A While ago I learnt of the passing of someone who had been born unable to swallow, like myself but wasn’t a child, but an ADULT. That got me thinking and ok if you’re a child everything is geared up to help you,

but if like me your classed as an adult, your it seems in the forgotten land of, What did you say you have?

I am not sure what info if any we will find about being born unable to swallow and classed as an adult, but with your help then maybe just maybe we can find something worth reading.

 

This page here above the start will be at some point given over in memory of the Adult TOF or TEF who has left us behind, and who’s passing made me think further down the road. 

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On this page there are some cutting edge interesting up to date data, you just need the time to read and listen, some would say WOW.

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Achalasia

Achalasia is rare. It may occur at any age but is most common in middle-aged or older adults. The problem may be inherited in some people.

Achalasia is an uncommon swallowing disorder that affects about 1 in every 100,000 people. The major symptom of achalasia is usually difficulty with swallowing. Most people are diagnosed between the ages of 25 and 60 years. Although the condition cannot be cured, the symptoms can usually be controlled with treatment.

PLEASE NOTE, Children are also known to have this too.

The tube that carries food from the mouth to the stomach is the oesophagus. Achalasia makes it harder for the oesophagus to move food into the stomach.

Achalasia is an oesophagal motor disorder characterised by increased lower oesophagal sphincter (LES) pressure, diminished to absent peristalsis in the distal portion of the oesophagus composed of smooth muscle, and lack of a coordinated LES relaxation in response to swallowing.

Achalasia

Barium swallow studies of achalasia are presented below. Barium swallow study demonstrating characteristics of achalasia, including the bird’s beak deformity and a dilated oesophagus.

Barium swallow achalasia,

Detail of a barium swallow study demonstrating the classic bird’s beak deformity of the distal oesophagus.

Primary achalasia is the most common subtype and is associated with loss of ganglion cells in the oesophagal myenteric plexus. These important inhibitory neurones induce LES relaxation and coordinate proximal-to-distal peristaltic contraction of the oesophagus.

Secondary achalasia is relatively uncommon. This condition exists when a process other than the intrinsic disease of the oesophagal myenteric plexus is the aetiology. Examples of maladies causing secondary achalasia include certain malignancies, diabetes mellitus, and Chagas disease. Sir Thomas Willis first described achalasia in 1674. Willis successfully treated a patient by dilating the LES with a cork-tipped whalebone. Not until 1929 did Hurt and Rake first realise that the primary pathophysiology resulting in achalasia was a failure in LES relaxation. Treatment options for achalasia include pharmacologic, mechanical, botulinum toxin, and surgical-based therapies.

For more photo’s etc http://emedicine.medscape.com/article/363551-overview

Causes

There is a muscular ring at the point where the oesophagus and stomach meet. It is called the lower oesophagal sphincter (LES). Normally, this muscle relaxes when you swallow to allow food to pass into the stomach. In people with achalasia, it does not relax as well. In addition, the normal muscle activity of the oesophagus (peristalsis) is reduced.

This problem is caused by damage to the nerves of the oesophagus. Other problems can cause similar symptoms, such as cancer of the oesophagus or upper stomach, and a parasite infection that causes.

esophagealachalasia_large

Symptoms include

Backflow (regurgitation) of food

 Chest Pain which may increase after eating or may be felt in the back, neck, and arms

https://www.nlm.nih.gov/medlineplus/ency/article/003079.htm

Cough

Difficulty swallowing liquids and solids

Heartburn (link has Video)

https://www.nlm.nih.gov/medlineplus/ency/article/003114.htm

Unintentional weight loss

Exams and Tests

Physical exam may show signs of

Anemia

https://www.nlm.nih.gov/medlineplus/ency/article/000560.htm

Malnutrition

https://www.nlm.nih.gov/medlineplus/ency/article/000404.htm

 Tests include

 Manometry a test to measure how well the esophagus is working

EDG (USA) or upper endoscopy, a test to examine the lining of the stomach and esophagus. It uses a flexible tube and camera.

X-Ray, taken to examine the esophagus, stomach, and small intestine.

Treatment

The goal of treatment is to reduce the pressure at the sphincter muscle and allow food and liquids the passport easily into the stomach. Therapy may involve:

Injection with botulinum toxin (Botox). This may help relax the sphincter muscles. However, the benefit wears off within a few weeks or months.

Medications, such as long-acting nitrates or calcium channel blockers. These drugs can be used to relax the lower esophagus sphincter.

Surgery (called a myotomy). In this procedure, the lower sphincter muscle is cut.

Widening (dilation) of the esophagus at the location of the narrowing. This is done during EGD.

Achalasia can sometimes be treated with medication that helps the lower esophageal sphincter relax. If medication is ineffective, however, esophageal dilatation can correct the problem. To open the esophagus, a balloon dilator is passed through the mouth down to the level of the lower esophageal sphincter, using an endoscope. The balloon is inflated, thus stretching the sphincter.

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If achalasia recurs after balloon dilatation, surgery may be necessary to correct the defect. This surgery can often be done laparoscopically. Laparoscopic surgery involves a number of small incisions made in the upper abdomen, into which the surgeon inserts a long, thin camera and surgical instruments.

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The surgeon then makes a long incision in the esophagus at the level of the esophageal sphincter. This releases the sphincter and allows it to relax. This surgery is very effective in curing achalasia, with over 90% of patients obtaining relief from symptoms post-operatively. Recovery is generally rapid, and most patients are able to leave the hospital within 1 to 3 days. Infrequently, the operation cannot be accomplished laparoscopically, and a larger incision is required. In these cases, hospitalization times may be longer.

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Prognosis

The outcomes of surgery and nonsurgical treatments are similar. Sometimes more than one treatment is necessary

 Possible Complications

https://www.nlm.nih.gov/medlineplus/ency/article/000267.htm

For better understanding click below.

http://www.uptodate.com/contents/achalasia-beyond-the-basics#H22

I found this thought I would include it here, Patient Comments: Achalasia – Treatment

http://www.medicinenet.com/achalasia/patient-comments-1789.htm

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Video explaining Acid reflux

Acid reflux may cause heartburn and other symptoms. Dr Sarah Jarvis teaches us how we can treat and prevent the symptoms.

https://youtu.be/VkhuF5QjNA8?rel=0

A few interesting finds

Doctor Michael Meyers co-Author of:

(Doctor Michael Meyers Supports this Website)

Surgical treatment of esophagogastric dysfunction forty years after reverse gastric tube esophagopathy for congenital esophageal anomaly.

Author information

  • Division of Surgical Oncology, Department of Surgery, University of North Carolina School of Medicine at Chapel Hill, Chapel Hill,

Abstract

BACKGROUND:

In 1968, Burrington first described the use of the reverse gastric tube esophagopathy for oesophagal replacement in children with oesophagal atresia or acquired stenosis. There are few documented cases of long-term follow-up of these patients.

CASE REPORT:

We describe a 41-year-old female who presented with progressive dysphagia 40 years after reverse gastric tube for a congenital oesophagal stenosis as an infant. Repeated endoscopic dilations were unsuccessful in relieving her symptoms, and she subsequently underwent a modified Ivor-Lewis esophagogastrostomy with resection of the reverse gastric tube and reconstruction using her remaining gastric remnant.

CONCLUSIONS:

This report describes what we believe to be the longest recorded follow-up after reverse gastric tube esophagopathy and highlights the potential for long-term complications after surgery for congenital anomalies.

Copyright © 2011. Published by Elsevier Inc. (This is OK as been given the OK by the Dr to share)

Hospital officials say it was the first known oesophagal transplant in the world
www.pressherald.com/2012/02/02/hollis-girl-welcomed-home-after-historic-transplant/

Minimally invasive esophagectomy has advanced to the point where it offers significant advantages
www.ehospitalistnews.com/index.php?id=100713&tx_ttnews[tt_news]=55596&cHash=fde3de4796c53d65cfb23d1025a05600

Full text is available as a scanned copy of the original print version.
www.ncbi.nlm.nih.gov/pmc/articles/PMC1476897/

A review of the experience with oesophagal atresia and tracheoesophageal fistula over a 25-year period
www.ncbi.nlm.nih.gov/pmc/articles/PMC1503623/

Long-term Functional results and quality of life after colon interposition for long-gap oesophageal atresia

Out of a series of 146 patients with oesophageal atresia 9 (6.2%) underwent colon interposition from 1963 to 1971. All eight surviving patients were seen at follow-up after a mean of 22 years. Three patients were free of specific symptoms according to the criteria of DeMeester, two had moderate and three severe distress. The mean time for consuming a standardised test meal was 15 minutes, compared to 8 minutes in healthy controls. Patients required 1-9 minutes to transport liquid barium through the transplant, compared to < 10 seconds in control subjects. Histological evaluation revealed a normal architecture of the colonic and ileal epithelium in three patients who underwent endoscopy. In none of these patients were contractions in the colon graft related to the act of swallowing recorded on manometry.

An unimpaired quality of life was indicated by the Spitzer index which scored a mean of nine out of ten points. However, on a 100 point visual analogue scale patients scored their global quality of life 66 and the mean Gastrointestinal Quality of Life Index was 92.2, compared to 107.6 in healthy control subjects (p < 0.05). This impairment was exclusively due to specific symptoms which scored 49.3 in patients and 59 in healthy individuals (p < 0.05). Physical and social functions, emotions, and inconvenience of a medical treatment were similar to control subjects. We conclude that colon interposition for long-gap oesophageal atresia achieves acceptable long-term functional results. However, specific symptoms lead to a considerable impairment in quality of life.

Most exciting technological break though coming…
www.theguardian.com/business/2014/aug/24/medical-implants-drive-3d-printer-growth

Articles are written by UK doctors and are based on research evidence, UK and European Guidelines
www.patient.co.uk/doctor/oesophageal-atresia

 Esophageal Dilation (I could not find a picture of higher up dilation with balloon so this gives you an idea)

What is Oesophagal Dilation?
OOesophagealdilation is a procedure that allows your doctor to dilate, or stretch, a narrowed area of your oesophagus [swallowing tube]. Doctors can use various techniques for this procedure. Your doctor might perform the procedure as part of a sedated endoscopy. Alternatively, your doctor might apply a local anaesthetic spray to the back of your throat and then pass a weighted dilator through your mouth and into your oesophagus.

Why is it Done?
The most common cause of narrowing of the oesophagus, or structure, is scarring of the oesophagus from reflux of acid occurring in patients with heartburn. Patients with a narrowed portion of the oesophagus often have trouble swallowing; food feels like it is “stuck” in the chest region, causing discomfort or pain. Less common causes of oesophagal narrowing are webs or rings (which are thin layers of excess tissue), cancer of the oesophagus, scarring after radiation treatment or a disorder of the way the oesophagus moves [motility disorder].

 How Should I Prepare for the Procedure?
An empty stomach allows for the best and safest examination, so you should have nothing to drink, including water, for at least six hours before the examination. Your doctor will tell you when to start fasting.

Tell your doctor in advance about any medications you take, particularly aspirin products or anticoagulants (blood thinners). Most medications can be continued as usual, but you might need to adjust your usual dose before the examination. Your doctor will give you specific guidance. Tell your doctor if you have any allergies to medications as well as medical conditions such as heart or lung disease. Also, tell your doctor if you require antibiotics prior to dental procedures because you might need antibiotics prior to oesophagal dilation as well.

 What Can I Expect during Esophageal Dilation?
Your doctor might perform oesophagal dilation with sedation along with an upper endoscopy. Your doctor may spray your throat with a local anaesthetic spray, and then give you sedatives to help you relax. Your doctor then will pass the endoscope through your mouth and into the oesophagus, stomach and duodenum. The endoscope does not interfere with your breathing. At this point, your doctor will determine whether to use a dilating balloon or plastic dilators over a guiding wire to stretch your oesophagus. You might experience mild pressure in the back of your throat or in your chest during the procedure. Alternatively, your doctor might start by spraying your throat with a local anaesthetic. Your doctor will then pass a tapered dilating instrument through your mouth and guide it into the oesophagus.

 What Can I Expect after Esophageal Dilation?
After the dilation is done, you will probably be observed for a short period of time and then allowed to return to your normal activities. You may resume drinking when the anesthetic no longer causes numbness to your throat unless your doctor instructs you otherwise. Most patients experience no symptoms after this procedure and can resume eating the next day, but you might experience a mild sore throat for the remainder of the day.

If you received sedatives, you probably will be monitored in a recovery area until you are ready to leave. You will not be allowed to drive after the procedure even though you might not feel tired. You should arrange for someone to accompany you home, because the sedatives might affect your judgment and reflexes for the rest of the day.

 What are the Potential Complications of Esophageal Dilation?
Although complications can occur even when the procedure is performed correctly, they are rare when performed by doctors who are specially trained. A perforation, or hole, of the esophagus lining occurs in a small percentage of cases and may require surgery. A tear of the esophagus lining may occur and bleeding may result. Complications from heart or lung diseases are potential risks if sedatives were used.

It is important to recognize early signs of possible complications. If you have chest pain, fever, difficulty swallowing, bleeding or black bowel movements after the test, tell your doctor immediately.

 Will Repeat Dilations be Necessary?
Depending on the degree of narrowing of your esophagus and its cause, it is common to require repeat dilations. This allows the dilation to be performed gradually and decreases the risks of the procedure. Once the stricture, or narrowed esophagus, is completely dilated, repeat dilations may not be required. If the stricture was due to acid reflux, acid-suppressing medicines can decrease the risk of stricture recurrence.

Reprinted from the American Society for Gastrointestinal Endoscopy (ASGE).

http://www.asge.org/patients/patients.aspx?id=392

 

Esophageal Dilation due to a narrowing of the esophagus      

What is Esophageal Dilation?
Esophageal dilation is a procedure that allows your doctor to dilate, or stretch, a narrowed area of your esophagus [swallowing tube]. Doctors can use various techniques for this procedure. Your doctor might perform the procedure as part of a sedated endoscopy

www.youtube.com/watch?v=UPlMtKpld78?rel=0

Dilation of an Esophageal-Jejunal Anastomotic Stricture (To give you an insight as to what happens)

 Published on Feb 13, 2014

Dilation of an Esophageal-Jejunal Anastomotic Stricture with the CRE™ Wireguided 12/15 mm Balloon, featuring Dr. Vanbiervliet.

www.youtube.com/watch?v=w9yO4hJhOjY?rel=0

Dumping syndrome is common after gastric surgery.

Dumping syndrome is common after gastric surgery. It is a group of symptoms that may result from having part of your stomach removed or from other surgery involving the stomach. The symptoms range from mild to severe and often subside with time. Although you may find dumping syndrome alarming at first, it is not life threatening. You can control it by making changes in what and how you eat. By controlling dumping syndrome, you will also be avoiding the foods that tend to make you gain weight.

Causes of Dumping Syndrome

After gastric surgery, it can be more difficult to regulate movement of food, which dumps too quickly into the small intestine. Eating certain foods makes dumping syndrome more likely. For example, refined sugars rapidly absorb water from the body, causing symptoms. Symptoms may also happen after eating dairy products and certain fats or fried foods.

Dumping Syndrome: Symptoms of the Early Phase

An early dumping phase may happen about 30 to 60 minutes after you eat. Symptoms can last about an hour and may include:

  • A feeling of fullness, even after eating just a small amount
  • Abdominal cramping or pain
  • Nausea or vomiting
  • Severe diarrhea
  • Sweating, flushing, or light-headedness
  • Rapid heartbern

 Dumping Syndrome: Causes of the Early Phase

Symptoms of an early phase happen because food is rapidly “dumping” into the small intestine. This may be due to factors such as these:

  • The small intestine stretches.
  • Water pulled out of the bloodstream moves into the small intestine.
  • Hormones released from the small intestine into the bloodstream affect blood pressure.

Dumping Syndrome: Symptoms of the Late Phase

A late dumping phase may happen about 1 to 3 hours after eating. Symptoms may include:

  • Fatigue or weakness
  • Flushing or sweating
  • Shakiness, dizziness, fainting, or passing out
  • Loss of concentration or mental confusion
  • Feelings of hunger
  • Rapid heartbeat

Dumping Syndrome: Causes of the Late Phase

The symptoms of this late phase may happen due to a rapid rise and fall in blood sugar levels. The cause of this rapid swing in blood sugar may be worse when eating sweets or other simple

carbohydrates.

Dumping Syndrome Treatment

Many people find that taking steps like these greatly reduces symptoms of dumping syndrome.

Foods to avoid. Avoid eating sugar and other sweets such as:

  • Candy
  • Sweet drinks
  • Cakes
  • Cookies
  • Pastries
  • Sweetened breads

Also avoid dairy products and alcohol. And avoid eating solids and drinking liquids during the same meal. In fact, don’t drink 30 minutes before and 30 minutes after meals.

 Foods to eat.

To help with symptoms, also try these tips:

  • Use fiber supplements, such as psyllium (Metamucil or Konsyl), methylcellulose (Citrucel), or guar gum (Benefiber).
  • Use sugar replacements, such as Splenda, Equal, or Sweet’N Low, instead of sugar.
  • Go for complex carbohydrates, such as vegetables and whole-wheat bread, instead of simple carbohydrates, such as sweet rolls and ice cream.
  • To prevent dehydration, drink more than 4 cups of water or other sugar-free, decaffeinated, noncarbonated beverages throughout the day.

How to eat. 

Here are some other ways to lessen symptoms of dumping syndrome:

  • Eat five or six small meals or snacks a day.
  • Keep portions small, such as 1 ounce of meat or 1/4 cup of vegetables.
  • Cut food into very small pieces. Chew well before swallowing.
  • Combine proteins or fats along with fruits or starches. (For example, combine fruit with cottage cheese.)
  • Stop eating when you first begin to feel full.
  • Drink liquids 30 to 45 minutes after meals.
  • Reclining after eating may help prevent light-headedness.

When to Call the Doctor About Dumping Syndrome

It is important to manage dumping syndrome so you stay well-nourished and don’t lose too much weight. Talk to your health care provider about any symptoms you have and what else you can do.

In some cases, medication or surgery may help correct the symptoms of dumping syndrome.

Can cancer of the esophagus be found early?

Looking for a disease in someone without symptoms is called screening. The goal of screening is to find a disease like cancer in an early, more curable stage, in order to help people live longer, healthier lives.In the United States, screening the general public for esophageal cancer is not recommended by any professional organization at this time. This is because no screening test has been shown to lower the risk of dying from esophageal cancer in people who are at average risk.

However, people who have a high risk of esophageal cancer, such as those with Barrett’s esophagus, are often followed closely to look for early cancers and pre-cancers.

Testing people at high risk

Many experts recommend that people with a high risk of esophageal cancer, such as those with Barrett’s esophagus, have upper endoscopy regularly. For this test, the doctor looks at the inside of the esophagus through a flexible lighted tube called an endoscope. The doctor may remove small samples of tissue (biopsies) from the area of Barrett’s so that they can be checked for dysplasia (pre-cancer cells) or cancer cells.Doctors aren’t certain how often the test should be repeated, but most recommend testing more often if areas of dysplasia are found. This testing is repeated even more often if there is high-grade dysplasia (the cells appear very abnormal).

If the area of Barrett’s is large and/or there is high-grade dysplasia, treatment of the abnormal area might be advised because of the high risk that an adenocarcinoma is either already present (but was not found) or will develop within a few years. Treatment options for high-grade dysplasia might include surgery to remove part of the esophagus with the abnormal area, endoscopic mucosal resection (EMR), photodynamic therapy (PDT), and radiofrequency ablation (RFA). The outlook for these patients is relatively good after treatment.

Careful monitoring and treatment (if needed) may help prevent some esophageal cancers from developing. It may also detect some cancers early, when they are more likely to be treated successfully.

 

From Barrett’s to cancer

Signs and symptoms of esophagus cancer

Cancers of the oesophagus are usually found because of the symptoms they cause. Diagnosis in people without symptoms is rare and usually accidental (because of tests are done for other medical problems). Unfortunately, most oesophagal cancers do not cause symptoms until they have reached an advanced stage when they are harder to treat.

Trouble swallowing

The most common symptom of oesophagal cancer is a problem swallowing, with a feeling like the food is stuck in the throat or chest, or even choking on food. The medical term for trouble swallowing is dysphagia. This is often mild when it starts and then gets worse over time as the opening of the oesophagus gets narrower.

When swallowing becomes harder, people often change their diet and eating habits without realising it. They take smaller bites and chew their food more carefully and slowly. As cancer grows larger, the problem can get worse. People then may start eating softer foods that can pass through the oesophagus more easily. They may avoid bread and meat since these foods typically get stuck. The swallowing problem may even get bad enough that some people stop eating solid food completely and switch to a liquid diet. If cancer keeps growing, at some point even liquids might be hard to swallow.

To help pass food through the oesophagus, the body makes more saliva. This causes some people to complain of bringing up lots of thick mucus or saliva.

Chest pain

Sometimes, people complain of pain or discomfort in the middle part of their chest. Some people describe a feeling of pressure or burning in the chest. These symptoms are more often caused by problems other than cancer, such as heartburn, so they are rarely seen as a signal that a person might have cancer.

Swallowing may become painful if the cancer is large enough to limit the passage of food through the oesophagus. Pain may be felt a few seconds after swallowing, as food or liquid reaches the tumour and has trouble getting past it.

Weight loss

About half of people with oesophagal cancer lose weight (without trying to). This happens because their swallowing problems keep them from eating enough to maintain their weight. Other factors include a decreased appetite and an increase in metabolism from cancer.

Other symptoms

Other possible symptoms of cancer of the oesophagus can include:

  • Hoarseness
  • Chronic cough
  • Vomiting
  • Hiccups
  • Pneumonia
  • Bone pain
  • Bleeding into the oesophagus. This blood then passes through the digestive tract, which may turn stools black. Over time, this blood loss can lead to anemia (low red blood cell levels), which can make a person feel tired.

Having one or more of the symptoms above does not mean you have esophageal cancer.

In fact, many of these symptoms are more likely to be caused by other conditions. Still, if you have any of these symptoms, especially trouble swallowing, it’s important to have them checked by a doctor so that the cause can be found and treated if needed.

http://www.cancer.org/cancer/esophaguscancer/detailedguide/esophagus-cancer-signs-and-symptoms

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Oesophageal cancer expert discusses how to tackle growing rates of the disease

March 5, 2016

A researcher who created a test to diagnose oesophageal cancer explains why the disease is on the rise in the UK, as part of an awareness campaign. Professor George Hanna is the Director of NIHR-Diagnostic Evidence Cooperative at Imperial College London, and he and his team devised a breath test that can diagnose oesophageal cancer in minutes.

Oesophageal cancer is a form of cancer that affects the pipe that connects the mouth to the top of the stomach.   It is the ninth most common type of cancer in the UK, with more than 8,500 new cases diagnosed each year. February marks the start of Oesophageal Cancer Awareness Month, an initiative led by the charity Action against Heartburn, to encourage people suffering from symptoms such persistent heartburn to visit their GP to check for underlying causes.

As part of Oesophageal Cancer Awareness Month, Maxine Myers caught up with Professor Hanna to find out why cases of this disease are rising in the UK and how his breath test could save lives.

1) Why is oesophageal cancer such a big concern in the UK?

The UK has the highest incidences of oesophageal cancer in Western Europe, with 7,000 people dying each year from the disease.  In particular oesophageal adenocarcinoma, a form of the disease is rising rapidly in men over the age of 60.  Like many types of cancer, certain lifestyle factors can increase your risk. For example, the disease is common among people who smoke, drink heavily, are overweight or obese and have a diet low in fruit and veg.  People who have long-term persistent heartburn can also be at risk. This is because it can cause chronic inflammation in the cells lining the oesophagus and chemical changes to the DNA inside them.  This is known as Barrett’s Oesophagus which can lead to cancer.

2) Why is it difficult to detect it?

Oesophageal cancer is very difficult to detect because early symptoms are non-specific and common, such as heartburn. By the time specific symptoms appear, such as difficulty and pain with swallowing, the disease is at a later stage.  As a result, only 20 per cent of patients are eligible for treatment that can cure their cancer and 80 per cent of patients are referred for palliative treatment, medical care that is aimed at controlling the disease and alleviating symptoms. The long-term survival rate is just 13 per cent for oesophageal cancer.

3) How is it currently diagnosed?

The diagnostic test for oesophageal cancer is an endoscopy.  This is a procedure where the inside of the body is examined using a probe with a light source and video camera at the end via the mouth and down the gullet.  This is an invasive and expensive test that can also lead to complications such as tearing of an organ and infections. Only two per cent of patients who are referred for an endoscopy by GPs are diagnosed with oesophageal cancer.

4) Can you tell me a bit more about your cancer breath test?

We have devised a cancer breath test to help diagnose oesophageal and gastric cancer.  The test is 90 per cent accurate and provides results in minutes, which can take up to four to six hours to process using other methods.  To take the test, patients breathe into a device similar to a breathalyser which is connected to a bag.  The test looks for chemical compounds in exhaled breath that are unique to patients with oesophageal and gastric cancer.  In our first clinical trial at Imperial College Healthcare NHS Trust in 2011 to 2013, we found that the test could discriminate between malignant and benign oesophageal cancer in over 200 patients.

5) How did you come up with devising a breath test?

There is some evidence which shows that dogs can sniff out cancer as they can smell minute odours known to be associated with many malignant cancers.  We wanted to see whether we can replicate that with a device.

6) How can your breath test help patients?

The test can be used to diagnose patients with early non-specific symptoms which can give them more treatment options and could increase their chances of survival. It can also help reduce the number of invasive endoscopies carried out on patients.   The test also has the potential to be used to screen patients who are most at risk of developing oesophageal cancer,  for example, men over the age of 60.

7) What are the next steps with your breath test?

We are currently running a larger study involving three other hospital trusts in London to see whether the breath test can produce similar results with a bigger group of patients. We have already recruited the patients for the trial from cancer centres throughout the UK.  We hope to use the results from the trial to create a smaller sensor device that can be used by GPs to refer patients for further investigations.

 http://healthlogics.site/oesophageal-cancer-expert-discusses-how-to-tackle-growing-rates-of-the-disease/

2011 Jan;26

Barrett’s oesophagus: A historical perspective, an update on core practicalities and predictions on future evolutions of management.

Interpretation of exploding knowledge about Barrett’s oesophagus is impaired by the use of several conflicting definitions. Because any histological type of esophageal columnar metaplasia carries a risk for esophageal adenocarcinoma, the diagnosis of Barrett’s esophagus should no longer require demonstration of intestinal-type metaplasia. Endoscopic recognition and grading of Barrett’s esophagus remains a significant source of ambiguity. Reflux disease is a key factor for the development of Barrett’s esophagus, but other factors must underlie its development since it occurs in only a minority of reflux disease patients. Neither antireflux surgery nor proton pump inhibitor (PPI) therapy has major impacts on cancer risk. Within a year, a major trial should indicate whether low-dose aspirin usefully reduces cancer risk. The best referral centres have transformed the accuracy of screening and surveillance for early curable esophageal adenocarcinoma by use of enhanced and novel endoscopic imaging, visually-guided, rather than blind biopsies and by a partnership with expert pathologists. General endoscopists now need to upgrade their skills and equipment so that they can rely mainly on the visual targeting of biopsies on mucosal areas of concern in their surveillance practice. General pathologists need to greatly improve their interpretation of biopsies. Endoscopic therapy now achieves very high rates of cure of high-grade dysplasia and oesophagal adenocarcinoma with minimal morbidity and risk. Such results will only be achieved by skilled interventional endoscopists. Esophagectomy should now be mainly restricted to patients whose cancer has extended into and beyond the submucosa. Weighing risks and benefits in the management of Barrett’s esophagus is difficult, as is the process of adequately informing patients about their specific cancer risk.

www.researchgate.net/publication/49722362_Barretts_esophagus_A_historical_perspective_an_update_on_core_practicalities_and_predictions_on_future_evolutions_of_management

2013 Mar

Endoscopic resection (endoscopic submucosal dissection/endoscopic mucosal resection) for superficial Barrett’s esophageal cancer.

Recently developed endoscopic resection (endoscopic submucosal dissection [ESD]/ endoscopic mucosal resection) has dramatically changed the therapeutic approach for Barrett’s oesophagal cancer. The rationale for endoscopic resection is that lesions confined to the mucosal layer have a negligible risk of developing lymph node metastasis and can be successfully eradicated by endoscopic treatment as a curative treatment with minimal invasiveness. According to some reports that analysed the rate of lymph-node involvement relative to the depth of mucosal or submucosal tumour infiltration, endoscopic resection is clearly indicated for intramucosal carcinoma and might be extended to lesions with invasion into the submucosa (<200 μm, sm1) because of the low risk for lymph node metastasis. Most Japanese experts recommend ESD for Barrett’s oesophagal cancer after accurate diagnosis of the margin of cancer using narrow band imaging with magnifying endoscopy because of its high curative rate. However, few studies have evaluated the long-term outcomes of endoscopic resection for Barrett’s oesophagal cancer in Japan. Further investigations should be conducted to establish endoscopic resection for Barrett’s oesophagal cancer.

www.researchgate.net/publication/264344065_Endoscopic_resection_%28endoscopic_submucosal_dissectionendoscopic_mucosal_resection%29_for_superficial_Barrett’s_esophageal_cancer

2014:

Surveillance in Barrett esophagus.

The only known precursor of the esophageal adenocarcinoma (EAC) is represented by Barrett’s oesophagus (BE). EAC incidence has increased sharply in the last 4 decades. The annual conversion rate of BE to cancer is small but significant; therefore the identification of patients at a higher risk of cancer represents a dilemma. The endoscopic surveillance of BE aims to detect dysplasia and in particular high-grade dysplasia and intramucosal cancers that can be endoscopically treated before progressing to invasive cancer with lymph node metastases. Using standard white light endoscopy (WLE), these high-risk lesions are often subtle and hard to detect. In addition to high-definition standard endoscopy, chromoendoscopy (CE), virtual chromoendoscopy (e.g. narrow band imaging), and confocal laser endomicroscopy might increase the diagnostic efficiency for the detection of dysplastic lesions and can also increase the diagnostic efficiency for the detection of BE dysplasia or cancer. This ability to detect subtle mucosal abnormalities that harbour high-grade dysplasia (HGD) or intramucosal carcinoma might enable endoscopists skilled in the assessment of BE to perform targeted rather than random biopsies. The standard protocol will remain the careful examination by using conventional high-resolution endoscopes, combined with a longer inspection time, which is associated with an increased detection of dysplasia until these modalities have been demonstrated to enhance efficiency or be cost effective. Many of the limitations of the current clinical standard may be overcome in the future by the use of multi-modal imaging combined with molecular information.

www.researchgate.net/publication/264393893_Barretts_Esophagus_and_Cancer_Risk_How_Research_Advances_Can_Impact_Clinical_Practice

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NOV 26-11-15

This is a SOUND CLOUD so turn on your sound, this is cutting edge and worth taking time out to hear.

Disruptive: Cancer Vaccine & Hydrogel Drug Delivery

How can a materials science approach lead to medical breakthroughs?

In this episode of Disruptive, Wyss Core Faculty Member Dave Mooney discusses programmable nanomaterials approaches to fighting disease. Mooney explains how a cancer vaccine, developed by his team and currently in a clinical trial at the Dana-Farber Cancer Institute, can train one’s own immune system to target specific cancer cells. He also describes the development of novel hydrogels that find application in drug delivery systems and tissue regeneration. Chris Gemmiti, a member of the Wyss Institute’s Business Development team, joins the conversation to discuss the Wyss process of translation and what is involved in bringing the hydrogel drug delivery technology from bench-to-bedside.

https://soundcloud.com/wyssinstitute/disruptive_ep4/s-aLpBe

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Date: Aug 25, 2015

Inciting an immune attack on cancer cells

A new minimally invasive vaccine that combines cancer cells and immune-enhancing factors could be used clinically to launch a destructive attack on tumours

(BOSTON) — New research led by Wyss Core Faculty member David Mooney, Ph.D., in collaboration with researchers at the Dana-Farber Cancer Institute could potentially yield a new platform for cancer vaccines. Leveraging a biologically inspired sponge-like gel called “cryogel” as an injectable biomaterial, the vaccine delivers patient-specific tumour cells together with immune-stimulating biomolecules to enhance the body’s attack against cancer. The approach, a so-called “injectable cryogel whole-cell cancer vaccine,” is reported online in Nature Communications on August 12.

Cryogel

This scanning electron microscopy image shows the thawed cryogel with its well-organized interconnected porous architecture ready to be infused with cancer cells and immune factors. Credits: Ellen Roche, James Weaver, Sidi A. Bencherif / Wyss Institute at Harvard University

Mooney, who leads a Wyss Institute team developing a broad suite of novel cancer vaccines and immunotherapies, is also the Robert P. Pinkas Family Professor of Bioengineering at the Harvard John A. Paulson School of Engineering and Applied Sciences.

His team’s latest approach differs from other cancer cell transplantation therapies—which harvest tumor cells and then genetically engineer them to trigger immune responses once they are transplanted back into the patient’s body—in that the new cryogel vaccine’s properties are used to evoke the immune response in a far simpler and more economical way.

Cryogels are a type of hydrogel made up of cross-linked hydrophilic polymer chains that can hold up to 99 percent water. They are created by freezing a solution of the polymer that is in the process of gelling. When thawed back again to room temperature, the substance turns into a highly interconnected pore-containing hydrogel, which is similar in composition to bodily soft tissues in terms of their water content, structure, and mechanics. By adjusting their shape, physical properties, and chemical composition, Mooney’s team generated sponge-like, porous cryogels that can be infused with living cells, biological molecules or drugs for a variety of potential therapeutic applications including cancer immunotherapy.

“Instead of genetically engineering the cancer cells to influence the behaviour of immune cells, we use immune-stimulating chemicals or biological molecules inserted alongside harvested cancer cells in the porous, sponge-like spaces of the cryogel vaccine,” said Mooney.

The cryogels can be delivered in a minimally invasive manner due to their extreme flexibility and resilience, enabling them to be compressed to a fraction of their size and injected underneath the skin via a surgical needle. Once injected, they quickly bounce back to their original dimensions to do their job.

Cancerous cells

Cancerous melanoma cells shown with their cell bodies (green) and nuclei (blue) are nestled in tiny hollow lumens within the polymeric cryogel (red) structure. Credits: Thomas Ferrante, Sidi A. Bencherif / Wyss Institute at Harvard University

“After injection into the body, the cryogels can release their immune-enhancing factors in a highly controlled fashion to recruit specialised immune cells which then make contact and read unique signatures of the patient’s tumour cells, also contained in the cryogels. This has two consequences: immune cells become primed to mount a robust and destructive response against patient-specific tumour tissue and the immune tolerance developing within the tumour microenvironment is broken,” said Sidi Bencherif, the study’s co-first author and a Research Associate in Mooney’s research group.

In experimental animal models of melanoma tumours, results show that utilising the cryogel to deliver whole cells and drugs triggers a dramatic immune response that can shrink tumours and even prophylactically protect animals from tumour growth. With the pre-clinical success of the new cancer cell vaccination technology, Mooney and his team are going to explore how this cryogel-based method could be more broadly useful to treat a number of different cancer types.

“This promising new approach is a great example of the power of collaboration across disciplines, bringing together expertise from the Wyss Institute and Dana-Farber spanning bioengineering, cancer biology and immunology,” said Mooney.

“This new injectable form of this biomaterials-based cancer vaccine will help to expand the cancer immunotherapy arsenal, and it’s a great example of how engineering and materials science can be used to mimic the body’s own natural responses in a truly powerful way,” said Don Ingber, the Wyss Institute’s Founding Director, who also is the Judah Folkman Professor of Vascular Biology at Harvard Medical School and Boston Children’s Hospital, and Professor of Bioengineering at SEAS.

Wyss Institute for Biologically Inspired Engineering at Harvard University

http://wyss.harvard.edu/viewpressrelease/216/

Watch this Video, this is What these Guys are working towards for you and me.

https://www.youtube.com/user/wyssinstitute

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July 20th, 2015  (READ THIS)

A study by researchers from Broad, Dana-Farber, and Brigham and Women’s Hospital suggest that esophageal adenocarcinoma takes different paths in development than was previously suspected.

blog-EAC_v2

 A NEW STUDY by researchers from the Broad Institute of MIT and Harvard, Dana-Farber Cancer Institute, and Brigham and Women’s Hospital suggests that esophageal adenocarcinoma (EAC) progresses differently than previously suspected.

Researchers took samples from EAC patients that included cancer tissue as well as premalignant, surrounding tissue affected by Barrett’s esophagus – a complication of gastroesophageal reflux disease and known precursor to EAC. They then sequenced the exomes, or protein-coding regions of the genome, in cells from those samples. Using an algorithm known as  ABSOLUTE, along with other computational methods, they were able to trace mutation patterns in the samples, revealing the lineage of cells and reconstructing cancer’s evolutionary tree. The information helped them determine the key genetic events that occurred along the path from Barrett’s to full-blown cancer.

Previously, the prevailing theory about EAC progression was that cancer developed following a gradual accumulation of genetic mutations. However, the team found that in over 60% of cases studied, EAC was instead catalysed by a single genomic event – “whole genome doubling,” during which the entire complement of chromosomes was duplicated. The researchers suspect that this whole genome doubling may be enabling a more rapid progression to cancer. In addition to identifying this potentially more direct route to cancer, the authors also found that a key mutation occurred earlier than previously believed: it had been thought that mutations to the tumor suppressor gene TP53 happened late in EAC progression, leading to dysplasia – an intermediary state between Barrett’s and cancer in which cells begin to exhibit abnormal changes in appearance. However, the new study found that TP53 is deactivated much earlier in the process, long before the tissue becomes dysplastic.

Why: Many patients have Barrett’s, but only a small percentage of them go on to develop EAC and it is difficult to identify which Barrett’s sufferers are most at risk. As a result, EAC is often identified late, when prognoses are poor. The identification of a mutation (as in TP53) that could be detected early, or a trigger event (such as whole genome doubling) that could be further investigated open new possibilities for diagnostics and prevention.

“We know that if you find cancer early when it’s localised, the cure rates are much better than when it has progressed,” explains co-senior author, Adam Bass a physician/scientist at Dana-Farber and Brigham and Women’s and associate member. “Overall, this study should change some ideas about how this cancer develops, and if we have a better sense of how these cancers emerge, we may be able to develop new screening approaches that might be more effective in addressing what’s really happening in patients.”

Who: Executing this genomic study of EAC required a perfect pipeline of team and technology. Pathologists such as co-first author Matthew Stachler, a postdoctoral fellow in Bass’ lab, were needed to collect samples and precisely identify and separate tissue from Barrett’s, cancer, and various intermediate disease stages. Those painstakingly-derived samples were then shepherded through the exome sequencing process by scientists from, Broad and finally analyzed by computational biologists led by co-senior authors Scott Carter, who created ABSOLUTE, and Gad Getz, who directs the Cancer Genome Computational Analysis group at the Broad as well as the Bioinformatics Program at the Massachusetts General Hospital Cancer Center and Department of Pathology.

www.broadinstitute.org/blog/barrett%E2%80%99s-cancer

 

An ABSOLUTEly new view of the cancer genome. May 3rd, 2012

Scientists hoping to unlock cancer’s secrets face a formidable challenge. Sophisticated research tools have allowed them to peer into the genomes of cancer cells and identify many DNA alterations that may underlie malignancy, yet quantifying those changes is no simple task.

For example, the genome of a cancer cell is drastically disorganised, often with large missing chunks or extra copies of whole chromosomes. Some tumour cells have several-fold the amount of DNA as healthy cells. In addition, tumour samples used in research are never 100% pure – they always contain some fraction of genetically unaltered cells. These are just some of the things that can complicate the search for genetic alterations in cancer.

Researchers at the Broad Institute of MIT and Harvard developed a new computational method, called ABSOLUTE, to help overcome these complications. ABSOLUTE infers each sample’s purity and “ploidy” – the number of genomes in each cancer cell – from relative measures of DNA mass to calculate genetic changes on an absolute (per-cell) basis, giving a more informative picture of the alterations underlying cancer. The work appears in the April 29 online issue of Nature Biotechnology.

“Most biology, including cancer, happens in cells,” said Scott Carter, a computational biologist in the Broad’s Cancer Program and first author of the new work. When tissue samples are prepared for analysis, cell membranes are broken and per-cell data is lost. “To associate what you’re actually measuring with the underlying biology, you need to go back to the unit of cells.”

In large-scale studies to look for DNA alterations in hundreds or thousands of cancer samples, it is impractical to directly and accurately measure the purity and ploidy of each sample. So scientists have thus far used a relative measure of DNA changes that does not directly assess purity and ploidy. The approach can reveal segments of the genome with more or less DNA than other segments, but it cannot discern changes on a per-cell basis, leaving much valuable information hidden.

“You start out measuring these relative changes in DNA mass, but to shed light on cancer, you really want to know the changes specific to the cancer cells,” said Carter.

ABSOLUTE infers purity and ploidy and enables measurements on a per-cell basis. The new method, which is currently being used in several large cancer genome projects, also sheds light on the evolution and population structure of cells within tumours. “ABSOLUTE provides a new window into the genetic changes underlying cancer, on a cellular level,” said Gad Getz, senior author of the new study and director of cancer genome computational analysis at the Broad. “This invaluable tool also gives an unprecedented look at the cellular makeup of tumours in large-scale studies.”

Before applying the new method, scientists extract DNA from a tumour sample containing both normal and malignant cells. Microarrays or DNA sequencing are used to measure the relative amounts of genetic material at each location along the genome, measures that will vary due to local “copy number” changes – extra or missing DNA known as duplications or deletions. The sophisticated statistical analysis of ABSOLUTE is then applied to the relative data, giving a few likely options for per-cell values represented by the data points in the results.

For example, chromosome 10 in a cancer sample might appear in the relative data to be present at 70% the amount in a healthy cell, which could suggest a deletion. But ABSOLUTE creates data models that assign more likely values to that segment – whole numbers such as zero, one, two, or three copies per cell.

ABSOLUTE also exposes alterations that cannot possibly be clonal, or in every tumour cell. As a tumour grows, cancer cells mutate further, sometimes spawning “subclones” with unique genetic alterations that are difficult to discern using existing methods. ABSOLUTE can reveal the presence of these subclonal populations of cells harbouring unique mutations. This knowledge can help scientists classify interesting mutations as clonal or subclonal, which can have important research and clinical implications: clonal mutations are important targets for designing therapeutics, and subclonal mutations could foster resistance to targeted treatments.

The team applied its new method to analyse copy number changes in microarray data from 3,155 samples across 25 cancer types, including samples of glioblastoma multiforme and ovarian carcinoma from The Cancer Genome Atlas (TCGA) project. The analysis illustrated that whole-genome doubling, in which the entire genome of a tumour cell is doubled, is common among cancers. In some cancer types, more than half of all samples harboured doubled genomes. The approach also allowed the team to examine the timing of copy number changes relative to genome doublings and showed that genome doubling can have effects on the trajectories of tumour evolution.

With sequenced genomes from 214 samples of ovarian cancer from the TCGA project, the scientists were then able to apply ABSOLUTE and to assign per-cancer-cell values not only to copy number alterations, but also to point mutations, or single-letter misspellings of DNA. This effort identified changes present only in subclones within the tumours.

Patterns in the point-mutation data also allowed the team to classify mutated genes as tumour suppressors or oncogenes. “This analysis gives us a window into the function of mutations,” said Carter. He explained that the method could be useful in helping identify new functional genes among data from other cancer studies.

By providing valuable information on purity and ploidy, ABSOLUTE allows researchers to select the purest samples to use in whole-genome sequencing studies and design the appropriate sequencing strategy to detect mutations in those samples. The method was used in recent studies by Broad researchers of prostate, head and neck, and colorectal cancers.

The team continues to improve the method and apply it to ongoing cancer genome efforts. The researchers are also working to collect samples from cancer patients before and after treatment to detect changes induced by cancer therapies and observe the evolution of subclones.

ABSOLUTE provides a revealing new look at the genome of cancer cells, one that is already helping unveil the mysteries underlying this disease. For Carter, bringing the data back to the “unit of cells” is crucial to making biological insights. “We hope this new tool will enable more enlightening studies of DNA’s role in cancer.”

www.broadinstitute.org/news/4139

(today’s date is 29 th August 2015)

Published on August 25, 2015, at 4:11 AM

Researchers reveal new electrical mechanism that can control molecular switches regulating cancer cell growth

 The molecular switches regulating human cell growth do a great job of replacing cells that die during the course of a lifetime. But when they misfire, life-threatening cancers can occur. Research led by scientists at The University of Texas Health Science Center at Houston (UTHealth) has revealed a new electrical mechanism that can control these switches.

This information is seen as critical in developing treatments for some of the most lethal types of cancer including pancreatic, colon and lung, which are characterised by uncontrolled cell growth caused by breakdowns in cell signalling cascades.

The research focused on a molecular switch called K-Ras. Mutated versions of K-Ras are found in about 20 percent of all human cancers in the United States and these mutations lock the K-Ras switch in the on position.

“When K-Ras is locked in the on position, it drives cell division, which leads to the production of cancer,” said John Hancock, M.B., B.Chir, Ph.D., ScD, the study’s senior author and chairman of the Department of Integrative Biology and Pharmacology at UTHealth Medical School. “We have identified a completely new molecular mechanism that further enhances the activity of K-Ras.”

Findings appear in Science, a journal of the American Association for the Advancement of Science.

The study focused on the tiny electrical charges that all cells carry across their limiting (plasma) membrane. “What we have shown is that the electrical potential (charge) that a cell carries is inversely proportional to the strength of a K-Ras signal,” Hancock said.

With the aid of a high-powered electron microscope, the investigators observed that certain lipid molecules in the plasma membrane respond to an electrical charge, which in turn amplifies the output of the Ras signalling circuit. This is exactly like a transistor in an electronic circuit board.

Yong Zhou, Ph.D., first author and assistant professor of integrative biology and pharmacology at UTHealth Medical School, said, “Our results may finally account for a long-standing but unexplained observation that many cancer cells actively try to reduce their electrical charge.”

Initial work was done with human and animal cells and findings were subsequently confirmed in a fruit fly model for membrane organisation.

“This has huge implications for biology,” Hancock said. “Beyond the immediate relevance to K-Ras in cancer, it is a completely new way that cells can use an electrical charge to control a multitude of signalling pathways, which may be particularly relevant to the nervous system.”

Source: medicalxpress.com/news/2015-08-scientists-electrical-cancer-cell-growth.html

University of Texas Health Science Center at Houston

A New Treatment for Medication-Refractory Gastroesophageal Reflux Disease

www.muschealth.org/

David Adams, M.D., Head of the Division of Gastrointestinal and Laparoscopic Surgery at the Medical University of South Carolina, discusses the new LINX® reflux management system (Torax Medical, Minneapolis-St. Paul, MN), a device consisting of a “necklace” of magnetized titanium beads that can be placed around the lower esophageal sphincter to provide better closure and prevent reflux in patients with medication-refractory gastroesophageal reflux.

Up Dated 2016

WATCH:-  https://www.youtube.com/watch?v=WZ4iUkzHU6U

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Stroke Survivors Develop Seizures, Study Confirms

15 percent experience at least one seizure within 3 years, researchers say
THURSDAY, Feb. 18, 2016

Seizures are common in the years following a stroke, a new study found, with nearly one in six survivors requiring hospital care after a seizure. Researchers noted that the seizure rate following stroke was more than double the rate compared to people who’d experienced traumatic brain injuries such as concussions. Researchers noted that the seizure rate following stroke was more than double the rate compared to people who’d experienced traumatic brain injuries such as concussions.The researchers also noted that people who had a certain type of stroke had an even higher risk for seizure. “One in four patients with a hemorrhagic-type stroke will develop seizures,” said study lead author Dr Alexander Merkler, a fellow in neurocritical care at Weill Cornell Medical College in New York City. A hemorrhagic stroke is a type that occurs when a blood vessel in the brain bursts. This type of stroke is much less common than an ischemic stroke, which occurs when a blood vessel in the brain is blocked, according to the American Stroke Association.

https://www.nlm.nih.gov/medlineplus/news/fullstory_157343.html

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Barrett’s Esophagus 2016

Written by Carmella Wint and Elizabeth Boskey, PhD
Medically Reviewed by Graham Rogers, MD on April 14, 2016

Barrett’s esophagus is a condition in which the cells that make up your esophagus begin to look like the cells that make up your intestines. This often happens when cells are damaged by exposure to acid from the stomach. This condition often develops after years of experiencing gastroesophageal reflux (GERD). In some cases, Barrett’s esophagus can develop into esophageal cancer.

The exact cause of Barrett’s esophagus is not yet known. However, the condition is most often seen in people with GERD. GERD occurs when the muscles at the bottom of the esophagus do not work properly. The weakened muscles won’t prevent food and acid from coming back up into the esophagus.

It’s believed that the cells in the esophagus can become abnormal with long-term exposure to stomach acid. Barrett’s esophagus can develop without GERD, but patients with GERD are 3 to 5 times more likely to develop Barrett’s esophagus.Approximately 5 to 10 percent of people with GERD develop Barrett’s esophagus. It affects men almost twice as often as women and is usually diagnosed after the age of 55.

Over time, the cells of the esophageal lining may develop into precancerous cells. These cells may then change into cancerous cells. However, having Barrett’s esophagus doesn’t mean you will get cancer.

(Click on red Writing to view other details)  It’s estimated that only about 0.5 percent of people with Barrett’s esophagus develop cancer.

READ THE FULL REPORT

http://www.healthline.com/health/barretts-esophagus#Overview1

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The “acid” in “acid reflux”

 May 17, 2016   

Surprising mechanism of acid reflux damage identified by UT Southwestern/Dallas VA researchers

Dr Stuart Spechler and Dr Rhonda Sousa, both with UT Southwestern and the Dallas VA Medical Center, co-direct the Esophageal Diseases Center at the Dallas VA Medical Center.

Click on the RED wording which I have underlined

Dr. Stuart Spechler and Dr. Rhonda Sousa, both with UT Southwestern and the Dallas VA Medical Center, co-direct the Esophageal Diseases Center at the Dallas VA Medical Center.

DALLAS – May 17, 2016 – The “acid” in “acid reflux” may not be the direct cause of damage to the esophagus as previously suspected, according to researchers at UT Southwestern Medical Center and Dallas VA Medical Center.

For more than 80 years, it has been assumed that stomach acid backing up into the esophagus damaged the lining of the esophagus by causing chemical burns, but their research suggests that the damage in patients with gastroesophageal reflux disease (GERD) actually occurs through an inflammatory response prompted by the secretion of proteins called cytokines.   

 “Although this radical change in the concept of how acid reflux damages the esophagus of GERD patients will not change our approach to its treatment with acid-suppressing medications in the near future, it could have substantial long-term implications,” said senior author Dr. Stuart Spechler, Professor of Internal Medicine at UT Southwestern and Chief of the Department of Gastroenterology at the Dallas VA Medical Center.

“Someday we might treat GERD with medications that target the cytokines or inflammatory cells that really cause the damage to the esophagus,” said co-senior author Dr. Rhonda Souza, Professor of Internal Medicine at UT Southwestern and staff physician with the Department of Gastroenterology at the Dallas VA Medical Center.

Dr Spechler and Dr Souza co-direct the Esophageal Diseases Center at the Dallas VA Medical Center, which conducted the research. The research appears online in the Journal of the American Medical Association.

The research builds on previous work in mice demonstrating that it takes several weeks from the time stomach acid is introduced into the esophagus before damage occurs.

“A chemical burn should develop immediately, as it does if you spill battery acid on your hand,” said Dr. Spechler, who holds the Berta M. & Cecil O. Patterson Chair in Gastroenterology.

For more on this report click below

http://www.utsouthwestern.edu/newsroom/news-releases/year-2016/may/acid-reflux-damage.html

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esophageal cancer with a shorter survival

October 21, 2016

Presence of certain oral bacterium in esophageal cancer samples associated with shorter survival

Bottom Line: Among Japanese patients with esophageal cancer, those whose cancer tested positive for DNA from the bacterium Fusobacterium nucleatum had shorter cancer-specific survival compared with those whose cancer had no DNA from the bacterium.

Journal in Which the Study was Published: Clinical Cancer Research, a journal of the American Association for Cancer Research. Author: Hideo Baba, MD, PhD, a professor in the Department of Gastroenterological Surgery in the Graduate School of Medical Sciences at Kumamoto University, Japan. Background: More than 100 trillion bacteria naturally inhabit every person’s body; they are collectively referred to as the microbiome, Baba explained.

http://medicalxpress.com/news/2016-10-presence-oral-bacterium-esophageal-cancer.html

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CEACCP

CEACCP stands for Continuing Education in Anaesthesia, Critical Care and Pain (UK and Ireland)

 

Key points

An acquired tracheo-oesophageal fistula bypasses laryngeal protection and leads to repeated pulmonary aspiration.

Cuff-related necrosis and malignancy are currently the major causes.

Diagnosis involves the identification of lesion site and size.

Careful preoperative optimisation and weaning from ventilation improve outcome.

Repair requires skills in thoracic and upper-gastrointestinal anaesthesia.

Oesophageal stenting offers palliation for malignant acquired tracheo-oesophageal fistulae.

The formation of an acquired tracheo-oesophageal fistula (TOF) is a rare but serious complication of malignancy and trauma. An established patient tract from the airway to the upper-gastrointestinal tract bypasses the normal protection offered by the laryngeal reflexes. As a consequence, this situation can present the anaesthetist with significant difficulties. The proximity of the oesophagus, trachea, upper mediastinal contents and large blood vessels can further complicate surgery and anaesthesia.

Much Much more on this click on the link below.

http://m.ceaccp.oxfordjournals.org/content/6/3/105.full#T1

 

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