads to misdiagnoses or ignorance.

When young patients present with signs and symptoms of a stroke, along with a history of skin lesions, renal insufficiency or failure, and heart attacks, Fabry disease is a consideration. Recent research suggests that Fabry mutations may be more frequent than previously thought in cryptogenic stroke patients, but these patients invariably had other signs of Fabry disease including proteinuria and acroparesthesias.

The diagnosis of Fabry disease has considerable implications regarding treatment, management, and counseling. Specifically, physicians may be alert to the involvement of other organs besides those of the CNS and thus make early intervention possible. With early identification, counseling and prenatal diagnosis may be offered to family members.

Fabry disease include episodes of pain, particularly in the hands and feet (acroparesthesias); clusters of small, dark red spots on the skin called angiokeratomas; a decreased ability to sweat (hypohidrosis); cloudiness of the front part of the eye (corneal opacity); and hearing loss. Fabry disease also involves potentially life-threatening complications such as progressive kidney damage, heart attack, and stroke. Milder forms of the disorder may appear later in life and affect only the heart or kidneys.

A number of patients have gastrointestinal difficulties characterized by frequent bowel movements shortly after eating. This disorder is due to a deficiency of a lipid breakdown enzyme known as ceramidetrihexosidase, also called alpha-galactosidase A. Its function is to cleave to a molecule of galactose from a lipid that arises primarily from old red blood cells. The pain in the hands and feet usually responds to medications such as Tegretol (carbamazepine) and dilantin. Gastrointestinal hyperactivity may be treated with metoclopramide or Lipisorb (a nutritional supplement).

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The initiation of early gastric enteral nutrition (EN) in critically ill patients increases secretion of mucosal immune factors and enhances the integrity of the gastrointestinal wall to limit septic complications and possibly decrease the overall cost and length of intensive care unit (ICU) and hospital stays.1-4 Consequently, expert opinions recommend initiating EN within 24 hours of ICU admission.5-7 Only 42%-76% of critically ill patients achieve goal caloric rate and 43%-63% of patients are unable to tolerate gastric EN.8-17 The development of high gastric residual volumes (GRV) impedes the delivery of gastric EN, occurring in 30%-51% of patients.8-17 Patients with high GRV are at increased risk of aspiration and have lengthened ICU stays and higher mortality rates.17
Gastrointestinal motility dysfunction is the primary reason for intolerance and is associated with several factors, including medications (opioid agonists, dopamine), hyperglycemia, electrolyte disturbances, ischemia/ hypoxia, burns, trauma, surgery, sepsis, increased intracranial pressure, and the administration of calorically dense or hyperosmolar formulas.18-21 Impaired motility is attributed to alterations of the interstitial cells of Cajal, which are concentrated in the gastric antrum and act as the “pacemaker” of gastrointestinal motility and disturbances of the interdigestive motility pattern known as the migrating motor complex.22,23
Most experts recommend monitoring GRV as a method of assessing gastrointestinal motility and initiating therapy with a prokinetic agent (erythromycin or metoclopramide) when these volumes are elevated.4-7,20,21, 27 Unfortunately, definitions of elevated GRV vary widely across recommendations and studies, likely because data in ICU patients relating gastrointestinal motility function to GRV are few. Studies have demonstrated that prokinetic agents enhance motility and reduce GRV in ICU patients with intolerance to facilitate EN administration, but other clinical outcomes, such as aspiration, have not been adequately studied.28-33 The purpose of this study was to comparatively evaluate gastric emptying function, using the acetaminophen absorption method34,35 in patients with limited GRV and in those with increased GRV, and to subsequently determine if prokinetic therapy improves gastric motility in patients with intolerance.
MATERIALS AND METHODS
Patients
The study protocol was approved by the institutional review board of the University of Colorado at Denver and Health Sciences Center. Patients were enrolled from 1 of 3 ICUs at the University of Colorado Hospital (16-bed medical ICU, 16-bed surgical ICU, and 8-bed neurologic ICU), resulting in a heterogeneous study population. Written informed consent and authorization in compliance with the Health Insurance Portability and Accountability Act were obtained from the patient or next of kin/legal representative.
Critically ill, mechanically ventilated patients between the ages of 18 and 85 years were eligible for enrollment if they were receiving continuous naso- or orogastric administration of EN and were either tolerant or intolerant to EN. Tolerance was denned as the administration of EN at a feeding rate sufficient to supply at least 75% of the patient’s daily energy requirements (as determined by an ICU dietitian) and a cumulative GRV 120 mL in the 24-hour period preceding enrollment, with each individually measured GRV 30 mL. Intolerance was defined as a single aspirated GRV 150 mL within the 24-hour period preceding enrollment, unless this volume was measured within 4 hours of enteral administration of contrast media, sterile water, or medications. GRVs were measured by a bedside nurse every 4 hours, using the aspiration-by-syringe technique through an 18-Fr large-diameter tube. EN was administered through this tube. As outlined by an institution-specific EN administration protocol that existed before this study was initiated, EN is started as early as possible, according to physician discretion and after consultation with an ICU dietitian. The protocol starts gastric EN at a rate of 20 mL/h with increases of 20 mL/h every 8 hours until the goal rate is achieved. For patients receiving continuous administration of vasopressor agents (see exclusion criteria for definitions) or neuromuscular blocking agents, the rate is started at 10 mL/h and increased by 10 mL/h every 12 hours. The protocol stipulates that EN be discontinued for 4 hours after the development of intolerance and then restarted at half the previous rate and increased by 10 mL/h every 8 hours as tolerated. Volumes

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Parkinson’s disease, a progressive disorder of the central nervous system (CNS), is caused by the degeneration of dopaminergic neurons in the substantia nigra of the midbrain. These neurons normally project to the striatum, consisting of the caudate and putamen nuclei, whose neurons bear dopamine receptors. This projection of neurons is just one component of the complex network of interconnections among the deep gray-matter structures known as the basal ganglia (Figure 1). Neurochemical or structural pathologic conditions affecting the basal ganglia result in diseases of motor control, classified as movement disorders.
Parkinson’s disease has been reported to affect approximately 1 percent of Americans over 50 years of age,1 but unrecognized early symptoms of the disease may be present in as many as 10 percent of those over 60 years of age.2 Early- onset Parkinson’s disease, which often affects persons in their 20s, is receiving more attention because of its impact on employability. Epidemiologic studies conducted in the United States have found that Parkinson’s disease is more prevalent in men than in women (approximate ratio: 3:2).2
The disease was once thought to affect primarily whites, but recent studies have demonstrated equal prevalence in African Americans and whites living in the same geographic area.3 To date, no studies have determined the prevalence or incidence of Parkinson’s disease in Hispanics, and retrospective epidemiologic studies performed in various major cities have yielded contradictory information.4 Variations in the prevalence of the disease in individual racial groups in different geographic areas have suggested an increased risk associated with rural living.5 Pesticides and other toxins have been suspected, but none has been proved to be a definite causative factor.
On the other hand, the search for genetic causes has yielded at least four independent gene loci in various forms of familial Parkinson’s disease. The autosomal dominant adult-onset type is linked to a site on chromosome 4q,6 and the gene for autosomal recessive juvenile parkinsonism maps to chromosome 6q.7
Because most patients do not have a clear history of either familial or environmental risk factors, the disorder may be due to a combination of genetic and environmental “influences” or “causes.”
Parkinson’s disease severely compromises quality of life. Patients with this illness can find it difficult to read, write and drive. With advanced disease, they often cannot manage basic activities of daily living. Thus, Parkinson’s disease can result in loss of employment and, ultimately, loss of personal autonomy.
Clinical Presentation
The first step in evaluating a patient with problems suggestive of Parkinson’s disease is to determine which components of motor control are affected. The patient’s signs and symptoms are then clustered to determine whether the diagnosis is Parkinson’s disease or another movement disorder (Table 1).
Like some other CNS degenerative disorders, Parkinson’s disease begins insidiously. Persons close to the patient may notice the problem before the patient does. The patient’s facial expression may appear “depressed” or “apathetic,” and the voice may become softer in volume and monotonous in tone. The patient may complain of muscular “weakness” or “stiffness.” Involuntary movements, such as tremor or the turning in of a foot (dystonia), may become a problem. The symptoms may be noticed during routine activities, or they may be present only at certain times, such as when the patient is walking or writing.
In the initial stages of Parkinson’s disease, many patients do not have movement problems. Instead, they may complain of anxiety and difficulty sleeping. However, signs of motor system dysfunction become apparent on neurologic and physical examination.