ChromoZinc - The key to complete diabetic management

Reliance Formulation (Pvt.) Ltd. provides the doctor with a powerful armamentarium to fight and keep in control blood sugar. ChromoZinc is not a substitute to a doctor’s prescription in sugar control. ChromoZinc is the key to complete a doctor’s prescription in the management of diabetes.

ChromoZinc contains:

Chromium picolinate: 500 mcg
Zinc sulphate monohydrate: 27.5 mg
Methylcobalamin: 750 mcg
Alpha-lipoic acid: 100 mg,
Vitamin B6: 3 mg
Folic acid: 1mg

Chromium

A highly refined diet that contains too few micronutrients has been recognized as the dominant factor in the rising incidence of diabetes and other insulin related conditions. Among the missing micronutrients, chromium has the greatest impact on insulin response. Until recently, few physicians recognized the importance of supplementing chromium in the management of diabetes. However, research has revealed that chromium plays an important role` in amplifying insulin response in diabetics.

Chromium is now proven to be the key to complete the diabetes management. We all know that insulin is a hormone whose primary role is to regulate the body's response to carbohydrates, proteins and fats.

Insulin is produced in the pancreas. Following a meal the pancreas releases insulin into the bloodstream, as glucose, or blood sugar, levels from the digested meal begin to rise; Glucose is the primary fuel for energy production within all body tissues including the brain. But it can't get into cells without the help of insulin. The more the sugar that enters the blood, the more the insulin is required to transport it into cells. Eating refined carbohydrates and sugary foods quickly raises glucose levels making these foods particularly troublesome for anyone with a blood sugar imbalance such as diabetes.

While glucose transport is the primary role of insulin, chromium's main function is increasing insulin's efficiency in regulating blood sugar levels. But this hormone produces much more complex and far-reaching effects. These include the transport of amino acids and electrolytes into cells, several enzymatic activities and cellular growth. Numerous studies show that chromium alters lipoprotein abnormalities (unhealthy LDL and HDL levels) that are believed to increase the risk of cardiovascular disease. Chromium supplementation also appears useful in treating obesity in other research, increasing lean muscle mass and improving athletic performance.

Symptoms of chromium deficiency;

Ø Fasting hyperglycemia (too much of fasting blood sugar)
Ø Hypoglycemia (to little of blood sugar)
Ø Elevated percentage of fat in the body
Ø Peripheral neuropathy
Ø Fatigue
Ø Anxiety

A minimum of 200 mcg of chromium daily is needed for at least three months to have a noticeable effect on insulin response. Anyone with diabetes who uses insulin should consult with a healthcare provider about chromium supplements, since the insulin dosage may have to be adjusted. If required up to 500 mcg can be administered.

What is chromium picolinate?

This popular nutritional supplement is a combination of the element chromium and picolinic acid. Chromium is a naturally occurring mineral, trace amounts of which are found in everyday foods like meat, poultry, fish, and whole-grain breads. When foods are processed, they are stripped of natural chromium, making our diets generally very low in chromium; studies estimate an average daily chromium consumption of 33 mcg in an average non-vegetarian diet.
In 1968, it was demonstrated that when subjects do not receive adequate levels of chromium, insulin is not optimally effective, and damage to insulin-dependent systems can occur (Schroeder, 1968). This led the FDA to recommend a daily chromium intake of approximately 130 mcg (100 mcg chromium picolinate is equivalent to 23mcg elemental chromium), as infinitesimal amounts of chromium are needed to aid the transport of blood glucose across cell membranes

Zinc sulphate monohydrate

Diabetics should probably take zinc supplements! Zinc plays a key role in the regulation of insulin production by pancreatic tissues and glucose utilization by muscles and fat cells.

The abilities to synthesize and secrete insulin and use glucose are impaired in the zinc deficient state. Intestinal zinc absorption rates and plasma zinc levels in diabetic patients are reduced. Zinc is involved in the regulation of insulin receptor-initiated signal transduction mechanisms and insulin receptor synthesis.

Scientists at Notre Dame* and at the University of Illinois have discovered that zinc has an insulin-like effect on the manifestation of diabetes.

Insulin, they note, promotes the transport of glucose and amino acids (proteins) and decreases the breakdown of muscles while healthfully enhancing their buildup.“.... failure to enhance glucose transport, " they say, "into insulin-sensitive cells is a hallmark of diabetes [emphasis added.] They have found that zinc enhances this glucose movement.

Zinc Sulphate 200mg (45mg elemental Zinc) - Zinc is alos documented to be an essential element for normal growth and good vision.

Methylcobalamin

Methylcobalamin is a type of Vitamin B12. Vitamin B12 comes in several kinds including hydroxy-, cyano-, and adenosyl-, but only the methyl form is used in the central nervous system.

Deficiency states are fairly common and vitamin B12 deficiency mimics many other disease states of a neurological or psychological kind, and it causes anemia. Cyanocobalamin (the kind in vitamin supplements) is converted by the liver into methylcobalamin but not in therapeutically significant amounts. Vitamin B12 deficiency is caused by a wide range of factors including low gastric acidity (common in older people,) use of acid blockers such as PPI’s or H2A’s or excessive laxative use, lack of intrinsic factor, poor absorption from the intestines, lack of Calcium, heavy metal toxicity, or excessive Vitamin B12 degradation.

Methylcobalamin donates methyl groups to the myelin sheath that insulates nerve fibers and regenerates damaged neurons. In a B12 deficiency, toxic fatty acids destroy the myelin sheath but high enough doses of B12 can repair it.

Methylcobalamin supplements increase alertness and body temperature. Methylcobalamin may slightly help those with diabetic neuropathy. Methylcobalamin has been found to be helpful in Bell's palsy. Methylcobalamin taken orally is effective in the treatment of pernicious anemia, says a Japanese study. Methylcobalamin may inhibit the ototoxic (hearing damage) side effects of the antibiotic Gentamycin.

Despite intensive searches for therapeutic agents, few substances have been convincingly shown to enhance nerve regeneration in patients with peripheral neuropathies. Recent biochemical evidence suggests that an ultra-high dose of methylcobalamin (methyl-B12) may up-regulate gene transcription and thereby protein synthesis.

Alpha-Lipoic Acid

Alpha-lipoic acid, also known as thioctic acid, is a disulfide compound that is a cofactor in vital energy-producing reactions in the body.

It is also a potent biological antioxidant. Alpha-lipoic acid was once thought to be a vitamin for animals and humans. It is made endogenously in humans - the details of its synthesis are still not fully understood. There are, however, certain situations, for example, diabetic polyneuropathy, where alpha-lipoic acid might have conditional essentiality.

Recent research indicates that the antioxidant roles of alpha-lipoic acid may confer several health benefits. Alpha-lipoic acid is found widely in plant and animal sources.

Alpha-lipoic acid is approved in Germany as a drug for the treatment of polyneuropathies, such as diabetic and alcoholic polyneuropathies, and liver disease.

Actions And Pharmacology

Alpha-lipoic acid has biological antioxidant activity, antioxidant recycling activity and activity in enhancing biological energy production.

Mechanism Of Action

Alpha-lipoic acid and its reduced metabolite, dihydrolipoic acid (DHLA), form a redox couple and may scavenge a wide range of reactive oxygen species. Both alpha-lipoic acid and DHLA can scavenge hydroxyl radicals, the nitric oxide radical, peroxynitrite, hydrogen peroxide and hypochlorite. Alpha-lipoic acid, but not DHLA, may scavenge singlet oxygen, and DHLA, but not alpha-lipoic acid, may scavenge superoxide and peroxyl reactive oxygen species.

Further, alpha-lipoic acid and its redox couple DHLA have been found to have antioxidant activity in aqueous, as well as in lipophilic regions, and in extracellular and intracellular environments. Finally, with regard to alpha-lipoic acid's antioxidant activity, alpha-lipoic acid appears to participate in the recycling of other important biologic antioxidants, such as vitamins E and C, ubiquinone and glutathione.

Exogenous alpha-lipoic acid has been shown to increase ATP production and aortic blood flow during reoxygenation after hypoxia in a working heart model.

Pharmacokinetics

Alpha-lipoic acid is absorbed from the small intestine and distributed to the liver via the portal circulation and to various tissues in the body via the systemic circulation.

Indications and Usage

Alpha Lipoic acid shows evidence of being effective in the treatment of diabetic neuropathy and may be useful in treating some other aspects of diabetes. It may help prevent the oxidation of LDL cholesterol and may be protective, generally, against oxidative stress and, specifically, against atherosclerosis, ischemia-reperfusion injury and various radiologic and chemical toxins. It may also be useful in some inborn metabolic disorders. It has been suggested that lipoic acid may slow aging of the brain and that it may be an anti-aging substance, in general.

Research Summary on Alpha Lipoic acid

Supplemental alpha-lipoic acid may lower blood glucose levels. Those with diabetes on antidiabetic medication should have their blood glucose monitored and antidiabetic drug dose appropriately adjusted, if necessary, to avoid possible hypoglycemia.

In some experiments, alpha lipoic acid, administered for up to three months, significantly reversed the increase in nerve vascular resistance. Nerve conduction velocity was entirely restored in some nerve groups after three months of treatment.

In a larger, multi-center, double blind, randomized, placebo-controlled study of 328 patients with type 2 diabetes, significant improvements were recorded in several clinical measures of diabetic polyneuropathy, including pain, numbness, paresthesia and burning sensations. These results were evident after three weeks of intravenous lipoic acid given five times weekly in doses of 600 and 1200 milligrams.

There is evidence, too, that lipoic acid may help prevent or slow the development of the atherosclerosis for which diabetics are at higher risk. It may do this, in part, through a gene-regulatory mechanism that helps prevent endothelial cell activity that has been implicated in the progression of atherosclerosis.

With respect to atherosclerosis, in general, lipoic acid's antioxidant and metabolic effects appear to offer some protection, as demonstrated in various animal models. Recently, researchers demonstrated, in a 16-week randomized trial, that lipoic acid, in oral doses of 600 milligrams daily for eight weeks, significantly inhibits the oxidation of LDL-cholesterol in healthy human subjects. The supplements also significantly reduced levels of F-2 isoprostanes, markers of oxidative stress. In this study, lipoic acid proved to be superior to vitamin E in decreasing levels of plasma protein carbonyls. Protein oxidation and LDL-cholesterol oxidation are implicated in heart disease.
Claims that alpha lipoic acid slows aging of the brain and is an anti-aging substance generally seem to be related to its potent antioxidant properties. Direct proof of anti-aging is lacking, but there is some animal work suggestive of some possible anti-aging effects.

Contraindications

None known.

Precautions

Because of lack of long-term safety data, alpha-lipoic acid should be avoided by pregnant women and nursing mothers.

Those with diabetes and problems with glucose intolerance are cautioned that supplemental alpha-lipoic acid may lower blood glucose levels. Blood glucose should be monitored and antidiabetic drug dose adjusted, if necessary, to avoide possible hypoglycemia.

Adverse Reactions

To date, alpha-lipoic acid in doses up to 600 milligrams daily has been well tolerated.
Interactions

Supplemental alpha-lipoic acid may lower blood glucose levels. Those with diabetes on antidiabetic medication should have their blood glucose monitored and antidiabetic drug dose appropriately adjusted, if necessary, to avoid possible hypoglycemia.

Dosage and administration

Alpha-lipoic acid is available as a racemic mixture of D- and L- entantiomers. Some studies showing significant antioxidant effects have used doses of the racemic mixture of 600 milligrams daily.

Vitamin B6 (Pyridoxine)

Vitamin B6, also called pyridoxine, is one of eight water-soluble B vitamins. The B vitamins help the body to convert carbohydrates into glucose (sugar), which is "burned" to produce energy. These vitamins, often referred to as the B complex, are also essential in the metabolism of fats and protein. B complex vitamins also play an important role in maintaining muscle tone in the gastrointestinal tract and promoting the health of the nervous system, skin, hair, eyes, mouth, and liver

Uses

Heart Disease

Low dietary intake of vitamin B6 is associated with higher risk of having heart disease. This may be related to the fact that vitamin B6, together with vitamin B9 (folic acid) and vitamin B12, help to keep homocysteine levels under control. Homocysteine is an amino acid. Elevated levels of this amino acid are associated with increased risk of heart disease and increased risk of stroke. Preliminary evidence suggests that vitamin B6 may help control blood sugar in people with diabetes. In a study of people with diabetes, those who received pyridoxine alpha-ketoglutarate (a form of vitamin B6) for one month experienced significant reductions in fasting blood sugar levels compared to those who did not receive the supplement. More research in this area is needed before conclusions can be drawn about the relationship between vitamin B6 and diabetes.

Folic acid:

Folic acid deficiency is widespread and is associated with an increased risk for heart disease, cancer, depression and many other disorders. There is no question that folic acid is extremely important to health and well-being. Not only is it important for heart health, mental health and women's health, but also it is now also clear that it affects many other facets of health and disease. Researchers at the Cleveland Clinic Foundation have found that patients with end- stage renal disease have extremely high homocysteine levels and can be protected from cardiovascular events by supplementing with folic acid, vitamins B6 and B12. Diabetes patients tend to have high homocysteine levels and folate is especially important for them. Recent research has also shown that low folate levels (high homocysteine levels) are implicated in age-related hearing loss, psoriasis, and restless leg syndrome.

It is indeed astounding that one single vitamin, folic acid, can have such a profound effect on our health and yet perhaps it is not so surprising when one considers its vital role in DNA synthesis and homocysteine metabolism.

ChromoZinc, therefore, is the indispensable addition in a doctor’s armamentarium while managing diabetes mellitus and diabetic neuropathy.

Posted:
28th December 2006
Reliance Formulation (Pvt.) Ltd., Ahmedabad
For more details on ChromoZinc, please e-mail to

Mr. Mukesh Vankani – General Manager (Marketing & Sales)

Mr. Deepak Shah B. Pharma. M.B.A.

reliancehealthcare@yahoo.co.in

Pantab/ Pantab D – The best of the two worlds in Acid-Peptic Disorder

Pantab/ Pantab D – The best of the two worlds in acid-peptic disorder

Many patients and caretakers are not familiar with GERD and its potential consequences, even though it afflicts millions of individuals.

Reliance Health Care believes it is important to share this educational information about GERD with the public as well as with caretakers and physicians.

It is not intended to recommend any particular treatment plan or to replace the advice of physicians. It is important that individuals seek and rely on the advice of health care professionals regarding individual medical conditions

GERD is an acronym. It stands for Gastro Esophageal Reflux Disease. It is often called "reflux," "reflux esophagitis," or sometimes inaccurately referred to as "hiatus hernia." Gastro esophageal reflux is the term used to describe a backflow of acid from the stomach into the swallowing tube or esophagus.

Almost everyone experiences gastro-esophageal reflux at some time. The usual symptom is heartburn, an uncomfortable burning sensation behind the breastbone, most commonly occurring after a meal. In some individuals reflux is frequent or severe enough to cause more significant problems and to be considered a disease. When it reaches that point, it is a medical condition called GERD. So GERD isn’t just “something you ate.” It’s a real disease and a real problem for millions of sufferers.
FAQ’s on GERD

1. What is GERD?

GERD stands for Gastro Esophageal Reflux Disease. Gastro-esophageal reflux describes a backflow of acid from the stomach into the swallowing tube or esophagus. This acid can irritate and sometimes damage the delicate lining on the inside of the esophagus. Almost everyone experiences gastro-esophageal reflux at some time. The usual symptom is heartburn, an uncomfortable burning sensation behind the breastbone, most commonly occurring after a meal. In some individuals this reflux is frequent or severe enough to cause more significant problems that is a disease. Thus, gastro-esophageal reflux disease is a clinical condition that occurs when reflux of stomach acid into the esophagus is severe enough to impact the patient’s life and/or damage the esophagus.

2. I have never heard of GERD. Is it a new disease?

No. GERD has probably been around as long as heartburn. The term is relatively new (about 20 years), however, and has really come into common usage over the past few years. GERD is often called "reflux," "reflux esophagitis," or sometimes even "hiatus hernia” (although hiatus hernia is a specific diagnosis that may or may not have anything to do with GERD). GERD is the preferred term because it accurately describes the problem - reflux of stomach acid up into the esophagus where it can produce symptoms and sometimes damage. Many patients are not familiar with GERD and its potential consequences, and thus may not have heard the term previously.

3. What are some symptoms of GERD?

The four major symptoms of GERD are:
· Heartburn (uncomfortable, rising, burning sensation behind the breastbone).
· Regurgitation of gastric acid or sour contents into the mouth.
· Difficult and/or painful swallowing.
· Chest pain.

Heartburn is the most common symptom of GERD.

In some patients it may be accompanied by other GERD symptoms, such as regurgitation of gastric contents into the mouth, chest pain and difficulty swallowing. Pulmonary manifestations, such as asthma, coughing, or intermittent wheezing and vocal cord inflammation with hoarseness, occur in some GERD patients.

In addition, acid can be regurgitated into the lungs in some GERD patients, causing wheezing or cough. Acid refluxed into the throat can cause sore throat. If acid reaches the mouth, it can dissolve enamel of the teeth.

4. How do people get GERD? What causes GERD?

GERD is caused by reflux of stomach acid into the esophagus. In most patients this is due to a transient relaxation of the “gate” or sphincter that keeps the lower end of the esophagus closed when a person is not swallowing food or liquids. This transient relaxation happens a few times each day in people without GERD. Why it happens more frequently in GERD patients isn’t known. The esophagus is not able to cope with acid as well as the stomach and is easily injured. It's the acid refluxing into the esophagus that produces the symptoms and potentially damages the esophagus.

5. How many people are afflicted with GERD?

Recent statistics from the US Department of Health and Human Services indicate that about seven (7) million people in the US alone suffer from GERD.
(Source: Digestive Diseases in the United States: Epidemiology and Impact, National Digestive Diseases Data Working Group, James E. Everhart, MD, MPH, Editor, US Department of Health and Human Services, Public Health Service, National Institutes of Health, NIH Publication No. 94-1447, May 1994)

6. Who is afflicted with GERD?

GERD afflicts people of every socioeconomic class, ethnic group and age. However, the incidence does seem to increase quite dramatically above the age of 40. Greater than 50 percent of those afflicted with GERD are between the ages of 45-64 (both male and female).

7. Do children get GERD?

Yes. GERD is most common in adults over age 40 but virtually anyone can get GERD, even infants.

8. What is the difference between GERD and GORD?
The British spelling of esophagus is oesophagus. Hence, GERD is GORD in many European countries.

9. What is the difference between heartburn and GERD?

GERD is a disease and heartburn is its most common symptom. Heartburn is defined as a rising, burning sensation behind the breastbone caused by reflux of stomach acid into the esophagus. Nearly everyone has or will experience heartburn on occasion. Frequent heartburn that disrupts one's lifestyle suggests the diagnosis of GERD.

10. What is the difference between GERD and a hiatus hernia?

Hiatus hernia refers to dislocation of the stomach through the "hiatus" of the diaphragm and into the chest. This is a common condition that increases in frequency with age. It may or may not be associated with GERD. When GERD is severe enough to be complicated by erosive esophagitis, seen as breaks in the lining of the esophagus, a hiatus hernia is usually present. However, most patients with a hiatus hernia do not have GERD.

11. What is endoscopy and when is it used in GERD patients?

Endoscopy is a diagnostic test wherein a thin, flexible tube is swallowed by the patient to allow the physician to directly inspect the lining of the upper gastrointestinal tract. This procedure can be used to identify complications of GERD and to take small samples (biopsies) for further analysis. GERD patients who have certain symptoms, such as difficulty in swallowing or painful swallowing, should be considered for endoscopy. Patients who fail to respond to therapy are also candidates for endoscopy. Some physicians advocate endoscopy for all patients with long-standing GERD in order to rule out Barrett's esophagus.

12. What are the complications of GERD?

Only a minority of patients develops complications of GERD. These complications include breaks in the lining of the esophagus (esophageal erosions), esophageal ulcer, and narrowing of the esophagus (esophageal stricture). In some patients, the normal esophageal lining or epithelium may be replaced with abnormal (Barrett's) epithelium. This condition (Barrett's esophagus) has been linked to cancer of the esophagus and must be carefully watched.

Lung (pulmonary) aspiration, asthma and inflammation of the vocal cords or throat may also be caused by GERD.

13. What makes GERD symptoms worse?

The major factor is meals. Meals stimulate the stomach to produce more acid that can reflux up into the esophagus. In some patients, lying down or taking certain medications can worsen acid reflux.

14. Does eating spicy food cause GERD or make GERD worse?

Spicy foods do not cause GERD, although they do seem to worsen GERD symptoms in some people. Food (in general) can make GERD worse. This is because food fills the stomach and induces more transient relaxations of the lower esophageal sphincter. In addition, all meals stimulate acid production in the stomach to aid digestion and can increase reflux into the esophagus in GERD sufferers. Any very large meal might be expected to produce heartburn in some people. The spicy food story is so compelling, however, that GERD sufferers often relate a spicy (or greasy) meal to their symptoms. Often they are told to avoid certain foods whether or not these foods have anything to do with their symptoms. In this way, many GERD sufferers end up on a very restricted diet or end up blaming their symptoms on dietary indiscretion. If avoiding spicy foods and/or other dietary advice helps, that's great. If it doesn't, GERD sufferers shouldn't feel that they are doing something wrong. They should seek medical advice on managing their disease.

15. What about GERD and smoking?

Smoking doesn't cause GERD and there is little evidence that smoking significantly worsens GERD. Stopping smoking is a good idea anyway.

16. Do any medications make GERD worse?

Yes. Medicines that delay emptying of acid from the stomach or that increase acid backup into the esophagus can worsen GERD. If you have, or suspect you have, GERD and you require medication for other conditions, you should make sure you inform your doctor about all medications you are taking including prescription and over-the-counter medications.

17. What should people with GERD avoid?

GERD is a disease that is caused by gastric acid. However, certain foods can trigger symptoms in some patients. Lying down after a meal, wearing tight-fitting clothing, and even performing certain activities, such as bending over, can also trigger symptoms in patients. A good way to identify these "triggers" is to keep a diary of GERD symptoms noting when they occur. If symptoms follow a pattern and occur after certain foods or activities, these foods or activities should be avoided. A diary will also help patients continue to enjoy those foods or activities that do not seem to provoke symptoms, so that their lifestyle is not restricted unnecessarily. Patients should review their symptoms with their doctor, who can evaluate their condition and advise an appropriate treatment plan.

18. Can GERD cause cancer?

Severe, long-standing GERD can damage the esophagus and cause a condition known as Barrett's esophagus wherein the normal lining of the esophagus is replaced by a lining more like that of the stomach or intestine. It is thought that this replacement may be an attempt by the body to protect itself from further injury by acid. The risk of esophageal cancer appears to increase significantly in patients with Barrett's esophagus. The only way to diagnose Barrett's esophagus is by endoscopy. Some studies suggest that intensive treatment of Barrett's esophagus can reduce the amount of abnormal lining in the esophagus. It is not yet clear whether such treatment will prevent esophageal cancer in GERD patients, but this is under active investigation.

19. Are there long-term consequences of GERD?

Long-standing GERD can lead to damage of the esophagus. This damage usually consists of breaks in the lining of the esophagus. In some cases ulcers can develop. In some patients, such damage can result in scarring and narrowing of the esophagus, making swallowing painful or difficult. A condition called Barrett's esophagus is thought to result from long-standing GERD in some patients. Barrett's esophagus is a risk factor for the development of esophageal cancer. In some patients, acid backup caused by GERD is thought to result in damage to the vocal cords or teeth and may even cause asthma.

20. Is there relationship between GERD and asthma?

Many investigators believe that there is a link between asthma and reflux of stomach acid up into the throat and then down into the lungs in some patients. It appears that some patients who suffer from asthma might benefit from treatment of GERD. This is a topic of active research at the moment.

21. Can GERD cause inflammation of the throat?
In some patients, acid can reflux into the throat causing inflammation of the back of the throat which can lead to pharyngitis, or into the vocal cords, which can lead to laryngitis and hoarseness. Although there are many other causes for sore throat and laryngitis, GERD should be suspected in a patient with chronic sore throat or other GERD symptoms or when no other cause can be found.

22. Can GERD be cured?

Unfortunately, GERD, in general, cannot be cured at present. In some cases, it may be a temporary condition associated with a specific aggravating factor such as pregnancy. In such cases, GERD will go away on its own when the pregnancy has ended. In most cases GERD is a chronic condition. However, it can be effectively managed with medications and lifestyle modifications in almost everybody. In severe cases, surgery is an option. Surgery does not cure the underlying problem, but wraps part of the stomach around the lower end of the esophagus to help keep acid from getting back up into the esophagus. A doctor can evaluate the condition and advise on an appropriate treatment plan.

23. I think I have GERD. What should I do?

See your doctor. Your doctor can establish the diagnosis and work with you to get you symptom-free. Primary care and physicians of many specialties are becoming increasingly familiar with GERD. Gastro-enterologists and some gastrointestinal surgeons are usually very familiar with GERD and its treatment.

24. Where can I go for more information about GERD?

If you think you might have GERD - see your doctor OR gastro-enterologists who can determine if you have GERD and, if so, can evaluate its severity.
GERD in Children Studies* show that GERD is common and may be overlooked in infants and children. It can cause repeated vomiting, coughing, and other respiratory problems. Children's immature digestive systems are usually to blame, and most infants grow out of GERD by the time they are 1 year old. Still, you should talk to your child's doctor if the problem occurs regularly and causes discomfort. Your doctor may recommend simple strategies for avoiding reflux, like burping the infant several times during feeding or keeping the infant in an upright position for 30 minutes after feeding. If your child is older, the doctor may recommend avoiding

• Sodas that contain caffeine
• Chocolate and peppermint
• Spicy foods like pizza
• Acidic foods like oranges and tomatoes
• Fried and fatty foods
• Avoiding food 2 to 3 hours before bed may also help.

The doctor may recommend that the child sleep with head raised. If these changes do not work, the doctor may prescribe medicine for your child. In rare cases, a child may need surgery.*( Jung AD. Gastroesophageal reflux in infants and children. American Family Physician. 2001;64(11):1853–1860.)

How is GERD treated?

If you have had heartburn or any of the other symptoms for a while, you should see your doctor. You may want to visit an internist, a doctor who specializes in internal medicine, or a gastroenterologist, a doctor who treats diseases of the stomach and intestines. Depending on how severe your GERD is, treatment may involve one or more of the following lifestyle changes and medications or surgery.

• Lifestyle Changes
• If you smoke, stop.
• Do not drink alcohol.
• Lose weight if needed.
• Eat small meals.
• Wear loose-fitting clothes.
• Avoid lying down for 3 hours after a meal.
• Raise the head of your bed 6 to 8 inches by putting blocks of wood under the bedposts—just using extra pillows will not help.
  Medications
  
  Your doctor may recommend over-the-counter antacids, which you can buy without a prescription, or medications that stop acid production or help the muscles that empty your stomach.
  
  Antacids, such as Diovol Suspension, are usually the first drugs recommended to relieve heartburn and other mild GERD symptoms. Many brands on the market use different combinations of three basic salts—magnesium, calcium, and aluminum—with hydroxide or bicarbonate ions to neutralize the acid in your stomach. Antacids, however, have side effects. Magnesium salt can lead to diarrhea, and aluminum salts can cause constipation. Aluminum and magnesium salts are often combined in a single product to balance these effects.

Calcium carbonate antacids can also be a supplemental source of calcium. They can cause constipation as well.

Foaming agents, work by covering your stomach contents with foam to prevent reflux. These drugs may help those who have no damage to the esophagus.

H2 blockers, such as cimetidine, famotidine, nizatidine and ranitidine impede acid production. They are available on prescription strength. These drugs provide short-term relief, but over-the-counter H2 blockers should not be used for more than a few weeks at a time. They are effective for about half of those who have GERD symptoms. Many people benefit from taking H2 blockers at bedtime in combination with a proton pump inhibitor.

Proton pump inhibitors include omeprazole (Romecid), lansoprazole, pantoprazole (Pantab), rabeprazole and esomeprazole which are all available by prescription. Proton pump inhibitors are more effective than H2 blockers and can relieve symptoms in almost everyone who has GERD.

Another group of drugs, prokinetics, helps strengthen the sphincter and makes the stomach empty faster. This group includes bethanechol, metoclopramide and domperidone.

Because drugs work in different ways, combinations of drugs may help control symptoms. People who get heartburn after eating may take both antacids and H2 blockers. The antacids work first to neutralize the acid in the stomach, while the H2 blockers act on acid production. By the time the antacid stops working, the H2 blocker will have stopped acid production. Your doctor is the best source of information on how to use medications for GERD.

What if symptoms persist?

If your heartburn does not improve with lifestyle changes or drugs, you may need additional tests.

A barium swallow radiograph uses x rays to help spot abnormalities such as a hiatal hernia and severe inflammation of the esophagus. With this test, you drink a solution and then x rays are taken. Mild irritation will not appear on this test, although narrowing of the esophagus—called stricture—ulcers, hiatal hernia, and other problems will.

Upper endoscopy is more accurate than a barium swallow radiograph and may be performed in a hospital or a doctor's office. The doctor will spray your throat to numb it and slide down a thin, flexible plastic tube called an endoscope. A tiny camera in the endoscope allows the doctor to see the surface of the esophagus and to search for abnormalities. If you have had moderate to severe symptoms and this procedure reveals injury to the esophagus, usually no other tests are needed to confirm GERD. The doctor may use tiny tweezers (forceps) in the endoscope to remove a small piece of tissue for biopsy. A biopsy viewed under a microscope can reveal damage caused by acid reflux and rule out other problems if no infecting organisms or abnormal growths are found.
In an ambulatory pH monitoring examination, the doctor puts a tiny tube into the esophagus that will stay there for 24 hours. While you go about your normal activities, it measures when and how much acid comes up into your esophagus. This test is useful in people with GERD symptoms but no esophageal damage. The procedure is also helpful in detecting whether respiratory symptoms, including wheezing and coughing, are triggered by reflux.

Surgery

Surgery is an option when medicine and lifestyle changes do not work. Surgery may also be a reasonable alternative to a lifetime of drugs and discomfort

Fundoplication, usually a specific variation called Nissen fundoplication, is the standard surgical treatment for GERD. The upper part of the stomach is wrapped around the LES to strengthen the sphincter and prevent acid reflux and to repair a hiatal hernia.

This fundoplication procedure may be done using a laparoscope and requires only tiny incisions in the abdomen. To perform the fundoplication, surgeons use small instruments that hold a tiny camera. Laparoscopic fundoplication has been used safely and effectively in people of all ages, even babies. When performed by experienced surgeons, the procedure is reported to be as good as standard fundoplication. Furthermore, people can leave the hospital in 1 to 3 days and return to work in 2 to 3 weeks.

In 2000, the U.S. Food and Drug Administration (FDA) approved two endoscopic devices to treat chronic heartburn. The Bard EndoCinch system puts stitches in the LES to create little pleats that help strengthen the muscle. The Stretta system uses electrodes to create tiny cuts on the LES. When the cuts heal, the scar tissue helps toughen the muscle. The long-term effects of these two procedures are unknown.

Implant

Recently the FDA approved an implant that may help people with GERD who wish to avoid surgery. Enteryx is a solution that becomes spongy and reinforces the LES to keep stomach acid from flowing into the esophagus. It is injected during endoscopy. The implant is approved for people who have GERD and who require and respond to proton pump inhibitors. The long-term effects of the implant are unknown.

What are the long-term complications of GERD?

Sometimes GERD can cause serious complications. Inflammation of the esophagus from stomach acid causes bleeding or ulcers. In addition, scars from tissue damage can narrow the esophagus and make swallowing difficult. Some people develop Barrett's esophagus, where cells in the esophageal lining take on an abnormal shape and color, which over time can lead to cancer.

Also, studies have shown that asthma, chronic cough, and pulmonary fibrosis may be aggravated or even caused by GERD.
For information about Barrett's esophagus, please see the Barrett's Esophagus fact sheet from the National Institute of Diabetes and Digestive and Kidney Diseases.

Points to Remember
Heartburn, also called acid indigestion, is the most common symptom of GERD. Anyone experiencing heartburn twice a week or more may have GERD.
You can have GERD without having heartburn. Your symptoms could be excessive clearing of the throat, problems swallowing, the feeling that food is stuck in your throat, burning in the mouth, or pain in the chest.
In infants and children, GERD may cause repeated vomiting, coughing, and other respiratory problems. Most babies grow out of GERD by their first birthday.
If you have been using antacids for more than 2 weeks, it is time to see a doctor. Most doctors can treat GERD. Or you may want to visit an internist—a doctor who specializes in internal medicine—or a gastro-enterologist—a doctor who treats diseases of the stomach and intestines.
Doctors usually recommend lifestyle and dietary changes to relieve heartburn. Many people with GERD also need medication. Surgery may be an option.

Non-cardiac chest pain

What is noncardiac chest pain?

Chest pain that is not caused by a heart problem is called noncardiac chest pain. Because it is very important to determine the cause, always see your health care provider if you have chest pain.

How does it occur?

Many causes of chest pain are not related to a heart problem. These include:
Swallowing disorders such as esophageal spasm, caused by the muscles of the lower esophagus squeezing painfully due to acid reflux or stress
Gastrointestinal disorders such as heartburn, which is stomach acid backing up into the esophagus.

Lung disease such as bronchitis or pneumonia
Problems affecting the ribs and chest muscles such as muscle strain or inflammation of the ribs or muscles
Anxiety or panic attacks
Inflammation of the sack around the heart (pericarditis) or of the lining of the lungs (pleuritis/pleurisy).
How is it diagnosed?

Keeping track of your chest pain will help your health care provider make the diagnosis. Write down:

• What the pain feels like, such as stabbing, dull, or burning
• When it happens and how long it lasts
• Where it hurts
• What makes it better or worse
• Any other symptoms, such as nausea, vomiting, sweating, or trouble breathing.
  

Your provider will ask about your symptoms and medical history and examine you. You may have the following tests:

• Electrocardiogram (ECG)
• Exercise stress test
• Echocardiogram (ultrasound scan of the heart)
• Cardiac angiogram
• Blood tests
• X - rays
• tests of your esophagus.
  How is it treated?
  
  After your provider has confirmed that the chest pain is not caused by a heart problem, he or she will recommend treatment for the problem that is causing the pain.
  

What is non-cardiac chest pain?

Many people, both young and old, have intermittent chest pain. Chest pain can be alarming, as it might indicate severe heart disease or even a heart attack. However, many people (and most young people) have chest pain that is not caused by the heart - this is called non-cardiac chest pain.

What causes non-cardiac chest pain?

The most common cause of non-cardiac chest pain arises from a nearby organ, the esophagus. Esophageal causes of non-cardiac chest pain include gastro-esophageal reflux disease (GERD) and esophageal spasm. GERD results from stomach acid backing up into the esophagus, which produces heartburn and chest pain. Esophageal spasm is caused by chaotic muscle contractions of the lower esophagus aggravated by acid reflux, stress or unknown factors.
Another common cause of non-cardiac chest pain is musculo-skeletal problems, especially fibromyositis (muscle inflammation). Finally, anxiety and panic attacks can produce chest pain that resembles the pain experienced during a heart attack.
Who is affected by non-cardiac chest pain?Both men and women are affected by non-cardiac chest pain. However, the syndrome is twice as common in women, especially young and middle-aged women.
What are the symptoms?Non-cardiac chest pain may resemble cardiac pain, therefore, you need to see a physician for this problem. The chest pain is usually in the middle of the chest and is characterized by a dull, burning or pressure sensation. The pain usually does not radiate into the neck, shoulders or arms.
Non-cardiac chest pain secondary to esophageal causes is made worse during or after meals, when lying on the back (supine position), exercising or when experiencing anxiety. Associated symptoms are often found including heartburn, acid regurgitation or difficulty swallowing and a feeling of food sticking in the middle of the chest (dysphagia).

Non-cardiac chest pain secondary to musculoskeletal disorders can be located anywhere on the chest wall (multiple painful sites are common). Patients may also complain of muscle and joint aches, fatigue and difficulty sleeping.
The chest pain associated with anxiety and panic attacks is accompanied by a feeling of impeding doom, shortness of breath, heart palpitations, sweating and insomnia.

How do you find out if you have non-cardiac chest pain?You must see your physician so he or she can exclude heart disease. This may require further testing including an exercise stress test, cardiac ultrasound or a cardiac angiogram.

After heart disease is confidently excluded, your medical history and physical exam should give your doctor the appropriate clues to the non-cardiac causes of your chest pain.

These causes may be GERD, esophageal spasm, musculoskeletal problems or anxiety/panic attacks.

Further testing for esophageal problems may be necessary. These tests may include fiberoptic endoscopy to visualize and exam the esophagus for injury from acid, manometry to identify abnormal esophageal contractions, and pH testing to identify excessive acid reflux into the esophagus.

What is the treatment for non-cardiac chest pain?

• Most patients can have complete relief of their symptoms if the appropriate cause of non-cardiac chest pain is identified.
  For the following conditions, treatment may include:
  GERD
  Lifestyle changes
  Drugs to control acid reflux such as antacids, H2 blockers, cisapride, proton pump inhibitors
  -Esophageal spasms
  -Treat associated GERD/anxiety
  -Medications such as anticholinergics, calcium channel blockers
  -Musculo-skeletal disorders
  -Heat
  -Stretching exercises
  -Non-steroidal anti-inflammatory drugs (NSAIDs)
  -Anxiety/panic attacks
  -Anxiolytics
  Imipramine
  Alprazolam

-Surgery is rarely required to treat any of the above causes of non-cardiac chest pain.

Psychological interventions for noncardiac chest pain

Katherine L. Margo

Clinical Scenario

A 35-year-old man comes to you for follow-up after his third emergency department visit for continued intermittent chest pain. He has no cardiac risk factors and his electrocardiography (ECG) and stress test results were normal in the emergency department. You suspect a noncardiac cause for his chest pain.
Clinical Question

What is the best way to treat noncardiac chest pain?

Evidence-Based Answer

Noncardiac chest pain can be caused by gastroesophageal reflux disease (GERD), panic disorder, or a number of other psychological conditions. Psychotherapy, particularly cognitive behavior therapy, has been shown to reduce the number of days with chest pain significantly over a three-month period, whatever the cause. (1)

Practice Pointers

The cause of chest pain for patients presenting to emergency departments most commonly is noncardiac. Epidemiologic studies have not been conclusive, but noncardiac chest pain is thought to affect about 25 percent of the U.S. population, with equal distribution among men and women. As such, it also is seen commonly in primary care and pain is not related to cardiac disease does not prevent patients with noncardiac chest pain from experiencing significant functional impairment. This translates into high medical care usage, including hospitalization and inappropriate cardiac medication. The cause of noncardiac chest pain is most commonly GERD or panic disorder, although other gastrointestinal motility diseases and psychiatric diseases also figure prominently. (2,3) Even when the cause is gastrointestinal, there often is significant psychiatric comorbidity, as there is with GERD without noncardiac chest pain. (4) Chest pain in children rarely is related to the heart and is thought to be most commonly musculoskeletal, although children with chest pain can have increased anxiety-related symptoms. (2)

Patients who are evaluated in the emergency department and diagnosed with non-cardiac chest pain often are not treated for their chest pain in that setting. The assumption is that the anxiety evident in the patient will be eased with the reassurance that they do not have heart disease. This does not seem to be true. Patients with noncardiac chest pain show more cardiac awareness and cardioprotective behavior than those with actual cardiac disease, and noncardiac chest pain may persist for years. (5) Noncardiac chest pain can be difficult to treat. Empiric treatment with high-dose omeprazole (Romecid, Romecid D) or pantaprazole 9Pantab, Pantab D) can benefit patients in whom GERD is suspected. (6) Trazodone and imipramine also have been investigated as possible treatments for non-cardiac chest pain, although the studies were small. (4)

The authors of this Cochrane review (1) analyzed psychotherapy as treatment for noncardiac chest pain and found a modest benefit. Patients received from one to 12 sessions of therapy. Although the interventions varied, almost all included breathing exercises, and most also included cognitive restructuring and relaxation exercises. In some studies, the intervention also included problem solving, physical exercise, and graded exposure. Cognitive behavior therapy can be carried out in individual or group settings and can be administered by a physician, nurse, psychologist, or other trained professional.

What is Pantab?
Pantab contains pantoprazole. Pantoprazole is in a class of medications called proton-pump inhibitors. It works by decreasing the amount of acid made in the stomach.
Pantab is mainly indicated in acid-peptic disorder, including gastroesophageal reflux disease (GERD). Pantoprazole is used to treat, a condition in which backward flow of acid from the stomach causes heartburn and injury of the food pipe (esophagus). It is also used to treat conditions where the stomach produces too much acid, such as Zollinger-Ellison syndrome.

CLINICAL PHARMACOLOGY
Pharmacokinetics
PANTAB is prepared as an enteric- coated tablet so that absorption of pantoprazole begins only after the tablet leaves the stomach. Peak serum concentration (Cmax) and area under the serum concentration time curve (AUC) increase in a manner proportional to oral and intravenous doses from 10 mg to 80 mg. Pantoprazole does not accumulate and its pharmacokinetics are unaltered with multiple daily dosing. Following oral administration, the serum concentration of pantoprazole declines biexponentially with a terminal elimination half- life of approximately one hour. In extensive metabolizers (see Metabolism section) with normal liver function receiving an oral dose of the enteric- coated 40 mg pantoprazole tablet, the peak concentration (Cmax) is 2.5 µg/ mL, the time to reach the peak concentration (tmax) is 2.5 h and the total area under the plasma concentration versus time curve (AUC) is 4.8 µg· hr/ mL. When pantoprazole is given with food, its tmax is highly variable and may increase significantly. Following intravenous administration of pantoprazole to extensive metabolizers, its total clearance is 7.6- 14.0 L/ h and its apparent volume of distribution is 11.0- 23.6L.


Absorption:

The absorption of pantoprazole is rapid, with a Cmax of 2.5 µg/ mL that occurs approximately 2.5 hours after single or multiple oral 40- mg doses. Pantoprazole is well absorbed; it undergoes little first- pass metabolism resulting in an absolute bioavailability of approximately 77%. Pantoprazole absorption is not affected by concomitant administration of antacids. Administration of pantoprazole with food may delay its absorption up to 2 hours or longer; however, the Cmax and the extent of pantoprazole absorption (AUC) are not altered. Thus, pantoprazole may be taken without regard to timing of meals.
Distribution The apparent volume of distribution of pantoprazole is approximately 11.0- 23.6L, distributing mainly in extracellular fluid. The serum protein binding of pantoprazole is about 98%, primarily to albumin.

Metabolism:

Pantoprazole is extensively metabolized in the liver through the cytochrome P450 (CYP) system. Pantoprazole metabolism is independent of the route of administration (intravenous or oral). The main metabolic pathway is demethylation, by CYP2C19, with subsequent sulfation; other metabolic pathways include oxidation by CYP3A4. There is no evidence that any of the pantoprazole metabolites have significant pharmacologic activity. CYP2C19 displays a known genetic polymorphism due to its deficiency in some sub- populations (e. g. 3% of Caucasians and African- Americans and 17- 23% of Asians). Although these sub- populations of slow pantoprazole metabolizers have elimination half- life values of 3.5 to 10.0 hours, they still have minimal accumulation (=<>

Elimination:

After a single oral or intravenous dose of 14 C- labeled pantoprazole to healthy, normal metabolizer volunteers, approximately 71% of the dose was excreted in the urine with 18% excreted in the feces through biliary excretion. There was no renal excretion of unchanged pantoprazole.

Pharmacodynamics:

Mechanism of Action Pantoprazole is a proton pump inhibitor (PPI) that suppresses the final step in gastric acid production by forming a covalent bond to two sites of the (H +, K +)- ATPase enzyme system at the secretory surface of the gastric parietal cell. This effect is dose- related and leads to inhibition of both basal and stimulated gastric acid secretion irrespective of the stimulus. The binding to the (H + ,K + )- ATPase results in a duration of antisecretory effect that persists longer than 24 hours for all doses tested. Antisecretory Activity Under maximal acid stimulatory conditions using pentagastrin, a dose- dependent decrease in gastric acid output occurs after a single dose of oral (20- 80 mg) or a single dose of intravenous (20- 120 mg) pantoprazole in healthy volunteers. Pantoprazole given once daily results in increasing inhibition of gastric acid secretion. Following the initial oral dose of 40 mg pantoprazole, a 51% mean inhibition was achieved by 2.5 hours. With once a day dosing for 7 days the mean inhibition was increased to 85%. Pantoprazole suppressed acid secretion in excess of 95% in half of the subjects. Acid secretion had returned to normal within a week after the last dose of pantoprazole; there was no evidence of rebound hypersecretion.

INDICATIONS AND USAGE:

Short- Term Treatment of Erosive Esophagitis Associated With Gastroesophageal Reflux Disease (GERD)

PANTAB ® (pantoprazole sodium) Delayed- Release Tablets are indicated for the short- term treatment (up to 8 weeks) in the healing and symptomatic relief of erosive esophagitis. For those patients who have not healed after 8 weeks of treatment, an additional 8-week course of PANTAB may be considered.

Maintenance of Healing of Erosive Esophagitis:

PANTAB Delayed- Release Tablets are indicated for maintenance of healing of erosive esophagitis and reduction in relapse rates of daytime and nighttime heartburn symptoms in patients with gastroesophageal reflux disease (GERD). Controlled studies did not extend beyond 12 months.

Pathological Hypersecretory Conditions Including Zollinger-Ellison Syndrome PANTAB Delayed-Release Tablets are indicated for the long-term treatment of pathological hypersecretory conditions, including Zollinger-Ellison syndrome.

Treatment of Erosive Esophagitis:

The recommended adult oral dose OF PANTAB /PANTAB-D is 1 tablet/capsule given once daily for up to 8 weeks. For those patients who have not healed after 8 weeks of treatment, an additional 8- week course of PANTAB may be considered.

Maintenance of Healing of Erosive Esophagitis:

The recommended adult oral dose is one PANTAB 40 mg Delayed- Release Tablet, taken daily.

Pathological Hypersecretory Conditions including Zollinger-Ellison Syndrome:

The dosage of PANTAB in patients with pathological hypersecretory conditions varies with the individual patient. The recommended adult starting dose is 40 mg twice daily. Dosage regimens should be adjusted to individual patient needs and should continue for as long as clinically indicated. Doses up to 240 mg daily have been administered. Some patients have been treated continuously with PANTAB for more than 2 years.

No dosage adjustment is necessary in patients with renal impairment, hepatic impairment, or for elderly patients. No dosage adjustment is necessary in patients undergoing hemodialysis.

PANTAB Delayed- Release Tablets should be swallowed whole, with or without food in the stomach. If patients are unable to swallow a 40 mg tablet, two 20 mg tablets may be taken. Concomitant administration of antacids does not affect the absorption of PANTAB.

Patients should be cautioned that PANTAB Tablets should not be split, chewed or crushed.

HOW SUPPLIED

PANTAB ® (pantoprazole sodium) Tablets is supplied as 40 mg in a strip of 10 tablets

SIDE EFFECTS:

Worldwide, more than 11,100 patients have been treated with pantoprazole in clinical trials involving various dosages and duration of treatment. In general, pantoprazole has been well tolerated in both short- term and long- term trials.

In two U. S. controlled clinical trials involving pantoprazole 10-, 20-, or 40- mg doses for up to 8 weeks, there were no dose- related effects on the incidence of adverse events. The following adverse events considered by investigators to be possibly, probably or definitely related to drug occurred in 1% or more in the individual studies of GERD patients on therapy with PANTAB.

In a 24- month carcinogenicity study, Sprague- Dawley rats were treated orally with doses of 0.5 to 200 mg/ kg/ day, about 0.1 to 40 times the exposure on a body surface area basis, of a 50- kg person dosed at 40 mg/ day. In the gastric fundus, treatment at 0.5 to 200 mg/ kg/ day produced enterochromaffin- like (ECL) cell hyperplasia and benign and malignant neuroendocrine cell tumors in a dose- related manner. In the forestomach, treatment at 50 and 200 mg/ kg/ day (about 10 and 40 times the recommended human dose on a body surface area basis) produced benign squamous cell papillomas and malignant squamous cell carcinomas. Rare gastrointestinal tumors associated with pantoprazole treatment included an adenocarcinoma of the duodenum at 50 mg/ kg/ day, and benign polyps and adenocarcinomas of the gastric fundus at 200 mg/ kg/ day. In the liver, treatment at 0.5 to 200 mg/ kg/ day produced dose- related increases in the incidences of hepatocellular adenomas and carcinomas. In the thyroid gland, treatment at 200 mg/ kg/ day produced increased incidences of follicular cell adenomas and carcinomas for both male and female rats.
Sporadic occurrences of hepatocellular adenomas and a hepatocellular carcinoma were observed in Sprague- Dawley rats exposed to pantoprazole in 6- month and 12- month toxicity studies.

In a 24- month carcinogenicity study, Fischer 344 rats were treated orally with doses of 5 to 50 mg/ kg/ day, approximately 1 to 10 times the recommended human dose based on body surface area. In the gastric fundus, treatment at 5 to 50 mg/ kg/ day produced enterochromaffin- like (ECL) cell hyperplasia and benign and malignant neuroendocrine cell tumors. Dose selection for this study may not have been adequate to comprehensively evaluate the carcinogenic potential of pantoprazole.

In a 24- month carcinogenicity study, B6C3F1 mice were treated orally with doses of 5 to 150 mg/ kg/ day, 0.5 to 15 times the recommended human dose based on body surface area. In the liver, treatment at 150 mg/ kg/ day produced increased incidences of hepatocellular adenomas and carcinomas in female mice. Treatment at 5 to 150 mg/ kg/ day also produced gastric fundic ECL cell hyperplasia.

A 26- week p53 +/- transgenic mouse carcinogenicity study was not positive.
Pantoprazole was positive in the in vitro human lymphocyte chromosomal aberration assays, in one of two mouse micronucleus tests for clastogenic effects, and in the in vitro Chinese hamster ovarian cell/ HGPRT forward mutation assay for mutagenic effects. Equivocal results were observed in the in vivorat liver DNA covalent binding assay. Pantoprazole was negative in the in vitro Ames mutation assay, the in vitro unscheduled DNA synthesis (UDS) assay with rat hepatocytes, the in vitro AS52/ GPT mammalian cell- forward gene mutation assay, the in vitro thymidine kinase mutation test with mouse lymphoma L5178Y cells, and the in vivorat bone marrow cell chromosomal aberration assay.
Pantoprazole at oral doses up to 500 mg/ kg/ day in male rats (98 times the recommended human dose based on body surface area) and 450 mg/ kg/ day in female rats (88 times the recommended human dose based on body surface area) was found to have no effect on fertility and reproductive performance.

Pregnancy:

Teratogenic Effects Pregnancy Category B Teratology studies have been performed in rats at oral doses up to 450 mg/ kg/ day (88 times the recommended human dose based on body surface area) and rabbits at oral doses up to 40 mg/ kg/ day (16 times the recommended human dose based on body surface area) and have revealed no evidence of impaired fertility or harm to the fetus due to pantoprazole. There are, however, no adequate and well- controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if clearly needed.

Nursing Mothers:

Pantoprazole and its metabolites are excreted in the milk of rats. It is not known whether pantoprazole is excreted in human milk. Many drugs which are excreted in human milk have a potential for serious adverse reactions in nursing infants. Based on the potential for tumorigenicity shown for pantoprazole in rodent carcinogenicity studies, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the benefit of the drug to the mother.

Pediatric Use:

Safety and effectiveness in pediatric patients have not been established.

Use in Women:

Erosive esophagitis healing rates in the 221 women treated with PANTAB (pantoprazole sodium) Delayed- Release Tablets in U. S. clinical trials were similar to those found in men. In the 122 women treated long- term with PANTAB 40 mg or 20 mg, healing was maintained at a rate similar to that in men. The incidence rates of adverse events were also similar for men and women.

Use in Elderly:

In short- term U. S. clinical trials, erosive esophagitis healing rates in the 107 elderly patients (≥65 years old) treated with PANTAB were similar to those found in patients under the age of 65? The incidence rates of adverse events and laboratory abnormalities in patients aged 65 years and older were similar to those associated with patients younger than 65 years of age

PATIENT INFORMATION

Patients should be cautioned that PANTAB Delayed-Release Tablets should not be split, crushed or chewed. The tablets should be swallowed whole, with or without food in the stomach. Concomitant administration of antacids does not affect the absorption of pantoprazole.

Pantab D

Pantab D is a combination of pantoprazole 40mg and domperidone 10 mg.

Many times in GERD, doctors enhance the effect of pantoprazole by adding domperidone, a gastric prokinetic.

Prokinetics are drugs, which enhance the motility of the g.i. tract. Hypo-motility, leading to gastric stasis is a common problem in acid-peptic disorder. Domperidone is also used to treat nausea and vomiting.

Description:

Domperidone (dom-PER-i-done) is a medicine that increases the movements or contractions of the stomach and bowel. Domperidone is also used to treat nausea and vomiting caused by other drugs used to treat Parkinson's Disease.

Domperidone is to be given only by or under the immediate supervision of your doctor. It is available in the following dosage forms:

Pharmacological Action:

Domperidone is a dopamine-receptor blocking agent. Its action on the dopamine-receptors in the chemo-emetic trigger zone produces an anti-emetic effect.

Domperidone does not cross the blood-brain barrier to any appreciable degree and so exerts relatively little effect on cerebral dopaminergic receptors.

Domperidone has been shown to increase the duration of antral and duodenal contractions to increase gastric emptying.

Domperidone does not alter gastric secretions and has no effect on intracranial pressure or on the cardiovascular system.

Domperidone is rapidly absorbed, with peak plasma concentrations at approximately 1 hour after oral administration.

The absolute bio-availability of oral domperidone is low (approximately 15%) due to first-pass hepatic and intestinal metabolism.Domperidone is 91 to 93% bound to plasma proteins. The plasma half-life after a single oral dose is 7 to 9 hours in healthy subjects but is prolonged in patients with severe renal insufficiency.Domperidone undergoes rapid and extensive hepatic metabolism by hydroxylation and N-dealkylation. In vitro metabolism experiments with diagnostic inhibitors revealed that CYP3A4 is a major form of cytochrome P-450 involved in the N-dealkylation of domperidone, whereas CYP3A4, CYP1A2 and CYP2E1 are involved in domperidone aromatic hydroxylation.
Urinary and faecal excretion amount to 31% and 66% of the oral dose, respectively. The proportion of drug excreted unchanged is small (approximately 1% of urinary and 10% of faecal excretion).

Indications:

Domperidone is indicated for:
Delayed gastric emptying of functional origin with gastro-esophageal reflux and/or dyspepsia
Control of nausea and vomiting of central or local origin.
As an anti-emetic in patients receiving cytostatic and radiation therapy.
Facilitates radiological examination of the upper gastro-intestinal tract.

CONTRA-INDICATIONS:

DOMPERIDONE is contra-indicated in patients with known hypersensitivity to domperidone.

Domperidone should not be used whenever stimulation of gastric motility is to be avoided or could be harmful, eg. in the presence of gastro-intestinal hemorrhage, obstruction or perforation.

Domperidone is also contra-indicated in patients with a prolactin-releasing pituitary tumor (prolactinoma).
The safety of use during pregnancy and lactation has not been established

In very severe GERD, with nausea and vomiting, Pantab D would the preference of choice.

For more details on Pantab and Pantab D, please e-mail to

Mr. Ghanashyambhai Patel – Director (Marketing and Sales)
Mr. Mukesh Vankani – General Manager (Marketing & Sales)
Mr. Deepak Shah B. Pharma. M.B.A.

At

reliancehealthcare@yahoo.co.in

Relidep Range for anxiety depression control

Relidep Range for anxiety and depression control

The Relationship BetweenDepression and Anxiety

"If you're facing terror every day, it's gonna bring Hannibal to his knees"
Jim Ballenger, a leading expert on anxiety

Although depression is often considered to be a "low energy'' state, the opposite is usually true.

Inside, the depressed person often experiences a lot of anxiety. This can lead to them having panic attacks.

Of course, having panic attacks can itself be a depressing thing. Any lack of control within our lives can contribute to depression.

The Link Between Depression and Anxiety

Depression and anxiety disorders are not the same though, although at first glance they seem very similar. Depression generates emotions such as hopelessness, despair and anger. Energy levels are usually very low, and depressed people often feel overwhelmed by the day-to-day tasks and personal relationships so essential to life.

A person with anxiety disorder, however, experiences fear, panic or anxiety in situations where most people would not feel anxious or threatened. The sufferer may experience sudden panic or anxiety attacks without any recognized trigger, and often lives with a constant nagging worry or anxiousness. Without treatment, such disorders can restrict a person’s ability to work, maintain relationships, or even leave the house.

Both anxiety and depression are frequently treated in much the same manner, which may explain why the two disorders are so often confused. Antidepressant medication is often used for anxiety, while behavioral therapy frequently helps people overcome both conditions.

Why Are Depression and Anxiety Linked?

Although no one knows exactly why, a great number of depressions are also accompanied by anxiety. In one study, 85 percent of those with major depression were also diagnosed with generalized anxiety disorder while 35 percent had symptoms of a panic disorder. Other anxiety disorders include obsessive-compulsive disorder and post-traumatic stress disorder (PTSD). Because they so often go hand in hand, anxiety and depression are considered the fraternal twins of mood disorders.

Believed to be caused in part by a malfunction of brain chemistry, generalized anxiety is not the normal apprehension that one feels before taking a test or awaiting the outcome of a biopsy. A person with an anxiety disorder suffers from what President Franklin Roosevelt called "fear itself."

For a reason that is only partially known, the brain's fight-or-flight mechanism becomes activated, even when no real threat exists. Being chronically anxious is like being stalked by an imaginary tiger. The feeling of being in danger never goes away.

"Even more than the depression, it was my anxiety and agitation that became the defining symptoms of my illness. Like epileptic seizures, a series of frenzied anxiety attacks would descend upon me without warning. My body was possessed by a chaotic, demonic force which led to my shaking, pacing and violently hitting myself across the chest or in the head. This self-flagellation seemed to provide a physical outlet for my invisible torment, as if I were letting steam out of a pressure cooker."Douglas Bloch, M.A., author of "Healing From Depression"

Being both anxious and depressed is a tremendous challenge. Clinicians have observed that when anxiety occurs "comorbidly" with depression, the symptoms of both the depression and anxiety are more severe compared to when those disorders occur independently. Moreover, the symptoms of the depression take longer to resolve, making the illness more chronic and more resistant to treatment. Finally, depression exacerbated by anxiety has a much higher suicide rate than depression alone. (In one study, 92 percent of depressed patients who had attempted suicide were also plagued by severe anxiety. This where brands like Relidep Plus and Relidep Plus H are useful) Like alcohol and barbiturates, depression and anxiety are a deadly combination when taken together.

Unfortunately, over 60 percent of major depressions are accompanied by varying levels of anxious feelings and behavior. (During his illness, Douglas Bloch says extreme anxiety interfered with his recovery and increased the risk of suicide.)
Here are some techniques that are commonly used to treat mild to severe anxiety.

1. Medications

The medications most often used to treat anxiety are a class of drugs known as benzodiazepines (also called "minor tranquilizers"). These include alprazolam, lorazepam and clonazepam and chlordiazepoxide. The main problem with these substances is their potential for tolerance, physical dependence, and the likely recurrence of panic and anxiety symptoms when the medication is stopped. Hence, they are best used for treating short-term anxiety and panic. Because anxiety is so often associated with depressive disorders, it is essential to treat the underlying depression along with the anxiety disorder. When the depression is healed, symptoms of anxiety often diminish. For some people, the herb Kava provides relief from anxiety without the problem of addiction."

2.Exercise and relaxation techniques

Because anxiety clearly has a physical component (especially when it manifests as a panic attack), techniques for relaxing the body are an important part of the treatment plan. These include abdominal breathing, progressive muscle relaxation (relaxing the body's muscle groups) and biofeedback. You can learn these practices from any mental health professional that teaches relaxation or stress reduction. Regular exercise also has a direct impact on several physiological conditions that underlie anxiety. Exercise reduces skeletal muscle tension, metabolizes excess adrenaline and thyroxin in the bloodstream (chemicals which keep one in a state of arousal) and discharges pent-up frustration and anger.

3.Cognitive-behavioral therapy

Cognitive-behavioral therapy is a psychotherapy that helps you to alter anxious self-talk and mistaken beliefs that give the body anxiety-producing messages. For example, saying to yourself, "What if I have an anxiety attack when I'm driving home?" will make it more likely that an attack will ensue. Overcoming negative self-talk involves creating positive counterstatements such as "I can feel anxious and still drive," or "I can handle it." What often underlies our negative self-talk is a set of negative beliefs about ourselves and the world. Examples of such mistaken beliefs are, "I am powerless," "Life is dangerous," and "It's not okay to show my feelings." Replacing these beliefs with empowering truths can help to heal the roots of anxiety (see the chart on cognitive distortions at the end of this section).

4.Monitoring diet and nutrition

Stimulants such as caffeine and nicotine can aggravate anxiety and leave one more prone to anxiety and panic attacks. Other dietary factors such as sugar, certain food additives and food sensitivities can make some people feel anxious. Seeing a nutritionally oriented physician or therapist may help you to identify and eliminate possible offending substances from your diet. He or she can also help you to research supplements and herbs (e.g., GABA, kava, B vitamins, chamomile and valerian teas) that are known to calm the nervous system. If you are suffering from a serious anxiety disorder, you may want to locate a clinic in your area that specializes in the treatment of anxiety. Your local hospital or mental health clinic can give you a referral. In addition, you may wish to call (800) 64-PANIC to receive helpful material from the National Institute of Mental Health.



Relidep/ Relidep Plus/ Relidep Plus H and Chronic Fatigue Syndrome[CFS]

Using Antidepressants/anxiolytics to Treat Chronic Fatigue Syndrome
By Charles Lapp, MD,Hunter-Hopkins Center,Duke University

Antidepressants have proven to be useful in treating chronic fatigue syndrome (CFS). They can help improve sleep, energy levels and cognitive impairment, and alleviate pain.

It needs to be emphasized that these drugs are helpful not because patients are primarily depressed (although depression may occur as a result of the illness), but because they often have low levels of the neurotransmitters serotonin and dopamine.

I find that almost all of my patients benefit from treatment with antidepressants. Following is a brief discussion of research on the benefits of antidepressants and the process that I use when deciding which drug to try with a patient.
Review of ResearchA small number of trials have been conducted to assess the possible value of antidepressants for CFS, and for the most part have provided evidence of their usefulness in treating specific symptoms.

A minority of patients in a six-week treatment study of phenelzine, a monoamine oxidase inhibitor (MAOI), reported significant improvement, although some had to drop out of the trial due to side effects.Trials of moclobemide, another MAOI, with CFS patients have showed significant reductions in fatigue.

Unfortunately, moclobemide is not available in the United States and India.

Nortriptyline[Sensival] a tricyclic antidepressant, was tested in a single-case, double-blind study for CFS. A 60 mg-per day dose significantly reduced CFS symptom scores.

In controlled trials, TCAs have also proven beneficial in the treatment of fibromyalgia (FM), an illness that shares many clinical features with CFS.

Despite encouraging results from earlier case studies, a trial of fluoxetine conducted in the Netherlands with 44 CFS patients with concomitant depression and 52 with CFS but no evidence of depression failed to show significant beneficial effects. The researchers suggested that the fact that even the depressed group failed to improve indicates chemical changes in the brain in CFS that are very dissimilar to depression.

Pain control is another factor that I consider. TCA’s increase levels of norepinephrine in the central nervous system, which will increase the patient's pain threshold. This is why amitriptyline and imipramine are often used to treat FM and CFS. However, while TCA’s have a soporific effect, it reduces deep sleep and in the long run may not be the best choice for patients having trouble sleeping. Venlafaxine is a serotonin and norepinephrine reuptake inhibitor that may also increase the pain threshold.


Relidep
The reliable antidepressant

Relidep: Amitriptyline 10/25/50/75

Relidep Plus: Amitriptyline 25 mg + Chlordiazepoxide 10 mg

Relidep Plus – H: Amitriptyline 12.5 mg + Chlordiazepoxide 5mg


Amitriptyline

Use:

Amitriptyline is a tricyclic antidepressant. Depressive illness of psychotic or endogenous nature and in selected patient with neurotic depression. May help alleviate anxiety component of depression.

Outpatient adults: Initially, 25 mg 3 times/day. Depending on tolerance and response, increase to a total of 150 mg/day with increases made preferably in late afternoon and/or bedtime doses.

Hospitalized patients may require 100 mg/day initially, increased gradually to 200 mg/day if necessary. A small number may need up to 300 mg/day.

Adolescent and elderly patients: Lower dosages are recommended for these patients and 50 mg/day given in divided doses or in a single evening or bedtime dose may be satisfactory.

For maintenance, reduce dosage to the lowest amount that maintains relief of symptoms- usually 50-100 mg/day in divided doses, or in suitable patients, in a single dose, preferably at bedtime.

Contraindications:

Not to be given concomitantly with MAOIs; discontinue MAOI therapy at least 14 days before starting amitriptyline and acute recovery phase following MI, acute CHF.

Precautions:

History of seizures, impaired liver function, hepatic damage, blood dyscrasias, urinary retention, constipation, narrow-angle glaucoma or increased intraocular pressure, cardiovascular disorders, hyperthyroidism. Pregnancy, lactation. Not recommended for depressed patients <>Side effects:

Anticholinergic effects (e.g. dry mouth, blurred vision, urinary retention, constipation, palpitations, tachycardia, associated sublingual adenitis or gingivitis). Weight loss or gain. Tinnitus, drowsiness, nervousness, insomnia, Hypotension, dizziness, rash sweating, confusion, mania, psychosis, heart block, arrhythmias, extrapyramidal symptoms. Gastric upset. Endocrine effects (e.g. changes in libido, impotence, gynecomastia, galactorrhea). Rarely, bone marrow depression, hepatic toxicity, seizures, peripheral neuropathy, severe cardiovascular effects in patients with cardiac disease, photosensitivity, Dysarthria, stuttering, renal failure. Withdrawal symptoms.

Interactions:

Possible hyperpyretic crisis if given with or within 14 days of MAOI therapy. May enhance the response to alcohol, other CNS depressants and anticholinergics (paralytic ileus). Use cautiously with sympathomimetics. May block the antihypertensive effect of guanethidine or similar agents. Delirium with ethchlorvynol and also with disulfiram. Cimetidine may reduce the hepatic metabolism of some tricyclic antidepressants.

Patient tips:

Caution regarding drowsiness, blurred vision (NB driving). Restrict alcohol intake. Antidepressant activity may take up to 30 days to develop adequately. Photosensitivity.

Chlordiazepoxide

Pharmacology:

Anxiolytic

Chlordiazepoxide possesses sedative, hypnotic, anxiolytic and muscle relaxant properties. These effects appear to be mediated through facilitation of the actions of gamma aminobutyric acid (GABA) in the CNS. Chlordiazepoxide acts selectively on polysynaptic neuronal pathways and may inhibit or augment transmission, depending on the endogenous function of GABA. It does not produce ganglionic blockade or reduce affective responses at therapeutic dosage as do phenothiazine drugs and reserpine. Amine oxidase inhibition has not been demonstrated with chlordiazepoxide.

Following oral administration, the drug appears in the blood stream in 0.5 to 1 hour; peak blood levels occur in 2 to 4 hours. After i.m. administration effects of the drug appear in 15 to 30 minutes, and following i.v. administration, within 3 to 30 minutes. Following administration of radioactive chlordiazepoxide to rats, distribution of the drug or its metabolites has been shown to be fairly even throughout all body tissues. Chlordiazepoxide readily passes the placental barrier, with the concentration of the drug in the fetal circulation approaching or equaling that in maternal circulation. Chlordiazepoxide has a volume of distribution of 0.3 L/kg and is 96% protein bound. The plasma half-life of a single dose of chlordiazepoxide in healthy subjects has been reported to range from 5 to 30 hours. Pharmacologically active metabolites of chlordiazepoxide include desmethylchlordiazepoxide, demoxepam, desmethyldiazepam and oxazepam. Less than 1% is excreted in the urine unchanged.

Indications:

Symptomatic relief of mild anxiety and tension and for reduction of tension states that may accompany muscle spasm. As an adjunct in tension states associated with insomnia, pre and postoperative apprehension, tension headache, premenstrual tension and stress, and functional gastrointestinal, cardiovascular, gynecological, and dermatological disorders with an emotional overlay. May be useful in the alleviation of alcohol withdrawal syndromes, although drug dependence may result, substituting for alcohol dependence. May also reduce anxiety associated with psychosis, but is not a specific management of psychosis.

Dosage

Optimum dosage varies with diagnosis and patient response; therefore, individual adjustment of dose is important, with minimum effective dose being used.

Oral:

Adults:Usually 10 to 40 mg daily in divided doses. In severe cases, 25 mg 3 or 4 times a day may be given.

Elderly or debilitated patients:5 mg 2 to 4 times daily.
Preoperative apprehension:5 to 10 mg, 3 to 4 times daily on days prior to surgery.

Dosage of Relidep/ Relidep Plus/ Relidep H: as per directions of treating and precsribing physician

For further details, please e-mail

Mr. Mukesh Vankani – General Manager [Marketing and Sales]

Or

Mr. Deepak Shah B. Pharm MBA

Relidep Range for anxiety depression control

Relidep Range for anxiety and depression control

The Relationship BetweenDepression and Anxiety

"If you're facing terror every day, it's gonna bring Hannibal to his knees"
Jim Ballenger, a leading expert on anxiety

Although depression is often considered to be a "low energy'' state, the opposite is usually true.

Inside, the depressed person often experiences a lot of anxiety. This can lead to them having panic attacks.

Of course, having panic attacks can itself be a depressing thing. Any lack of control within our lives can contribute to depression.

The Link Between Depression and Anxiety

Depression and anxiety disorders are not the same though, although at first glance they seem very similar. Depression generates emotions such as hopelessness, despair and anger. Energy levels are usually very low, and depressed people often feel overwhelmed by the day-to-day tasks and personal relationships so essential to life.

A person with anxiety disorder, however, experiences fear, panic or anxiety in situations where most people would not feel anxious or threatened. The sufferer may experience sudden panic or anxiety attacks without any recognized trigger, and often lives with a constant nagging worry or anxiousness. Without treatment, such disorders can restrict a person’s ability to work, maintain relationships, or even leave the house.

Both anxiety and depression are frequently treated in much the same manner, which may explain why the two disorders are so often confused. Antidepressant medication is often used for anxiety, while behavioral therapy frequently helps people overcome both conditions.

Why Are Depression and Anxiety Linked?

Although no one knows exactly why, a great number of depressions are also accompanied by anxiety. In one study, 85 percent of those with major depression were also diagnosed with generalized anxiety disorder while 35 percent had symptoms of a panic disorder. Other anxiety disorders include obsessive-compulsive disorder and post-traumatic stress disorder (PTSD). Because they so often go hand in hand, anxiety and depression are considered the fraternal twins of mood disorders.

Believed to be caused in part by a malfunction of brain chemistry, generalized anxiety is not the normal apprehension that one feels before taking a test or awaiting the outcome of a biopsy. A person with an anxiety disorder suffers from what President Franklin Roosevelt called "fear itself."

For a reason that is only partially known, the brain's fight-or-flight mechanism becomes activated, even when no real threat exists. Being chronically anxious is like being stalked by an imaginary tiger. The feeling of being in danger never goes away.

"Even more than the depression, it was my anxiety and agitation that became the defining symptoms of my illness. Like epileptic seizures, a series of frenzied anxiety attacks would descend upon me without warning. My body was possessed by a chaotic, demonic force which led to my shaking, pacing and violently hitting myself across the chest or in the head. This self-flagellation seemed to provide a physical outlet for my invisible torment, as if I were letting steam out of a pressure cooker."Douglas Bloch, M.A., author of "Healing From Depression"

Being both anxious and depressed is a tremendous challenge. Clinicians have observed that when anxiety occurs "comorbidly" with depression, the symptoms of both the depression and anxiety are more severe compared to when those disorders occur independently. Moreover, the symptoms of the depression take longer to resolve, making the illness more chronic and more resistant to treatment. Finally, depression exacerbated by anxiety has a much higher suicide rate than depression alone. (In one study, 92 percent of depressed patients who had attempted suicide were also plagued by severe anxiety. This where brands like Relidep Plus and Relidep Plus H are useful) Like alcohol and barbiturates, depression and anxiety are a deadly combination when taken together.

Unfortunately, over 60 percent of major depressions are accompanied by varying levels of anxious feelings and behavior. (During his illness, Douglas Bloch says extreme anxiety interfered with his recovery and increased the risk of suicide.)
Here are some techniques that are commonly used to treat mild to severe anxiety.

1. Medications

The medications most often used to treat anxiety are a class of drugs known as benzodiazepines (also called "minor tranquilizers"). These include alprazolam, lorazepam and clonazepam and chlordiazepoxide. The main problem with these substances is their potential for tolerance, physical dependence, and the likely recurrence of panic and anxiety symptoms when the medication is stopped. Hence, they are best used for treating short-term anxiety and panic. Because anxiety is so often associated with depressive disorders, it is essential to treat the underlying depression along with the anxiety disorder. When the depression is healed, symptoms of anxiety often diminish. For some people, the herb Kava provides relief from anxiety without the problem of addiction."

2.Exercise and relaxation techniques

Because anxiety clearly has a physical component (especially when it manifests as a panic attack), techniques for relaxing the body are an important part of the treatment plan. These include abdominal breathing, progressive muscle relaxation (relaxing the body's muscle groups) and biofeedback. You can learn these practices from any mental health professional that teaches relaxation or stress reduction. Regular exercise also has a direct impact on several physiological conditions that underlie anxiety. Exercise reduces skeletal muscle tension, metabolizes excess adrenaline and thyroxin in the bloodstream (chemicals which keep one in a state of arousal) and discharges pent-up frustration and anger.

3.Cognitive-behavioral therapy

Cognitive-behavioral therapy is a psychotherapy that helps you to alter anxious self-talk and mistaken beliefs that give the body anxiety-producing messages. For example, saying to yourself, "What if I have an anxiety attack when I'm driving home?" will make it more likely that an attack will ensue. Overcoming negative self-talk involves creating positive counterstatements such as "I can feel anxious and still drive," or "I can handle it." What often underlies our negative self-talk is a set of negative beliefs about ourselves and the world. Examples of such mistaken beliefs are, "I am powerless," "Life is dangerous," and "It's not okay to show my feelings." Replacing these beliefs with empowering truths can help to heal the roots of anxiety (see the chart on cognitive distortions at the end of this section).

4.Monitoring diet and nutrition

Stimulants such as caffeine and nicotine can aggravate anxiety and leave one more prone to anxiety and panic attacks. Other dietary factors such as sugar, certain food additives and food sensitivities can make some people feel anxious. Seeing a nutritionally oriented physician or therapist may help you to identify and eliminate possible offending substances from your diet. He or she can also help you to research supplements and herbs (e.g., GABA, kava, B vitamins, chamomile and valerian teas) that are known to calm the nervous system. If you are suffering from a serious anxiety disorder, you may want to locate a clinic in your area that specializes in the treatment of anxiety. Your local hospital or mental health clinic can give you a referral. In addition, you may wish to call (800) 64-PANIC to receive helpful material from the National Institute of Mental Health.



Relidep/ Relidep Plus/ Relidep Plus H and Chronic Fatigue Syndrome[CFS]

Using Antidepressants/anxiolytics to Treat Chronic Fatigue Syndrome
By Charles Lapp, MD,Hunter-Hopkins Center,Duke University

Antidepressants have proven to be useful in treating chronic fatigue syndrome (CFS). They can help improve sleep, energy levels and cognitive impairment, and alleviate pain.

It needs to be emphasized that these drugs are helpful not because patients are primarily depressed (although depression may occur as a result of the illness), but because they often have low levels of the neurotransmitters serotonin and dopamine.

I find that almost all of my patients benefit from treatment with antidepressants. Following is a brief discussion of research on the benefits of antidepressants and the process that I use when deciding which drug to try with a patient.
Review of ResearchA small number of trials have been conducted to assess the possible value of antidepressants for CFS, and for the most part have provided evidence of their usefulness in treating specific symptoms.

A minority of patients in a six-week treatment study of phenelzine, a monoamine oxidase inhibitor (MAOI), reported significant improvement, although some had to drop out of the trial due to side effects.Trials of moclobemide, another MAOI, with CFS patients have showed significant reductions in fatigue.

Unfortunately, moclobemide is not available in the United States and India.

Nortriptyline[Sensival] a tricyclic antidepressant, was tested in a single-case, double-blind study for CFS. A 60 mg-per day dose significantly reduced CFS symptom scores.

In controlled trials, TCAs have also proven beneficial in the treatment of fibromyalgia (FM), an illness that shares many clinical features with CFS.

Despite encouraging results from earlier case studies, a trial of fluoxetine conducted in the Netherlands with 44 CFS patients with concomitant depression and 52 with CFS but no evidence of depression failed to show significant beneficial effects. The researchers suggested that the fact that even the depressed group failed to improve indicates chemical changes in the brain in CFS that are very dissimilar to depression.

Pain control is another factor that I consider. TCA’s increase levels of norepinephrine in the central nervous system, which will increase the patient's pain threshold. This is why amitriptyline and imipramine are often used to treat FM and CFS. However, while TCA’s have a soporific effect, it reduces deep sleep and in the long run may not be the best choice for patients having trouble sleeping. Venlafaxine is a serotonin and norepinephrine reuptake inhibitor that may also increase the pain threshold.


Relidep
The reliable antidepressant

Relidep: Amitriptyline 10/25/50/75

Relidep Plus: Amitriptyline 25 mg + Chlordiazepoxide 10 mg

Relidep Plus – H: Amitriptyline 12.5 mg + Chlordiazepoxide 5mg


Amitriptyline

Use:

Amitriptyline is a tricyclic antidepressant. Depressive illness of psychotic or endogenous nature and in selected patient with neurotic depression. May help alleviate anxiety component of depression.

Outpatient adults: Initially, 25 mg 3 times/day. Depending on tolerance and response, increase to a total of 150 mg/day with increases made preferably in late afternoon and/or bedtime doses.

Hospitalized patients may require 100 mg/day initially, increased gradually to 200 mg/day if necessary. A small number may need up to 300 mg/day.

Adolescent and elderly patients: Lower dosages are recommended for these patients and 50 mg/day given in divided doses or in a single evening or bedtime dose may be satisfactory.

For maintenance, reduce dosage to the lowest amount that maintains relief of symptoms- usually 50-100 mg/day in divided doses, or in suitable patients, in a single dose, preferably at bedtime.

Contraindications:

Not to be given concomitantly with MAOIs; discontinue MAOI therapy at least 14 days before starting amitriptyline and acute recovery phase following MI, acute CHF.

Precautions:

History of seizures, impaired liver function, hepatic damage, blood dyscrasias, urinary retention, constipation, narrow-angle glaucoma or increased intraocular pressure, cardiovascular disorders, hyperthyroidism. Pregnancy, lactation. Not recommended for depressed patients <>Side effects:

Anticholinergic effects (e.g. dry mouth, blurred vision, urinary retention, constipation, palpitations, tachycardia, associated sublingual adenitis or gingivitis). Weight loss or gain. Tinnitus, drowsiness, nervousness, insomnia, Hypotension, dizziness, rash sweating, confusion, mania, psychosis, heart block, arrhythmias, extrapyramidal symptoms. Gastric upset. Endocrine effects (e.g. changes in libido, impotence, gynecomastia, galactorrhea). Rarely, bone marrow depression, hepatic toxicity, seizures, peripheral neuropathy, severe cardiovascular effects in patients with cardiac disease, photosensitivity, Dysarthria, stuttering, renal failure. Withdrawal symptoms.

Interactions:

Possible hyperpyretic crisis if given with or within 14 days of MAOI therapy. May enhance the response to alcohol, other CNS depressants and anticholinergics (paralytic ileus). Use cautiously with sympathomimetics. May block the antihypertensive effect of guanethidine or similar agents. Delirium with ethchlorvynol and also with disulfiram. Cimetidine may reduce the hepatic metabolism of some tricyclic antidepressants.

Patient tips:

Caution regarding drowsiness, blurred vision (NB driving). Restrict alcohol intake. Antidepressant activity may take up to 30 days to develop adequately. Photosensitivity.

Chlordiazepoxide

Pharmacology:

Anxiolytic

Chlordiazepoxide possesses sedative, hypnotic, anxiolytic and muscle relaxant properties. These effects appear to be mediated through facilitation of the actions of gamma aminobutyric acid (GABA) in the CNS. Chlordiazepoxide acts selectively on polysynaptic neuronal pathways and may inhibit or augment transmission, depending on the endogenous function of GABA. It does not produce ganglionic blockade or reduce affective responses at therapeutic dosage as do phenothiazine drugs and reserpine. Amine oxidase inhibition has not been demonstrated with chlordiazepoxide.

Following oral administration, the drug appears in the blood stream in 0.5 to 1 hour; peak blood levels occur in 2 to 4 hours. After i.m. administration effects of the drug appear in 15 to 30 minutes, and following i.v. administration, within 3 to 30 minutes. Following administration of radioactive chlordiazepoxide to rats, distribution of the drug or its metabolites has been shown to be fairly even throughout all body tissues. Chlordiazepoxide readily passes the placental barrier, with the concentration of the drug in the fetal circulation approaching or equaling that in maternal circulation. Chlordiazepoxide has a volume of distribution of 0.3 L/kg and is 96% protein bound. The plasma half-life of a single dose of chlordiazepoxide in healthy subjects has been reported to range from 5 to 30 hours. Pharmacologically active metabolites of chlordiazepoxide include desmethylchlordiazepoxide, demoxepam, desmethyldiazepam and oxazepam. Less than 1% is excreted in the urine unchanged.

Indications:

Symptomatic relief of mild anxiety and tension and for reduction of tension states that may accompany muscle spasm. As an adjunct in tension states associated with insomnia, pre and postoperative apprehension, tension headache, premenstrual tension and stress, and functional gastrointestinal, cardiovascular, gynecological, and dermatological disorders with an emotional overlay. May be useful in the alleviation of alcohol withdrawal syndromes, although drug dependence may result, substituting for alcohol dependence. May also reduce anxiety associated with psychosis, but is not a specific management of psychosis.

Dosage

Optimum dosage varies with diagnosis and patient response; therefore, individual adjustment of dose is important, with minimum effective dose being used.

Oral:

Adults:Usually 10 to 40 mg daily in divided doses. In severe cases, 25 mg 3 or 4 times a day may be given.

Elderly or debilitated patients:5 mg 2 to 4 times daily.
Preoperative apprehension:5 to 10 mg, 3 to 4 times daily on days prior to surgery.

Dosage of Relidep/ Relidep Plus/ Relidep H: as per directions of treating and precsribing physician

For further details, please e-mail

Mr. Mukesh Vankani – General Manager [Marketing and Sales]

Or

Mr. Deepak Shah B. Pharm MBA