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This product will be the fourth unit dose gastrointestinal product available under the Xactdose label that is marketed by Baltimore-based Alpharma USPD.
COPYRIGHT 2000 Reproduced with permission of the copyright holder. Further reproduction or distribution is prohibited without permission.
COPYRIGHT 2008 Gale, Cengage Learning

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Main outcome measures Rates of clinically important gastrointestinal bleeding and nosocomial pneumonia (compared between the two study arms and expressed with odds ratios specific for individual studies and meta-analytic summary odds ratios).
Results Meta-analysis A (five studies) comprised 398 patients; meta-analysis C (three studies) comprised 311 patients; meta-analysis D (two studies) comprised 226 patients: and meta-analysis E (eight studies) comprised 1825 patients. Meta-analysis B was not carried out as the literature search selected only one clinical trial. In meta-analysis A ranitidine was found to have the same effectiveness as placebo (odds ratio of bleeding 0.72, 95% confidence interval 0.30 to 1.70, P = 0.46). In placebo controlled studies (meta-analyses C and D) ranitidine and sucralfate had no influence on the incidence of nosocomial pneumonia. In comparison with sucralfate, ranitidine significantly increased the incidence of nosocomial pneumonia (meta-analysis E: 1.35, 1.07 to 1.70, P = 0.012). The mean quality score in the four analyses (on a 0 to 10 scale) ranged from 5.6 in meta-analysis E to 6.6 in meta-analysis A.
Conclusions Ranitidine is ineffective in the prevention of gastrointestinal bleeding in patients in intensive care and might increase the risk of pneumonia. Studies on sucralfate do not provide conclusive results. These findings are based on small numbers of patients, and firm conclusions cannot presently be proposed.
Introduction
Ranitidine and sucralfate are widely used to prevent stress ulcers in patients admitted to intensive care units.[1] A meta-analysis published by Cook et al in 1996 showed that [H.sub.2] receptor antagonists (such as cimetidine and ranitidine together) are more effective than placebo for this clinical indication.[2] With regard to sucralfate, this meta-analysis found a small but significant reduction in overt bleeding but no effect on clinically important events. The meta-analysis did not resolve the question of an increased risk of nosocomial pneumonia related to the use of [H.sub.2] receptor antagonists.
Several arguments emphasise the need for up to date information on this issue. Firstly, ranitidine has become the main [H.sub.2] receptor antagonist used for prophylaxis for stress ulcers, and cimetidine has generally been abandoned[1]; secondly, new findings have been published on effectiveness and complications of ranitidine; and, thirdly, a meta-analytic comparison of ranitidine versus placebo has never been carried out, and, as the comparison of sucralfate and placebo made by Cook et al gave no proof of the effectiveness of this drug, ranitidine and sucralfate might both be ineffective. Another problem is that the most recent randomised studies on this topic did not include a group with no prophylaxis and compared supposedly active treatments with one another.[3 4]
We conducted a literature search to identify randomised trials, and we carried out a meta-analysis to update the results of Cook’s study with regard to effectiveness and infectious complications.
Methods
Searching
Our Medline search covered the period from 1966 to 20 June 2000 and was based on four key words (stress, pneumonia, ranitidine, sucralfate) and on the extraction of studies published in English. Randomised studies were identified by using the key words “randomized controlled trial” or “random” according to a validated literature search.[5]
This search was supplemented by examining the Iowa-IDIS system (Iowa Drug Information, Iowa University, United States) from 1966 to December 1999 and Drugdex (CD Rom Drugdex, vol 104, Micromedex, Englewood, Colorado, United States).
Selection
We carried out five meta-analyses that evaluated data on effectiveness in terms of rates of bleeding (meta-analysis A: ranitidine v placebo; meta-analysis B: sucralfate v placebo) and incidence of nosocomial pneumonia (meta-analysis C: ranitidine v placebo; meta-analysis D: sucralfate v placebo; meta-analysis E: ranitidine v sucralfate). Eligible studies were included in meta-analysis A or B if they met the following criteria: patients were admitted to an intensive care unit or were undergoing mechanical ventilation, or both; randomised design; assessment of gastrointestinal bleeding. In meta-analyses C, D, and E the inclusion criterion gastrointestinal bleeding was replaced by the assessment of pneumonia.

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The level of acid inside the stomach increases because some factors interfere in its production. For example, following a treatment with NSAIDs for a long time could increase the level of produced acid inside your stomach. To prevent ulcer from occurring your current doctor will prescribe some antacids, inhibitors of the proton pump (Omeprazole, Lansoprazole, and Pantoprazole), and H2-Receptor antagonists (Famotidine, Cimetidine, Nizatidine, and Ranitidine).

There is also a bacterium responsible for peptic ulcer: Helicobacter Pylori. For killing the bacterium, the doctor will prescribe antibiotic drugs. The most efficient antibiotic drugs are: Metronidazole, Tetracycline, Clarithromycin and Amoxicillin. This treatment must be followed for at least two weeks. Bismuth salicylate is also useful for killing the bacterium and is available over the counter. It also protects the stomach from the damage produced by the acid.

Also, a lifestyle change must be done. Smoking and drinking alcohol and coffee must be eliminated or at least reduced. Stress is also a factor that contributes to the extent of ulcer, so you should avoid getting stressed.

Try to avoid the following aliments because they only injure your stomach line: pepper, chilly, peppermint, citrus fruits, cocoa, chocolate, cola, and fried fatty foods. This list can be adjusted according to your tolerances but the doctors should be consulted about it too. Cranberries, apples, onions kill the H. Pylori; fruits and vegetable that are rich in fiber are also good for you. If you have an alcohol problem your doctor can advise you on receiving appropriate care.

Pay attention to the foods that cause you pain and burnings and try not to eat them any more.

For protecting the line of your stomach and duodenum, you will receive antacids like TUMS and ROLAIDS that will preserve the lining from the acids action.

Also if ulcer lesions are present, Sucralfate is helpful because it covers them up and helps them heal faster.

The most indicated drugs in ulcer are the proton pumps because they decrease gastric acid production. They are: esomeprazole, lansoprazole, omeprazole, pantoprazole, and rabeprazole.

There are some rare cases when treatment is not effective and other measures must be applied. Surgery is a solution for treating peptic ulcers but only the doctor will be able to pronounce whether you need a surgery or not.

For more resources about Ulcer or especially about Peptic Ulcer please click this link http://www.ulcer-center.com/Peptic-Ulcer.htm

- Acute vomiting that fails to respond to appropriate symptomatic therapy

- Untreated vomiting that persists longer than two weeks

Consistent

Intermittent or episodic

Approach to Vomiting

- Primary GI

Gastric

Small intestinal

Colonic

- Secondary GI

Systemic illness that affects GI function

Secondary GI Causes of Vomiting

SYSTEM

- Kidneys

- Liver

- Exocrine pancreas

- Endocrine pancreas

- Adrenals

- Peritoneum

- CNS

- Thyroid

- Uterus

- Systemic infection

Disease:

- Renal failure

- Hepatic disease

- Pancreatitis

- DKA

- Addisons

- Peritonitis

- Cerebral or vestibular disease

- Hyperthyroidism

- Pyometra

- Sepsis

Overview:

Gastric Causes of Chronic Vomiting

- Chronic gastritis

Lymphocytic/plasmacytic

Eosinophilic

Associated with GHLOs

Parasitic

Reflux gastritis

- Gastric foreign body

- Gastric ulceration

- Gastric motility disorders

- Gastric neoplasia

Overview:

Intestinal Causes of Chronic Vomiting

- Inflammatory bowel disease (IBD)

- Intestinal neoplasia

- Duodenal ulcers

- Fungal enteritis

- Chronic intussusception

- Foreign bodies

- Colitis

Chronic Vomiting: History

- Characterize vomiting

Onset

Duration

Frequency

Progression

Relationship to eating

Specific features (blood, foreign material, undigested food, projectile, etc.)

Response to changes in diet or feeding schedule, medication, other changes

Associated clinical signs-

Appetite changes

Weight loss

Diarrhea

Changes in attitude (lethargy)

PU/PD

Cough, tachypnea, dyspnea

Other

- Potential exposures prior to onset:

Medications

Plants

Toxins

Garbage

Potential foreign bodies

Other sick animals

- Dietary history

- Deworming history

- Vaccination status

- Past medical history

- Past surgical history

Approach to Vomiting:

- Primary GI

Gastric

Small intestinal

Colonic

- Secondary GI

Systemic illness that affects GI function

Chronic Vomiting:

Diagnostic Steps

- CBC, biochemistry profile, UA

- Fecal

- Survey abdominal radiographs

- Cats:

T4 if over 6 yrs, FeLV, FIV

occult heartworm test

- Elimination diet

- Endoscopy

- Abdominal ultrasound

- Barium series

- Laparatomy

Approach to Chronic Vomiting

CBC, biochemistry profile, UA, fecal

Survey abdominal radiographs

Cats: T4 if over 6 yrs, FeLV, FIV (occult heartworm test)

Mild Signs:

- Elimination diet

Significant Clinical Signs:

- Endoscopy

- Abdominal ultrasound

- Barium series

- Laparotomy

Overview:

Gastric Causes of Chronic Vomiting

- Chronic gastritis

Lymphocytic/plasmacytic

Eosinophilic

Associated with GHLOs

Parasitic

Reflux gastritis

- Gastric foreign body

- Gastric ulceration

- Gastric motility disorders

- Gastric neoplasia

Chronic Gastritis

Classified by etiology, breed, and/or histopathology

Types of Chronic Gastritis

Lymphocytic/plasmacytic gastritis (Chronic non-specific gastritis, IBD)

Eosinophilic gastritis

Granulomatous gastritis

Atrophic gastritis

Gastritis associated with GHLOs

Parasitic gastritis

Reflux gastritis

Etiopathogenesis of Chronic Lymphocytic/Plasmacytic Gastritis

- Non-specific reaction to many insults

- Either wall defects allow antigen absorption from stomach stimulating immune response OR breakdown in immune tolerance (auto-immune gastritis)

- Mucosal damage allows back-diffusion of acid

- Gastric inflammation compromises motility, secretions and plasma proteins lost into lumen

Chronic Lymphocytic/Plasmacytic Gastritis: Clinical Features

- Persistent intermittent vomiting exacerbated by eating

- Diarrhea occurs if animal has concurrent IBD of intestines

- PE, CBC, chemistries, UA, fecal, and survey radiographs typically NAF

Chronic Lymphocytic/Plasmacytic Gastritis: Diagnosis

- Obtain endoscopic biopsies or full-thickness biopsies by laparotomy

- Infiltration of the gastric mucosa predominantly with lymphocytes and plasma cells

- Mucosa may be normal thickness (simple gastritis), increased (hypertrophic), or decreased (atrophic)

Note: Mucosal hypertrophy can cause outflow obstruction

Chronic Lymphocytic/Plasmacytic Gastritis: Treatment

PRIMARY THERAPY

- /- NPO or no food for 24-48 hours

- Multiple small daily meals

Easily digested diet (i/d)

Novel protein diet (e.g. venison and rice)

Hydrolyzed protein diet (z/d, HA)

- Gastric protectant (Sucralfate)

- Treat for ulceration if indicated

SECONDARY THERAPY

- Prednisolone 1-2 mg/kg PO q12 hr, tapered

- Usually reserve antiemetics for acute exacerbations

Eosinophilic Gastritis

- Clinical signs like L/P gastritis

- Inflammatory infiltrate dominated by eosinophils

- May have peripheral eosinophilia

- May be associated with:

Generalized eosinophilic gastroenteritis (dogs and cats)

Eosinophilic granulomas (dogs)

Hypereosinophilic syndrome (cats)

Eosinophilic Gastritis

- Suspected etiologies

Parasites

Dietary hypersensitivity

Hypereosinophilic syndrome (cats) neoplastic-

Eosinophilic Gastritis: Treatment

- Therapeutic deworming

- Treat as for L/P gastritis except use prednisolone as part of primary therapy

- Cats usually require higher doses of steroids for control (2-3 mg/kg q12 hr)

- If refractory, add azathioprine

- Resect granulomatous masses

Eosinophilic Gastritis: Prognosis

- Eosinophilic gastritis /- enteritis: Good prognosis for control of clinical signs

- Hypereosinophilic syndrome in cats: Very guarded prognosis

Many people with this disease have no symptoms. Hashimoto’s Disease is often referred to as Hashimoto’s thyroiditis, autoimmune thyroiditis, lymphadenoid goiter, struma lymphomatosa, and chronic lymphocytic thyroiditis. Hashimoto’s Thyroiditis is not uncommon. Many people with Hashimoto’s thyroiditis have other endocrine disorders, such as diabetes, an underactive adrenal gland, or underactive parathyroid glands, and other autoimmune diseases, such as pernicious anemia, rheumatoid arthritis, Sjgren’s syndrome, or systemic lupus erythematosus (lupus). In many cases, Hashimoto’s thyroiditis usually results in hypothyroidism, although in its acute phase, it can cause a transient thyrotoxic state. Hashimoto’s disease progresses slowly over a number of years and causes chronic thyroid damage, leading to a drop in thyroid hormone levels in your blood. Less commonly, Hashimoto’s disease occurs with hypoparathyroidism, adrenal insufficiency, and fungal infections of the mouth and nails in a condition called type 1 polyglandular autoimmune syndrome. The thyroid gland typically becomes and the antibodies the body normally produces to protect the body and fight foreign substances such as bacteria, are found to ‘attack’ their own thyroid tissue. Treatment with synthetic thyroid hormone replacement medication usually is simple and effective. Natural treatment options also exist.

Causes of Hashimoto’s disease

The common causes and risk factor’s of Hashimoto’s disease include the following:

The exact cause of Hashimoto’s disease is unknown.

A reaction of the immune system against the thyroid gland.

If someone in your family has had thyroid disease, you may have an increased risk for Hashimoto’s disease.

Hashimoto’s thyroiditis is most common among women, particularly older women, and tends to run in families.

It may rarely be associated with other endocrine disorders caused by the immune system.

A combination of factors including heredity, and age may determine your likelihood of developing the disorder.

Hashimoto’s Thyroiditis is seen more frequently in people taking extra iodine in their diets.

Symptoms of Hashimoto’s disease

Some sign and symptoms related to Hashimoto’s disease are as follows:

Fatigue.

Enlarged neck or presence of goiter.

Small or atrophic thyroid gland.

Dry skin.

Joint stiffness.

Excessive sleepiness.

Dry, coarse hair.

Facial swelling.

Hair loss.

Heavy and irregular menses.

Hoarse voice.

An elevated blood cholesterol level.

Intolerance to cold.

Most often, people with Hashimoto’s Thyroiditis suffer from symptoms of Hypothyroidism (fatigue, lethargy, decreased metabolic rate).

Treatment of Hashimoto’s disease

Here is list of the methods for treating Hashimoto’s disease:

Iron supplements.

If Hashimoto’s disease causes thyroid hormone deficiency, you may need replacement therapy with thyroid hormone.

Antibiotics to fight infection.

Hormones to suppress or replace thyroid function.

Sucralfate, an ulcer medication.

Long-term prognosis is very good. Most people with the disease can be easily treated.

Cholestyramine (Questran), a medication used to lower blood cholesterol levels.

Replacement therapy with thyroid hormone is given if the hormone is deficient or may be given if there is evidence of mild thyroid failure.

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Medical treatments in the short-term management of reflux esophagitis

In a poster focused on short-course gemifloxacin therapy in CAP patients with certain risk factors, researchers analyzed data from Oscient’s Phase III trial comparing a five-day course of therapy to a seven-day course of therapy of FACTIVE in CAP. A retrospective examination of the 510 patients enrolled in the study showed that 21.5% (55/256) in the five-day group and 21.7% (55/254) in the seven-day group had risk factors as defined by IDSA guidelines, including diabetes, chronic obstructive pulmonary disease and congestive heart failure. Of the 110 patients with risks factors, 75% were 65 years or older. A comparison of clinical resolution at follow-up in this sub-population showed a 90.9% response rate in the five-day group and a 92.7% response rate in the seven-day group. Gemifloxacin was generally well-tolerated with a low incidence of adverse events. FACTIVE is currently approved in the U.S. for the seven-day treatment of mild to moderate CAP.
“Understanding the impact of risk factors on clinical outcome in CAP is an important consideration when treating patients, as many are older and suffer from heart disease or other co-morbid conditions,” stated Thomas File, M.D., Professor of Internal Medicine and Head of the Infectious Disease Section, Northeastern Ohio Universities College of Medicine and an author on the poster. “The clinical results seen with gemifloxacin in this trial, especially when looking at this specific sub-population, are supportive of the drug’s utility in treating these patients.”
Support for this poster was provided through an unrestricted education grant from Oscient Pharmaceuticals.
About Oscient Pharmaceuticals
Oscient Pharmaceuticals Corporation is a biopharmaceutical company committed to the clinical development and commercialization of novel therapeutics to address unmet medical needs. The Company is marketing FACTIVE(R) (gemifloxacin mesylate) tablets, approved by the FDA for the treatment of acute bacterial exacerbations of chronic bronchitis and community-acquired pneumonia of mild to moderate severity and ANTARA(R) 130 mg (fenofibrate) capsules, FDA-approved for the adjunct treatment of hypercholesterolemia (high blood cholesterol) and hypertriglyceridemia (high triglycerides) in combination with diet. Oscient has a novel antibiotic candidate, Ramoplanin, in advanced clinical development for the treatment of Clostridium difficile-associated disease (CDAD).
Important Safety Information about FACTIVE Tablets
The most common (more than 2% incidence) drug-related side effects reported in FACTIVE clinical trials were diarrhea (3.6%), rash (2.8%) and nausea (2.7%). In clinical trials, drug-related rash was reported in 2.8% of patients receiving gemifloxacin and was more commonly observed in patients less than 40 years of age, especially females. The incidence of rash increases with treatment longer than the maximum-labeled duration of 7 days. In clinical trials, the discontinuation rate due to drug-related adverse events was similar for FACTIVE tablets and comparators (2.2% versus 2.1%, respectively).
Gemifloxacin is contraindicated in patients with a history of hypersensitivity to gemifloxacin, fluoroquinolone antibiotic agents, or any of the product components. Patients receiving marketed fluoroquinolones have reported serious and occasionally fatal hypersensitivity and/or anaphylactic reactions, peripheral neuropathy, antibiotic-associated colitis and tendon ruptures. Gemifloxacin should be discontinued immediately at the first sign of any of these events.
Fluoroquinolones may prolong the QT interval in some patients. Gemifloxacin should be avoided in patients with a history of prolongation of the QTc interval, patients with uncorrected electrolyte disorders (hypokalemia or hypomagnesemia), and patients receiving Class IA or Class III antiarrhythmic agents. In clinical studies with gemifloxacin, CNS effects have been reported infrequently. As with other fluoroquinolones, gemifloxacin should be used with caution in patients with known or suspected CNS diseases. If CNS reactions occur, gemifloxacin should be discontinued and appropriate measures instituted.
No significant drug-drug interactions were seen with theophylline, digoxin, oral contraceptives, cimetidine, omeprazole, and warfarin, although patients receiving a fluoroquinolone concomitantly with warfarin should be monitored closely. Drug-drug interactions include probenicid, sucralfate, antacids containing aluminum or magnesium, iron, multivitamins containing metal cations, and didanosine. The safety and effectiveness of gemifloxacin in children, adolescents (less than 18 years of age), pregnant women, and lactating women have not been established. For complete safety and efficacy information, please see the full prescribing information available at www.factive.com.

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The authors of this Cochrane review studied the effectiveness of PPIs, [H.sub.2] blockers, prokinetics, and sucralfate (Carafate) in the short-term management (two to 12 weeks of therapy) of endoscopically proven reflux esophagitis. The authors reviewed 134 trials, which included 35,978 patients with gastroesophageal reflux disease, to assess the proportion of patients who had persistent reflux esophagitis symptoms or persistent esophagitis.
Five randomized controlled trials (RCTs) that evaluated the effectiveness of standard-dose PPI therapy in 645 participants at eight weeks showed a statistically significant benefit in which esophagitis persisted in 16.8 percent of those on PPIs compared with 71.7 percent on placebo. In other words, 1.7 patients needed short-term treatment with a PPI to benefit, and three patients needed short-term treatment to experience global symptom relief. Head-to-head comparisons between PPIs showed equal effectiveness at standard doses; the only exception was esomeprazole (Nexium), which showed a small benefit compared with omeprazole (Prilosec) in one trial where esophagitis persisted in 35.2 percent of those taking omeprazole versus 29.6 percent taking esomeprazole. However, the dose of esomeprazole was higher than the dose of omeprazole in this trial.
Ten RCTs that evaluated 1,241 participants at six weeks showed a statistically significant benefit of taking an [H.sub.2] blocker (esophagitis persistence 59.0 versus 79.7 percent in [H.sub.2] blocker and placebo groups, respectively), with a number needed to treat to benefit (NNTB) of 5. Pooled data from 26 RCTs showed a statistically significant benefit of taking PPI therapy compared with [H.sub.2] blocker or [H.sub.2] blocker plus prokinetics (esophagitis persistence 31.5 versus 61.5 percent in PPI and in the [H.sub.2] blocker or [H.sub.2] blocker plus prokinetics group, respectively) with an NNTB of 3. There was no statistically significant benefit of prokinetic therapy compared with placebo, or of administering mucosal-protecting agent therapy compared with antacid or placebo.
There were no statistically significant differences in reported adverse events for PPIs or [H.sub.2] blockers compared with placebo. The most commonly reported side effects included diarrhea, constipation, and headache; no studies examined adverse events in prokinetic agents compared with placebo. However, a recent nested case control study of 13,556 patients with hip fractures and 135,386 control-group participants older than 50 years concluded that long-term PPI therapy (up to four years), particularly at high doses, is associated with an increased hip fracture risk; this risk increased with increasing cumulative exposure to PPIs. (1)
The American College of Gastroenterology (ACG) recommends PPIs for reflux esophagitis, and, although [H.sub.2] blockers are less effective, they may be used for less severe cases. (2) The ACG recommends maintenance therapy at therapeutic or higher daily dosing and cites that up to 50 percent of patients have chronic symptoms that require maintenance or lifelong therapy; the goal of maintenance is to control patients’ bothersome symptoms and prevent complications (e.g., esophageal stricture). In light of recent evidence of increased risk of osteoporotic hip fracture with prolonged PPI therapy, it is reasonable to stop treatment in patients who do not continue to require therapy.
REFERENCES
(1.) Yang YX, Lewis JD, Epstein S, Metz DC. Long-term proton pump inhibitor therapy and risk of hip fracture. JAMA. 2006;296(24):2947-2953.
(2.) DeVault KR, Castell DO; American College of Gastroenterology. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Am J GastroenteroL 2005;100(1):190-200.
JANELLE GUIRGUIS-BLAKE, MD
Source: Khan M, Santana J, Donnellan C, Preston C, Moayyedi P. Medical treatments in the short term management of reflux oesophagitis. Cochrane Database Syst Rev. 2007;(2):CD003244.
Author disclosure: Nothing to disclose.
COPYRIGHT 2008 American Academy of Family Physicians
COPYRIGHT 2008 Gale, Cengage Learning