(bold print from the FDA web site)
Proton Pump Inhibitors (PPI): Class Labeling Change
including Nexium, Dexilant, Prilosec, Zegerid, Prevacid, Protonix, Aciphex, Vimovo, Prilosec OTC, Zegerid OTC, and Prevacid 24HR
[UPDATED 3/22/2011] FDA has determined an osteoporosis and fracture warning on the over-the-counter (OTC) proton pump inhibitor (PPI) medication “Drug Facts” label is not indicated at this time. Following a thorough review of available safety data, FDA has concluded that fracture risk with short-term, low dose PPI use is unlikely.
The National Institute of Health (NIH) argues gastroesophageal reflux disease (GERD) is the most common reason for doctor visits. Besides heartburn and indigestion, many unknowingly suffer from atypical GERD masquerading as mucus problems, loss of dental enamel, headache, stiff neck, insomnia, cough, asthma, etc. Relief is generally from commonly used stomach acid reducers, the proton pump inhibitors (PPI’s): Prilosec*, Zegerid*, Prevacid*, AcipHex, Protonix, Nexium and Dexilant (*available over-the-counter [OTC]). The Food and Drug Administration (FDA) allows medicines OTC only after addressing safety concerns. When PPI’s became available (1980’s), time limits (long since rescinded) were placed on continuous patient use while concerns with pneumonia, impaired protein, iron or B12 absorption, interference with Plavix, and other affects have also been alleviated. Relationships with infectious diarrhea and low magnesium levels remain unconfirmed. About 3% of patients can experience headache, upset stomach or diarrhea. See tbe bold print above revealing short term PPI use has very recently been "cleared", so currently (FDA) has an alert concerning osteoporosis with long term PPI use. However the American Journal of Gastroenterology recently reported analysis of 1,600 studies and found no significant bone risk identified with ongoing PPI use. Medication benefits need to exceed (or “match”) the risk. Extensively studied, PPI’s have exceeded safety expectations. The goal of therapy is to control symptoms, prevent serious complications of GERD (like bleeding, ulceration, scar tissue, Barrett’s esophagus, cancer of the esophagus) and improve quality-of-life. PPI’s are available for long term use when significant benefits exceed potential risks. Other medications and surgical procedures could be options.
Saturday, February 18. 2012
Vagus Nerve and Neurogenic Inflammation: Their Role in GERD
The autonomic nervous system (ANS or visceral nervous system) is part of the peripheral nervous system that acts as a control system functioning largely below the level of consciousness while it controls visceral (the “inner parts” of the body) functions. The ANS affects heart rate, digestion, respiration rate, salivation, perspiration, diameter of the pupils, urination and sexual arousal. Whereas most of its actions are involuntary, some, such as breathing, work in tandem with the conscious mind.
It is classically divided into two subsystems: the parasympathetic nervous system (PSNS) and the sympathetic nervous system (SNS). Relatively recently, a third subset of neurons have been named ‘non-adrenergic and non-cholinergic’ neurons (because they use nitric oxide as a neurotransmitter) have been described and found to be integral in autonomic function, particularly in the gut and the lungs. The enteric nervous system is sometimes considered part of the autonomic nervous system, and sometimes considered an independent system. Besides output to the various organs of the body, the vagus nerve conveys sensory information about the state of the body's organs to the central nervous system. Up to 80-90% of the nerve fibers in the vagus nerve are sensory nerves communicating the state of the viscera to the brain. The vagus nerve is also called the pneumogastric nerve because it innervates both the lungs and the stomach.
The lower esophagus is richly invested with vagal nerve endings and failure/relaxation of the lower esophageal sphincter allows digestive contents to leak in a retrograde fashion from the intestine and stomach. This allows corrosive digestive juices including acid and proteolytic enzymes to encounter, irritate and stimulate vagal nerve endings which over time become eroded and sensitized.Our brain receives the information via this communication network and, rightly so, becomes alarmed thus triggering involuntary protective reflex responses. Reilly's syndrome confirms that changes in vascular tone, and reticuloendothelial system via neurogenic inflammatory response produces protection in vulnerable tissues. This is where it gets really interesting. Either the severity of the reflux or the intensity of the body’s response to this dangerous insult can result in a clinical syndrome that has manifestations far-reaching beyond the origin of the endangered tissues. Thus regurgitation of digestive/intestinal contents into the lower esophagus can trigger vagal nerve response that results in tissues swelling, injury, scarring and mucus production in the paranasal sinuses as well as the larynx and pharynx without the affected tissues ever having come in direct contact with regurgitated digestive secretions. Artificial placement of acid into the lower esophagus is proven to result in inflammatory reaction of the paranasal sinuses. This is but one example of a myriad of potential effects that can occur anywhere in the distribution of the vagus nerve, or even the entire craniosacral nervous system. This phenomenon of vagal activation in the presence of regurgitated digestive contents explains the resolution of cardiac palpitations with successful therapy for gastroesophageal reflux disorder (GERD).
It is classically divided into two subsystems: the parasympathetic nervous system (PSNS) and the sympathetic nervous system (SNS). Relatively recently, a third subset of neurons have been named ‘non-adrenergic and non-cholinergic’ neurons (because they use nitric oxide as a neurotransmitter) have been described and found to be integral in autonomic function, particularly in the gut and the lungs. The enteric nervous system is sometimes considered part of the autonomic nervous system, and sometimes considered an independent system. Besides output to the various organs of the body, the vagus nerve conveys sensory information about the state of the body's organs to the central nervous system. Up to 80-90% of the nerve fibers in the vagus nerve are sensory nerves communicating the state of the viscera to the brain. The vagus nerve is also called the pneumogastric nerve because it innervates both the lungs and the stomach.
The lower esophagus is richly invested with vagal nerve endings and failure/relaxation of the lower esophageal sphincter allows digestive contents to leak in a retrograde fashion from the intestine and stomach. This allows corrosive digestive juices including acid and proteolytic enzymes to encounter, irritate and stimulate vagal nerve endings which over time become eroded and sensitized.Our brain receives the information via this communication network and, rightly so, becomes alarmed thus triggering involuntary protective reflex responses. Reilly's syndrome confirms that changes in vascular tone, and reticuloendothelial system via neurogenic inflammatory response produces protection in vulnerable tissues. This is where it gets really interesting. Either the severity of the reflux or the intensity of the body’s response to this dangerous insult can result in a clinical syndrome that has manifestations far-reaching beyond the origin of the endangered tissues. Thus regurgitation of digestive/intestinal contents into the lower esophagus can trigger vagal nerve response that results in tissues swelling, injury, scarring and mucus production in the paranasal sinuses as well as the larynx and pharynx without the affected tissues ever having come in direct contact with regurgitated digestive secretions. Artificial placement of acid into the lower esophagus is proven to result in inflammatory reaction of the paranasal sinuses. This is but one example of a myriad of potential effects that can occur anywhere in the distribution of the vagus nerve, or even the entire craniosacral nervous system. This phenomenon of vagal activation in the presence of regurgitated digestive contents explains the resolution of cardiac palpitations with successful therapy for gastroesophageal reflux disorder (GERD).
Thursday, February 16. 2012
Back Pain and GERD...Are They Connected?
This is an intriguing, mystifying subject but I have found numerous examples of back pain resolution concurrent with eradication of gastroesophageal reflux symptoms. Ten years ago I encountered the first example of dramatic back pain relief in a patient in his early 60s, disabled as a result of persistent pain following lumbar laminectomy. He realized subsequent to the surgery that he had limitations which, if exceeded, brought on significant worsening of his back pain condition. After the process of adjusting the dosage of his medication to successfully control atypical GERD symptoms he came to the office with pain in his forearms. He reported he had been using a "weed whip" in preparation for a visit from an out-of-state relative and had used the apparatus for several hours breaking only for lunch and then resuming activities after lunch for another several hours. He awoke next morning with severe pain in both of his forearms, and thus presented to the office. I was shocked when I heard the history considering the fact that he had previously reported limitations of 15 to 20 min. doing this particular behavior; if he exceeded these arbitrary limits his back pain progressed to the point of being insufferable. He stated, "My back doesn't bother me anymore. I can do almost anything I want to, it doesn't hurt anymore". Needless to say I was shocked. I cautioned him about being too physically aggressive, due to the danger of aggravating his pre-existing back pain. He continued to have dramatic relief and increased exercise tolerance as he reported shoveling gravel and in the winter months shoveling snow. After discussions with the late Dean of the College of Osteopathic Medicine at Michigan State University, Dr. Allan Jacobs, the conclusion was he no longer suffered from piriformis muscle spasm mediated through sacral segments 2,3,4. I have seen, on numerous occasions, individuals discontinue muscle relaxants and other pain relieving medications, including narcotics, since they were no longer needed. Generally, pain relief has been an anecdotal finding since people come to me with with problems such as rhinitis, sinus issues, headache, chest pain, coughing, throat clearing, and asthma. If they have pain, it often improves concurrently with resolution of atypical GERD symptoms. Remember, GERD is caused when digestive secretions migrate from the stomach and intestine back into the esophagus.The vagus nerve is richly invested in the lower esophagus and goes into "alarm mode". The vagus nerve communicates with the brain and the spinal cord to coordinate bodily functions and contributes to your automatic pilot (autonomic nervous system). This information thus continues on through the spinal cord as the craniosacral nervous system. Data departs from the spinal cord at sacral cord levels 2,3,4. As unusual as it seems or sounds, it appears that many people with back pain are experiencing muscle spasm as a result of regurgitation and reflux of digestive contents into the esophagus stimulating the vagus nerve. The vagus nerve commands tissues to produce mucus, vasodilate, extravasate and cause smooth muscle contraction. It thus appears that the piriformis muscle, innervated by sacral segments 2,3,4, can be influenced (adversely) into chronic spasm and pain as a result of regurgitation of digestive contents. On several occasions I have seen measureable, in some cases dramatic, eradication of pain, (including back pain) with successful treatment for extra esophageal manifestations of atypical GERD.
Thursday, February 9. 2012
Unrecognized Symptoms of GERD
A man in his 60s came when his dentist discovered dental enamel was being eroded by acid. He neither tasted nor felt the acid. He denies ever having had heartburn or indigestion. Questioning revealed long-standing neck pain, belching, and discomfort in the sternum area of his chest. He also reported "irregular heart beat”. His primary care provider had recently performed 24-hour Holter monitor EKG to evaluate the cardiac palpitations. He reported being particularly annoyed by “runny nose” when he eats. I'm not sure which of these bothersome symptoms had been reported to his internist but I find each of them to be very significant.
(1)-GERD without heartburn is called atypical or silent GERD; when respiratory problems predominate the moniker is laryngopharyngeal reflux (LPR).
(2)-Erosion of dental enamel is clearly associated with gastroesophageal reflux disease (GERD).
(3)-Neck pain (pain in the cervical region, torticollis) is commonly encountered in GERD patients and in my experience nearly always resolves with successful treatment.
(4)-Irregular pulse beat or cardiac palpitation is commonly associated with GERD. A large study at the Veterans Administration Hospital found a very strong correlation between GERD and atrial fibrillation.... eight times more common than would've been expected by chance alone.
(5)-Runny nose at mealtime, in medical terminology gustatory rhinitis, is common in reflux patients and it can be very difficult to eradicate but often improves with successful treatment.
(6)-belching (eructation) is commonly associated with GERD; so are hiccups (singultus).
(1)-GERD without heartburn is called atypical or silent GERD; when respiratory problems predominate the moniker is laryngopharyngeal reflux (LPR).
(2)-Erosion of dental enamel is clearly associated with gastroesophageal reflux disease (GERD).
(3)-Neck pain (pain in the cervical region, torticollis) is commonly encountered in GERD patients and in my experience nearly always resolves with successful treatment.
(4)-Irregular pulse beat or cardiac palpitation is commonly associated with GERD. A large study at the Veterans Administration Hospital found a very strong correlation between GERD and atrial fibrillation.... eight times more common than would've been expected by chance alone.
(5)-Runny nose at mealtime, in medical terminology gustatory rhinitis, is common in reflux patients and it can be very difficult to eradicate but often improves with successful treatment.
(6)-belching (eructation) is commonly associated with GERD; so are hiccups (singultus).
Sunday, January 22. 2012
GERD, Heartburn and the FDA
Gastroesophageal Reflux Disease (GERD) has become inescapably linked with heartburn and indigestion largely because of Food and Drug Administration (FDA) regulations regarding the advertising of prescription drugs. When drug manufacturers petitioned the FDA for permission to advertise “the Purple Pill” type medications they used the most commonly recognized symptoms of GERD, heartburn and indigestion, to plead their case. The designations atypical-GERD or silent-GERD identifies non-heartburn symptoms or problems associated with GERD because heartburn/indigestion is not present in every case of GERD. These unexpected non-heartburn symptoms are common as well as diverse. Such atypical symptoms were not requested for approval thus not approved in the FDA advertising rules for GERD medications. Thus sophisticated advertising, because of FDA statues, mandates heartburn is inevitably associated with GERD. It is just not “advertised” that GERD is common even without heartburn.
Two major neglected concepts I have encountered while studying the body’s response to GERD:1) reflux of digestive contents happens commonly without heartburn; 2) manifestations of the body’s response to the threat posed by GERD are extremely variable. The caustic, harsh digestive juices are very dangerous when they escape the friendly confines of the stomach and travel backward into the esophagus. The vagus nerve traverses the head, neck, chest and abdominal cavity connecting organs thus allowing communication and ultimately regulation of bodily functions. The lower esophagus is richly invested with vagal nerve fibers. The vagus nerve is an internal smoke, burglar and CO2 alarm. It connects with the “head-to-tail” craniosacral nervous system, a division of the “automatic pilot” autonomic nervous system. When the vagus nerve (10th cranial) is activated interesting and unanticipated events can result; some are profoundly life altering. It is most always the vagus nerve that is responsible for typical fainting spells. This often is identified as vagovasal syncope. An unappealing event takes place (the sight of blood, etc.) and the susceptible individual releases chemicals internally that result in a dramatic drop in blood pressure plus slowing of the heart rate. The resultant lack of blood flow to the brain causes the person to temporarily lose consciousness. This is an example of rapid discharge of stored neurotransmitter chemicals when the protective vagus nerve is set in motion. In GERD an ongoing intermittently-amplified, protective response occurs with or without heartburn. The vagus nerve connection explains how, in the research lab,acid artificially placed in the lower esophagus results in sinusitis.
The University Of Virginia School Of Medicine points out, "When GERD presents as a chronic cough or other extraesophageal symptom, G.I. symptoms may be silent. The patient's complaint may focus on the respiratory or other organ system. It is marked by an absence of any report of heartburn or related G.I. problem." They go on to reveal, “Other extraesophageal symptoms or conditions associated with GERD include chronic cough, bronchitis, recurrent pneumonia, globus sensation, hiccups, pharyngitis, sinusitis, otitis media, and erosion of dental enamel."
On the earlier pages of my website under “Meet the Doctor” is chapter of my book christened by the web site GRANDTIMES.com, “GERD: The Surprising Source of Many Physical Disorders”.
My goal is to demonstrate that a cause (reflux of digestive contents) has effects (swelling, congestion, mucus production). I hope you understand that treatment as near to the real source (cause) of the symptom/problem/"disease" means the more likely you are to succeed.
Two major neglected concepts I have encountered while studying the body’s response to GERD:1) reflux of digestive contents happens commonly without heartburn; 2) manifestations of the body’s response to the threat posed by GERD are extremely variable. The caustic, harsh digestive juices are very dangerous when they escape the friendly confines of the stomach and travel backward into the esophagus. The vagus nerve traverses the head, neck, chest and abdominal cavity connecting organs thus allowing communication and ultimately regulation of bodily functions. The lower esophagus is richly invested with vagal nerve fibers. The vagus nerve is an internal smoke, burglar and CO2 alarm. It connects with the “head-to-tail” craniosacral nervous system, a division of the “automatic pilot” autonomic nervous system. When the vagus nerve (10th cranial) is activated interesting and unanticipated events can result; some are profoundly life altering. It is most always the vagus nerve that is responsible for typical fainting spells. This often is identified as vagovasal syncope. An unappealing event takes place (the sight of blood, etc.) and the susceptible individual releases chemicals internally that result in a dramatic drop in blood pressure plus slowing of the heart rate. The resultant lack of blood flow to the brain causes the person to temporarily lose consciousness. This is an example of rapid discharge of stored neurotransmitter chemicals when the protective vagus nerve is set in motion. In GERD an ongoing intermittently-amplified, protective response occurs with or without heartburn. The vagus nerve connection explains how, in the research lab,acid artificially placed in the lower esophagus results in sinusitis.
The University Of Virginia School Of Medicine points out, "When GERD presents as a chronic cough or other extraesophageal symptom, G.I. symptoms may be silent. The patient's complaint may focus on the respiratory or other organ system. It is marked by an absence of any report of heartburn or related G.I. problem." They go on to reveal, “Other extraesophageal symptoms or conditions associated with GERD include chronic cough, bronchitis, recurrent pneumonia, globus sensation, hiccups, pharyngitis, sinusitis, otitis media, and erosion of dental enamel."
On the earlier pages of my website under “Meet the Doctor” is chapter of my book christened by the web site GRANDTIMES.com, “GERD: The Surprising Source of Many Physical Disorders”.
My goal is to demonstrate that a cause (reflux of digestive contents) has effects (swelling, congestion, mucus production). I hope you understand that treatment as near to the real source (cause) of the symptom/problem/"disease" means the more likely you are to succeed.
Tuesday, January 17. 2012
Reilly's syndrome, Neurogenic Inflammation and Gastric Asthma
Reilly's syndrome (page 258) Illustrated Dictionary of Eponymic Syndromes and Diseases and their Synonyms by Stanley Jablonski (National Library of Medicine)
Synonyms: Reilly's phenomenon, splanchnic vasoplegia, sympathetic irritation syndrome
A syndrome in which experimental irritation of the sympathetic nervous system with various agents, such as allergens, bacterial toxins, and physical irritants, produces vasomotor disorders, increased capillary permeability, edema, and lesions of the reticuloendothelial system.
This little-known syndrome is crucial in the understanding of gastroesophageal reflux disease (GERD), particularly when one considers non-esophageal manifestations of GERD.
The Journal of Respiratory Diseases published an article by Doctors Theodoropoulos & Ledford, “Is GERD a factor in your patient's asthma?". On page 239 they describe vagally mediated reflexes triggered by exposure to stomach acid, or mechanical distention, of the lower esophagus that may explain asthma exacerbations. The epithelial layer of the esophageal mucosa, already thinned by acid erosion, has exposed vagal nerve endings. As stomach contents are refluxed into the esophagus receptors are stimulated and transmit the signal via a neural network to the vagal nerve thereby stimulating bronchospasm. Mast cell degranulation may also contribute to smooth muscle contraction resulting in bronchoconstriction; plasma extravasation, vasodilation, and edema may be present. They go on to point out, “Vagally mediated reflexes and neurogenic inflammation have been proposed explanations for asthma exacerbations occurring in the absence of aspiration. Intra-esophageal installations studies in humans and dogs are consistent with the hypothesis of the vagal reflex triggered by exposure to acid or mechanical distention of the lower esophagus. These observations are supported by embryological evidence that the distal esophagus originates from the lung bud and that the lower esophagus and airway share innervation by the vagus nerve”.
This paradigm explains the inflammation in non-allergic asthma. This has been called "gastric asthma" by some authorities and Reilly's syndrome explains the justification. Here's to seeking the truth. Treat the "cause" and the "effects" go away.
Synonyms: Reilly's phenomenon, splanchnic vasoplegia, sympathetic irritation syndrome
A syndrome in which experimental irritation of the sympathetic nervous system with various agents, such as allergens, bacterial toxins, and physical irritants, produces vasomotor disorders, increased capillary permeability, edema, and lesions of the reticuloendothelial system.
This little-known syndrome is crucial in the understanding of gastroesophageal reflux disease (GERD), particularly when one considers non-esophageal manifestations of GERD.
The Journal of Respiratory Diseases published an article by Doctors Theodoropoulos & Ledford, “Is GERD a factor in your patient's asthma?". On page 239 they describe vagally mediated reflexes triggered by exposure to stomach acid, or mechanical distention, of the lower esophagus that may explain asthma exacerbations. The epithelial layer of the esophageal mucosa, already thinned by acid erosion, has exposed vagal nerve endings. As stomach contents are refluxed into the esophagus receptors are stimulated and transmit the signal via a neural network to the vagal nerve thereby stimulating bronchospasm. Mast cell degranulation may also contribute to smooth muscle contraction resulting in bronchoconstriction; plasma extravasation, vasodilation, and edema may be present. They go on to point out, “Vagally mediated reflexes and neurogenic inflammation have been proposed explanations for asthma exacerbations occurring in the absence of aspiration. Intra-esophageal installations studies in humans and dogs are consistent with the hypothesis of the vagal reflex triggered by exposure to acid or mechanical distention of the lower esophagus. These observations are supported by embryological evidence that the distal esophagus originates from the lung bud and that the lower esophagus and airway share innervation by the vagus nerve”.
This paradigm explains the inflammation in non-allergic asthma. This has been called "gastric asthma" by some authorities and Reilly's syndrome explains the justification. Here's to seeking the truth. Treat the "cause" and the "effects" go away.
Posted by Kurt Barrett, D.O.
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Monday, November 21. 2011
Halitosis and GERD
Could bad breath be an unidentified complication of gastroesophageal reflux disease (GERD)? Bacterial overgrowth from a mucus-rich environment can cause halitosis. In atypical/silent GERD, heartburn/indigestion, as a warning, is absent or infrequent. However, with or without heartburn, our natural defense mechanisms includes production of a mucus barrier to prevent the acid and refluxed digestive enzymes from harming the esophagus (and airways as well). Vagus nerve fibers in the esophagus recognize danger and trigger mucus production and more. As the protective mucus response grows it can “spill over” beyond the endangered esophagus clinging to dental/oral/ear/nasal structures. This mucus rich environment, in addition to being a nuisance, can allow bacterial over-growth causing the characteristic odor. Even extreme attempts at oral hygiene can fail. Those afflicted might (or might not!) have other unrecognized symptoms or events caused by refluxed stomach juices: nasal drip/itching/congestion, runny nose,”allergies”, sinus pressure, sneezing, throat clearing, hoarseness/voice changes, lump sensation in the throat, choking, sore throat, difficulty swallowing, hiccups, dental problems, ear discomfort, headache, neck pain/stiffness, chronic cough, unexplained chest pain/chest soreness could be present in GERD. A variety of symptoms can be present at any age, even in infants. Non-heartburn, atypical-GERD symptoms are often harder to treat/resolve. Therapy intended for heartburn relief alone often leave away-from-the-esophagus (called extra-esophageal) symptoms untouched. I first realized GERD could have far reaching implications when, after numerous failed therapies, I found it the cause of my daughter’s long-standing phlegm and choking episodes. If the underlying cause is treated symptoms disappear.
Friday, July 29. 2011
Idiopathic Pulmonary Fibrosis (IPF) Treated for GERD Survive Longer
The American Journal of Respiratory and Critical Care Medicine (7/21/2011) reported use of reflux medications was an independent predictor of improved x-ray findings as well as longer survival. These findings support the hypothesis that reflux plays an important role in IPF.
This adds to the evidence that lung (pulmonary) problems are closely associated with GERD. A study released in 2011 reveals that patients with IPF DOUBLE THEIR LIFE EXPECTANCY with therapy for GERD even in the absence of classic symptoms.
This adds to the evidence that lung (pulmonary) problems are closely associated with GERD. A study released in 2011 reveals that patients with IPF DOUBLE THEIR LIFE EXPECTANCY with therapy for GERD even in the absence of classic symptoms.
Sunday, July 24. 2011
Back Pain and GERD?????
Four recent cases of extraordinary outcomes that share the fact they no longer require narcotics for back pain control.
1) cc: 70 y/o female chief complaint: for years coughing up phlegm every morning for 2-3 hours. Therapy initiated including pantoprazole 40 mg, 2 tabs twice daily; cough GONE, discontinued 7 yr hx of Vicodin 3-4x day for back pain (had back surgery in past)...I met her in fall 2010...she remains in remission on high dose ranitidine 3x day
2) 70+ female came in March referred by her minister, chief complaint: long standing cough, rhinorrhea/post nasal drip, voice problems and finally unable to sing in church...I started her on lifestyle change and samples of Dexilant 60mg instructed to use 1 daily for 3 days then 1 twice daily....at follow up in 3 weeks she had reduced her Kadian (morphine) from 80 mg to 40 mg and at follow up last week (July) has been off ALL narcotics 3 weeks. Her back surgery was in 2003, she has had 12 or more invasive pain procedures over the years....the pain clinic provider willingly helped her taper off the morphine but ..."rolled her eyes" when told by the patient what patient believed to be the reason her pain resolved..
3)19 y/o male, post surgical, cervical fracture at age 14 chief complaint: neck pain, bilateral lumbar radicular pain (pain down both legs)....failed pain clinic referral by neurosurgery with PT, narcotics, muscle relaxants, tricyclics....Dexilant 60 mg 3/day completely resolves ALL signs and symptoms....has relapsed several times off Dexilant or on reduced dose over the last 6-8 months
4) 70+ male, Vetrans Administration patient chief complaint: left side radicular (down the leg) pain (10/10)...9 months duration when he came to me...on omeprazole 20 mg for heartburn..titrated to Dexilant 60mg 2-3 daily...pain 0/10....has relapsed several times when he "runs out of pills"....(Dexilant)...told by VA doctor (per patient)..."heartburn does not cause leg pain and leg pain does not cause heartburn."
I have more cases like these. All are documented in the chart and could be validated by checking pharmacy records. I first saw this type response over 10 years ago.
What is the mechanism?
I believe vagal afferents alert the brain of the danger in the distal esophagus, craniosacral nervous system is activated and through recruitment and amplification of the protective mechanisms (NB Reilly's syndrome) sacral roots 2,3,4 carry the message to swell, exstravasate, vasodilate and muscle constriction result in piriformis m. spasm that can impinge on siatic n. thus causing radicular pain. Reduction in the vagal stimulation reduces the autonomic "output" and symptoms including pain resolve. Central sensitization is also part of the mechanism.
I have sent this to the National Institute of Health to encourage them to become involved.
Dr. Barrett
1) cc: 70 y/o female chief complaint: for years coughing up phlegm every morning for 2-3 hours. Therapy initiated including pantoprazole 40 mg, 2 tabs twice daily; cough GONE, discontinued 7 yr hx of Vicodin 3-4x day for back pain (had back surgery in past)...I met her in fall 2010...she remains in remission on high dose ranitidine 3x day
2) 70+ female came in March referred by her minister, chief complaint: long standing cough, rhinorrhea/post nasal drip, voice problems and finally unable to sing in church...I started her on lifestyle change and samples of Dexilant 60mg instructed to use 1 daily for 3 days then 1 twice daily....at follow up in 3 weeks she had reduced her Kadian (morphine) from 80 mg to 40 mg and at follow up last week (July) has been off ALL narcotics 3 weeks. Her back surgery was in 2003, she has had 12 or more invasive pain procedures over the years....the pain clinic provider willingly helped her taper off the morphine but ..."rolled her eyes" when told by the patient what patient believed to be the reason her pain resolved..
3)19 y/o male, post surgical, cervical fracture at age 14 chief complaint: neck pain, bilateral lumbar radicular pain (pain down both legs)....failed pain clinic referral by neurosurgery with PT, narcotics, muscle relaxants, tricyclics....Dexilant 60 mg 3/day completely resolves ALL signs and symptoms....has relapsed several times off Dexilant or on reduced dose over the last 6-8 months
4) 70+ male, Vetrans Administration patient chief complaint: left side radicular (down the leg) pain (10/10)...9 months duration when he came to me...on omeprazole 20 mg for heartburn..titrated to Dexilant 60mg 2-3 daily...pain 0/10....has relapsed several times when he "runs out of pills"....(Dexilant)...told by VA doctor (per patient)..."heartburn does not cause leg pain and leg pain does not cause heartburn."
I have more cases like these. All are documented in the chart and could be validated by checking pharmacy records. I first saw this type response over 10 years ago.
What is the mechanism?
I believe vagal afferents alert the brain of the danger in the distal esophagus, craniosacral nervous system is activated and through recruitment and amplification of the protective mechanisms (NB Reilly's syndrome) sacral roots 2,3,4 carry the message to swell, exstravasate, vasodilate and muscle constriction result in piriformis m. spasm that can impinge on siatic n. thus causing radicular pain. Reduction in the vagal stimulation reduces the autonomic "output" and symptoms including pain resolve. Central sensitization is also part of the mechanism.
I have sent this to the National Institute of Health to encourage them to become involved.
Dr. Barrett
Letter to National Institute of Health
To the National Institute of Health:
If you recall I have documented over 20 cases of esophageal specialized intestinal metaplasaia that have shown normalization with absence of metaplastic histology on surveillance endoscopy. These results were obtained as the result of treating patients with GERD to SUPPRESSION OF NON-ESOPHAGEAL symptoms. "Quieting" the amplified autonomic response to GERD with successful therapy results in remarkable outcomes. Vagal stimulation is clearly involved whether aspiration happens or not is usually irrelevant (the aspiration vs autonomic/vagal debate)., The first step in improved quality of life is realizing that GERD may be the generator of diverse symptoms/signs/problems. Once the dx of atypical GERD is entertained, followup with the conviction that attention to details and titration/escalation of therapy OFTEN is rewarded with dramatic resolution of issues that are sometimes unanticipated!
Last week I spoke at the local community center, "The Many Faces of GERD" was the title of the presentation and over 100 preregistered were in attendance.
In the question period, most all questions dealt with extra-esophageal problems like cough, throat clearing, non-cardiac chest pain, adult onset asthma, chronic sinus problems, etc. According to testimonials, on the infrequent occasion these symptoms were felt to be associated with reflux, the treatment was sub-therapeutic having been exposed to various agents in ordinary doses. If history repeats, 10-20% of those in attendance will end up in my office and my best estimate is 80% of those will ultimately have have significant symptom resolution.
I spoke in June to the Michigan Sleep Alliance. As a result a 3 month old was brought to me suffering with "failure to thrive, poor sleep {always <2 hr duration}, constant nasal mucus, sneezing spells, aggression based crying and frequent (2 -3 times a week?)Dr visits.
I suggested life style changes and started the infant on ranitidine suspension for GERD. I saw the child this week for follow up and ALL symptoms markedly improved or gone, no Dr. visits and a 2# weight gain in the 4 1/2 weeks since therapy institued. Mom reports after the 1st dose the infant slept 4 hours. The next day with 3 daily doses the child slept 8 hours as she continues to nightly.
We need to educate the provider population and alert them to the frequent occurrence of non-esophageal GERD symptoms. I am here to testify that dosage titration of anti-secretory medications rather than an arbitrary twice daily fixed dose can frequently alleviate symptom burden. I too have found individuals that fail to respond to the therapeutic strategy but I find many more that do respond with individualized, titrated "high dose" treatment and attention to lifestyle changes and the addition of barrier antacids.
If what I claim is true, then a study with the end point of symptom suppression in atypical GERD by titration of anti secretory therapy would be revealing and likely trans formative in establishing a new paradigm. A properly designed study would almost certainly be terminated prematurely because it would be inappropriate to with hold treatment in the control group.
I personally feel it unethical to NOT TREAT these patients by ignoring their symptoms (as many have been when they finally find me). How can such favorable outcomes be disseminated? How can our medical community be allowed to remain ignorant of this epidemic/pandemic and these truths? This is not confined to our community since I receive requests for guidance/insight/help from people all over the USA and occasionally other countries. Anything going on in the NIH in this regard?
Thank you for listening
Kurt A Barrett DO
PS I write letters, publish articles when I can, speak anytime a group will have me, respond to phone calls and maintain a web site with altruistic motives with the intent of EDUCATION.
www.DRKURTBARRETT.com
Sunday, November 14. 2010
Silent/Atypical GERD......The Great Masquerader
A family member had struggled with minor respiratory issues for 20 years. While home from college, in the cold Thanksgiving air, on a short walk in the neighborhood, she gasped, choked and turned blue. “I’m okay”, she stoically claimed, “I just have to get out of the cold air and then I’ll be fine. I always do this.” I was shocked. I quizzed her, tested and treated her for asthma (the most likely culprit).She DID NOT respond. We questioned all sorts of physicians. I suspected something “wrong” with her esophagus based on “sounds “…sort of a belch/burp/hiccup combination she emitted. But I didn’t know how to treat the apparent condition. No answers ANYWHERE.
Time went on....years later she called to ask, “For the last two days, for the first time in my life, I’ve had heartburn. What can I do?” I suddenly realized she had something I had vaguely heard of called atypical gastroesophageal reflux disease (GERD). The hallmark of “ordinary GERD” is heartburn but in her kind, atypical/silent GERD, they have little or NO HEARTBURN. The absence of classic symptoms makes the consideration of a digestive problem seem highly unlikely. Since that day in 2000 I have continued to study GERD and the body’s response to stomach contents regurgitating from the stomach and intestine backwardly into the esophagus. It seems each day I learn something new (patient experiences teach me if I'm willing to listen!) or better understand this complex, fascinating, extremely common disorder that some call "The Great Masquerader”. GERD is the known cause of adenocarcinoma of the esophagus which happens to be the MOST RAPIDLY GROWING OCCURRENCE OF ANY CANCER IN THE UNITED STATES. The incidence of cancer of the esophagus is doubling every five years. The University of Virginia School of Medicine states: ”Symptoms related to GERD represent one of the most common, often confusing, health problems seen in primary care. The frequency of GERD has increased in recent years…”
I have read and I find that GERD is associated with about 80% of the following conditions when chronic or recurring: asthma, “allergies”, bronchitis, cough, emphysema, otitis media, sinusititis, hoarseness, sore throat, non-cardiac chest pain, ear pain, throat clearing, hiccups and a feeling of a lump in the throat (globus sensation). There is more too: day time fatigue, poor quality sleep, insomnia, neck pain, and bloody nose, coughing up blood, chronic burping, dental pain/problems, hives and worsening acne of all forms. The Institute of Medicine (IOM) reports that it takes, “about 17 years for a new treatment for a given disease to make its way into routine patient care”. I this guess means we’re about half way there from a time line. Please remember, as some obscure philosopher once said, “The eyes only see what the mind already knows”.
Time went on....years later she called to ask, “For the last two days, for the first time in my life, I’ve had heartburn. What can I do?” I suddenly realized she had something I had vaguely heard of called atypical gastroesophageal reflux disease (GERD). The hallmark of “ordinary GERD” is heartburn but in her kind, atypical/silent GERD, they have little or NO HEARTBURN. The absence of classic symptoms makes the consideration of a digestive problem seem highly unlikely. Since that day in 2000 I have continued to study GERD and the body’s response to stomach contents regurgitating from the stomach and intestine backwardly into the esophagus. It seems each day I learn something new (patient experiences teach me if I'm willing to listen!) or better understand this complex, fascinating, extremely common disorder that some call "The Great Masquerader”. GERD is the known cause of adenocarcinoma of the esophagus which happens to be the MOST RAPIDLY GROWING OCCURRENCE OF ANY CANCER IN THE UNITED STATES. The incidence of cancer of the esophagus is doubling every five years. The University of Virginia School of Medicine states: ”Symptoms related to GERD represent one of the most common, often confusing, health problems seen in primary care. The frequency of GERD has increased in recent years…”
I have read and I find that GERD is associated with about 80% of the following conditions when chronic or recurring: asthma, “allergies”, bronchitis, cough, emphysema, otitis media, sinusititis, hoarseness, sore throat, non-cardiac chest pain, ear pain, throat clearing, hiccups and a feeling of a lump in the throat (globus sensation). There is more too: day time fatigue, poor quality sleep, insomnia, neck pain, and bloody nose, coughing up blood, chronic burping, dental pain/problems, hives and worsening acne of all forms. The Institute of Medicine (IOM) reports that it takes, “about 17 years for a new treatment for a given disease to make its way into routine patient care”. I this guess means we’re about half way there from a time line. Please remember, as some obscure philosopher once said, “The eyes only see what the mind already knows”.
Sinusitis Caused by Acid Instillation into Lower Esophagus
Gastrosource reported October, 2010, “...sinusitis was induced in healthy volunteers by introducing hydrochloric acid into the lower esophagus”. This explains chronic sinus patients returning to normal health when successfully treated for GERD (gastroesophageal reflux disorder). Reflux of digestive contents occurs when the one-way safety valve at the bottom of the esophagus fails to close correctly. Heartburn is the usual response to the reversed flow of harsh, acidic, digestive juices. However, many GERD sufferers do not signal this problem with heartburn. Called atypical/silent GERD, patients have little or no heartburn. They have numerous manifestations, i.e., hoarseness, lump feeling in the throat, runny nose, post nasal drip, ear pain, fatigue, chest pain, short of breath, cough, etc. (atypical GERD has been called “The Great Masquerader”).
This compelling information, as novel as it may seem, clearly reinforces the minority position maintained for well over 15 years, that GERD can cause a variety of recurring, often hard to treat, non-digestive problems. The vagus nerve links internal organs allowing for mutual communication. The “excited” response from the lower esophagus is mimicked by the sinuses via vagus communication; both organ tissues leak fluid, swell, make mucus and become inflamed. This is good for the esophagus but the unintended response causes sinus problems and more. Treat the cause (GERD) and these noxious, unhealthy symptoms vanish. Atypical/silent GERD is exceptionally common and can be ongoing for years. Great relief results from the expanded understanding, acknowledgement and successful treatment for atypical/silent GERD. I encourage questions about this condition.
Posted by Kurt Barrett, D.O.
in GERD and Respiratory Problems
at
08:52
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Thursday, May 13. 2010
What about P.P.I. Side Effects?
A "new" study was recently released and made the CBS NEWS and others. What I've seen so far is not new information. Some is actually "junk science"...i.e., clostridium difficle is an acid resistant spore and hence the pH of the gut should NOT BE RELEVANT since it is not altered by the presence or absence of acid. We can talk about the bias in the retrospective studies because it seems that some of these findings result from the disease state (GERD) not the from the treatment. The only people that take these drugs in these cases are PEOPLE WITH GERD. We have no information on what results would be if non-GERD patients took the same treatment.
That said, ALL meds have some risk. We need to do every thing we can to minimize that risk. The benefit /risk determination needs to be ascertained on a case by case basis. Concern for children should be acknowledged but given the lack of adverse results in the short run (months up to 5 years) I believe the risk (small) is clearly justified given the benefit. Similarily, I would not withhold penicillin in the child with fever and sore throat based on the possibility that anaphylactic reaction could result. The small risk seems acceptable since benefit in both cases is substantial.
I might add that I have treated hundreds of patients with P.P.I.s (Proton Pump Inhihitors) for over 25 years and I remain very impressed with their remarkable benefits and safety.
That said, ALL meds have some risk. We need to do every thing we can to minimize that risk. The benefit /risk determination needs to be ascertained on a case by case basis. Concern for children should be acknowledged but given the lack of adverse results in the short run (months up to 5 years) I believe the risk (small) is clearly justified given the benefit. Similarily, I would not withhold penicillin in the child with fever and sore throat based on the possibility that anaphylactic reaction could result. The small risk seems acceptable since benefit in both cases is substantial.
I might add that I have treated hundreds of patients with P.P.I.s (Proton Pump Inhihitors) for over 25 years and I remain very impressed with their remarkable benefits and safety.
Sunday, April 4. 2010
Why Didn't MY DOCTOR tell me?
Gastroesophageal reflux disease (GERD) is becoming MORE common in our society. And this statement is made despite the fact that I meet people of all ages that have GERD related symptoms and have NO SENSE that gastric reflux is at the root of their problems. Their doctors don't either because the prevailing wisdom is you must have heartburn or indigestion to even consider GERD.
"Why didn't my doctor tell me about this?". My answer is that most of us patients and physicians, are overwhelmed by the "information glut". The concept that GERD causes more than heartburn is a newer concept and "hides" in this information onslaught. As a primary care, general practioner, and due to a family members illness, I have been enlightened as to the suprisingly frequent occurence of GERD. I try to look at the bigger picture of what ails my patient. I see specialists, due to, perhaps(?) the dogma of their classic training, that fail to "connect-the-dots". The pulmonologists, who treats the lung, fails to realize that there is OFTEN (over half the time!) a prominent association with GERD. I see infants who sneeze, cough, scream in pain and can't sleep at night under go a transformation...sometimes immediately...when GERD is recognized and treated. The dad of a 7 month old, who had the peditrician refuse to accept GERD as a cause of symptoms state, "He is like a different kid" immediately upon initiation of therapy for GERD. Same situation with a 4 month old. An adolescent who has been in the habit of having such severe coughing spells (presumed to be due to her asthma) that she ends up vomiting. In reality her asthma is precipited from acid reflux and so is her vomiting. I find people that could not finish a meal without coughing and now with appropriate GERD therapy only cough with illness. Perhaps if you realize that some people have a "runny nose" when they eat you can expand that understanding to see that eating can cause cough. BOTH conditions are caused by digestive contents arising from the stomach and intestine, flowing in reverse into the esophagus. These harsh digestive contents come in contact with an irritated lining of the esophagus caused from previous similar events BUT OFTEN THERE IS NO HEARTBURN. Even without heartburn, the body and the brain rightly recognize these events as dangerous. The response appears as sneezing, runny nose, mucus production, coughing and in some cases vomiting. The individual may (or may not) have difficulty swallowing. The esophagus correctly recognizes this reflux of digestive contents as "toxic" or harmful and thus responds in the only way it can devise to protect the person. The stimulation of the acid/digestive contents contacting the gentle, fragile lining of the food tube evokes the clinical responses. The physiological response induces mucus making tissues to pour out mucus type secretions to line, dilute and thus protect the esophagus. The severity of the danger in the esophagus results in " all out" stimulation of mucus producing tissues. Thus mucus producing tissues else where in the body "hear" the message to make mucus/secrete. Thus tissues remote to the actual insult become actively involved as if they were protecting themselves!
"Why didn't my doctor tell me about this?". My answer is that most of us patients and physicians, are overwhelmed by the "information glut". The concept that GERD causes more than heartburn is a newer concept and "hides" in this information onslaught. As a primary care, general practioner, and due to a family members illness, I have been enlightened as to the suprisingly frequent occurence of GERD. I try to look at the bigger picture of what ails my patient. I see specialists, due to, perhaps(?) the dogma of their classic training, that fail to "connect-the-dots". The pulmonologists, who treats the lung, fails to realize that there is OFTEN (over half the time!) a prominent association with GERD. I see infants who sneeze, cough, scream in pain and can't sleep at night under go a transformation...sometimes immediately...when GERD is recognized and treated. The dad of a 7 month old, who had the peditrician refuse to accept GERD as a cause of symptoms state, "He is like a different kid" immediately upon initiation of therapy for GERD. Same situation with a 4 month old. An adolescent who has been in the habit of having such severe coughing spells (presumed to be due to her asthma) that she ends up vomiting. In reality her asthma is precipited from acid reflux and so is her vomiting. I find people that could not finish a meal without coughing and now with appropriate GERD therapy only cough with illness. Perhaps if you realize that some people have a "runny nose" when they eat you can expand that understanding to see that eating can cause cough. BOTH conditions are caused by digestive contents arising from the stomach and intestine, flowing in reverse into the esophagus. These harsh digestive contents come in contact with an irritated lining of the esophagus caused from previous similar events BUT OFTEN THERE IS NO HEARTBURN. Even without heartburn, the body and the brain rightly recognize these events as dangerous. The response appears as sneezing, runny nose, mucus production, coughing and in some cases vomiting. The individual may (or may not) have difficulty swallowing. The esophagus correctly recognizes this reflux of digestive contents as "toxic" or harmful and thus responds in the only way it can devise to protect the person. The stimulation of the acid/digestive contents contacting the gentle, fragile lining of the food tube evokes the clinical responses. The physiological response induces mucus making tissues to pour out mucus type secretions to line, dilute and thus protect the esophagus. The severity of the danger in the esophagus results in " all out" stimulation of mucus producing tissues. Thus mucus producing tissues else where in the body "hear" the message to make mucus/secrete. Thus tissues remote to the actual insult become actively involved as if they were protecting themselves!
Posted by Kurt Barrett, D.O.
in GERD and Respiratory Problems
at
05:39
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Sunday, March 14. 2010
"Insomnia-What Role Might GERD Play?"
The numbers of sleep associated issues related to GERD are impressive BUT in my experience they are routinely ignored or overlooked. GERD patients can present (with or WITHOUT heartburn) complaining of: drowiness, daytime fatigue, frequent nocturnal awakenings, awakening non-refreshed, snoring, and/or experiencing unpleasant feelings of legs (or arms).
I speak to the Michigan Sleep Alliance (in Kalamazoo, Michigan) on March 18, 2010. The title of the presentation is, "Insomnia-What Role Might GERD Play?"
The National Health and Wellness Survey, with 66,000 participants, found 18% of this group were diagnosed with GERD.
The participants diagnosed with GERD reported:
-they required "more medical care"
-decreased Quality-Of-Life scores
-lowered work productivity
-reduced sense of well being
-87% had "sleep issues"!.....
-48% revealed trouble staying asleep.....
-56% claimed difficulty initiating sleep....
I find that physicians and providers only treat GERD when associated with heartburn. Their goal of therapy is, generally, to reduce heartburn. Beyond heartburn and indigestion little is recognized or acknowledged by primary and even gastroenterology specalists.
THE EYES ONLY SEE WHAT THE MIND ALREADY KNOWS.
I speak to the Michigan Sleep Alliance (in Kalamazoo, Michigan) on March 18, 2010. The title of the presentation is, "Insomnia-What Role Might GERD Play?"
The National Health and Wellness Survey, with 66,000 participants, found 18% of this group were diagnosed with GERD.
The participants diagnosed with GERD reported:
-they required "more medical care"
-decreased Quality-Of-Life scores
-lowered work productivity
-reduced sense of well being
-87% had "sleep issues"!.....
-48% revealed trouble staying asleep.....
-56% claimed difficulty initiating sleep....
I find that physicians and providers only treat GERD when associated with heartburn. Their goal of therapy is, generally, to reduce heartburn. Beyond heartburn and indigestion little is recognized or acknowledged by primary and even gastroenterology specalists.
THE EYES ONLY SEE WHAT THE MIND ALREADY KNOWS.
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